Notes in Anesthesiology Dr. Azam's.... : Flow Charts, Diagrams & Important Tables

Dr. Azam’s....
Notes in Anesthesiology
Postgraduates appearing
Updated up to December 2013, 3rd Edition for MD, DNB & DA Exams
Flow Charts, Diagrams

& Important Tables
Edited by:
Dr. Azam
Consultant Anesthesiologist
& Critical Care Specialist
www.drazam.com
2
Dr Azam’s Notes in Anesthesiology 2013
Dedication
To Mohammed Shafiulla, my father, my oxygen, companion, and best friend; for

being my major pillar of support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless gratitude, for the sake of your
children. I owe you a debt I can never repay.
I also would like to thank my mom (Naaz Shafi), my wife (Roohi Azam), my two lovely
kids (Falaq Zohaa & Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book.
Finally, I would like to thank my teachers (Dr.Manjunath Jajoor & team) & Dr T. A. Patil . The
dream begins with a teacher who believes in you, who tugs and pushes and leads you to the next
plateau, sometimes poking you with a sharp stick called "truth."

A NOTE TO THE READER
Anesthesiology is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience
broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the
most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the
method and duration of administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences, neither the author nor the publisher nor any other party
who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect
accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information
contained in this work. Readers are encouraged to confirm the information contained herein with other sources. It is the responsibility of the
licensed prescriber, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual
patient. Neither the publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this
publication.
Dr. Azam

Whole lung lavage Left DLT
! !"#$%&%!' Independent lung ventilation Left DLT Right DLT
!()*+*,'(-./0/1(2+3,'043523,'(10436/4)/4(37' BB, ipsilateral bronchial blocker; DLT, Double-lumen tube; EBT, contralateral single-lumen endobronchial tube.
6+465730+/-'
860+930(.'6/2)7(2(-0':(*);'<=3'3-.'<>3?' Right lung Left lung

19
@(504/)A+7'3BB4(B30+/-'3-.'360+930+/-'' Apical posterior

Apical
Upper lobe Posterior 22

16 50
13
Anterior 10 Anterior
<E0/0/1+6' Upper lobe
C(360+9('/1+.3-0'*)(6+(*'' I4/0(3*(*''
(FF(60*''
D1EB(-'F4(('43.+637*'7+G('AE.4/1E7' J73*03*(,''
43.+637*,'*+-B7(0'DH'3-.'AE.4/B(-' I73*2+-/B(-'360+930/4,')73*2+-' Lower lobe Superior
)(4/1+.(''' AE3754/-+.3*('(06;'''' Lingula
Superior 9 Inferior
Lateral Superior
Middle lobe
Medial Anterior
basal
Medial
K+4(60'(FF(60'' #-.+4(60'(FF(60'' K+4(60'(FF(60'' #-.+4(60'(FF(60'' Anterior basal
basal Posterior Lateral
- K(*04/E'K@8' J-ME2('+-360+930+/-'' - </773B(-'' - </2)7(2(-0''
basal basal
- I(4/1+.3*('7+)+.'' - N'3-0+)4/0(+-3*('' - J73*0+-'' - S3B(23-'F360/4'' Lateral
- #-L54(' - OP'IK'' - Q+R4/-(60+-'' - T+-+-*' 3-.' /0A(4' basal Posterior
(-./0A(7+52'' - <3'8"I3*('' ' )4/0(+-*'' basal
' - <372/.57+-'' '
' Lower lobe
Millers: Page # 1842

Figure 59-20 Diagram of the tracheobronchial tree. Mean lengths and diameters are shown in millimeters. Note that the right middle lobe bronchus exits
Flow Chart: ARDS Pathophysiology A directly anteriorly while the superior segments (some authors refer to these as the “apical” segments) of the lower lobes exit directly posteriorly. Using the
apical designation on the right side the segmental bronchi in a rostral to caudal sequence give the mnemonic “A PALM A MAPL.” (From Youngberg JA: Cardi
Vascular and Thoracic Anesthesia. Philadelphia, Churchill Livingstone, 2000.)
5
Classification & characteristics of various Mapleson circuit
Mapleson Other Names Configuration1 Spontaneous Controlled Comments

Class
A Magill attachment Equal to minute Very high and Poor choice during controlled
ventilation ( 80 mL/ difficult to ventilation. Enclosed Magill system is
kg/min) predict a modification that improves
efficiency. Coaxial Mapleson A (Lack
breathing system) provides waste-
gas scavenging.
B 2 x minute 2–2½ x minute
ventilation ventilation
C Waters' to-and-fro 2 x minute 2–2½ x minute

D Bain circuit 2–3 x minute 1–2 x minute Bain coaxial modification: fresh gas
ventilation ventilation tube inside breathing tube.
E Ayre's T-piece 2–3 x minute 3 x minute Exhalation tubing should provide a

ventilation ventilation (I:E larger volume than tidal volume to
=1:2) prevent rebreathing. Scavenging is
difficult.
F Jackson-Rees' 2–3 x minute 2 x minute A Mapleson E with a breathing bag
modification ventilation ventilation connected to the end of the
breathing tube to allow controlled
ventilation and scavenging.

4. Classify vaporizers. Discuss the effect of altered barometric pressure on the performance of Dr Azam’s Notes in Anesthesiology 2013
vaporizers?
Vapour: A Vapour is the gaseous form of a substance which is liquid at room temperature
Vaporizer: A vaporizer is an instrument designed to change a liquid anesthetic agent in to its vapour and to add a controlled amount of this vapour to the
fresh gas flow.
Classification of vaporizer:
Oldest Classification:
Older Classification: New Classification:
A. Method of regulating Output Concentration
A. Method of regulating Output Concentration A. Method of regulating Output Concentration
1. Variable Bypass
1. Variable Bypass 1. Variable Bypass
2. Measured Flow
2. Measured Flow 2. Measured Flow
B. Method of Vaporization
B. Method of Vaporization B. Method of Vaporization
1. Flow Over
1. Flow Over 1. Flow Over
2. Bubble Through
2. Bubble Through 2. Bubble Through
3. Flow over or Bubble Through
3. Injection 3. Injection
C. Location
C. Resistance C. Temperature Compensation
1. Outside the Breathing System
1. Plenum 1. Mechanical
2. Inside the Breathing System
2. Low resistance 2. Supplied Heat
3. Computerized
D. Temperature Compensation
1. None D. Temperature Compensation
2. By Supplied Heat 1. Thermocompensation
3. By Flow Alteration 2. Supplied Heat
E. Specificity E. Specificity
1. Agent Specific 1. Agent Specific
2. Multiple Agent 2. Multiple Agent

Enumerate the effects of chronic smoking & the anesthetics implications.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Preoperative Preparation:
• Stop Smoking Time course Bene3icial effects
• Dilate the airway using: 12-24 hours Decrease carbon monoxide and nicotine levels
• Beta agonist 48-72 hours Normalizes carboxy Hb levels. Improves ciliary
• Anti-cholinergics
function, tissue oxygenation.
• Theophylline
• Steroids 1-2 weeks Decrease sputum production & improves smaller
• Cromolyn Sodium airway function.
• Loosen the Secretions by: 4-6 weeks Improves PFT
• Airway hydration ( Humidification/Nebulization) 6-8 weeks Normalizes immune function, drug metabolism and
• Systemic hydration orally - 3 Liters hepatic enzyme activity
• Mucolytic agents & Expectorant drugs 8-12 weeks Reduces overall post-operative pulmonary
• Antibiotics
Remove secretions: complications.
•
• Postural drainage
• Coughing
• Chest physiotherapy(percussion & Vibration) Post-operative Management:
Ancillary Measures: Goals:
• Treatment of co-existing disease • To promote adequate analgesia
• Treatment of Cor-Pulmonale • To minimize the incidence of postoperative complications
• Pre-operative Digitalization • To prevent infections
Patient Education, motivation & facilitation of • Chest physiotherapy & deep breathing exercise.
post operative care: Continuation: • Consider CPAP - Decreases WOB, Improves LV Compliance.
• Psychological preparation • Continuous administration of Local anesthetic with low dose opioids via
• Incentive spirometry & deep breathing exercise epidural catheter for post operative pain relief.
• Exposure to secretion removal maneuvers
• Exercise
• Weight gain/reduction
• Diet supplements.
8
9. Describe the innervations of Larynx. Briefly discuss various palsies following Nerve Dr Azam’s Notes in Anesthesiology 2013
injury. Continuation:
Neurological lesions:
Vocal Cord palsy
General Causes
Vagus Nerve Recurrent Laryngeal nerve
• DM
Supra-nuclear lesions: • Syphilis
in the motor cortex • viral Disease
Left RLN Palsy:
• Aneurysm of Right recurrent laryngeal nerve:
aorta • Aneurysm of subclavian artery
• Lungs: TB, • Lungs: TB, apical carcinoma
Nuclear lesions: Malignancy Bilateral RLN Palsy:
• stroke • Esophagus: •Pulmonary tuberculosis
• Tumor malignancy • Esophageal malignancy
• MS
Peripheral
neurological
lesions
Intra Cranial: Lesions in the neck:

• Posterior fossa • Trauma
tumors • metastatic nodes
• Basal fractures

57. What are the major causes of Hypoxemia? What is Hypoxic Pulmonary Vasoconstriction? How
can general anesthesia worsens V/Q mismatch?
Five Causes of Hypoxemia (↓ PaO2):

1. Hypoventilation
2. Low inspired Oxygen
3. Right to Left shunt
4. Ventilation-Perfusion mismatch
5. Diffusion impairment
Hypoventilation: Low inspired Oxygen:

• P(A-a)O2 is normal Right to Left shunt: Ventilation-Perfusion
• A decrease in Barometric
• PaCO2 is elevated ( Hypercapnia) pressure (High Altitude) • Healthy Individuals: mismatch:
• A portion of the bronchial • V/Q mismatch is the
• A decrease in FIO2 - circulation (blood supply most common cause of
Causes of Hypoventilation: accidental disconnection
• Depression of CNS by drugs to the conducting zone hypoxemia in disease
of the ETT, leak or of the airways) venous state.
• Upper airway obstruction exhausted central supply blood drains into the
• Disease of Neuromuscular of O2 pulmonary vein
junction
• A portion of coronary
• Disease of respiratory muscles circulation venous blood Diffusion impairment:
• Abnormality of the chest wall drains through the
• Disease of motor neurons of the • PaCO2 is normal
thebesian veins into the
brain stem/Spinal cord left ventricles
• P(A-a)O2 is normal at rest
• Inflammation, trauma or but may be elevated
• Congenital abnormalities:
hemorrhage in the brain stem • TOF,
during exercise
• VSD + PAS
• Intrapulmonary
Hypoxic pulmonary vasoconstriction is a paradoxical, physiological fistulas
phenomenon in which pulmonary arteries constrict in the presence of
hypoxia without hypercapnia, redirecting blood flow to alveoli with a higher
oxygen content.
10

Pathophysiology of Bronchial Asthma:
!
!""#$%&'()*+,$&-.&'/( 01&2.3-'$4,&'(!"#$!"%!&''
!-,&%#-&'(( 52-(!-,&%#-&'(( Severity of expiratory airflow obstruction & Grading:
()%#'' 2"3-&#!+"''
*+,,-"' *+,,)#!+"'
FEV FEF 25-‐75
Severity Pao2 (mm Hg) Pa Co2 (mm Hg)
."!/0,'10"1-$'' 45-$&!%-'' (% predicted) (% predicted)
6+,1' 1) Mild 65-‐80 60-‐75 > 60 < 40
*%7&8+9-"!&'''
(asymptomatic)
294'
2) Moderate 50-‐64 45-‐59 > 60 < 45
3) Marked 35-‐49 30-‐44 < 60 > 50

:-,-0%-'+3'#$!99-$'09-"#%'
G-)$+9-"!&'$-3,-5'HC090,;' 4) Sever (status < 35 < 30 < 60 > 50
!; <-)=+#$!"-%'6>?'(>?'4>'
!!; @!%#0/!"-' asthamaticus)
!!!; *$+%#09,0"1!"%'AB?'4B?'(B'
!C; D$017=!"!"'
C; E8$+/F+50"-'.B' 5
Anesthesia for Thoracic Surgery 1839
C!; *,0#-,-#'0&#!C0#!"9'30&#+$''
Table 59-13 Characteristics of the Cohen, Arndt, and Fuji Bronchial Blockers
Cohen Blocker Arndt Blocker Fuji Uniblocker

@7I-!$$!#0F,-'!"3,0//0#+$7'0!$J07'''
' Size 9 Fr 5 Fr, 7 Fr, and 9 Fr 5 Fr, 9 Fr
Section V Adult Subspecialty Management

Balloon shape Spherical Spherical or elliptical Spherical
Guidance mechanism Wheel device to deflect the tip Nylon wire loop that is coupled with the None, preshaped tip
K; D$+"&8+,I0%/'' fiberoptic bronchoscope
B; 41-/0'+3'F$+"&8!0,'L'!"3,0//0#+$7''
Smallest recommended ETT for coaxial use 9 Fr (8.0 ETT) 5 Fr (4.5 ETT), 7 Fr (7.0 ETT), 9 Fr (8.0 ETT) 9 Fr (8.0 ETT)
''''''&-,,'!"3!,#$0#!+"'
M; N)&)%'%-&$-#!+"'!'#8!&='0"1'#-"0&!+)%'' Murphy eye Present Present in 9 Fr Not present
Center channel 1.6 mm ID 1.4 mm ID 2.0 mm ID
ETT, single endotracheal tube; ID, internal diameter.

From Campos JH: Which device should be considered the best for lung isolation: Double-lumen endotracheal tube versus bronchial blockers. Curr Opin Anaesthesiol 20:
:-%),#%'!"'' 30, 2007, with permission.
O; 2"&$-0%-'!"'0!$J07'$-%!%#0"&-''
P; (-&$-0%-'!"'3+$&-1'-5I!$0#+$7' K; @7I-$!"3,0#!+"'+3',)"9%?'0"1'#8+$05''
exposure. Bronchial blockers are most commonly used intralumi- blockade, the Arndt blocker can be advanced independently of
C+,)/-'0"1'3,+J'$0#-%'' B; 2"&$-0%-1'J+=%'+3'F$-0#8!"9H'QRD';'' nal (coaxial) with an SLT. They can also be placed separately the wire loop by observing its entrance into the right mainstem
M; .,#-$0#!+"'!"'$-%I!$0#+$7'/)%&,-' thorough the glottis or tracheostomy exterior to an SLT. This bronchus under fiberoptic visualization. The optimal position of
3)"&#!+"'' allows the use of a smaller SLT and is often an option in pediat- the Arndt blocker in the left or in the right bronchus is achieved
>; 680"9-%'!"'-,0%#!&'$-&+!,''''' rics. Another advantage of the bronchial blockers is when post- when the blocker balloon’s outer surface is seen with the fiberop-
operative mechanical ventilation is being considered after
prolonged thoracic or esophageal surgery. In many instances
these patients have an edematous upper airway at the end of the
procedure. If a bronchial blocker is used there is no need to
change the SLT and there is no compromise of the airway if
mechanical ventilation is needed in the postoperative period.
Table 59-13 describes the characteristics of current bronchial
blockers. The smallest internal diameter (ID) of an endotracheal
tube that will allow passage of both a bronchial blocker and a
fiberoptic bronchoscope depends on the diameters of the bron-
choscope and blocker. For standard adult 9-Fr blockers, an 11
endotracheal tube greater than or equal to 7.0 mm ID can be used 1
with a bronchoscope less than 4.0 mm in diameter. Larger bron-
Dr Azam’s Notes in Anesthesiology 2013 choscopes will require an endotracheal tube greater than 7.5 mm 2
ID. All blockers need to be well lubricated before placement.
V 1834 Adult Subspecialty Management
Table 59-9 Options for Lung Isolation
Options Advantages Disadvantages
Double-lumen tube Quickest to place successfully Size selection more difficult

1. Direct laryngoscopy Repositioning rarely required Difficult to place in patients with difficult airways
2. Via tube exchanger Bronchoscopy to isolated lung or abnormal tracheas
3. Fiberoptically Suction to isolated lung Not optimal for postoperative ventilation
CPAP easily added Potential laryngeal trauma
Can alternate OLV to either lung easily Potential bronchial trauma
Placement still possible if bronchoscopy not
available
Bronchial blockers (BB) Size selection rarely an issue More time needed for positioning
Arndt Easily added to regular ETT Repositioning needed more often
Cohen Allows ventilation during placement Bronchoscope essential for positioning
Fuji Easier placement in patients with difficult airways Nonoptimal right lung isolation due to RUL
and in children anatomy
Postoperative two-lung ventilation by withdrawing Bronchoscopy to isolated lung impossible
blocker Minimal suction to isolated lung
Selective lobar lung isolation possible Difficult to alternate OLV to either lung
CPAP to isolated lung possible
Univent tube Same as BBs Same as for BBs

Less repositioning compared with BBs ETT portion has higher air flow resistance than
regular ETT
ETT portion has larger diameter than regular ETT
Endobronchial tube Like regular ETTs, easier placement in patients Bronchoscopy necessary for placement
with difficult airways Does not allow for bronchoscopy, suctioning or
Longer than regular ETT CPAP to isolated lung
Short cuff designed for lung isolation Difficult right lung OLV
Endotracheal tube (ETT) advanced into bronchus Easier placement in patients with difficult airways Does not allow for bronchoscopy, suctioning or
CPAP to isolated lung
Cuff not designed for lung isolation
Extremely difficult right OLV
CPAP, continuous positive airway pressure; ETT, endotracheal tube; OLV, one-lung ventilation; RUL, right upper lobe.
12

7. A 30 year old female ASA grade I following exploratory laparotomy is not maintaining oxygen
saturation in the post operative period. Discuss the causes & Management.
Definition: Hypoxia is defined as inadequate oxygen supply to the cells and tissues of the body. Decreased FRC:
Values: Sao2 < 90%, PaO2 < 60% • Seen in Pulmonary edema (Treatment will be fluid
restriction, diuretics & oxygen therapy Positive
Causes of Post operative Hypoxia & its treatment: ( 12 Causes) pressure ventilation.), Infections( Antibiotics),Obesity
Low Inspired concentration of O2: (incentive spirometer & deep breathing exercises),
• When FIO2 is < 0.21%. The treatment would be giving high inspired oxygen through Venturi aspiration(postural drainage, nebulization incentive
mask. spirometer & deep breathing exercises.)
Airway obstruction: Right to left intrapulmonary shunts:
• Pharyngeal obstruction: Treatment would be Head tilt & chin lift.! • Most common cause is Atelectasis. Treatment would
• Laryngeal obstruction: treatment: Lift the chin while the head is on a pillow or displace !jaw be Deep breathing exercise, Chest physiotherapy
forward. Alternating lifting and relaxing the chin will, relax the strap muscle of the neck. humidification of inspired gases, coughing &
• Attempt to facilitate ventilation of gentle positive pressure via mask. When conservative incentive spirometer.
measures are not effective in breaking spasm within 1min, then a muscle relaxant should be Drug Overdosage:
given I.V. Scoline 1.5mg/kg injected • Like opioids, muscle relaxants, in adequate reversal.
• Bronchospasm: Bronchodilators like Beta agonist, Anticholinergics, Theophylline Treatment would be titrated dosage of opioids & to
andSteroids wait for adequate reversal.
Post operative shivering: Pulmonary Embolism:
• May also cause hypoxia. Treatment is Oxygen therapy • Lower limb surgeries, prolonged
Sudden reduction in cardiac output: immobilization.treatment would be DVT stocking,
• Can contribute to hypoxemia. Treatment: Watch out for bleeding & dehydration. Give IV early mobilization, DVT prophylaxis.
fluids, blood replacement. Pneumothorax:
Diffusion Hypoxia: • Result of direct injury to lungs or rib fracture.
• At the end of surgery when both oxygen & nitrous oxide stopped at the same time. Where • Treatment is 100% oxygen, insertion of chest tube &
N2O diffuses back into the alveoli. Treatment is to give oxygen after cutting off N2O. intercostal drainage & IPPV.
Type of Surgery:
• Patients with abdomino-thoracic procedures will not respire adequately because of pain on
deep inspiration. Treatment would be adequate analgesia with opioids or NSAIDS or
through the epidural.
Ventilation Perfusion Mismatch:
• Usually seen under Anesthesia. GRID: Question needs answered under
following headings:
1. Definition
2. values
3. 12 Causes of Post operative Hypoxia &
its management.
13

3. Pulmonary Function Test Dr Azam’s Notes in Anesthesiology 2013
Non-Specific - Bed Side Test
Specific Test - PFT
Test of Ventilation Test of Distribution of Ventilation Test of Diffusion Test of Perfusion Other Tests
Single Breath N2 elimination Test

Multi-breath N2 wash out test Carbon Monoxide Diffusing
Radio-active Xenon distribution Capacity
radio-active Xenon
Static Test injection!
Dynamic Test
Radio-nucleotide
Non-Specific - Bed Side Function:
Macro-aggragated iodine
•Anatomical • Breath Holding test
Measurements • Sniderʼs Match Blowing test •Split Lung Function Test
•Do not evaluate • De Bonoʼs Whistle test •Bronchospirometery
Measures rate of flow of Gas • Auscultation over the trachea
Function •radio-active Scanning
• Sphygmomanometer •Pulmonary artery occlusion
• Walk test test
4 Volumes 4 Capacities MBC/MVV
• Stair case test. •ABG
TV VC FEV
IRV TLC PEFR •A-a Gradient
ERV FRC MMEFR 25 to 75 % •Raw
RV IC Respiratory Muscle Strength •Compliance
Fixed Obstruction
Variable Extra-Thoracic Obstruction
E-Expiration is normal
Flow
Volume Variable Intra-Thoracic Obstruction
Loops I-Inspiration is normal
Restrictive Lung Disease
14
Dr Azamʼs Notes in Anesthesia

FRC Dynamic Tests
Pulmonary Function Test
• Spirometer can measure - VT,IRV, • Volume of air remaining in the lung MBC or MVV
ERV, VC, IC, FEV & MBC after normal expiration • Max volume of air that can be breathed per
• Cannot be measured by Spirometer • measured by: minute by voluntary effort
- RV, TLC & FRC • N2 washout technique • normal - 160L/min to 180 L/min
• Helium dilution MBC is decreased in:
Static Test • Body Plethysmograph • old age
VT - Tidal Volume • FRC increased: • emphysema
• Total Volume of air inspired & Expired in each breath • Obstruction of airways • bronchospasm
• measured by wrightʼs Respirometer • Emphysema • bronchiolar obstruction
• PEEP
IRV - Inspiratory reserve volume FVC & FEV
• FRC decreased:
• Volume of air that can be inspired after normal FVC
• Under Anesthesia
inspiration. • Assess the expiratory ability
• post op old age
ERV - Expiratory reserve volume • max volume of air that can be
• obesity
• Volume of air that can be expired after normal exhaled forcefully and rapidly after
• smoking
expiration maximum inspiration
• Lithotomy
• It reflects the thoracic muscles, abdominal muscle • measured by Spirometer and fast
• Abdominal distention
& thoracic mobility moving Kymograph
• Lap surgeries
RV - Residual Volume • FVC done over 4 sec
TLC • reflects the relationship between
• Volume of air remaining in the lung
after maximum expiration • Total volume of air in lung after Flow & resistance
maximum inspiration. FEV1
• Measured by
• TLC decreased: • Max volume of gas exhaled during
• N2 washout technique
• Pulmo fibrosis the 1st second of FVC maneuver
• Helium dilution technique
VC - Vital Capacity • obesity • FEV1 = 83% of VC
• weakness of inspiratory muscle
• Most commonly measured
• volume of air that can be expired after maximum inspiration FVC is decreased in:
• can be measured by - spirometer • Atelectasis
• BSA: Male- 2.6l/m2 Female - 2.1l/m2 • Fibrosis
• A given VC is abnormal if < 80% of predicted value • muscle weakness
• VC: decreased - in pregnancy, Pulm fibrosis • abdominal swelling
• Emphysema • pain
• ch.Bronchitis In healthy patients
• asthma FVC=VC
• Abdominal pain
• can be < 70 to 75% in upper abdominal surgery
• < 50 to 55% in lower abdominal surgery
• Position: Lithotomy Vc < 18% 15
• VC= 3 X VT for effective cough
• Decrease in VC means decreased ability to cough and post operative complications Dr Azam’s Notes in Anesthesiology 2013
PEFR:
• After max inspiration patient exhales as forcefully
as he can and the max flow rate is measured
and expressed in lt/min and lt/sec
• Normal: Condition FEV1 FVC FEV1 /FVC
• 450-600 L/min
Airway obstruction (asthma, bronchitis) Decreased Normal Decreased
• 300 - 500 L/min
• Measured by Wrightʼs Respirometer Stiff lungs (pneumonia, pulmonary edema) Decreased Decreased Normal
! ! Pneumotachygraph
Respiratory muscle weakness (myasthenia, Decreased Decreased Normal
PEFR is decreased in:
myopathies)
• Obstructed Airway
Values less that 200 lt/min suggest impaired cough
and increased likely hood of post op pulmonary
complications
MMEFR ( 25% to 75%): Obstructive Restrictive
• Flow measured in middle half of FVC FEVI Decreased Decreased
• obtained by dividing the volume of gas FVC Normal Decreased
between 25 - 75% by corresponding FEV1/FVC Decreased Normal
elapsed time FRC Increased Decreased
• Normal = 4 to 5 L/sec TLC Increased Decreased
Importance
(Raw)airway resistance Increased Normal
• more sensitive of small airway
obstruction or disease MMEFR Decreased Normal
MBC Decreased Normal
Respiratory Muscle weakness: PEFR Decreased Decreased
• It is evaluated and measured by
maximum static respiratory
pressure
• PImax = -125 cm of H2O - normal Flow-‐Volume Loops
• If PImax = -25 inability to take deep • Provide a graphic analysis of flow at various lung volumes
breath • Used to differen:ators between pa:ents with upper airway and lower airway obstruc:on
• PEmax = + 200 cm of H2O - normal • Flow is charted on Y-‐axis
• If PEmax = + 40 cm of H2O • Volume is charted on X axis
severely impaired coughing ability • Pa:ent is asked to inhale fully to TLC and then perform a FVC maneuver. This is followed
• seen in Emphysema
immediately by a maximum inspira:on back to TLC
• predictor of successful weaning
• The ra:o of expiratory flow to inspiratory flow at 50% of VC is normally 1 (mid VC ra:o)
• Evaluation of NM disorder
16
20. Classify Anti-Hypertensive drugs. Describe anesthetic management of hypertensive episode
during anesthesia
Oral Anti-Hypertensive Drugs - Classification
Vasodilators:
Sympatholytics:
Diuretics: Calcium Channel Blockers:
• Benzothiazepines: Diltiazem
Adrenergic receptor blockers:
• Phenylalkalamines: Verapamil
I. Beta Blockers:
Thiazide: • Dihydropyridines: Amlodipine,
1. Atenolol
• Chlorthiazide Nifidipine, Nicardipine, Felodipine
2. Metoprolol
• Hydrochlorthiazide 3. Acebutolol
• Chlorthalidone 4. Timolol
• Indapamide ACE Inhibitors:
5. Esmolol
• Metalazone • Captopril, Enalapril,
6. Nadolol
II. Alpha Blockers: Lisinopril,Ramipril
Potassium Sparing:
A. α1 + α2 Phenoxybenzamine
• Spironolactone
B. α1 Prazosin, Doxazosin
• Triamterene
Terazosin
• Amiloride Angiotensin-receptor Antagonist:
III. α + β • Losartan, Valsartan, Telmisartan
A. Labetalol
Loop Diuretics: B. carvedilol
• Furosemide
• Torasemide Central α2 Agonist: Direct Vasodilators:
• Ethacrynic acid • Hydralazine, Minnoxidil
• Clonidine
• Bumetanide
• Methyldopa
• Guanabenz
Post gangalionic blockers:

• Guanithidine
• Reserpine
17

Indications Drugs Dose Onset Duration

For patient with good LV function ↑ HR Esmolol IV 0.5mg/kg over /min 1min 12-‐20min
CI in bronchospastic disease 50-‐300µg/kg/min
Labetalol 5-‐20mg 1-‐2min 4-‐8hr

Propanol 1-‐3mg 1-‐2min 4-‐6hr
Ca+2 channel blockers Nicardipine 0.25-‐0.5mg 1-‐5min 3-‐4 hr
Myocardial ischemia ← reGlex Nifedipine (S/L) 10mg 5-‐10min 4h
tachycardia
Mod to severe HTN – most rapid Nitroprusside 0.5-‐10µg/kg/min 30-‐60 sec 1-‐5min
Nitroglycerine 0.5-‐10µg/kg/min 1min 3-‐5min
Sustained control of BP ← delayed onset Hydralazine 5-‐20mg 5-‐20min 4-‐8hr
reGlex tachycardia Phentolamine 1-‐mg 1-‐10min 20-‐40mm
Enalaprilat 0.625-‐1mg 6-‐14min 4-‐6h
ACE Inhibitors Fenoldopam 0.1-‐0.6 µg/kg/min 5 min 5 min
18

Goldman's Cardiac Risk Index -‐ 1977.
i. Age > years 5
ii. MI in previous 6 months 10
iii. S3 gallop or ↑ JVP (0-‐3 cm) 11
iv. Important aortic stenosis 3
v. Rhythm other than sinus, Pac on last preoperative 7
vi. >5 PVC/min at any time before 7
vii. PaO2, < 60 or PaCO2 > 50mm Hg, 3

K<3.00 mEq/L or HCO3 < 20 mEq/l
BUN > 50 or Cr> 3 mg/dl. Abnormal SGOT, signs of chronic liver disease, bed ridden from
non-cardiac cause
viii. Intraperitoneal, Intrathoracic, aortic surgery 3
ix. Emergency operation 4
Total 53
Class I 0-5 points (low risk)

Class II 6-12 points (intermediate risk)
Class III 13-25 points (high risk)
Class IV ≥ 26 points (very high)
19

Detsky’s ModiGied Cardiac Risk Index-‐ 1986
Risk of perioperative reinfarction in patients with recent MI:
i. Age > 70 years 5
ii. MI < 6 months 10
iii. MI > 6 months 5 Duration since last MI Re-infarction rate
iv. Unstable angina 10
v. Pulmonary edema < 1 week 10 with in 3 months 30%
vi. Pulmonary edema in the past 5
vii. Non sinus rhythm PAC 5 3 - 6 months 15%
viii. CCVSA class III 10
ix. CCVSA class IV 20
> 6 months 6%
x. Critical As 20
xi. Emergency operation 5
xii. Poor general status 5
Total 120
Lee’s revised Cardiac Risk Index-‐-‐ 1999.
!!!!!!
(Assign one point to each of the following variables)
i. High risk type of surgery (intra-peritoneal, intra-thoracic or suprainguinal vascular
procedures.
ii. History of IHD (history of MI, positive exercise test, current complaint of ischemic chest pain
or use of nitrate therapy of ECG with Q waves)
iii. History of CHF
iv. History of cerebro-vascular disease
v. Insulin therapy for diabetes
vi. Preoperative serum creatinine > 2.0 mg/gl
Class I = 0 factors,
Class II = 1 factor
Class III = 2 factors
Class IV = >2 factors
20

Algorithm of cardiac evaluation for non cardiac surgery as recommended by ACC/AHA 2007 Dr Azam’s Notes in Anesthesiology 2013
guidelines on perioperative CVS evaluation.
21

Cardiac Risk* Stratification for Noncardiac Surgical Procedures
Risk Stratification Procedure Examples
Vascular (reported cardiac risk often more than 5%) Aortic and other major vascular surgery
Peripheral vascular surgery
Intermediate (reported cardiac risk generally 1% to 5%) Intraperitoneal and intrathoracic surgery
Carotid endarterectomy
Head and neck surgery
Orthopedic surgery
Prostate surgery
Low (reported cardiac risk generally less than 1%) Endoscopic procedures
Superficial procedure
Cataract surgery
Breast surgery
Ambulatory surgery
* Combined incidence of cardiac death and nonfatal myocardial infarction.

These procedures do not generally require further preoperative cardiac testing.
22
6. Supraglottic devices
Supraglottic airway devices are devices that ventilate patient by delivering/anesthetic gases/O2 above the level of the vocal cords and are designed to
overcome the disadvantages of Et - Intubation.
Advantages: Classification of SGA(Supraglottic Airway):

• Avoidance of laryngoscopy Based on:
• Less invasive for respiratory tract • Presence or absence of cuff
• Better tolerated by patients • Oral/nasal route of insertion
• Placement is easier • Anatomic location of the distal portion (sealing mechanism)
• Improved hemodynamic stability in
emergence • Cuffed perilaryngeal sealers: E.g Ambu laryngeal mask, SSLM(softseal laryngeal mask), ILA(intubating
• Less coughing laryngeal airway), LMA, ILMA(intubating laryngeal mask airway).
• Less sore throat • Cuffed pharyngeal sealers: E.g CobraPLA (Cobra perilaryngeal airway)
• Less incidence of bronchospasm • Cuff less pre-shaped sealer: E.g SLIPA
• Hands free airway
23

Supraglottic devices.continuation:
Cuffed perilaryngeal sealers Cuffed pharyngeal sealers Cuff less pre-shaped sealers
Without directional sealing With directional sealing Without esopheageal sealing With esopheageal sealing
cuff cuff
Devices LMA, ILMA, SSLM, AMBU LM, ILA PLMA Proseal LMA COPA, COBRA PLA, Laryngeal tube, combitube, SLIPA, I-GEL
easy tube
Sealing relies on simple opposition of the cuff sealing site is at or around the Pharyngeal cuff seals at the base of the tongue Anatomically preshaped hollow
mechanism that surrounds the larynx entrance of the larynx airway which seals the outlet
from the pharynx at the base of
the tongue to the esophagus,
as a result of the resilience of
the walls of the shaped airway
Advantages • Minimal risk of precipating • Higher seal pressure • Better sealing pressures • Minimizes aspiration risk • Easier to use,
laryngospasm, • Decreased risk of • Pressure exerted • Provides access to • Able to insert through limited
• Well tolerated at lower anesthetic levels regurgitation perpendicular to airway esophagus mouth opening
channel • Hollow structure provides
protection for aspiration
• Pre-shaped provides specific
positioning and a stable
airway
Disadvantages • Low seal pressure • Harder to insert • No sealing of the • Increased mucosal trauma • Difficult to select proper size
• Little storage space for regurgitated • More easily rotated out of downward outlet increasing due to stiffer tube • Less flexibility in positioning
liquid position the risk of GE aspiration. • Congestion of tongue with • Not for use in abnormal
• Increased risk of GE insufflation. • Folding of tip can occur • No protection from excessive increase in cuff airway anatomy.
upon insertion, occluding the aspiration pressure and potential lingual
drainage tube. • Increased need for nerve damage
repositioning • Increased need for
repositioning
24

Diagrams & Flow charts
25
dosages of most medications should be decreased in the elderly, and the dosing
interval Venturi
should Mask:
be increased (Table 23.3). Dr
POSTOPERATIVE ANESTHESIA CARE UNIT (PACU) AND Azam’s
COMMON Notes inPROBLEMS
POSTOPERATIVE Anesthesiology
433 2013 L
Flow rates & percentages:

OXYGEN OXYGEN FLOW AIR ENTRAINMENT
Anesthetic Management
CONCENTRATION(%) (L/min) (L/min) Table 27.3 Suggested medical therapies for hypertension.
24 Blue 2-4 50-100
Preoperative
28 White
Examination 4-6 40-60 Mild to moderate hypertension t #FUBCMPDLFST MBCFUBMPM FTNPMPM NFUPQSPMPM
The purpose of the preoperative

32 Orange 6-8 examination is to56(1) determine the baseline
t $BMDJVNDIBOOFMCMPDLFST OJDBSEJQJOF
t /JUSPQBTUF
physical 36
and mental status of8-10
yellow the patient, and (2)40identify and optimize any t )ZESBMB[JOF
medical 40
comorbidities
Red prior 8-12
to undergoing a surgical
24-36 procedure. The elderly Severe or refractory hypertension t *7BOUJIZQFSUFOTJWFJOGVTJPOT
60 Green 12 33 (consider intra-arterial BP monitoring) − Nicardipine
patient has on average three or more comorbid conditions at any given time. − Nitroglycerine
− Nitroprusside
Table 23.3 Comparative elimination half-life of drugs. Table 27.4 Causes of postoperative tachycardia.
Noxious stimuli t 1BJO BOYJFUZ

Young Old
t &OEPUSBDIFBMUVCF
t %JTUFOEFECMBEEFS
Fentanyl 250 min 925 min
Physiologic derangements t "DJEPTJT
Alfentanil 90 min 130 min t )ZQPYFNJB
t )ZQPUFOTJPOBOEIZQPWPMFNJB
Diazepam 24 h 72 h
t )ZQPHMZDFNJB
Midazolam 2.8 h 4.3 h t *ODSFBTFEJOUSBDSBOJBMQSFTTVSF
t .ZPDBSEJBMJTDIFNJB
Vecuronium 16 min 45 min
Medications t #FUBBESFOFSHJDWBTPQSFTTPST
t %PQBNJOF
t %PCVUBNJOF
t #SPODIPEJMBUPST
Anesthetics t ,FUBNJOF
t *TPGMVSBOF
includes treating the underlying cause, fluid bolus, draining the bladder, and pain
control. Symptomatic treatment may be necessary to allow offending medications
to wear off. Cardiac arrhythmias are also common causes of tachycardia. If atrial
fibrillation occurs, consider beta blockade, calcium channel blockers, and poten-
tially cardioversion if the patient becomes hemodynamically unstable.
The most common causes of postoperative bradycardia are increased
parasympathetic flow or decreased sympathetic output, which may addition-
ally manifest as hypotension concomitant with the bradycardia. In cases of sus-
26
pected increased parasympathetic output, consider muscarinic blocking agents
such as atropine and glycopyrrolate. In cases of decreased sympathetic output,
beta-mimetic agents such as ephedrine are useful. Table 27.5 outlines the most
Diagrams: Respiratory System Dr Azam’s Notes in Anesthesiology 2013
The pre-operative respiratory care:
• Stop Smoking
• Dilate the airway using:
• Beta agonist
• Theophylline
• Steroids
• Cromolyn Sodium
• Loosen the Secretions by:
• Airway hydration ( Humidification/Nebulization)
• Systemic hydration orally - 3 Liters
• Mucolytic agents & Expectorant drugs
• Antibiotics
• Remove secretions:
• Coughing
• Chest physiotherapy(percussion & Vibration)
Ancillary Measures:
ECMO circuit: • Treatment of co-existing disease
It utilizes a modified heart lung bypass machine, • Treatment of Cor-Pulmonale
consisting of a venous blood drainage reservoir, a • Pre-operative Digitalization
Patient Education, motivation & facilitation of post
blood pump, the membrane oxygenator where the operative care:
exchange of O2 and CO2 takes place, and a heat • Physiological preparation
exchanger to maintain temperature. • Incentive spirometry & deep breathing exercise
• Exercise
27

Diagrams Dr Azam’s Notes in Anesthesiology 2013
Obstructive Restrictive
FEVI Decreased Decreased
FVC Normal Decreased
FEV1/FVC Decreased Normal
FRC Increased Decreased
TLC Increased Decreased
(Raw)airway Increased Normal
resistance
MMEFR Decreased Normal
PEFR Decreased Decreased
Relationship of FRC and CC:

Condition FEV1 FVC FEV1 /FVC
• FRC = CC !Neonate and infants
Airway obstruction (asthma, bronchitis) Decreased Normal Decreased • FRC = CC !in supine position at 45 years (40-45)
Stiff lungs (pneumonia, pulmonary edema) Decreased Decreased Normal • FRC = CC !in upright position at 65 yrs.
myopathies)
28

Describe pathophysiology, clinical features diagnosis & management of fat embolism? Dr Azam’s Notes in Anesthesiology 2013
Continuation:
Diagnostic criteria:
Gurd and Wilson criteria: Lindeque Criteria: !

1. PaO2< 60 mmHg on room air.
Major features– petechial rash, respiratory 2. PaCO2> 55 mmHg or pH<7.3
insufficiency, cerebral signs.
3. Spontaneous respiratory rate
Minor features– Pyrexia, tachycardia, retinal
changes, jaundice, renal changes. >35 breaths/minute.
4. Clinical signs of increase work
• Positive diagnosis requires at least one of breathing (dyspnea and
major and four minor clinical features. accessory muscle action).
TREATMENT:
1. Fluid resuscitation: The severity of FES is directly related to degree and duration
of associated shock. Shock by producing pulmonary damage of its own can
intensify the lung injury caused by FES. Aggressive fluid resuscitation must be GRID: Question needs answered under
initiated early to restore intravascular volume, improve preload establish optimal following headings:
cardiac output. Appropriate monitoring should be used to avoid fluid overload. 1. Definition
2. Albumin has been recommended for volume resuscitation along with balanced 2. Etiology
electrolyte solution, as it not only restore blood volume but also binds fatty acids, 3. Pathophysiology - Theories
reducing their potential for lung damage. 4. Clinical features
3. Ventilatory support: Lung is the primary target organ in FES necessitating the use 5. Diagnosis
of aggressive ventilatory therapy. Mechanical ventilation preferably with PEEP must 6. Management.
be instituted whenever simple oxygen administration with or without CPAP is
insufficient to maintain adequate oxygen saturation.
4. Drugs: Steroids-Limits free fatty acid induced inflammatory reaction in lungs.
5. Aprotinin – A protease inhibitor decreases aggregation of platelet and release of
serotonin and thus limits lung injury.
29

Diagrams regulationPOSTOPERATIVE
from anesthetics and theCARE
ANESTHESIA higher rate
UNIT ofDr
(PACU)heat
AND loss from
COMMON
Azam’s patients with PROBLEMS 2013
POSTOPERATIVE
Notes in Anesthesiology 435
L
burns, traumatic injuries, or cachexia can all lead to a significant drop in body
temperature and subsequent shivering. The physiologic impairments of both
Time course Bene3icial effects Table 27.6
hypothermia and shivering Causesbelow
are detailed of postoperative
in Table 27.9.mental status changes.
12-24 hours Decrease carbon monoxide and nicotine levels The treatment of hypothermia and shivering includes forced air warming
Hypoxemia
48-72 hours Normalizes carboxy Hb levels. Improves ciliary devices, patient reassurance, and meperidine in severe cases of shivering.
Metabolic derangements
Decrease sputum production & improves smallerDischarge Criteria
Cerebral hypoperfusion
1-2 weeks
Discharge from the Extremes
PACU isofbased
age on an array of clinical factors outlined below:
airway function.
Emotionally significant operations
4-6 weeks Improves PFT
General ConditionPresence of intraoperative recall
6-8 weeks Normalizes immune function, drug metabolism and
The patient should Scopolamine
be oriented or to time, place, situation, and follow commands.
atropine
hepatic enzyme activity
Patient should be non-cyanotic
Substance abuse
and non-pallorous, and muscle strength needs
8-12 weeks Reduces overall post-operative pulmonary
to be appropriate. Nausea, pain, and any other major early postop complica-
complications. Pain, nausea, pruritus
434 L
ANESTHESIA STUDENT SURVIVAL GUIDE tions should be absent or under control.
Table 27.9 Effects of hypothermia and shivering.

Table 27.5 Common causes of postoperative bradycardia. providing supplemental oxygen, benzodiazepines, arm restraints, and phys-
Hypothermia
Medications t /FPTUJHNJOF FESPQIPOJVN ostigmine if reaction is related to scopolamine or atropine (central anticholin-
t *ODSFBTFEPYZHFODPOTVNQUJPO DBSCPOEJPYJEFQSPEVDUJPO
t 1IFOZMFQISJOF OPSFQJOFQISJOF ergic syndrome).
t &MFWBUFTQFSJQIFSBMWBTDVMBSSFTJTUBODF
t 0QJPJET
t 4VDDJOZMDIPMJOF
Postoperative neuropathy is a less common injury that may present post-
t *NQBJSTQMBUFMFUGVODUJPO EFDSFBTFEDMPUUJOHGBDUPST
t #FUBCMPDLFST operatively. Spinal cord injury can occur with positioning during intubation or
t *ODSFBTFEJOGFDUJPOSBUFT
t -PDBMBOFTUIFUJDT with hematoma after neuraxial anesthesia, but this is very rare. More commonly
t .BZMFBEUPDBSEJBDEZTSIZUINJBT
t (BOHMJPOJDCMPDLFST Shivering
t )JHITQJOBMFQJEVSBMBOFTUIFTJB seen are peripheral nerve injuries. These stretch or compression injuries may
t *ODSFBTFEPYZHFODPOTVNQUJPO VQUP
Physical causes t $BSPUJETJOVTNBTTBHF involve the ulnar nerve (compression of ulnar nerve at the postcondylar groove
t *ODSFBTFEDBSCPOEJPYJEFQSPEVDUJPO VQUP
t 7BMTBMWBNBOFVWFS oft humerus), peroneal nerve (compression of nerve against fibular head while in
*NQBJSTNPOJUPSJOHEFWJDFT
t (BHHJOH
t 3FDUBMFYBN
lithotomy), femoral nerve (due to exaggerated lithotomy position with “candy
t .BZMFBEUPNZPDBSEJBMJTDIFNJB
t *ODSFBTFEPDVMBSQSFTTVSF cane” stirrups), brachial plexus (due to over abduction of arms past 90° in the
t .BZQSFDJQJUBUFWFOUJMBUPSZDPNQSPNJTF
t %JTUFOEFECMBEEFS
supine position or the neck being too far to one side), and long thoracic nerve
t 4UJNVMBUJPOPGQIBSZOY
(occurs with pneumonectomies, leading to winged scapula and paralyzed ser-
Metabolic derangements t 4FWFSFBDJEFNJB
t )ZQPYFNJB ratus anterior muscle). Most symptoms resolve in 6–12 weeks, although per-
manent injuries may occur.
Corneal abrasions can be caused by ocular drying (eyes open during pro-
ischemia include CHF, valvular disease, low ejection fraction, smoking history, cedure), contact with eye during facemask ventilation or intubation, 30or the
anemia, hypertension, and emergency surgery. Causes may include tachycardia patient scratching his or her own eye upon awakening (hence the reason we ask
Dr Azam’s
(decreases timeNotes in Anesthesiology
in diastole, 2013 hypoperfusion), hypotension,
leading to coronary the patient not to rub his or her eyes on the way to the recovery room). Signs
9. Describe the innervations of Larynx. Briefly discuss various palsies following Nerve Dr Azam’s Notes in Anesthesiology 2013
injury. Continuation:
Neurological lesions:
Vocal Cord palsy
General Causes
Vagus Nerve Recurrent Laryngeal nerve
• DM
Supra-nuclear lesions: • Syphilis
in the motor cortex • viral Disease
Left RLN Palsy:
• Aneurysm of Right recurrent laryngeal nerve:
aorta • Aneurysm of subclavian artery
• Lungs: TB, • Lungs: TB, apical carcinoma
Nuclear lesions: Malignancy Bilateral RLN Palsy:
• stroke • Esophagus: •Pulmonary tuberculosis
• Tumor malignancy • Esophageal malignancy
• MS
Peripheral
neurological
lesions
Intra Cranial: Lesions in the neck:

• Posterior fossa • Trauma
tumors • metastatic nodes
• Basal fractures
31

"!#$%!&!'()!**+,!
Pathophysiology: Amniotic fluid embolism:

! !"#$%&$'()*+$,(-".%*$/"(
-----".%*$/"(
0-'12#$'2*(%./&3+'&$%#(( 4+"%32*(%./&3+'&$%#((
53$&$'2*(6+*"%#237(8-//-*(%./&3+'&$%#! 9+*"%#237(:-//-*(82/%/62/"((
!'+&-(9+*"%#237(4;<(=(476%>-"$2((
?-8-3-(#-+3%*%@$'( ?6%#&2#-%+/(3-/%*+&$%#(( B:C((

$"62$3"-#&A,-2&1(
32

B) Biochemical and other investigation abnormalities:

A four point scoring system for lung injury has been formulated and is
! !"#$%&'()!(!
as follows:
1. Chest radiograph score Score
!!!"#$%&'(&!)*&+,-%*).!/! !!!0%1#&&%,2!)*&+,-%*).!/!
No alveolar consolidation 0
Alveolar consolidation in one quadrant 1
Alveolar consolidation in two quadrants 2 !!!!!3,2%&,*)!4&*,15!!!!!!!!!!!
9:2%&,*)!4&*,15!6;(2(&8! ?(2(&!4&*,15! "%,7(&+!4&*,15!
Alveolar consolidation in three quadrants 67%,7(&+8!
3
Alveolar consolidation in all four quadrants
4 "#$$)'%7!)*&+,:! "#$$)'%7!25%! "#$$)'%7!*))!',2&',7'1! "#$$)'%7!*))!
*4(<%!)%<%)!(=!<(1*)! 1&'1(25&+('>!;#71)%7! %:1%$2!1&'1(25+&('>! 7#4-)(22'1!&%-'(,!!!
1(&>!
2. Hypoxemia score Value Score
PaO2 / FiO2 > 300 0
Nerve Supply to Larynx:
PaO2 / FiO2 225-299 1
PaO2 / FiO2 175-224 2
PaO2 / FiO2 100-174
3
PaO2 / FiO2 < 100
4
3. Respiratory system compliance Value Score
score (when ventilated)
Compliance > 80ml/cm. H2O 0
Compliance 60-79 ml/cm. 1
Compliance H2O 2
Compliance 40-59ml/cm. H2O
3
Compliance 20-39/cm. H2O
< 19 ml/cm. H2O 4
4. Peep score (when ventilated) Value Score
PEEP < 5cm. H2O 0
PEEP 6-8 cm. H2O 1
PEEP 9-11 cm. H2O 2
PEEP 12-14 cm. H2O
3
PEEP > 15 cm. H2O
4
33

34

38. Enumerate Post operative complications? Dr Azam’s Notes in Anesthesiology 2013
• Post operative respiratory Complications are: Mechanism for Post operative pulmonary complications:
1. Airway obstruction: • VC is ↓ by 25% ( <15ml/kg - vital capacity): Decrease ability to
a. Laryngospasm, bronchospasm - Treatment of cause, Oxygen cough.
supplementation, bronchodilators. • Residual Volume ↑ by 13% following GA
2. Hypoxemia: SaO2 < 90% • ERV ↓ by 25% after lower abdominal surgery & 60% after upper
• Immediate ( 1 to 2 Hrs): abdominal and thoracic surgery.
• Opioids, • Risk increases as duration of surgery exceeds 3 hours to 4hrs.
• Loss of pulmonary vasoconstriction,
• shivering Pathogenesis:
• V/Q mismatch, Post operative decrease in Vital capacity
• Diffusion Hypoxia
• Late ( > 2 Hrs):
• Atelectasis,
• Pulmonary Embolism,
• Pneumothorax,
• Pulmonary Edema Poor cough &
3. Cor-Pulmonale: Digitalization & Diuretics retention of Atelectasis
Secretions
4. Pulmonary infection:
• Pneumonia
5. Hypoventilation.
• Hypercarbia: Alveolar hypoventilation secondary to pain, inadequate
analgesia, inadequate reversal of NMB. - Oxygen supplementation. Pneumonia
6. Aspiration:
Arterial Hypoxemia
7. Atelectasis:
• Decreased FRC,
• Pain,
• splinting of diaphragm,
• decrease sputum clearance.
8. Delayed ambulation Acute Respiratory Failure
9. DVT & PE:
• Polycythemia Treatment of PPC: • Non - Invasive Ventilation - CPAP.
• intraoperative hypothermia & Dehydration: • Oxygen supplementation • Early Mobilization
• LMWH, TED Stockings, early mobilization and • Incentive Spirometry & Deep • Early Nutrition
Hydration breathing exercises Cor-pulmonaleDiuretics, Digoxin
•
10. Need for Mechanical ventilation, prolonged ICU stay/ • Chest Physiotherapy - Percussion & Avoiding Respiratory depressants.
•
hospital stay vibration. • Antibiotics & Analgesics 35
• Bronchodilators • Invasive ventilation - Lastly
There is a report suggesting that pressure-controlled ventilation Preoperative Spirometry
Diagrams may lead to improved oxygenation in COPD patients.129 Pressure-
controlled ventilation will avoid sudden increases in peak airway
Dr Studies
Azam’s Notes in Anesthesiology 2013
consistently show that when the previous factors are con-
trolled, patients with better spirometric lung function preopera-
pressures that may result from surgical manipulation in the chest. tively are more likely to desaturate and have lower Pa2 values
Table 59-18 Suggested Ventilation Parameters for One-Lung Ventilation

Problems During OLV Etiology
Parameter Suggested Guidelines/ Exceptions
Tidal volume 5-6 mL/kg Maintain:

Hypoxemia Intrapulmonary shunt during one- Peak airway pressure < 35 cm H2O
Plateau airway pressure < 25 cm H2O
lung ventilation
Positive end-expiratory pressure 5 cm H2O Patients with COPD: no added PEEP
Respiratory rate 12 breaths/min Maintain normal PaCO2; Pa-ETCO2 will usually increase 1-
Sudden severe Surgical compression of the heart 3 mm Hg during OLV
hypotension or great vessels Mode Volume or pressure controlled Pressure control for patients at risk of lung injury (e.g., bullae,
A pneumonectomy, post lung transplantation)
Sudden changes in Movement of endobronchial tube/

ventilating pressure blocker, air leak Severity of expiratory airflow obstruction & Grading:
or volume
FEV FEF 25-‐75 Pao2 (mm Pa Co2 (mm
Severity
Arrhythmias Direct mechanical irritation of the (% predicted) (% predicted) Hg) Hg)
1) Mild 65-‐80 60-‐75 > 60 < 40
heart
(asymptomatic)
Bronchospasm Direct airway stimulation, 2) Moderate 50-‐64 45-‐59 > 60 < 45
increased frequency of reactive
airways disease 3) Marked 35-‐49 30-‐44 < 60 > 50
Massive hemorrhage Surgical blood loss from great 4) Sever (status < 35 < 30 < 60 > 50
vessels or inflamed pleura asthamaticus)
Hypothermia Heat loss from the open

hemithorax
36

V Diagrams
1834 Adult Subspecialty Management

available

regular ETT
37

• Complications related to single lung ventilation:

Pulmonary Cardiovascular CO2 Insufflation
Effects Effects Effects
Hypoxaemia Hypotension Hypotension
Hypercapnia Hypertension Bradycardia
Impaired HPV Arrhythmias Co2 air embolism
Pulmonary Mediastinal Shift Subcutaneous

Edema Emphysema
Atelectasis
Pneumonia
Complications more with Rt Lung as Vascular supply is 10%
more compared to the left side. Anesthesia for Thoracic Surgery 1839 59
Size 9 Fr 5 Fr, 7 Fr, and 9 Fr 5 Fr, 9 Fr
Section V Adult Subspecialty

fiberoptic bronchoscope
Murphy eye Present Present in 9 Fr Not present

30, 2007, with permission.
38

Classification & characteristics of various Mapleson circuit
Mapleson Other Names Configuration1 Spontaneous Controlled Comments

Class
A Magill attachment Equal to minute Very high and Poor choice during controlled
ventilation ( 80 mL/ difficult to ventilation. Enclosed Magill system is
kg/min) predict a modification that improves
efficiency. Coaxial Mapleson A (Lack
breathing system) provides waste-
gas scavenging.
B 2 x minute 2–2½ x minute
C Waters' to-and-fro 2 x minute 2–2½ x minute

D Bain circuit 2–3 x minute 1–2 x minute Bain coaxial modification: fresh gas
ventilation ventilation tube inside breathing tube.
E Ayre's T-piece 2–3 x minute 3 x minute Exhalation tubing should provide a

ventilation ventilation (I:E larger volume than tidal volume to
=1:2) prevent rebreathing. Scavenging is
difficult.
F Jackson-Rees' 2–3 x minute 2 x minute A Mapleson E with a breathing bag
modification ventilation ventilation connected to the end of the
breathing tube to allow controlled
ventilation and scavenging.
39

4. Classify vaporizers. Discuss the effect of altered barometric pressure on the performance of Dr Azam’s Notes in Anesthesiology 2013
vaporizers?
Vapour: A Vapour is the gaseous form of a substance which is liquid at room temperature
Vaporizer: A vaporizer is an instrument designed to change a liquid anesthetic agent in to its vapour and to add a controlled amount of this vapour to the
fresh gas flow.
Classification of vaporizer:
Oldest Classification:
Older Classification: New Classification:
A. Method of regulating Output Concentration
A. Method of regulating Output Concentration A. Method of regulating Output Concentration
1. Variable Bypass
1. Variable Bypass 1. Variable Bypass
2. Measured Flow
2. Measured Flow 2. Measured Flow
B. Method of Vaporization
B. Method of Vaporization B. Method of Vaporization
1. Flow Over
1. Flow Over 1. Flow Over
2. Bubble Through
2. Bubble Through 2. Bubble Through
3. Flow over or Bubble Through
3. Injection 3. Injection
C. Location
C. Resistance C. Temperature Compensation
1. Outside the Breathing System
1. Plenum 1. Mechanical
2. Inside the Breathing System
2. Low resistance 2. Supplied Heat
3. Computerized
D. Temperature Compensation
1. None D. Temperature Compensation
2. By Supplied Heat 1. Thermocompensation
3. By Flow Alteration 2. Supplied Heat
E. Specificity E. Specificity
1. Agent Specific 1. Agent Specific
2. Multiple Agent 2. Multiple Agent
40

Enumerate the effects of chronic smoking & the anesthetics implications.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Preoperative Preparation:
• Stop Smoking Time course Bene3icial effects
• Dilate the airway using: 12-24 hours Decrease carbon monoxide and nicotine levels
• Beta agonist 48-72 hours Normalizes carboxy Hb levels. Improves ciliary
• Theophylline
• Steroids 1-2 weeks Decrease sputum production & improves smaller
• Cromolyn Sodium airway function.
• Loosen the Secretions by: 4-6 weeks Improves PFT
• Airway hydration ( Humidification/Nebulization) 6-8 weeks Normalizes immune function, drug metabolism and
• Systemic hydration orally - 3 Liters hepatic enzyme activity
• Mucolytic agents & Expectorant drugs 8-12 weeks Reduces overall post-operative pulmonary
• Antibiotics
Remove secretions: complications.
•
• Coughing
• Chest physiotherapy(percussion & Vibration) Post-operative Management:
Ancillary Measures: Goals:
• Treatment of co-existing disease • To promote adequate analgesia
• Treatment of Cor-Pulmonale • To minimize the incidence of postoperative complications
• Pre-operative Digitalization • To prevent infections
Patient Education, motivation & facilitation of • Chest physiotherapy & deep breathing exercise.
post operative care: Continuation: • Consider CPAP - Decreases WOB, Improves LV Compliance.
• Psychological preparation • Continuous administration of Local anesthetic with low dose opioids via
• Incentive spirometry & deep breathing exercise epidural catheter for post operative pain relief.
• Exercise
41
57. What are the major causes of Hypoxemia? What is Hypoxic Pulmonary Vasoconstriction? How
can general anesthesia worsens V/Q mismatch?

1. Hypoventilation
2. Low inspired Oxygen
3. Right to Left shunt
4. Ventilation-Perfusion mismatch
5. Diffusion impairment
Hypoventilation: Low inspired Oxygen:

• P(A-a)O2 is normal Right to Left shunt: Ventilation-Perfusion
• A decrease in Barometric
• PaCO2 is elevated ( Hypercapnia) pressure (High Altitude) • Healthy Individuals: mismatch:
• A portion of the bronchial • V/Q mismatch is the
• A decrease in FIO2 - circulation (blood supply most common cause of
Causes of Hypoventilation: accidental disconnection
• Depression of CNS by drugs to the conducting zone hypoxemia in disease
of the ETT, leak or of the airways) venous state.
• Upper airway obstruction exhausted central supply blood drains into the
• Disease of Neuromuscular of O2 pulmonary vein
junction
• A portion of coronary
• Disease of respiratory muscles circulation venous blood Diffusion impairment:
• Abnormality of the chest wall drains through the
• Disease of motor neurons of the • PaCO2 is normal
thebesian veins into the
brain stem/Spinal cord left ventricles
• P(A-a)O2 is normal at rest
• Inflammation, trauma or but may be elevated
• Congenital abnormalities:
hemorrhage in the brain stem • TOF,
during exercise
• VSD + PAS
• Intrapulmonary
Hypoxic pulmonary vasoconstriction is a paradoxical, physiological fistulas
phenomenon in which pulmonary arteries constrict in the presence of
hypoxia without hypercapnia, redirecting blood flow to alveoli with a higher
oxygen content.
42

Pathophysiology of Bronchial Asthma:
!
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()%#'' 2"3-&#!+"''
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FEV FEF 25-‐75
Severity Pao2 (mm Hg) Pa Co2 (mm Hg)
."!/0,'10"1-$'' 45-$&!%-'' (% predicted) (% predicted)
6+,1' 1) Mild 65-‐80 60-‐75 > 60 < 40
*%7&8+9-"!&'''
(asymptomatic)
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2) Moderate 50-‐64 45-‐59 > 60 < 45
3) Marked 35-‐49 30-‐44 < 60 > 50

:-,-0%-'+3'#$!99-$'09-"#%'
G-)$+9-"!&'$-3,-5'HC090,;' 4) Sever (status < 35 < 30 < 60 > 50
!; <-)=+#$!"-%'6>?'(>?'4>'
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!!!; *$+%#09,0"1!"%'AB?'4B?'(B'
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C; E8$+/F+50"-'.B' 5
Anesthesia for Thoracic Surgery 1839
C!; *,0#-,-#'0&#!C0#!"9'30&#+$''

@7I-!$$!#0F,-'!"3,0//0#+$7'0!$J07'''
' Size 9 Fr 5 Fr, 7 Fr, and 9 Fr 5 Fr, 9 Fr

K; D$+"&8+,I0%/'' fiberoptic bronchoscope
B; 41-/0'+3'F$+"&8!0,'L'!"3,0//0#+$7''
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M; N)&)%'%-&$-#!+"'!'#8!&='0"1'#-"0&!+)%'' Murphy eye Present Present in 9 Fr Not present

:-%),#%'!"'' 30, 2007, with permission.
O; 2"&$-0%-'!"'0!$J07'$-%!%#0"&-''
P; (-&$-0%-'!"'3+$&-1'-5I!$0#+$7' K; @7I-$!"3,0#!+"'+3',)"9%?'0"1'#8+$05''
C+,)/-'0"1'3,+J'$0#-%'' B; 2"&$-0%-1'J+=%'+3'F$-0#8!"9H'QRD';'' nal (coaxial) with an SLT. They can also be placed separately the wire loop by observing its entrance into the right mainstem
M; .,#-$0#!+"'!"'$-%I!$0#+$7'/)%&,-' thorough the glottis or tracheostomy exterior to an SLT. This bronchus under fiberoptic visualization. The optimal position of
3)"&#!+"'' allows the use of a smaller SLT and is often an option in pediat- the Arndt blocker in the left or in the right bronchus is achieved
>; 680"9-%'!"'-,0%#!&'$-&+!,''''' rics. Another advantage of the bronchial blockers is when post- when the blocker balloon’s outer surface is seen with the fiberop-
operative mechanical ventilation is being considered after
prolonged thoracic or esophageal surgery. In many instances
these patients have an edematous upper airway at the end of the
procedure. If a bronchial blocker is used there is no need to
change the SLT and there is no compromise of the airway if
mechanical ventilation is needed in the postoperative period.
Table 59-13 describes the characteristics of current bronchial
blockers. The smallest internal diameter (ID) of an endotracheal
tube that will allow passage of both a bronchial blocker and a
fiberoptic bronchoscope depends on the diameters of the bron-
choscope and blocker. For standard adult 9-Fr blockers, an 43
endotracheal tube greater than or equal to 7.0 mm ID can be used 1
with a bronchoscope less than 4.0 mm in diameter. Larger bron-
Dr Azam’s Notes in Anesthesiology 2013 choscopes will require an endotracheal tube greater than 7.5 mm 2
ID. All blockers need to be well lubricated before placement.

available

regular ETT
44

7. A 30 year old female ASA grade I following exploratory laparotomy is not maintaining oxygen
saturation in the post operative period. Discuss the causes & Management.
Definition: Hypoxia is defined as inadequate oxygen supply to the cells and tissues of the body. Decreased FRC:
Values: Sao2 < 90%, PaO2 < 60% • Seen in Pulmonary edema (Treatment will be fluid
restriction, diuretics & oxygen therapy Positive
Causes of Post operative Hypoxia & its treatment: ( 12 Causes) pressure ventilation.), Infections( Antibiotics),Obesity
Low Inspired concentration of O2: (incentive spirometer & deep breathing exercises),
• When FIO2 is < 0.21%. The treatment would be giving high inspired oxygen through Venturi aspiration(postural drainage, nebulization incentive
mask. spirometer & deep breathing exercises.)
Airway obstruction: Right to left intrapulmonary shunts:
• Pharyngeal obstruction: Treatment would be Head tilt & chin lift.! • Most common cause is Atelectasis. Treatment would
• Laryngeal obstruction: treatment: Lift the chin while the head is on a pillow or displace !jaw be Deep breathing exercise, Chest physiotherapy
forward. Alternating lifting and relaxing the chin will, relax the strap muscle of the neck. humidification of inspired gases, coughing &
• Attempt to facilitate ventilation of gentle positive pressure via mask. When conservative incentive spirometer.
measures are not effective in breaking spasm within 1min, then a muscle relaxant should be Drug Overdosage:
given I.V. Scoline 1.5mg/kg injected • Like opioids, muscle relaxants, in adequate reversal.
• Bronchospasm: Bronchodilators like Beta agonist, Anticholinergics, Theophylline Treatment would be titrated dosage of opioids & to
andSteroids wait for adequate reversal.
Post operative shivering: Pulmonary Embolism:
• May also cause hypoxia. Treatment is Oxygen therapy • Lower limb surgeries, prolonged
Sudden reduction in cardiac output: immobilization.treatment would be DVT stocking,
• Can contribute to hypoxemia. Treatment: Watch out for bleeding & dehydration. Give IV early mobilization, DVT prophylaxis.
fluids, blood replacement. Pneumothorax:
Diffusion Hypoxia: • Result of direct injury to lungs or rib fracture.
• At the end of surgery when both oxygen & nitrous oxide stopped at the same time. Where • Treatment is 100% oxygen, insertion of chest tube &
N2O diffuses back into the alveoli. Treatment is to give oxygen after cutting off N2O. intercostal drainage & IPPV.
Type of Surgery:
• Patients with abdomino-thoracic procedures will not respire adequately because of pain on
deep inspiration. Treatment would be adequate analgesia with opioids or NSAIDS or
through the epidural.
Ventilation Perfusion Mismatch:
• Usually seen under Anesthesia. GRID: Question needs answered under
following headings:
1. Definition
2. values
3. 12 Causes of Post operative Hypoxia &
its management.
45

3. Pulmonary Function Test Dr Azam’s Notes in Anesthesiology 2013
Non-Specific - Bed Side Test
Specific Test - PFT
Test of Ventilation Test of Distribution of Ventilation Test of Diffusion Test of Perfusion Other Tests
Single Breath N2 elimination Test

Multi-breath N2 wash out test Carbon Monoxide Diffusing
Radio-active Xenon distribution Capacity
radio-active Xenon
Static Test injection!
Dynamic Test
Radio-nucleotide
Non-Specific - Bed Side Function:
Macro-aggragated iodine
•Anatomical • Breath Holding test
Measurements • Sniderʼs Match Blowing test •Split Lung Function Test
•Do not evaluate • De Bonoʼs Whistle test •Bronchospirometery
Measures rate of flow of Gas • Auscultation over the trachea
Function •radio-active Scanning
• Sphygmomanometer •Pulmonary artery occlusion
• Walk test test
4 Volumes 4 Capacities MBC/MVV
• Stair case test. •ABG
TV VC FEV
IRV TLC PEFR •A-a Gradient
ERV FRC MMEFR 25 to 75 % •Raw
RV IC Respiratory Muscle Strength •Compliance
Fixed Obstruction
Variable Extra-Thoracic Obstruction
E-Expiration is normal
Flow
Volume Variable Intra-Thoracic Obstruction
Loops I-Inspiration is normal
Restrictive Lung Disease
46
Dr Azamʼs Notes in Anesthesia

FRC Dynamic Tests
Pulmonary Function Test
• Spirometer can measure - VT,IRV, • Volume of air remaining in the lung MBC or MVV
ERV, VC, IC, FEV & MBC after normal expiration • Max volume of air that can be breathed per
• Cannot be measured by Spirometer • measured by: minute by voluntary effort
- RV, TLC & FRC • N2 washout technique • normal - 160L/min to 180 L/min
• Helium dilution MBC is decreased in:
Static Test • Body Plethysmograph • old age
VT - Tidal Volume • FRC increased: • emphysema
• Total Volume of air inspired & Expired in each breath • Obstruction of airways • bronchospasm
• measured by wrightʼs Respirometer • Emphysema • bronchiolar obstruction
• PEEP
IRV - Inspiratory reserve volume FVC & FEV
• FRC decreased:
• Volume of air that can be inspired after normal FVC
• Under Anesthesia
inspiration. • Assess the expiratory ability
• post op old age
ERV - Expiratory reserve volume • max volume of air that can be
• obesity
• Volume of air that can be expired after normal exhaled forcefully and rapidly after
• smoking
expiration maximum inspiration
• Lithotomy
• It reflects the thoracic muscles, abdominal muscle • measured by Spirometer and fast
• Abdominal distention
& thoracic mobility moving Kymograph
• Lap surgeries
RV - Residual Volume • FVC done over 4 sec
TLC • reflects the relationship between
• Volume of air remaining in the lung
after maximum expiration • Total volume of air in lung after Flow & resistance
maximum inspiration. FEV1
• Measured by
• TLC decreased: • Max volume of gas exhaled during
• N2 washout technique
• Pulmo fibrosis the 1st second of FVC maneuver
• Helium dilution technique
VC - Vital Capacity • obesity • FEV1 = 83% of VC
• weakness of inspiratory muscle
• Most commonly measured
• volume of air that can be expired after maximum inspiration FVC is decreased in:
• can be measured by - spirometer • Atelectasis
• BSA: Male- 2.6l/m2 Female - 2.1l/m2 • Fibrosis
• A given VC is abnormal if < 80% of predicted value • muscle weakness
• VC: decreased - in pregnancy, Pulm fibrosis • abdominal swelling
• Emphysema • pain
• ch.Bronchitis In healthy patients
• asthma FVC=VC
• Abdominal pain
• can be < 70 to 75% in upper abdominal surgery
• < 50 to 55% in lower abdominal surgery
• Position: Lithotomy Vc < 18% 47
• VC= 3 X VT for effective cough
• Decrease in VC means decreased ability to cough and post operative complications Dr Azam’s Notes in Anesthesiology 2013
PEFR:
• After max inspiration patient exhales as forcefully
as he can and the max flow rate is measured
and expressed in lt/min and lt/sec
• Normal: Condition FEV1 FVC FEV1 /FVC
• 450-600 L/min
Airway obstruction (asthma, bronchitis) Decreased Normal Decreased
• 300 - 500 L/min
• Measured by Wrightʼs Respirometer Stiff lungs (pneumonia, pulmonary edema) Decreased Decreased Normal
! ! Pneumotachygraph
PEFR is decreased in:
myopathies)
• Obstructed Airway
Values less that 200 lt/min suggest impaired cough
and increased likely hood of post op pulmonary
complications
MMEFR ( 25% to 75%): Obstructive Restrictive
• Flow measured in middle half of FVC FEVI Decreased Decreased
• obtained by dividing the volume of gas FVC Normal Decreased
between 25 - 75% by corresponding FEV1/FVC Decreased Normal
elapsed time FRC Increased Decreased
• Normal = 4 to 5 L/sec TLC Increased Decreased
Importance
(Raw)airway resistance Increased Normal
• more sensitive of small airway
obstruction or disease MMEFR Decreased Normal
Respiratory Muscle weakness: PEFR Decreased Decreased
• It is evaluated and measured by
maximum static respiratory
pressure
• PImax = -125 cm of H2O - normal Flow-‐Volume Loops
• If PImax = -25 inability to take deep • Provide a graphic analysis of flow at various lung volumes
breath • Used to differen:ators between pa:ents with upper airway and lower airway obstruc:on
• PEmax = + 200 cm of H2O - normal • Flow is charted on Y-‐axis
• If PEmax = + 40 cm of H2O • Volume is charted on X axis
severely impaired coughing ability • Pa:ent is asked to inhale fully to TLC and then perform a FVC maneuver. This is followed
• seen in Emphysema
immediately by a maximum inspira:on back to TLC
• predictor of successful weaning
• The ra:o of expiratory flow to inspiratory flow at 50% of VC is normally 1 (mid VC ra:o)
• Evaluation of NM disorder
48
20. Classify Anti-Hypertensive drugs. Describe anesthetic management of hypertensive episode
during anesthesia
Oral Anti-Hypertensive Drugs - Classification
Vasodilators:
Sympatholytics:
Diuretics: Calcium Channel Blockers:
• Benzothiazepines: Diltiazem
Adrenergic receptor blockers:
• Phenylalkalamines: Verapamil
I. Beta Blockers:
Thiazide: • Dihydropyridines: Amlodipine,
1. Atenolol
• Chlorthiazide Nifidipine, Nicardipine, Felodipine
2. Metoprolol
• Hydrochlorthiazide 3. Acebutolol
• Chlorthalidone 4. Timolol
• Indapamide ACE Inhibitors:
5. Esmolol
• Metalazone • Captopril, Enalapril,
6. Nadolol
II. Alpha Blockers: Lisinopril,Ramipril
Potassium Sparing:
A. α1 + α2 Phenoxybenzamine
• Spironolactone
B. α1 Prazosin, Doxazosin
• Triamterene
Terazosin
• Amiloride Angiotensin-receptor Antagonist:
III. α + β • Losartan, Valsartan, Telmisartan
A. Labetalol
Loop Diuretics: B. carvedilol
• Furosemide
• Torasemide Central α2 Agonist: Direct Vasodilators:
• Ethacrynic acid • Hydralazine, Minnoxidil
• Clonidine
• Bumetanide
• Methyldopa
• Guanabenz
Post gangalionic blockers:

• Guanithidine
• Reserpine
49


For patient with good LV function ↑ Esmolol IV 0.5mg/kg over /min 1min 12-20min
HR CI in bronchospastic disease 50-300μg/kg/min
Labetalol 5-20mg 1-2min 4-8hr

Propanol 1-3mg 1-2min 4-6hr
Ca+2 channel blockers Nicardipine 0.25-0.5mg 1-5min 3-4 hr
Myocardial ischemia ← reflex Nifedipine (S/L) 10mg 5-10min 4h
tachycardia
Mod to severe HTN – most rapid Nitroprusside 0.5-10μg/kg/min 30-60 sec 1-5min
Nitroglycerine 0.5-10μg/kg/min 1min 3-5min
Sustained control of BP ← delayed Hydralazine 5-20mg 5-20min 4-8hr
onset reflex tachycardia Phentolamine 1-mg 1-10min 20-40mm
Enalaprilat 0.625-1mg 6-14min 4-6h
ACE Inhibitors Fenoldopam 0.1-0.6 μg/kg/min 5 min 5 min
50

Goldman's Cardiac Risk Index -‐ 1977.
i. Age > years 5
iii. S3 gallop or ↑ JVP (0-‐3 cm) 11
iv. Important aortic stenosis 3
vi. >5 PVC/min at any time before 7
vii. PaO2, < 60 or PaCO2 > 50mm Hg, 3

BUN > 50 or Cr> 3 mg/dl. Abnormal SGOT, signs of chronic liver disease, bed ridden from
non-cardiac cause
viii. Intraperitoneal, Intrathoracic, aortic surgery 3
ix. Emergency operation 4
Total 53
Class I 0-5 points (low risk)

Class II 6-12 points (intermediate risk)
51

Detsky’s ModiGied Cardiac Risk Index-‐ 1986
Risk of perioperative reinfarction in patients with recent MI:
i. Age > 70 years 5
iii. MI > 6 months 5 Duration since last MI Re-infarction rate
iv. Unstable angina 10
v. Pulmonary edema < 1 week 10 with in 3 months 30%
vii. Non sinus rhythm PAC 5 3 - 6 months 15%
ix. CCVSA class IV 20
> 6 months 6%
x. Critical As 20
xi. Emergency operation 5
Total 120
Lee’s revised Cardiac Risk Index-‐-‐ 1999.
!!!!!!
(Assign one point to each of the following variables)
i. High risk type of surgery (intra-peritoneal, intra-thoracic or suprainguinal vascular
procedures.
ii. History of IHD (history of MI, positive exercise test, current complaint of ischemic chest pain
or use of nitrate therapy of ECG with Q waves)
iii. History of CHF
Class II = 1 factor
52

Algorithm of cardiac evaluation for non cardiac surgery as recommended by ACC/AHA 2007 Dr Azam’s Notes in Anesthesiology 2013
guidelines on perioperative CVS evaluation.
53

Cardiac Risk* Stratification for Noncardiac Surgical Procedures
Risk Stratification Procedure Examples
Vascular (reported cardiac risk often more than 5%) Aortic and other major vascular surgery
Peripheral vascular surgery
Intermediate (reported cardiac risk generally 1% to 5%) Intraperitoneal and intrathoracic surgery
Carotid endarterectomy
Head and neck surgery
Orthopedic surgery
Prostate surgery
Low (reported cardiac risk generally less than 1%) Endoscopic procedures
Superficial procedure
Cataract surgery
Breast surgery
Ambulatory surgery
* Combined incidence of cardiac death and nonfatal myocardial infarction.

These procedures do not generally require further preoperative cardiac testing.
54
6. Supraglottic devices
Supraglottic airway devices are devices that ventilate patient by delivering/anesthetic gases/O2 above the level of the vocal cords and are designed to
overcome the disadvantages of Et - Intubation.
Advantages: Classification of SGA(Supraglottic Airway):

• Avoidance of laryngoscopy Based on:
• Less invasive for respiratory tract • Presence or absence of cuff
• Better tolerated by patients • Oral/nasal route of insertion
• Placement is easier • Anatomic location of the distal portion (sealing mechanism)
• Improved hemodynamic stability in
emergence • Cuffed perilaryngeal sealers: E.g Ambu laryngeal mask, SSLM(softseal laryngeal mask), ILA(intubating
• Less coughing laryngeal airway), LMA, ILMA(intubating laryngeal mask airway).
• Less sore throat • Cuffed pharyngeal sealers: E.g CobraPLA (Cobra perilaryngeal airway)
• Less incidence of bronchospasm • Cuff less pre-shaped sealer: E.g SLIPA
• Hands free airway
55

Supraglottic devices.continuation:
Cuffed perilaryngeal sealers Cuffed pharyngeal sealers Cuff less pre-shaped sealers
Without directional sealing With directional sealing Without esopheageal sealing With esopheageal sealing
cuff cuff
Devices LMA, ILMA, SSLM, AMBU LM, ILA PLMA Proseal LMA COPA, COBRA PLA, Laryngeal tube, combitube, SLIPA, I-GEL
easy tube
Sealing relies on simple opposition of the cuff sealing site is at or around the Pharyngeal cuff seals at the base of the tongue Anatomically preshaped hollow
mechanism that surrounds the larynx entrance of the larynx airway which seals the outlet
from the pharynx at the base of
the tongue to the esophagus,
as a result of the resilience of
the walls of the shaped airway
Advantages • Minimal risk of precipating • Higher seal pressure • Better sealing pressures • Minimizes aspiration risk • Easier to use,
laryngospasm, • Decreased risk of • Pressure exerted • Provides access to • Able to insert through limited
• Well tolerated at lower anesthetic levels regurgitation perpendicular to airway esophagus mouth opening
channel • Hollow structure provides
protection for aspiration
• Pre-shaped provides specific
positioning and a stable
airway
Disadvantages • Low seal pressure • Harder to insert • No sealing of the • Increased mucosal trauma • Difficult to select proper size
• Little storage space for regurgitated • More easily rotated out of downward outlet increasing due to stiffer tube • Less flexibility in positioning
liquid position the risk of GE aspiration. • Congestion of tongue with • Not for use in abnormal
• Increased risk of GE insufflation. • Folding of tip can occur • No protection from excessive increase in cuff airway anatomy.
upon insertion, occluding the aspiration pressure and potential lingual
drainage tube. • Increased need for nerve damage
repositioning • Increased need for
repositioning
56

57
15. Inhalation Grid Dr Azam’s Notes in Anesthesiology 2013
PARAMETERS HALOTHANE ENFLURANE ISOFLURANE SEVOFLURANE DESFLURANE Nitrous Oxide N2O
HISTORY SUCKLING - 1951 E = Epilepsy S = Steal, L = • S = not to be used with • Priestly - 1772
Laryngospasm Soda Lime • Fresh Blue cylinder
• sevoflurane appeared (750 - Psi)
in the literature in 1971 • Pin Index = 3,5
• Introduced into clinical
practice initially in
Japan in 1990
BASIC 2-CHLORO,2-BROMO,111- Clear colourless 1,1,1,3,3,3-hexafluoro-2- • Laughing gas

PHARMACOLO TRIFLUROETHANE liquid with a (fluoromethoxy)propane • Colourless
GY sweet smell • Odorless
(should be • Obtained by heating
protected from Ammonium nitrate at
light). 240 degree
centigrade
PHARMACOKIN MAC = 0.75%, Boiling point = MAC = 1.63%, MAC = 1.17%, MAC = 2%(1.8%), MAC = 6.6%, Boiling MAC = 104%, Boiling
ETICS 50.2,Blood-gas coefficient = 2.54 Boiling point = Boiling point = Boiling point = point = 22.8,Blood- point = - 88,Blood-gas
Clear colourless liquid, available in 56.5,Blood-gas 48.5,Blood-gas 58.5,Blood-gas gas coefficient =0.42 coefficient = 0.46
Amber bottle. coefficient = coefficient = 1.40 coefficient = 0.69 (Blood -gas
PRESERVATIVE: 0.01% Thymol 1.90 ( Hence speeds coefficient close to
used to prevent decomposition to Induction & recovery) N2O)
light. Special vaporizer
organic odour TEC - 6
PHARMACODYNAMICS
CNS ↑ ICP, ↓ CMRO2 25% Convulsions, ↑ depress CNS, Not • Sevoflurane of 0.5 to 1.0 MAC – maintains • ↑ CBF,
CBF, ↓ CMRO2 epileptic & not an auto regulation! • ↑ ICP,
analgesic • ↑ CBF, • ↑ CMRO2
• ↑ ICP,
• ↓ CMRO2
58

RS • ↑ PaCO2, • Inhibit HPV, • irritating to airways • Pleasant to inhale, • ↓ TV,

• Bronchodilator, • ↓ MV, - leading to • ↓ MV, • Inhibits Carotid body
• ↓ TV, • Respiratory coughing & • ↑ RR. hypoxic drive
• ↑ RR, depressant laryngospasm • Abolishes HPV !Extremely irritating to airways, • Pulmonary
• ↑ alveolar ventilation • ↓ TV, • ↑ Secretion (bronchial & Salivary) vasoconstriction - ↑
• ↑ RR, • Potent respiratory depressant PVR
• ↓ FRC • ↓ TV,
• Hypoxemia • ↑ RR,
• ↓ MV
CVS • Sensitizes heart to catecholamines • ↑ heart rate • ↑ Heart rate • ↓ SVR • Direct Myocardial
• ↓ Myocardial oxygen consumption • ↓ BP • ↓ Myocardial O2 • Dose dependent decrease in CO! ↓ Myocardial depressant
& depressant • ↓ Cardiac consumption contractility
• ↓ coronary blood flow, output • Hypotension • ↓ SVR,
• ↓ Heart rate • ↓ LV after • Potent coronary • ↓ cardiac work
load vasodilator & • Causes coronary vasodilatation
Coronary Steal • DOES NOT SENSITIZES TO EXOGENOUS
Phenomenon MYOCARDIUM
• DOES NOT
SENSITIZES TO
EXOGENOUS
MYOCARDIUM
NEUROMUSCUL • Muscle relaxant • Relaxation of Analgesic

AR • Relaxes uterine muscles all abdominal
• Causes halothane shakes muscles
• Relaxes
uterine
muscles
• Augments
muscle
blocking
agents
KIDNEY • ↓ GFR
• ↓RBF
LIVER • ↓HBF, Minimal or No change in portal vein flow

• ↓ Clearance Compensated by
An Increase in hepatic artery blood flow
59

METABOLISM • 3 weeks to clear Only OXIDATIVE

• Oxidative & P-450 & 2EI ( Hepatic)
• reductive (<1%)
Enzymes Responsible:
• P-450 & 2EI ( Oxidative) • TFA- • TFA-trifluroacetic • Hexafluro isopropanol, • TFA-trifluroacetic
• CYP 2A6 & CYP 3A4 (Reductive) trifluroacetic acid Inorganic Fl acid
• Metabolites are TFA-trifluroacetic acid & •
acid & Inorganic Cl,Fl, Br Inorganic Fl
ELIMINATION • 60 to 80 % via Lung • Mostly Lung • Mostly Lung • Mostly Lung • By Lung
• 20% metabolized in liver
OTHERS • Hepatotoxicity - results in Hepatic • production of • Rapid awaking compound A • N2O Toxicity,
POINTS necrosis carbon [fluoromethyl-2,2- • N2O impurities
monoxide - difluoro-1- • irreversibly oxidizes
due to Soda (trifluoromethyl)vinyl cobalt atom of Vit
& Baralyme ether]also called PIFE B12 inhibiting B12-
leading to ↑ (pentafluoroisopropenyl dependent Enzyme
Temperature fluoromethyl ether) and • Bone marrow
Compound B [1,1,1,3,3- depression
pentafluoro-2-
(fluoromethoxy)-3-
methoxypropane] also
called PMFE
(pentafluoromethoxy
isopropyl fluoromethyl
ether) on contact with the
soda lime
60

CONTRAINDICA Malignant Hyperthermia (MH) Epilepsy, MH, & MH, Coronary Steal MH, Its toxic hence MH, Causes • It is 35 times more
TIONS Renal Failure avoided in Renal,hepatic, Laryngospasm - soluble than N2.
& brain tumors hence not used in • So fills & expand
children under 2 any air-containing
years of age cavities:
Air Embolism,
Pneumothorax,
Intracranial air, Lung
Cyst, Intraocular air
bubbles,
Tympanoplasty,
Endotracheal tube cuff
61

Venturi Mask: Flow rates & percentages:
OXYGEN OXYGEN FLOW AIR ENTRAINMENT
CONCENTRATION(%) (L/min) (L/min)
24 Blue 2-4 50-100
28 White 4-6 40-60
32 Orange 6-8 56
36 yellow 8-10 40
40 Red 8-12 24-36
60 Green 12 33
62

63
64

65

66

67

IV 1772 Anesthesia Management
Table 56-1 Anticoagulant Agents
Plasma Stop before Prolongation

Drug Site of Action Route Half-life Excretion Antidote Procedure of PT/aPTT
Unfractionated IIa/Xa IV/SC 1.5 hr Hepatic Protamine 6 hr No/Yes

heparin
LMWH Xa SC 4.5 hr Renal Protamine (partial 12-24 hr No/No

reversal)
Streptokinase Plg IV 23 min Hepatic Antifibrinolytics 3 hr Yes/Yes
t-PA Plg IV <5 min Hepatic Antifibrinolytics 1 hr Yes/Yes
Warfarin Vitamin K–dependent Oral 2-4 days Hepatic Vitamin K 2-4 days Yes/No
factors rfVIIa
PCCs
Plasma
Pentasaccharide Xa SC 14-17 hr Renal rfVIIa 4 days No/No
Bivalirudin IIa IV 25 min Hepatic None 2-3 hr Yes/Yes
Argatroban IIa IV 45 min Hepatic None 4-6 hr *Yes/Yes
Hirudin IIa IV 1.5 hr Renal PMMA, dialysis 8 hr *Yes/Yes
APC Va/VIIIa IV 2 hr Hepatic None 12 hr No/Yes
Ximelagatran IIa Oral 3 hr Renal None 24 hr Yes/Yes
*Argatroban and lepirudin may increase the normal PT 4 to 5 seconds.

APC, activated protein C; HIT, heparin-induced thrombocytopenia; IV, intravenous; LMWH, low molecular weight heparin; PCCs, prothrombin complex concentrates; Plg,
plasminogen; PMMA, polymethyl methylacrylate; rFVlla, recombinant factor VIIa; SC, subcutaneous; IIa, thrombin; t-PA, tissue plasminogen activator.
From Roberts HR, Monroe DM, Escobar MA: Current concepts of hemostasis: Implications for therapy. Anesthesiology 100:722-730, 2004, with permission.
albeit less sensitive, measure of heparin anticoagulation.54 ment of anti–factor Xa activity. Furthermore, should rapid reversal
68
Heparin’s anticoagulant effect is rapidly reversible by protamine of LMWH prove necessary, protamine proves only partially
55
Dr administration.
Azam’s Notes in Anesthesiology 2013 effective.57
More recently, low-molecular-weight heparins (LMWHs) Oral anticoagulant therapy in the form of coumarin deriva-
PT and aPTT most often are unaffected, necessitating measure- drug administration. However, given a half-life of 2 to 4 days,
Table 56-2 Antiplatelet Agents
Drug Site of Action Route Plasma Half-life Metabolism Antidote Stop before Procedure Prolongation of PT/aPTT
Aspirin COX 1-2 Oral 20 min Hepatic None 7 days No/No
Dipyridamole Adenosine Oral 40 min Hepatic None 24 hr No/No
Clopidogrel ADP Oral 7 hr Hepatic None 5 days No/No
Ticlopidine ADP Oral 4 days Hepatic None 10 days No/No
Abciximab GPIIb-IIIa IV 30 min Renal None 72 hr No/No
Eptifibatide GPIIb-IIIa IV 2.5 hr Renal None 24 hr No/No
Tirofiban GPIIb-IIIa IV 2 hr Renal Hemodialysis 24 hr No/No
ADP, adenosine diphosphate; COX, cyclooxygenase diphosphate; IV, intravenous; GP, glycoprotein.
From Roberts HR, Monroe DM, Escobar MA: Current concepts of hemostasis: Implications for therapy. Anesthesiology 100:722-730, 2004, with permission.
69

Anesthesia fo
Table 59-19 Therapies for Desaturation during One-Lung Ventilation cated (e.g., inotropes/vasopresso
Severe or precipitous desaturation: Resume two-lung ventilation (if epidural sympathetic blockade).
possible). vasodilators, and decrease MAC o
Gradual desaturation: less than or equal to 1 MAC.
1. Ensure that delivered FIO2 is 1.0. 5. Perform a recruitment maneuver o
2. Check position of double-lumen tube or blocker with fiberoptic eliminate any atelectasis, inflate th
bronchoscopy. more for 15 to 20 seconds. This ma
3. Ensure that cardiac output is optimal; decrease volatile anesthetics to < tension and will also cause a tran
1 MAC.
Pa2 as the blood flow is tempora
4. Apply a recruitment maneuver to the ventilated lung (this will
transiently make the hypoxemia worse).
nonventilated lung.
5. Apply PEEP 5 cm H2O to the ventilated lung (except in patients with 6. Apply PEEP to the ventilated lung. I
emphysema). a recruitment maneuver before ap
6. Apply CPAP 1-2 cm H2O to the nonventilated lung (apply a recruitment maximal benefit (see Chapter 15).
maneuver to this lung immediately before CPAP). expiratory volume of the ventilate
7. Intermittent reinflation of the nonventilated lung in patients with normal lung mech
8. Partial ventilation techniques of the nonventilated lung: increased elastic recoil due to rest
a. Oxygen insufflation possible to predict the optimal PEE
b. High-frequency ventilation a level of 5 cm H2O is a useful st
c. Lobar collapse (using a bronchial blocker)
increase the end-expiratory lung v
9. Mechanical restriction of the blood flow to the nonventilated lung
significant levels of auto-PEEP (e.g
Unlike CPAP, application of PEEP
tion of the nonventilated70lung and
during OLV. Clinically this is evident because emphysematous
PEEP has been shown to be as effe
lung volume reduction patients generally tolerate OLV very well. levels during OLV in patients wit
gory
aortichas a 2-year
valve leafletsmortality
by causingrisk greater than 75%;
abnormalities in surgical
the leaflets testing, electrocardiography,
pensatory mechanisms echocardiography,
for maintaining adequatechest radiogra-
cardiac output.
intervention is the only effective treatment in these patients. Dr Azam’s
phy, right- and left-heart catheterization, and pulmonaryNotes in Anesthesiology
function 2013
tests. The goal of the evaluation is to confirm a diagnosis of class
Table 60-13 Goals
Heart Transplantation for Anesthetic Care of Patients with Aortic Stenosis and Aortic
D HFRegurgitation
that has been maximally treated but will result in death in
According to the ACC/AHA guidelines, the only established sur- less than 1 year.
Systemic Vascular Pulmonary Vascular
gical treatment option for advanced HF is cardiac transplanta- In the United States, cardiac transplantation is performed
Left Ventricular Preload Heart Rate Contractile State Resistance Regurgitation
tion,364 which is associated with excellent 1-year survival rates in member centers of the United Network for Organ Sharing
(>85%), 5-year survival rates
Aortic stenosis ↑ (70%), and functional capacity. ↓ (sinus)367 (UNOS), an umbrella organization
Maintain ↑ responsible for coordinating
Maintain
Discovery of the immunosuppressive agent cyclosporine in the organ procurement, organ allocation, and statistical information.
Aortic reguritation ↑ ↑ Maintain ↓ Maintain
early 1980s made cardiac transplantation an accepted surgical The UNOS selection guidelines for cardiac transplantation give
option for end-stage
From Sukernik DE: 368
MR, MartinHF. Since then,
Anesthetic techniques
management for the for detecting
surgical priority
treatment of valvularto patients
heart with
diseases. end-stage
In Hensley HF and
FA, Martin a life GP
DE, Gravlee expectancy of
(eds): A Practical
Approach to Cardiac Anesthesia, 4th ed. Philadelphia, Lippincott Williams & Wilkins, less than
2008, pp 1316-347.
year, such as patients in cardiogenic shock or a low-
output state requiring mechanical or inotropic support, patients
Table 60-14 ACC/AHA Classification of Chronic Heart Failure with advanced symptomatic HF and peak oxygen uptake less than
10 mL/kg/min
Problems(withDuring achievement
OLV of an anaerobic
Etiology threshold),
Stage Description patients with NYHA class IV HF because of advanced hyper-
trophic Hypoxemia Intrapulmonary
or restrictive cardiomyopathy, patientsshunt
withduring one-lung
refractory
A—High risk for heart Hypertension, diabetes mellitus, CAD, family
ventilation
failure history of cardiomyopathy angina pectoris caused by inoperable coronary artery disease, and
patients with severe
Sudden life-threatening ventricular arrhythmias
Surgical compression thatheart
of the are or
B—Asymptomatic heart Previous MI, LV dysfunction, valvular heart
failure disease
refractory to all appropriate medical
hypotension and surgical treatment.370
great vessels
Usually, the patient’s EF is less than 20%. However, patients with
Sudden changes in
C—Symptomatic heart Structural heart disease, dyspnea and fatigue, NYHA class III HF who are at Movement of endobronchial tube/
risk for sudden death related to
failure impaired exercise tolerance ventilating pressure or blocker, air leak
malignant
volume
arrhythmias are sometimes placed on the waiting list.
D—Refractory end-stage Marked symptoms at rest despite maximal Assessing PVR and “reversibility” is also important. Patients
heart failure medical therapy with ischemic or idiopathic cardiomyopathy
Arrhythmias and irritation
Direct mechanical increasedof LAPthe heart
often have reversible elevated PVR, a condition that usually
ACC/AHA, American College of Cardiology/American Heart Association; CAD, Bronchospasm Direct airway stimulation, increased
coronary artery disease; LV, left ventricular; MI, myocardial infarction. normalizes during the first week after heart transplantation. A
frequency of reactive airways disease
From Hunt SA, Baker DW, Chin MH, et al: ACC/AHA guidelines for the evaluation pressure gradient across the vascular bed (also known as a
and management of chronic heart failure in the adult: Executive summary. A Report transpulmonary gradient and calculated
Massive hemorrhage Surgical as the difference
blood between
loss from great vessels
of the American College of Cardiology/American Heart Association Task Force on mean PAP and mean PCWP) that or is higher pleura
inflamed than 14 mm Hg indi-
Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation
and Management of Heart Failure): Developed in Collaboration with the
cates significant elevation of PVR. A reduction in PCWP to
Hypothermia Heat loss from the open hemithorax
International Society for Heart and Lung Transplantation; Endorsed by the Heart 20 mm Hg that occurs during treatment with pulmonary vasodila-
Failure Society of America. Circulation 104:2996-3007, 2001. tory medication and is associated with persistent high PAP sug-
71

Box 60-6 Pulmonary Vasodilator Agents Box 60-7 Pharmacologic Agents for Inotropic Support of the
Anesthesia for Cardiac Surgical Procedures 1941
RV
1. Phosphodiesterase III Inhibitors Table 60-16 Pulsatile Ventricular Assist Devices
Bgab[bmbhgh_frh\Zk]bZemri^BBBiahliah]b^lm^kZlê^Z]l 1. Isoproterenol
to an increase in myocardial cAMP, which increases the Ghglê^\mbo^β-adrenergic
Device Lengthagonist
of Support Position Ventricular Support Drive Mechanism
influx of intracellular Ca2+ and has a positive inotropic Ihlbmbo^\akhghmkhib\Zg]bghmkhib\Z`^gm
effect InefhgZkrZg]lrlm^fb\oZlh]beZmhk
Abiomed BVS Short term Extracorporeal LV, RV, BV Pneumatically driven atrial and
Ngbjn^f^\aZgblfh_bghmkhib\^__^\mlbg]î^g]^gmh_β- 5000 ventricular chambers
2. Dobutamine
receptor stimulation
β-Adrenergic receptor agonist with minimal α-adrenergic
;riZll β-adrenergic receptors in patients with preexist- Thoratec VAD activity
Short to medium term Extracorporeal LV, RV, BV Pneumatically driven sac
receptor agonist
ing heart failure
Ihlbmbo^\akhghmkhib\Zg]bghmkhib\Z`^gm
:]]bmbo^^__^\mpbma\Zm^\aheZfbg^l HeartMate IP Long term as a bridge to Intracorporeal, abdominal LV Pneumatically or electrically driven,
InefhgZkrZg]lrlm^fb\oZlh]beZmhk
InefhgZkroZlh]beZmbhg and VE transplantation or recovery or as (preperitoneal or intraperitoneal) flexible, textured polyurethane
<hkhgZkroZlh]beZmbhg 3. Epinephrine
destination therapy (HeartMate VE) diaphragm
α- and β-adrenergic receptor agonist
2. B-Type Natriuretic Peptide
β-Adrenergic
Novacor receptor Longpredominance at lower
term as a bridge to doses Intracorporeal, abdominal LV Polyurethane pump sac compressed
K^\hf[bgZgmanfZg;&mri^gZmkbnk^mb\iîmb]^
Ihm^gmkbàmo^gmkb\neZkbghmkhi^
Lbm^ h_ Z\mbhg3 `nZgreZm^ \r\eZl^ k^\îmhk h_ oZl\neZk transplantation or recovery (preperitoneal or intraperitoneal) by electrically driven pusher plates
AZllb`gbÖ\ZgmZkkarmafh`^gb\ihm^gmbZe
smooth muscle and endothelial cells
>__^\m3 bg\k^Zl^] bgmkZ\êeneZk \@FI Zg] lfhhma fnl\e^ BV, biventricular; BVS, biventricular support; IP, implantable pneumatic; LV, left ventricular; RV, right ventricular; VAD, ventricular assist device; VE, vented electric.
cell relaxation, dose-dependent reduction in PCWP and
systemic arterial pressure in patients with heart failure, the heart to assume some of its workload and permit the ventricle
increased permeability of vascular endothelium, inhibi- to rest, thereby potentially allowing reverse remodeling and
tion of the renin-angiotensin-aldosterone axis
=hl^3+&µg/kg bolus followed by a 0.01- to 0.03-µg/kg/min
or ofintracorporeal.
recovery Most extracorporeal
some contractile function. VADs,
The latest applications of whether pulsatile impairment, stroke, severe pulmonary hypertension, incurable
mechanical circulatory support include reversing ventricular dys-
infusion or nonpulsatile, are used for short- or
function after cardiac surgery, bridging patients to heart trans-
medium-term support. malignancy, and for the larger LVADs, a small body surface
IeZlfZaZe_&eb_^3*1fbgnm^l Pulsatile assist devices provide
plantation, and serving as destination therapy for patients who a pulsatile flow and can area (<1.5 m2).384 Nonetheless, the smaller size and ease of
3. Prostaglandin I2 (PGI2) are notgenerate
transplant a cardiac
candidates. output of 6 to 9 L/min,
• Complications relatedgiven toan single implantation
adequatelung ventilation:of the newer axial flow LVADs make this technology
>g]h`^ghnlikhlmZèZg]bg Studies have
venous shown that
return. the myocardium
Currently, can repair itself
U.S. FDA–approved pulsatile VADs potentially lifesaving for a wide range of patients, including
Lrgma^lbs^] [r ma^ \r\ehhqr`^gZl^ Zkf h_ ma^ ZkZ\ab- during a period of unloading, after which some patients experi-
donic acid metabolic pathway ence aninclude the Abiomed
improvement
Pulmonary
in quality of BVS 5000,
life.375-381 the VADs
Therefore, Thoratec CardiovascularthoseCO2
can VAD System, the withInsufflation
a small body surface area, such as women and
Ihm^gmoZlh]beZmhk be usedNovaco,
for short-and the HeartMate.
or long-term of The
supportEffects HeartMate
the ventricle. The useVE (vented electric) children.369,385
Effects Effects
Bgab[bmlg^nmkhiabeZ\mboZmbhg of VADs as bridges
is the only to cardiac transplantation
mechanical improves the
device currently sur-
approved by the FDA for Because decompensated HF refractory to medical manage-
LmZ[bebs^l\êef^f[kZg^l vival rates and outcomes of patients with decompensated HF.375-383
destination
In addition, evidence therapy.
suggests Hypoxaemia
that long-term support of the leftHypotension ment is the principal feature of candidates for LVAD insertion,
Hypotension
>gaZg\^l frh\Zk]bZe bghmkhir [r Z\mboZmbg` Z]^greZm^
cyclase and increasing intracellular cAMP ventricle withNonpulsatile
a VAD (i.e., an devices
LVAD) isare designed
superior with either centrifugal these patients may have different degrees of end-organ dysfunc-
to optimal
medicalortreatment
axial flow in patterns.
patients withThese pumps
end-stage
Hypercapnia generate
HF who are notcontinuous flow and tionBradycardia
caused by decreased cardiac output and perfusion pressure.
4. Nitric Oxide candidates for heart transplantation. 383
Thus, mechanical circula-Hypertension
Lê^\mbo^ inefhgZkr ]beZmhk4 e^ll ihm^gm maZg bgaZe^] have the advantage of being small,
tory support has become an important tool in the surgical man-
silent, valveless, and fully Sepsis, pneumonia, ischemia, arrhythmias, and uremia secondary
prostacyclin implantable. By working
agement of patients with failing hearts. in concert with the heart, they improve to renal insufficiency are common. Patients also often have reac-
:\mboZm^l`nZgreZm^\r\eZl^ the
Mostposition
VADs can of
Impaired
the left as
be classified ventricle
HPV Arrhythmias
on the Frank-Starling
either nonpulsatile or pul-
Co2 air embolism
curve. The tive pulmonary hypertension caused by chronic elevation of LAP.
Bfikho^lo^gmbeZmbhg&i^k_nlbhg]blmkb[nmbhg satile (Tables
Gh^__^\mhgma^\Zk]bZ\hklmkhd^bg]^q Jarvik60-16
2000and and60-17),
the depending
HeartMate on the
II type
VADs of blood
can produce high flow Heart catheterization should be performed in these patients to
flow that they promote. Alternatively,
Pulmonary when the site of the pumpMediastinal Shift Subcutaneous
<hfie^q Zg] ^qi^glbo^ m^\agheh`r g^\^llZkr _hk lZ_^ rates and generate virtually all of the cardiac
is taken into account, VADs can be categorized as extracorporeal output. They can also obtain information about PVR, the pulmonary vascular response
and effective use operate at lower speeds, Edema Emphysema
which allows the left ventricle to assume to vasodilators, cardiac output, and LV filling pressure.
Ikhehg`^] nl^ \Zg \Znl^ k^[hng] inefhgZkr
vasoconstriction
some of the workload. The Jarvik 2000 is an intraventricular Coagulopathy is common in HF patients receiving VAD
Mhqb\f^mZ[hebm^l3gbmkh`^g]bhqb]^Zg]f^ma^fhèh[bg Box device that is
60-8 Arginine implanted at the LV apex, with the outflow cannula support. Chronic, passive hepatic congestion may coincide with
Atelectasis
Vasopressin
5. Prostaglandin E1 (PGE1) placed in the descending thoracic aorta (Fig. 60-30). The Heart- RV failure and can interfere with coagulation factor–dependent
Endogenous peptide with osmoregulatory and vasomotor
>g]h`^ghnlikhlmZèZg]bg Mate II operates atPneumonia
properties
6000 to 15,000 rpm and provides up to 10 L/ synthetic function. In addition, because prolonged or intermit-
Lrgma^lbs^] [r ma^ \r\ehhqr`^gZl^ Zkf h_ ma^ ZkZ\ab- min of continuous
End-organ effect mediated by
cardiac output. An inflow graft delivers blood tent use of heparin is common in this patient population, VAD-
donic acid metabolic pathway
Ihm^gminefhgZkrZg]lrlm^fb\oZlh]beZmhk V1 receptor present in vascular smoothpump,
from the left ventricle to the
Complications muscle and an outflow
more with Rtgraft delivers
Lung supported supply
as Vascular patients is
have
10%a higher incidence of HIT than other
<e^Zk^]_khfma^\bk\neZmbhg]nkbg`bmlÖklmiZllmakhnà blood
Promotes from the more
vasoconstriction pump to the ascending aorta
compared to the left side.
by activating G protein and (Fig. 60-31). A patients undergoing cardiac surgery do.386,387 Testing for HIT anti-
the lung drivelineC,connects
phospholipase the pump
thereby releasing calcium to
fromthe
theexternal system driver. The bodies in VAD patients, as well as implementing an alternative
sarcoplasmic reticulum
cAMP, cyclic adenosine monophosphate; cGMP, cyclic guanosine
monophosphate; PCWP, pulmonary capillary wedge pressure.
Jarvik 2000 and the HeartMate II are used
V2 receptor present in the distal and collecting tubules
for long-term ventricu- anticoagulation regimen, may lead to desirable outcomes.388 In
lar support as a bridge to heart transplantation.
Promotes water resorption by increasing intracellular levels
addition, VAD systems are known to activate the coagulation,
of cAMP andNot all patients
activating withAadvanced HF are good candidates for thrombolytic, and inflammatory systems,389 and platelet
protein kinase 72 mor-
A cAMP,LVAD support.
cyclic adenosine Contraindications to LVAD placement include phology and function are significantly altered by VAD-induced
monophosphate.
active infection, irreversible renal dysfunction, severe liver surface activation.390
active infection, irreversible renal dysfunction, severe liver surface activation.390
Table 60-17 Nonpulsatile Ventricular Assist Devices
Device Flow Type Length of Support Position Ventricular Support Drive Mechanism
Levitronix CentriMag Centrifugal Short term Extracorporeal LV, RV, BV Electric
Tandem Heart Centrifugal Short term Extracorporeal LV Electric
Impella Axial Short term Extracorporeal LV Electric
Jarvik 2000 Axial Long term Intracorporeal LV Impeller electrically driven
DeBakey LVAD Axial Long term Intracorporeal LV Electric
HeartMate II Axial Short term Intracorporeal LV Electric
BV, biventricular; LV, left ventricular; LVAD, left ventricular assist device; RV, right ventricular.
Table 60-20 The RIFLE* Classification Scheme for Acute Renal Failure Neuroprotection Strategi
Numerous strategies have be
Urine Output
the incidence and severity of
GFR Criteria Criteria
patients. A recent review of
Risk Plasma creatinine increased 1.5× or GFR <0.5 mL/ kg/h × 6 hr ates,234 using methods prom
decrease >25% dence-based recommendatio
Injury Plasma creatinine increased 2× or GFR <0.5 mL/kg/hr × 12 hr strategies with current evide
decrease >50% level, to support their use: e
tions in bypass or surgical te
Failure Plasma creatinine increased 3×, acute <0.3 mL/kg/hr × 24 hr
arterial pressure during CPB,
plasma creatinine ≥350 µmol/L, or or anuria × 12 hr
acute rise ≥44 µmol/L
α-stat pH management durin
a class IIb rating, which Hog
Loss Persistent acute renal failure = complete
loss of kidney function >4 wk “Class IIb: interventions are
ESKD End-stage kidney disease (>3 mo) sidered ‘within’ the standard
cians can choose. Considered
*Acronym for risk, injury, failure, loss, and end-stage kidney disease (ESKD).
GFR, glomerular filtration rate.
by a majority of experts.”
From Kuitunen A, Vento A, Suojaranta-Ylinen R, Pettilä V: Acute renal failure after 73
cardiac surgery: Evaluation of the RIFLE classification. Ann Thorac Surg 81:542-546, Many therapies and strategie
2006. cation in Hogue and colleag
adequate evidence that they p
Anesthesia for Cardiac Surgical Procedures 1957
examining only neurocognitive dysfunction, have reported inci- than conventional magnetic resonance
Dr Azam’s imaging
Notes does and is better 2013
in Anesthesiology
dences approaching 60%.62 A large European study involving able to find multiple, “watershed” lesions.505
Box 60-14moreVasodilators
than 16,000 patients
Available reported
for thethe following of
Treatment injury rates: extremities. Occasionally during the perioperative period, the
OPCAB,
Perioperative 1.9%; CABG, 3.8%; aortic valve operations, 4.8%; CABG
Hypertension
cardiac anesthesiologist
Box 60-15 or surgeon
Aims of and Treatment must toreplace
Modalities Reduce aor peripheral
combined with valve procedures, 7.4%; mitral valve operations, catheter
Prevent(e.g., insert a femoral
the Development arterial catheter)
of Postoperative to ensure that the
Renal Dysfunction
Adenosine8.8%; and multiple-valve procedures, 9.7%.61 effects of vasoactive therapy are monitored accurately.
The impact of surgery-related CNS injury is profound. In 1. Maintain adequate oxygen delivery—by ensuring
α1-Adrenergic antagonistsdatabase study of 10,860 cardiac surgical
a single-institution adequate cardiac output, adequate oxygen-carrying
patients,agonists
those who had overt perioperative strokes had survival capacity, and proper hemoglobin saturation
α2-Adrenergic Renal Insufficiency
rates of 64% at 1 year and 44% at 5 years, whereas patients who 2. Suppression of renovascular constriction—by ensuring
Angiotensin-converting enzyme strokes
did not have perioperative inhibitors
had (enalaprilat)
survival rates of 94% at 1 adequate volume preload and use of infusions of mannitol,
year and 81%
Angiotensin II antagonistsat 5 years. 503
The impact of stroke on health care Perioperative renal
calcium entry dysfunction,
blockers, when it occurs, can have serious
and angiotensin-converting
resource utilization is also a cause for concern. Roach and col- consequences. In a multicenter study of more than 2000 patients
enzyme inhibitors
Atrial natriuretic peptide (nesiritide)
leagues56 found that 47% of patients who had a type I neurologic who underwent
3. Renal coronarydopaminergic
vasodilation—by revascularizationagents,with or without val-
β2-Adrenergic agonists
event (stroke or transient ischemic attack) were discharged from vularprostaglandins,
surgery, Mangano and atrialand coworkers
natriuretic peptide83
found postoperative
the hospital to acalcium
skilled nursing
channelfacility or rehabilitation center. renal dysfunction in 7.7%, including
Dihydropyridine-type blockers* 4. Maintain renal tubular flow—by loop30 (1.4%)and
diuretics patients in whom
Furthermore, 30% of patients with more subtle neurocognitive
Dopamine agonists(type II event) after cardiac surgery were discharged
dysfunction
dialysis was needed.
mannitol In that
(which may study,
act to preventmortality
tubular was higher in patients
obstruction,
to such facilities versus 8% without type I or type II events. Given with ARF requiring dialysis (63%) and those with
which can cause cellular swelling, ischemia, and renal dysfunc-
death)
Hydralazine
that the clinical manifestation of cerebral injury is primarily a tion
5. (19%)
Decrease than in patients
oxygen demand—by who hadthe useneither
of loop (0.9%). Additionally,
diuretics
Nitrovasodilators*
postoperative diagnosis, often with potentially irreversible and with
patients mild cooling
postoperative renal failure had significantly longer
neurologic sequelae
Phosphodiesterase enzymeand significant consequences for resource
inhibitors hospital and ICU
6. Attenuate staysreperfusion
ischemic than did patients
injury—as who had of
a result nothe
renal failure
utilization, preoperative risk stratification and intraoperative release of oxygen free radicals and calcium ions
or dysfunction in the postoperative period. Bove and associates,81
Prostaglandins
management are important focal points for efforts to ameliorate in From
a study of Kidney
moredysfunction
than 5000 patients who period.
underwent cardiac
Sear JW: in the postoperative Br J
and reduce CNStherapies
dysfunction and injury within
use tothe cardiac surgi-
A *Intravenous
cal
vasoactive
population.
in widespread treat surgery with
Anaesth CPB, found
95:20-32, 2005. that 1.9% required postoperative dialysis
perioperative hypertension.
and had an in-hospital mortality of 64%.
From Levy JH: Management of systemic and pulmonary
hypertension. Tex Heart Inst J 32:467-471, 2005. Preoperative risk factors that are commonly associated
with postoperative renal dysfunction after cardiac surgery include
preexisting renal insufficiency,500,501 type 1 diabetes mellitus, age
Because arterial vasoconstriction plays an important role older than 65 years, major vascular surgery, arteriopathy, genetic
in the development of hypertension after cardiac surgery, the predisposition, and recent exposure to nephrotoxic agents, such
therapeutic agent chosen should usually be one that effectively as radiocontrast dyes, bile pigments, aminoglycoside antibiotics,
reduces hypertension. Sodium nitroprusside, a nonspecific venous and nonsteroidal anti-inflammatory drugs. Also, several intraop-
and arterial vasodilator, is a common choice. However, theoreti- erative factors may predispose a patient to renal dysfunction,
cally, nitroprusside can cause coronary steal.497 Furthermore, in including the need for emergency surgery,81 CPB time 74 exceeding
76 501
patients with renal failure, elimination of sodium nitroprusside is 3 hours, and poor cardiac function. Other perioperative risk
Drreduced, thus in
Azam’s Notes making the patient
Anesthesiology 2013vulnerable to the toxic effects factors for renal dysfunction after cardiac surgery are hypovo-
nt
edema in patients with decreased myocardial reserve. Reactive
therapy hyperemia in tissues and organs distal to the clamp and
n V Adult Subspecialty Management

Use of vasodilator
Use of diverting circulatory support Dr Azam’s Notes in Anesthesiology 2013
Therapeutic Box 62-1Strategies
Physiologic Changes with Aortic Cross-Clamping* Degree of periaortic collateralization
Patients with preexisting impaired ventricular function
and Therapeutic Interventions and
Left ventricular function
Box 62-3 Physiologic Changes with Aortic Unclamping* and
Status of the coronary circulation
reduced coronary
Hemodynamicreserve Changes are most vulnerable to the stress Therapeutic Interventions
↑ Arterial Volume status
imposed on the cardiovascular
blood pressure abovesystemthe clampby aortic cross-clamping.
↓ Arterial blood pressure below the clamp Neuroendocrine activation
Rational therapeutic strategies to prevent the deleterious effect of Hemodynamic Changes
Duration of aortic cross-clamping
↑ Segmental wall motion abnormalities
aortic cross-clamping primarily
↑ Left ventricular wall tension
include measures to reduce after-
Body temperature ↓ Myocardial contractility
load, normalize
↓ Ejectionpreload,
fraction and maintain cardiac output. Vasodila- ↓ Arterial blood pressure
tors, positive and
↓ Cardiac output negative
† inotropes, and controlled volume
↑ Pulmonary artery pressure
depletion ↓(i.e.,
Renalphlebotomy)
blood flow may be used selectively. response to aortic cross-clamping at any level. The increase in
Patients withocclusion
↑ Pulmonary impaired
pressureventricular function requiring ↓ Central
arterial blood pressure venous
above the clamp ispressure
primarily due to the
sudden increase in impedance to aortic blood flow and the result-
supraceliac aortic cross-clamping are the most challenging.
↑ Central venous pressure
ant Myo- ↓ Venous
increase in systolic return
ventricular wall tension or afterload.
↑ Coronary blood flow
cardial ischemia, reflecting an unfavorable balance between However, factors such as myocardial contractility, preload, blood
↓ Cardiac output
volume, and activation of the sympathetic nervous system may
myocardial oxygen
Metabolic supply and demand, may result from
Changes the
also be important.97 Cross-clamping of the aorta at or above the
↓ Total-body oxygen consumption
hemodynamic consequences of aortic cross-clamping. Control- diaphragm resultsMetabolic Changes
in the most profound increases in arterial
↓ Total-body carbon dioxide production
led (i.e., slow clamp application) supraceliac aortic blood
cross-clamp- pressure ↑
unlessTotal-body
diverting oxygen
circulatory consumption
support or intrave-
↑ Mixed venous oxygen saturation nous vasodilators are used.
ing is important
↓ Total-bodyto oxygen
avoidextraction
abrupt and extreme stress on the heart. Changes in ↑ Lactate
cardiac output and filling pressure with aortic
Both afterload and preload
↑ Epinephrine reduction is often required. Afterload
and norepinephrine cross-clamping are not consistent and require an integrated
↓ Mixed venoustheoxygen
approach in an attempt to understand direction saturation
and magni-
reduction,Respiratory
most commonly alkalosis‡ accomplished with the use of tude sodium
of such changes (Fig. 62-5). Cross-clamping of the proximal
↑ Prostaglandins
nitroprusside (predominantly
Metabolic acidosis an arteriolar dilator), is necessary descending thoracic aorta increases mean arterial, central venous,
mean pulmonary ↑ Activated
arterial, complement
and pulmonary capillary wedge pres-
to “unload” the heart
Therapeutic and reduce ventricular wall tension.
Interventions In a
sure by 35%, 56%, 43%, and 90%, respectively, and decreases the
Afterload reduction
large series of patients
Sodium requiring cross-clamping of the descend-
nitroprusside cardiac index by 29%.↑ Myocardial
Heart rate and depressant factor(s)
left ventricular stroke work
ing thoracic Inhaled
aorta,anesthetics
stable left ventricular function was maintained are not significantly changed. Supraceliac aortic cross-clamping
↓ Temperature
increases mean arterial pressure by 54% and pulmonary capillary
with sodiumAmrinone
nitroprusside during
Shunts and aorta-to-femoral bypass
cross-clamping. Sodium nitro-
wedge pressure by 38%.98 Ejection fraction, as determined by
Metabolic acidosis
prusside allowed adequate intravascular volume before unclamp-
Preload reduction
two-dimensional echocardiography, decreases by 38%. Despite
normalization of systemic and pulmonary capillary wedge pres-
ing, which resulted in stable unclamping hemodynamics, although
Nitroglycerin
sure with anesthetic Therapeutic Interventions
agents and vasodilator therapy, supraceliac
Controlled phlebotomy
isoflurane can provide hemodynamics
Atrial-to-femoral bypass
comparable to that
aorticpro-
cross-clamping↓ Inhaled anesthetics
causes significant increases in left ventricu-
vided by Renal
sodiumprotectionnitroprusside during thoracic aorticlar end-systolic and end-diastolic area (69% and 28%, respec-
cross- ↓ Vasodilators
tively), as well as wall motion abnormalities indicative of ischemia
102
clamping, Fluid Though
administration not widely used, amrinone provides in 11 of 12 patients (Table 62-6). Aortic cross-clamping at the
Distal aortic perfusion techniques ↑ Fluidsimilaradministration
hemodynamic control equivalent to that of sodium nitroprusside
Selective renal artery perfusion
suprarenal level causes but smaller cardiovascular changes,
128 and clamping at ↑ theVasoconstrictor
infrarenal level is associated
drugs with only
during abdominalMannitol aortic surgery. A normal preload isminimal equally changes and no wall motion abnormalities.
important and Drugsinvolves careful
to augment renal fluid titration and vasodilator
perfusion The marked Reapply
increasescross-clamp
in ventricular for severe
filling hypotension
pressure
Other (preload) reported with high aortic cross-clamping have been
administration. Nitroglycerin is commonly used in thisattributed
Hypothermia
settingto bloodConsider mannitol
volume redistribution and increased afterload.
because it increases venous capacity to a greater extent
↓ Minute ventilation thansubstantial body of evidence supports the hypothesis of
The most
Consider sodium bicarbonate
sodium nitroprusside
Sodium bicarbonate does. Infusion of nitroglycerin blood during
volume redistribution during thoracic aortic cross-clamp-
*These changes are of greater significance with longer duration of
abdominal cross-clamping
aortic surgery and withmaintains ventricular functionblood
more proximal cross-clamping.
ing. The splanchnic*These
during
circulation,
changes are ofsource
an important greaterof functional
significance with longer duration of A
volume reserve, is central to this hypothesis.
cross-clamping and with more The splanch-
proximal cross-clamping.
†
Cardiac output may increase with thoracic cross-clamping. A
the cross-clamp
‡ period.
When ventilatory settings are unchanged from preclamp levels.
nic organs contain nearly 25% of the total blood volume, nearly
two thirds (>800 mL) of which can be autotransfused from the
75

fromtube,
cheal one compartment
or gas trapping to another
as a result (or into the surgical field)These
of bronchospasm. (see isoflurane, the clinician
desflurane, should andasksevoflurane
whether a are subdural or ext
probably
Dr Azam’s Notes in Anesthesiology 2013 n
V Fig. 63-1),
events also with resultant
should be sought mechanical
and remedied. injury Most to brain tissue, or cant to
practitioners hematoma
the clinician. is present
The net on the
CBF contralateral side that w
effect of introducing
reduction in perfusion pressure, leading to ischemic injury.
either immediate bur holes or immediate postpro
carefully maintain paralysis during craniotomies, unless a anesthetic depends on the interaction of several factors,
Several variables can interact to cause or aggravate intra- radiologic evaluation.
contraindication is present, because
Myocardial
a sudden cough Myocardial
can result the concentration of the anesthetic, the extent of prev
cranial hypertension (Fig. 63-4). For clinicians faced with the
oxygen demand oxygen supply 2. The CSF compartment: There is no pharmacologic m
in dramatic herniation of cerebral structures through the depression, simultaneous blood pressure changes actin
problem of managing Heart increased
rate ICP, Coronary
the objective
blood flow is, broadly O2 content lation of the CSF space, the time course and magn
craniotomy.
speaking, to reduce theContractility volume of the intracranial
Diastolic volume Heart rate contents. For
Hematocrit
junction with previous or anesthetic-induced auto
which are relevant to the neurosurgical operating
Thereafter, the anesthesiologist should
Diastolicconsider
volume O2 saturation abnormalities, and simultaneous changes in Paco2 in co
the arterial
mnemonic purposes, the
Bloodclinician
pressure can divide the intracranial The only relevant means for manipulating the size
side of the circulation.
space into four subcompartments (Table Attention to the effect
Coronary
63-1):
Coronary
of anesthetic
vasoconstriction
cells (including
thrombosis
drugs with any disease-related
compartment is by impairment
drainage. A tight 2 responsiv
in COsurgical field
and techniques on cerebral blood
neurons, glia, tumors, and extravasatedMyocardial flow (CBF)
collections (see Chapter
of blood), fluid 13) is Nitrous oxide (N O) is also
times can be improved by passage of a brain needl
2 a cerebral vasodilato
ischemia
an(intracellular
established part of neuroanesthesia.
and extracellular), CSF, and blood. Such attention is relevant effect of whichinto
surgeon is the most profound
a lateral ventricle towhendrainit CSF.
is admini
Lumb
because
Figure increases
62-18 Determinants in CBF
of myocardial generally
oxygen are
supply and demand associated with
that lead to myocardial increases
ischemia. sole anesthetic,
During the perioperative and
period, virtually every
drainage
determinant is altered by factors such as fluid shifts, blood loss, pain, catecholamines, altered coagulability, and ventilatory insufficiency. can
(Adapted frombe
least when it is administered
used to improve surgical exposure
Beattie
again
1-3
inFleisher
C, cerebral blood
LA: Periopeative volume
myocardial (CBV).
ischemia and infarction. The notable
Int Anesthesiol exception
Clin 30:1-17, 1992.) to this
ations with no substantial hazard of uncal or transf
rule occurs in the context of cerebral ischemia caused by
diate attention. Conventional practice is to monitor all vascular and cardiac morbidity; therefore, bodymagnum hypo- temperatureherniation.
should be
tension
surgery
Table 63-1 or vessel
patients in an occlusion,
ICU
Intracranial setting after
Compartments at which
surgery. Sometimes CBV
centers
and Techniques for may
carefully increase
monitored
Manipulation of as
and controlled in
3.
Table
all vascular
The
63-2 fluidsurgery
Factors
patients.
compartment:
That InfluenceThis compartment
Cerebral Blood Flow*can be ad
have set up specialized vascular step-down units in which lower- In a prospective randomized trial, the relative risk for early post-
theTheir
risk cerebral
Volume
patients can bevasculature dilates
evaluated frequently by in response
specialized nursingto aoperative
suddencardiac reduction
morbidity was reduced with steroids
by 55% and diuretics. The use of these agent
when normo-
in CBF.
staff. Thehowever,
There are, relationship generally
no clinical trials to support applies, however,
this practice, thermiaand attentionby use ofPao
was maintained 2 cussed
a forced-air subsequently.
warming system.165
and Compartment
most centers admit all vascular surgery patientsVolume
to the control of CBF is relevant in tosituations
postoperatively.
the ICU In theMethods
Control
a in
twofold
early postoperative period,
which volume
to threefold
vascular surgery patients have
Paco
4. 2The
greater incidence blood compartment:
of myocardial ischemia This is the compartme
compensation
Myocardial
Cells (including mechanisms
ischemia
neurons,and glia,
cardiac are exhausted,
morbidity
tumors, occur most
Surgical orwhenICP
removal is already
core temperature Cerebral
is less than 35°C. 166 metabolic rate
receives
Even mildthehypother-
anesthesiologist’s greatest attention be
frequently in the postoperative period. Patients should be care- mia of approximately 35°C is Arousal/pain
associated with a 200% to 700%
increased. The general
and extravasated blood) approach is to select anesthetics and
fully monitored for signs and symptoms of ischemia, but up to increase in norepinephrine levels,163,506
is the most
generalized
amenable
vasoconstric-
to rapid alteration. The bloo
Seizures
control
90% of these
Fluid the
episodesphysiologic
(intracellular areand
asymptomatic. parameters
extracellular)
501-505
in a manner
The determinants
Diuretics
507
tion, and that avoids
increased blood pressure inpartment
postoperativeshould
patients. be considered as two separate
163
Temperature
unnecessary
of myocardial oxygen increases
supply and indemand
CBF. shouldThe parameters
be optimized that influence
Shivering occurs and CBF
increases total-body nents:oxygen venous and arterial.
consumption,
for all patients (Fig. 62-18) to prevent ischemia beforeSteroids it develops.(principally
but onlytumors)
by about 40% in the typical Anesthetics
elderly vascular patient.152
are listed
β-Blocker andin Table
statin 63-2
therapy andbeare
should discussed
continued throughout in Chapter It is13.
important to control the stresspressure/status
Blood response in the postop- of autoregulation
the CSFpostoperative period. Dysrhythmias may beDrainage secondary erative period. This includes preventingWe suggest
the potential giving
triggers for first consideration to the venous
to ischemia or to sympathectomy associated with regional myocardial ischemia (pain, anemia, hypothermia, hemodynamic
Vasoactive agents
Arterial blood
anesthesia. Decrease CBFextremes, and ventilatory insufficiency). the Anesthetics
circulation. It is largely a passive compartment tha
In mechanically venti-
Selection
Besides myocardialof Anesthetics
ischemia and cardiac morbidity, other lated patients, the weaning period quently
isPressors overlooked.
especially Passive though it is, engorgement
stressful, and myo-
Venous blood coagulopathy, either from residualImprove cerebral venous drainage
compartment
Inotropes is a common cause of increased ICP or poor
508
problems include heparin or cardial ischemia occurs frequently during this time. Careful
from dilutional coagulopathy after massive transfusion. Even in sedation and expeditious weaning are desirable. When possible,
The
theCBF, question
cerebral
absence of flow;
blood which
of coagulopathy, CSF, anesthetics
cerebrospinal
bleeding through fresh are vascular
fluid. appropriate, extubation especially in room
in the operating tions instressful
the surgical
is Vasodilators
less field (Fig. 63-5). A head-up posture to
and is preferable
anastomoses may occur when significant postoperative hyperten- for carotid and lower extremity Blood vascular
viscositysurgery patients.
the context of unstable ICP, arises often. Chapter 13 provides rel-
sion is untreated. Hypovolemia occurs after aortic surgery as a For more invasive surgical procedures (TAA and abdominal
Neurogenic pathways (intra-axial and extra-axial)
evantof significant
result information in fluid
third-space detail,loss andandbleeding.
only Hypovo-
broad generalizations are
aortic aneurysm), postoperative mechanical ventilation is usually
lemia may lead to hypotension and hypoperfusion of the coro- necessary. 76
offered here. Generally, intravenous
nary arteries or lower extremity vascular grafts. Graft occlusion
anesthetic, analgesic, and *See Chapter 13 for detailed discussion.
Vascular surgery continues to challenge the anesthesiolo-
Dr Azam’s
in the lower Notes in Anesthesiology
extremities occurs in 3% to 2013
10% of patients27,28,323 gist, given the significant physiologic stress superimposed on a
after lower extremity or aortic surgery and should be recognized relatively elderly patient population with a high incidence of
however. Expired nitrogen analysis is theoretically Neurosurgicalattractive.
AnesthesiaThe 2049encourage the use of alternative access sites. Access to the brachial
expired nitrogen concentrations involved in anything less than Dr Azam’s Notes in Anesthesiology 2013
esser
catastrophic
Table 63-4VAE are very
Methods small,
for Rapid however,
Reduction and pushPressure
of Intracranial the available
and
apter Brain Volume*
instrumentation to the limits of its sensitivity (see Fig. 63-11).105 Table 63-6 Management of an Acute Air Embolic Event
anes- Figure 63-12 of shows
Further titration Paco2 the
(≥25 physiologic
mm Hg) and monitor response Prevent further air entry
mum to an air embolic event. Table 63-6 presents
CSF drainage (ventriculostomy, brain needle) an appropriate man- Notify surgeon (flood or pack surgical field)
mpo- agement response
Diuresis (usuallytomannitol)
such an event. Jugular compression

with CMR suppression (barbiturates, propofol) Lower the head
gencyRight Heart Catheter
MAP reduction (if dysautoregulation) Treat intravascular Air
they
Essentially all patients who undergo sitting posterior fossa pro-
Surgical control (i.e., removal of bone flap or lobectomy) Aspirate right heart catheter
ma,cedures
a *Aftershould
reviewhave
of the achecklist
right heart
in Tablecatheter.
63-3. Although catastrophic, Discontinue N2O
ictim
life-threatening VAE is rate;
CMR, cerebral metabolic relatively uncommon,
CSF, cerebrospinal a mean
fluid; MAP, catheter
arterialthat Fio2: 1.0
sulci
permitspressure.
immediate evacuation of an air-filled heart occasionally Pressors/inotropes
omi- Chest compression
is the sine qua non for resuscitation. The latitudes are much wider
a are
essed CSF drainage was discussed earlier. The use of additional
cs are osmotic diuretics is theoretically limited by an upper acceptable
osur- osmolarity limit of approximately 320 mOsm/L. In extremis, the
(in a use is frequently empirical, however, and repeated doses (e.g.,
ently 12.5 g) are administered until a clinical response is no longer
ential observed. Barbiturates have long been the most widely used drugs
m the for inducing a reduction in CMR, with the objective of causing a
coupled reduction in CBF and CBV. Propofol is gaining popular-
ential ity for this application. Although the use of barbiturates is sup-
given ported by intensive care unit (ICU) experience showing efficacy
es in in ICP control7 (if not outcome), no such experience has been
an be accumulated for propofol. A frequently fatal syndrome of meta-
(and bolic acidosis and rhabdomyolysis has been recognized in patients
nces, who have received prolonged propofol infusions in the ICU.8,9
urgi- MAP reduction occasionally reduces vascular engorgement and
rhage reduces total brain bulk, but should be applied with extreme
n for caution if patients have compromised intracranial collateral cir-
lcho- culation. This approach is most likely to be relevant in the event
y and of dysautoregulation occurring in the context of resection of arte- 77
riovenous malformations (AVMs) (see the later section on aneu-
on of rysms Dr Azam’sand Notes in Anesthesiology
arteriovenous 2013
malformations).
ncidence and severity of the problem. Prior surgical practices surgery
is slightlyis hyperosmolar
deferred, and with TCD,
respect angiography,
to plasma (295or Dr other
mOsm/L).
Azam’s imaging
ItNotes in is Anesthesiology 2013
ntailed maintaining the patient
Table 63-7 Relative Indicationsatforbed rest until
Intra-arterial approximately
Pressure Monitoring
has
performed.the disadvantage
175-177 that
Confirmed129 in large volumes it can cause
vasospasm is commonly treated with a hyper-
ay 14, when the period of spasm risk had passed. Early aneu- chloremic
the “triple metabolic
H” therapy acidosis.
described Theinphysiologic
the next significanceand
paragraph of some-
Table 63-8 World Federation of Neurosurgeons (WFNS)
this acidosis, which involves the extracellular, but not the intracel- Subarachnoid to that which occu
ysm clippingElevated
reducesICP
the period of hospitalization and reduces times
lular,by balloon
fluid space, isangioplasty or intra-arterial
unclear. At a minimum, it has thevasodilators.
potential to
Ischemia or incipient ischemia of neurologic tissue
he incidence of the medical complications (e.g., deep vein throm-
Hemorrhage
Forthe
Scale
patients proceeding to surgery,
drome is characte
Recent SAH confuse diagnostic picture when acidosis CPP should
is present. As be a main-
osis, atelectasis, pneumonia) associated with a lengthy period of tained intraoperatively in predominately
aGCS
high-normal range.Ringer’s
Despite the former contraction, and h
Recent head injury WFNSresult,Grade
many clinicians use Score lactated Motorsolu- Deficit
nforced bed rest.
Recent spinal cord injury
popularity
tion. Although of lactated
inducedRinger’shypotension,
solution (273 themOsm/L)
potential for induced
theoreti- L). The distinction
Intended or potential temporary vessel occlusion
Early intervention can make the surgeon’s task more diffi- I cally is not ideal for individual
hypotension to cause or aggravate 15 replacement of blood and
cerebral ischemia Absent
third
in a patient tant. SIADH, whic
Circulatory instability
ult. The brainTrauma
in the early post-SAH period is likely to be more with
II
spacesomeloss ordegree
insensible of losses,
vasospasm
14-13
it servesisasnow a reasonable
recognized.compro-
Absent
178,179
This hypervolemia, is
mise for meeting both needs simultaneously and is very suitable wasting is associa
dematous than after
Spinal cord a 2-week
injury delay. A mild degree of hydro-
(spinal shock) concern
in most extends
instances. even
It is tohypo-osmolar
a a patient classified
fluid, as World
however, and Federation
in a
Sitting position
ephalus is common after blood contaminates the subarachnoid III
of Neurosurgeons
healthy experimentalgrade
14-13
animal,Iit who maytohave
is possible reduceregions
Present
serum osmo- of cerebral Fluid restriction a
Possible barbiturate coma
pace. Ten percent toinduced
Possibility of 20% hypotension
of SAH patients may require CSF ischemia 41
that arecerebral
IVlarity and produce subclinical 12-7 when
edema with a the
largepatient
volume is normotensive.
ofPresent
lactatedor absent cially deleterious
iversion at some point
Possibility in their
of induced course.167 Early intervention also
hypertension Ringer’sIn solution.
the ICU, 128
the
In theregimens employed fluid
setting of large-volume to treat vasospasm
adminis- avoided. Although
V tration (e.g., significant blood6-3 loss, multiple trauma), we Present or absent
alternate, causes of hyponat
may enhance the risk of intraoperative aneurysmal rupture
Anticipated/potential major blood loss
usually involve some combination of hypervolemia, hemodilu-
Aneurysm clipping
ecause of the Arteriovenous
shorter period of time for clot to organize over the liter by
tion,Glasgow
GCS,
liter,
and Coma lactated
hypertension.
Scale.
Ringer’s solution and normal saline.
The science behind hypervolemic- drome) may be di
malformations The crystalloid versus colloid discussion is a recurrent one.
te of the initial bleed.
Vascular tumors All of this places a substantial premium This discussion usually arises in the context of a head injury istration of isoton
n techniques designed to major
Tumors involving reduce thesinuses
venous volume of the intracranial victim.
Table 63-9Although
Hunt-Hess there are numerous
Classification fervent Status
of Neurologic beliefsafter
regarding the end point.
Craniofacial reconstruction
ontents (see the section on control of intracranial pressure and
Extensive craniosynostosis procedures 10 to 14
this days
issue,
Subarachnoid theretohas
be been
Hemorrhage safely only beyond
a singlethe period of that
demonstration maximal
the vaso-
rain relaxation) to facilitate
Anticipated exposure
light anesthesia and minimize retraction
without paralysis reduction of colloid oncotic
spasm risk (i.e., days 4 to 10 post-SAH). pressure in the absence of a change Vasospasm. Th
ressures. of osmolarity
GradeThe rationale can contribute to an augmentation
Criteria* for early intervention is severalfold. First, the of cerebral
Brainstem manipulation/compression/dissection vasospasm has oc
Anticipated cranial nerve manipulation (especially CN V) edema in the setting of experimental head injury.130 The transcap-
Advantageous for postoperative intensive care sooner
I illary the aneurysm
membrane pressure
Asymptomatic, is clipped
orgradients
minimal orheadache
obliterated,
that can be the less
andproduced
slight nuchal likelihood
by rigidity been undertaken.
reoperativeHypervolemic
Evaluation therapy of reduction
rebleeding (and rebleeding
of colloid oncotic pressure is the areprincipal
very smallcause comparedof death for breakdown produ
Many patients Head
scheduled
injury for intracranial aneurysm clipping come IIwith those created
patients hospitalized Moderate to severe
after SAH
by changes headache,
165
in serum nuchal
). osmolarity.
Second, therigidity, no deficit
management
Nonetheless, other
of accumulated aroun
irectly from the ICU,
Diabetes and elements of their management in the
insipidus it seems that than cranial
those small nerve palsy
gradients have the potential—probably
the ischemia caused by vasospasm involves volume loading and A specific mechan
Incidental cardiac disease
CU may influence their immediate preoperative status. IIIin the setting
induced
of a blood-brain
hypertension.
Drowsiness, barrier
or mildinjury
Early occlusion
confusion, of intermediate
focalofdeficit
the aneurysm elimi- current A focus is on
CN, cranial nerve; ICP, intracranial pressure; SAH, subarachnoid hemorrhage. severity—to augment edema. It seems reasonable then to select a
nates
IV the risk of rebleeding
Stupor, moderate to severe associated with possibly
hemiparesis, this therapy.
early Vaso- lin A receptor anta
luid Management. Some patients develop the syndrome of
spasm seems to be related
decerebrate to and
rigidity the vegetative
presencedisturbances
of blood in the basal of established vaso
nappropriate secretion of antidiuretic hormone (SIADH) after
cisterns in the vicinity of the circle of Willis. Some of this blood dence of new infar
AH and are appropriately managed with fluid restriction. V Deep coma, decerebrate rigidity, moribund appearance
can be removed at the time of the aneurysm clipping, and intra- preliminary repor
However, hyponatremia after SAH is more likely to be the result
f the cerebral salt-wasting syndrome, which probably occurs as
cisternal fibrinolytics
*Serious systemic diseases, such(foraswhich therediabetes,
hypertension, is limited
severe proof of effi- related hypoperfus
arteriosclero-
result of the release of a natriuretic peptide by the brain (similar

sis, chronic
cacy 166 pulmonary disease, and severe vasospasm seen on arteriography,
) can be administered. Early operative clipping not only
result in placement of the patient in the next less favorable category.
WhenAthere
makes the therapy of vasospasm safer, but also may reduce the because of a chan
incidence and severity of the problem. Prior surgical practices surgery is deferred
175-177
entailed maintaining the patient at bed rest until approximately performed. 78
C
day 14, when the period of spasm risk had passed. Early aneu- the “triple H” ther
Dr Azam’s Notes in Anesthesiology 2013 rysm clipping reduces the period of hospitalization and reduces times by balloon a
the incidence of the medical complications (e.g., deep vein throm- For patients
into cells or K+ secretion in the distal nephron. there is anySeveral drugs are
uncertainty lipid insoluble
regarding the airway or or
arethehighly ionized
cervical spine, in the
direct laryngoscopy (with vigorous atlanto-occipital extension)
Cardiac
Table 63-10 Glasgow and
Coma Pulmonary Manifestations
Scale should probably be avoided, unless the exigencies of airway
Hypertension is a common complication of CRF and control ESRD. demand it (which often is the case). The nasal route can
Eyes open Never
Because hypervolemia 1
is the major cause of hypertension in Table if 65-7 Management Guidelines for Correction of Anemia of Chronic
be considered the clinical context warrants, bearing in mind that
uremia, normotension is usually restored by the use of diuretics
To pain 2 Renal Disease
risk of infection may be increased with skull base fracture and CSF
in predialysis patients or by dialysis in ESRD patients.
To speech 3 Despite Erythropoietin
leak. The anesthesiologist needs to use discretion (e.g., in the pres-
therapy, patients continue to be hypertensive because
Spontaneously 4 of the
vasodilators required for the management of overwhelming ence of anStarting
obvious facial smash, the 50-150
dosage nasal route
U/kg/wkshould
IV or SCbe avoided
(once, twice, or
Best verbal responses None 1
hyperreninemia. Patients generally have left ventricular hypertro- because of the possibility of entering the cranium)
three times per and
week)be sensitive
Garbled/incomprehensible sounds
phy and accelerated atherosclerosis (disordered glucose and
2 to unusual
fat resistance
Target in passing the11-12
hemoglobin endotracheal
g/dL tube.
metabolism). Pericarditis can be observed in underdialyzed When a hypnotic muscle-relaxant sequence is used, the
Inappropriate words 3
Optimal rate of correction Increase hemoglobin by 1-2 g/dL over 4 wk
Confused but converses 4
patients versus patients with CRF who undergo regular dialysis. standard approach includes the use of cricoid pressure and in-line
Oriented
A unique form of pulmonary congestion and edema 5 axial
maystabilization.
DarbepoetinIn-line
alfa traction previously was favored, but has
occur even None
Best motor responses in the absence of volume overload and been supplanted
1 is associated by stabilization because
Starting dosage 0.45 µg/kgof administered
the perceived riskIVofor SC
as single
with normalExtension
or mildly(decerebrate
elevated intracardiac
rigidity) and pulmonary
2 overdistraction
capil- and cord injury in the eventonce
injection of weekly
gross instability.
lary wedge Abnormal
pressure. flexion
This entity, characterized
(decorticate rigidity) The
radiologically
3 bylargest of the clinical series that concluded that
0.75 µg/kg administered oral
as aintuba-
single IV or
peripheral vascular
Withdrawal congestion giving rise to a “butterfly
4 wing”
tion with anesthesia and relaxation is SC reasonable 227
used
injection once every in-line
2 wk
distribution,Localizes
is due topain
increased permeability of alveolar5 capillary
stabilization with the patient’s occiput held firmly on the back-
Target hemoglobin 12 g/dL
membranes.Obeys
This “low-pressure”
commands
pulmonary edema6
and the car-
board, limiting the amount of “sniff ” that was feasible (Fig. 63-15).
diopulmonary abnormalities associated with circulatory overload Optimal rate of correction Increase hemoglobin by 1-2 g/dL over 4-wk
There is no question that in-line stabilization, properly performed,
Total usually respond promptly to vigorous dialysis.9 3-15 period
makes laryngoscopy more difficult, but it decreases the amount
Iron
Hematologic Manifestations Monitor iron stores by TSat and serum ferritin
CRF usually causes a normochromic, normocytic anemia. Anemia If patient is iron-deficient (TSat <20%; serum ferritin <100 g/L), administer
is generally observed when the GFR decreases to less than 30 mL/ iron, 50-100 mg IV twice per week for 5 wk; if iron indices are still low,
min and is due to insufficient production of erythropoietin by the repeat the same course
diseased kidneys. Other factors are iron deficiency, either related If iron indices are normal but hemoglobin is still inadequate, administer IV
to or independent of blood loss from repeated laboratory testing, iron as outlined above; monitor hemoglobin, TSat, and ferritin.
Withhold iron therapy when TSat >50% or ferritin >800 ng/mL (>800 g/L)
blood retention in the dialyzer, or gastrointestinal bleeding.10
A Treatment of anemia with iron, darbepoetin alfa, and human IV, intravenously; SC, subcutaneously; TSat, percent transferrin saturation.
79

V 2080 Adult Subspecialty Management Dr Azam’s Notes in
Table 63-14 Common Pediatric Neurosurgical Disorders and Anesthetic Considerations
Age Group Lesion Pathogenesis Anesthetic Considerations
Neonates Intraventricular hemorrhage Subependymal vascular rupture Associated problems of prematurity

Depressed skull fracture Forceps injury Associated cerebral edema
Infants Hydrocephalus Varied Increased ICP, especially dangerous in shunt-dependent

revisions
Meningocele Outpouching of meninges through skull defect Large size creates airway management problems
Prone or lateral position
Substantial blood loss
Repair may increase ICP
Encephalocele Outpouching of meninges through skull defect
with brain tissue enclosed
Myelomeningocele Protrusion of spinal meninges and roots Prone or lateral position
through spina bifida Substantial blood loss
Respiratory restriction after covering large defects
Arnold-Chiari malformation Impaction of posterior fossa contents into Brainstem compression with head flexion
foramen magnum
With or without hydrocephalus Increased ICP
Latex allergy
With or without myelomeningocele Postoperative respiratory depression
Craniosynostosis Premature cranial suture fusion Substantial blood loss
Air embolism
Supine or prone position
Craniofacial dysostosis Developmental abnormality Lengthy procedures
Substantial blood loss
Brain retraction
Air embolism
Endotracheal tube damage
Vascular malformations Varied Congestive heart failure
Large blood loss
Elective hypotension
Subdural hematoma/effusion Trauma Associated injuries
Older children Posterior fossa tumors Ependymoma Malnutrition/dehydration

Astrocytoma Hydrocephalus
Increased ICP
Prone or sitting position
Air embolism
Brainstem compression
Postoperative cranial nerve dysfunction or brainstem
swelling or compression
ICP, intracranial pressure.
80

of 30 to 34.9 kg/m2), class 2 (35 to 39.9 kg/m2), and class 3 (40 to HDL levels, and hypertriglyceridemia.
Dr Azam’s Specific
Notes in Anesthesiology 2013 d
2 2
49.9
Table kg/m
64-2 ). Patientsandwith
Waist Circumference Risk a BMI of 50 kg/m or greater are con- are presented in Table 64-4. Weight gain with vi
sidered superobese. AsBody BMI increases beyond normal weight, the
2
Mass Index (kg/m )
major predictor of metabolic syndrome. The
08
97
risk of serious health problems developing rises greatly (Table
Waist uses waist circumference rather than BMI to d
Circumference Normal Weight Overweight Obese Class 1
86 64-2). Malnourishment and malnutrition are commonly offered mass component contributing to metabolic sy
<102 cm (!) Least risk Increased risk High risk
75 as explanations
<88 cm (")
for the fact that underweight patients are also at BMI has been shown to be a relatively insensitiv
64
53 increased risk for contracting illnesses. risk for obesity-associated metabolic and cardio
≥102 cm (!) Increased risk High risk Very high risk
42 ≥88 cm (") Waist circumference, but not BMI, reflects abdo
31
ous adipose tissue, as well as abdominal viscer
Weight (lb)
20
09 and is therefore a better index of central, or tru
Table 64-1 Levels of Risk Associated with Increasing Body Mass Index
98
Specific diseases are commonly associated with obesity,
In the United States, nearly 50 million p
87
76 andClassification
obesity is often accompanied
BMI (kg/mby 2 multiple comorbid states.7
) Risk of Health Problems Developing
bolic syndrome, for an age-adjusted prevalence o
65 Such states frequently include insulin resistance, type 2 diabetes such people, more than 83% meet the criteri
54 mellitus, obstructive sleep
Underweight <18.5apnea (OSA), hypoventilation,
Increased cardio- obesity. The incidence of metabolic syndrome in
43 vascular disease, hypertension, certain malignancies, and osteo-
32
arthritis.
Normal 7-14
Virtually all18.5-24.9
weight organ systems can be included in the
Least with more than 40% of the U.S. population affec
21
extended list of health risks associated with having an increased 60 years.15 Men are affected more commonly t
10 Overweight 25.0-29.9 Increased
9
BMI. A listing of the most common specific disease states along Hispanics and south Asians appear to be particu
with their obesity-associated risk is detailed in Table 64-3. As a
8 Obese
result of these concomitant conditions, obesity is also associated
Its frequency is lower in African American tha
1 6 Of the
Classdeath.
with early 30.0-34.9 High
health risks listed in Table 64-3, meta- Metabolic syndrome may result from the use of
bolic syndrome
Class 2 and OSA merit additionalVery
35.0-39.9 attention
high because they prescribed drugs, including corticosteroids, ant
d pose special concerns for the anesthetic care of the obese antipsychotic agents. The protease inhibitors use
Class 3 40.0-49.9 Extremely high
(in population.
immunodeficiency virus infection can induce
Superobese ≥50 Exceedingly high
drome secondary to insulin resistance.
Metabolic Syndrome
to 50 The clustering of a group of defined metabolic and physical
nches) abnormalities is now referred to as “metabolic syndrome.”15
ystem, Patients with metabolic syndrome commonly have abdominal
d risk obesity, reduced levels of high-density lipoprotein (HDL), hyper-
atients insulinemia, glucose intolerance, hypertension, and other charac- 81
5 and teristic features (Box 64-1).15 Clinical criteria for diagnosing

m.2 The metabolic syndrome require at least three of the following:
V 2106 Uremic frost
Adult Subspecialty Management
Anorexia
Table 65-1 Pain Conduction Pathways and Spinal Segment Projection of Pain of the Genitourinary System
OrganNausea and vomiting

Sympathetics, Spinal Segments Parasympathetics Spinal Levels of Pain Conduction
KidneyUremic fetor T8-L1 CN X (vagus) T10-L1
UreterGastroenteritis T10-L2 S2-4 T10-L2
Bladder T11-L2 S2-4 T11-L2 (dome), S2-4 (neck)
Prostate T11-L2 S2-4 T11-L2, S2-4

2.5 mg/100 mL). The serum creatinine concentration and clear-
Penis
ance are better indicators L1 and L2 S2-4
of general kidney function and GFR Tubular Function
S2-4
than similar measurements

Scrotum NS of urea nitrogen (Table 65-4).
NS There S2-4
are disease states,T10-L2
Testes however, in which even the serum creatinine
NS ConcentrationT10-L1
may
NS, not be affected
significant independent
for nociceptive function. of the GFR (Table 65-5). Urinary specific gravity is an index of the kidney’s concent
ability, specifically, renal tubular function. Determinati
urinary osmolality (i.e., measurement of the number of m
Table 65-4 Conditions Affecting Blood Urea Nitrogen (BUN) Independently of solute [osmoles] per kilogram of solvent) is a similar, mor
Glomerular
Patients Filtration
requiring Rate for renal and genitourinary surgery
anesthesia cificvagus
Left test.n.Excretion of concentrated
T10 urine (specific gravity
are frequently at the extremes of age. In addition to the physio-
Increased BUN
logic changes of aging in elderly patients, concomitant cardiovas- 1050 mOsm/kg) is indicative of excellent tubular fun
T11
Reduced effective circulating blood volume (prerenal azotemia)
cular and respiratory comorbidity is common. A medical history, whereas a urinary osmolality fixed at that of plasma (s
physicalCatabolic states (gastrointestinal
examination, and appropriate bleeding,
laboratorycorticosteroid use)
tests are neces- gravity 1.010; 290 mOsm/kg) indicates renal disease. The u
Celiac T12
High-protein
evaluate diets
sary to concomitant disease. In pediatric urologic ganglia dilution mechanism persists after concentrating defec
Tetracycline
patients, a careful history should exclude other nonurologic con- present, so a urinary osmolality
L1 of 50 to 100 mOsm/kg sti
genital lesions.
Decreased BUN be consistent with advanced renal disease.
Urologic procedures are performed mostly on the kidneys, L2
Liver disease
adrenals, ureters, urinary bladder, prostate, urethra, penis, scrotum,
testis, Malnutrition
and spermatic cord. Because their sensory nerve supply is Protein
Sicklethoracolumbar
primarily cell anemia and sacral outflow (Table 65-1), these Patients without renal disease may excrete 150 mg of prote
SIADH Left
structures are well adapted for regional anesthesia. aorticorenal day; greater amounts may be present after strenuous exer
SIADH, syndrome of inappropriate secretion of antidiuretic hormone. ganglion after standing for several hours. Massive proteinuria
Aortic 82
Innervation of the plexus
Genitourinary System
Anesthesia and the Renal and Genitourinary Systems 2111 6
MA
pos
Table 65-5 Conditions Affecting Serum Creatinine Independently of renal disease is present, patients consuming a diet high in animal fluo
Glomerular Filtration Rate Table
protein 65-8have
may Drugsmetabolic
Used or Encountered
acidosis.in Anesthesia Practice That
Significantly Depend on Renal Elimination L)2
Condition Mechanism No
Completely DependentThe electrocardiogram
Electrocardiogram. Partially Dependent(see Chapter 34)
hum
Conditions Causing Elevation reflects the toxic
Digoxin, effects
inotropes (used of potassium excess more closely than
IV anesthetics—barbiturates (1 L

Ketoacidosis Noncreatinine chromogen
determination
frequently;of the serum
monitoring of potassium concentration. ren
blood levels indicated in
Cephalothin, cefoxitin Noncreatinine chromogen chronic
Imaging renal failure)
Studies in r
Flucytosine Noncreatinine chromogen Computed Tomography Scan
Others—aminoglycosides, Kidneys. A stone proto-
of relaxants—pancuronium
Muscle exc
col computed
vancomycin,tomography (CT) scan of the kidneys, ureter, and nis
Other drugs—aspirin, cimetidine, Inhibition of tubular creatinine bladder has become and
cephalosporins, the study of choice for the detection of kidney gul
probenecid, trimethoprim secretion penicillins
stones because of its ability to detect stones of all kinds, including vas
Conditions Causing Decrease uric acid stones and nonobstructing
Anticholinergics—atropine, glycopyrrolate
stones in the ureter. Masses mo
Cholinesterase inhibitors—neostigmine, uri
in the kidney can be evaluated using either contrast-enhanced CT
edrophonium
Advanced age Physiologic decrease in muscle mass 6 hav
or renal ultrasound. Others—milrinone, hydralazine, enc
Cachexia Pathologic decrease in muscle mass cycloserine, sulfonamides, and
blo
Computed Tomography chlorpropamide CT angiography
Angiography. is
Liver disease Decreased hepatic creatine synthesis ran
and cachexia used for the evaluation of renal artery stenosis and is emerging
rapidly as a useful study. Although it is comparable to magnetic
resonance angiography as a noninvasive tool, it requires the use
of iodinated contrast material, which may cause renal dysfunction
in patients with chronic kidney disease.7
>750 mg/day) is always abnormal and usually indicates severe
glomerular damage. Magnetic Resonance Imaging with Magnetic Resonance
Angiography The use of magnetic resonance imaging (MRI)
Glucose with magnetic resonance angiography has revolutionized the
Glucose is freely filtered at the glomerulus and is subsequently evaluation of renovascular disease. The test is highly sensitive, but
reabsorbed in the proximal tubule. Glycosuria signifies that the tends to overestimate the degree of stenosis. Its accuracy in
ability of the renal tubules to reabsorb glucose has been exceeded detecting fibromuscular dysplasia causing renal artery stenosis
by an abnormally heavy glucose load and is usually indicative of has not been well validated. MRI also can be used to evaluate
diabetes mellitus. Glycosuria also may be present in hospitalized renal masses. Its main advantages of MRI are that it is a nonin-
83
patients without diabetes who are receiving intravenous glucose vasive test and does not require iodinated contrast material.
infusions.
Disorders of renin-angiotensin and aldosterone secretion occur dialysis and hemodialysis. Peritoneal dialysis
Dr Azam’s Notes incan be either 2013
Anesthesiology
and contribute to the hypertension that develops in patients with Anesthesia and the Renal and Genitourinary Systems 2117 65
severe renal disease. Reduced erythropoietin production leads to
anemia.
TableHeart
65-12 failure
PerioperativeandCauses
abnormalities
of Oliguria in liver function and Outcome analysis indicates that the overall mortality rate
blood coagulation also may occur in patients with renal shut- TableARF
from 65-13has
Urinary
not Composition of Oliguria
been significantly reduced in recent years
Prerenal
down. Hypovolemia
Infection is common and difficult to treat because the despite earlier and more frequent dialysis.
Physiologic Prerenal It is likely Acute
that there
Tubular
altered Dehydration
excretion of antibiotics leads to the rapid development of has been an increaseOliguria
in the survival Failure
rate of some categories
Necrosisof
toxic levels of these
Low cardiac output drugs.
states patients without any change in the overall rate because of an

Urinary in
increase sodium <10 mEq/L
the proportion of seriously<25
illmEq/L
patients who >35 mEq/L
are now
When established, oliguria is usually present for 10 to 18
Aortic/renal artery clamping
Thromboembolic phenomena treated inspecific
dialysis units. This conclusion
>1.024 is suggested by1.010-1.015
>1.015 the steady
days, but may persist for 30 to 45 days. During this period, hemo-
Hemorrhage
Urinary
improvement in mortality data of obstetric patients with renal
dialysisTransfusion
is required every 2 to 4 days. When diuresis occurs, the gravity
reaction failure. The low (15%) mortality rate for this group emphasizes
beginning of the recovery phase is signaled. During the diuretic that the most
Urinary osmolality >700
significant feature >500 mOsm/kg
determining
mOsm/kg survival is<350
the physi-
mOsm/kg
Renal
phase, urine volume gradually increases until 5 to 6 L of urine is
Ischemic injury from shock (cardiogenic, septic, hemorrhagic) cal status of the patient before the onset of renal failure.
Urinary/plasma >2.5 : 1 >1.8 : 1 ≤1.1 : 1
produced daily. Management of the patient is directed at main-
Nephrotoxins As noted earlier, many patients with ARF have normal or
osmolality
tainingAntibiotics
fluid and electrolyte balance in the face of these large high urinary flow rates. In these patients, the antecedent cause of
losses. Finally, concentrating
Chemotherapeutic agents ability gradually returns toward renal failure may be the
Urinary/plasma same
>100 : 1 as that in>20
patients
:1 with classic
3 : 1, oligu-
rarely >10 : 1
Radiocontrast dyes
normal. Complete return of all measurable parameters of renal ric renal
urea failure, but an oliguric or anuric phase is not identifiable.
function
Free hemoglobin and myoglobin
occurs in approximately two thirds of patients who Patients are unable to alter urinary volume and content appropri-
Cellular debris
survive.Acute
Fiftyinterstitial
percentnephritis
to 60% of patients with ARF do not survive ately, with an average>60
Urinary/plasma : 1 output often
daily >30 :greater
1, rarelythan<102.5: L/day.
1
creatinine <10 : 1
The more frequent incidence of nonoliguric and polyuric renal
67
long enough for recovery
Hypersensitivity reactionsor the development of CRF, however.
failure in recent
Fractional sodiumyears <1 compared with >1 the 1940s and>0.5 1950s is
Arrhythmias, bleeding, and infection are the most frequent causes
Acute glomerulonephritis
thought to be due, in part, to more vigorous early treatment of
of death.
Postrenal
excretion
patients withAnesthesia
incipient oliguric
and therenalRenalfailure.
and Genitourinary Systems 2125 6
Calculi
Tumors Hemodialysis
foam Clot
taperetention
placed to secure the epidural catheter was frequently Table 65-16 Changes on Immersion during Lithotripsy
in theSurgical
blast path The steady improvement in hemodialysis techniques (see
ligationof the shock waves and could absorb 80% of the Cardiovascular Increased Central in
blood volume
Chapter 67) from the first artificial kidney developed 1944 by
shockEdema
wave energy. 68 Increased Central venous pressure
Kolf and Berk to the current practice of home dialysis has
FromExcept when
Patafio O: piezoelectric
Acute renal lithotripters
failure and perioperative or Inlithotripters
oliguria. Malhotra V (ed):with resulted in additional yearsIncreased
of productive life Pulmonary artery
for patients withpressure
veryAnesthesia
low shock wave
for Renal andenergy are used,
Genitourinary Surgery.the
Newprocedure is painful
York, McGraw-Hill, 1996, and
CRF.Respiratory
This improvement, coupled with the 1976 Pulmonary
federal legislation
Section V Adul
p 38. Increased blood flow
requires some form of anesthesia. Shock waves produce sharp extending Medicare coverage to renal failure patients, has resulted
Decreased Vital capacity
stinging pain at the entry site in the flank along with a sensation in a large increase in the number of hemodialysis patients. Dialy-
Decreased Functional residual capacity
of deep visceral pressure discomfort. sis improves most of the signs and symptoms of uremia (e.g.,
Although shock waves pass through most tissues relatively volume overload, acid-base Decreased Tidal volume
and electrolyte imbalance, abnormal
unimpeded,orthey
matized postsurgical
do cause patients);
tissue ainjury,
decrease
theinextent
serum ofsodium
which mental function, peripheralIncreased
neuropathy, muscle Respiratory
weakness,rateand 84
and
depends calcium;
on Notes a decrease
the tissue in serum
exposed and2013proteins, particularly albumin;
the shock wave energy at the defective coagulation). Hypertension is improved except in
Dr Azam’s in Anesthesiology
a consistent increase in total reducing substance are
tissue level. Skin bruising and flank ecchymoses in serum,
common fre- at patients with high renin levels. Some patients have been undergo-
groups.155
con- Dr Azam’s Notes in Anesthesiologya 2013 result of
with Table 65-17 Anesthetic Implications of Radical Nephrectomy for Tumors in the gen
Table 65-18 Anesthetic Implications of Radical Prostatectomy prostatect
ver.144
85%-90% are for renal cell cancer periphera
omi- Disease of the elderly
neous ve
ut off 5%-10% extension to the IVC and right atrium CAD, COPD, and renal dysfunction epidural-g
iately Large-bore IV access, A-line, IJV line (preferably on left side if IVC is Significant blood loss
during ge
added to
involved)
eated Wide-bore IV access and invasive monitoring agulability
Paraneoplastic syndrome preemptiv
rtho- Acute normovolemic hemodilution versus autologous blood donation
postopera
ngton Hypercalcemia, eosinophilia; increased prolactin, erythropoietin, and Hyperextended position neuroend
ich is glucocorticoids Nerve injuries, soft tissue injury, joint dislocations block than
matic occurs fas
Men > women Venous air embolism
sia, althou
hetic
Anesthesia patient.162
may Chronic smoking history usually associated
The
or the CAD, COPD
Benefits of regional anesthesia versus general anesthesia debated
decreased
nabil- Not known to influence mortality lished clin
udent Renal failure
Epidural anesthesia with spontaneous ventilation decreases blood loss
satisfactor
ering CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; IJV,
was 1.34 d
newer internal jugular vein; IVC, inferior vena cava.
General or combined anesthesia with IPPV increases blood loss Alth
CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; IPPV, dural ane
intermittent positive-pressure ventilation. support su
85

of brainstem reflexes (Table 67-1) and the apnea test. Possible
Multiple blood transfusions can increase levels of uncon-
66 66 2013
Dr Azam’s Notes in Anesthesiology
Anesthesia and the Hepatobiliary System 2143 causes of reversibleAnesthesia cerebralanddysfunction
the Hepatobiliaryshould
System be
2145excluded
jugated bilirubin because approximately 10% of stored whole
(e.g., hypothermia, residual drug effects). For the apnea test, the
med the diag-
are blood
of undergoes
Organ hemolysis
Donors
Table 66-1 Modified Child-Turcotte-Pugh146
CPB, Koizumi and colleagues within after 24
Scoring System
noted ahours
decrease of transfusion
in PBF and (see
Table 66-2 Etiology of Postoperative Jaundice by Time Course
whom were patient breathes 100% oxygen for 10 minutes, during which time
Chapter HABF 55).
Parameters Each
without a0.5-L unit
concomitant of blood
change
Modified stored
in hepatic
Child-Turcotte-Pugh in citrate-phosphate-
oxygen Score* metabo-
Neurologic Determination the P is confirmed to be in the normal range (35 to 45 mm Hg).
hol use. In a Immediate Postoperative Jaundice (<3 wk)
and
d a 21% inci- dextrose-adenine
lism. Normothermic (CPDA-1) CPB was
1 yields
associated
2 7.5 g
with of ahemoglobin,
similar
3 decline which
in is2
Hemolysis
PBF, but HABF was maintained. Increasing thebilirubin.
dose of fentanyl 151 Subsequently,
Anesthesia mechanical ventilation is terminated, and blow-by
xtra-
of
ulation.
Death then converted
Both
Albumin (g/dL) to approximately >3.5 250 mg of <2.8 Multiple

1.8-3.5
is cannot be
dice units
from 10 to 50 µg/kg/hr significantly suppressed HABF and
of blood may therefore overwhelm the liver’s ability oxygen
to con- is administered with a T-piece. After 7 to 10 minutes, an
Hypotension/hypovolemia

ed solely on impaired hepatic oxygen metabolism in normothermic and
Prothrombin time
analysisDrugs
of arterial blood gases is performed. A P2 value greater
ther
sonographic jugatehypothermic
and
Seconds excrete
prolongedCPB,bilirubin.
suggesting Finally,
<4 the 4-6 reabsorption
possibility >6 of extravasated
of fentanyl-medi- Infection/sepsis
opotential
most underwent deceased
blood, as
ated occurs donors
peripheral
International withvenous
normalized areratio previously
retroperitoneal
<1.7
pooling and healthy
or
1.7-2.3 or
intra-abdominal
subsequent rela- hemato-
>2.3lowering than
of 60 mm Hg confirms
Bleeding/resorption lack of brainstem control of ventilation
of hematoma
re healthy
ence ofof post- individuals
mas, cardiac
may increase
Bilirubin who More
output.
†
(mg/dL) have experienced
the recently, <2 Okano
bilirubin load
2-3 brain
and death
coworkers
and >3 and
cause
147
assessedand represents
postoperative a positive apnea
Bile duct ligation/stricture/surgical injury test. No signs of spontaneous
stopathology Hepatic artery ligation
ot, thehave jaundice.
an extracranial
hepatosplanchnic malignancy
AscitesThis etiology is not
oxygenation oruncommon
Absent
untreatable
in 25 patients with
Slight-moderate
infection.
after no history respiratory
major trauma
Tense
of
or common
Retained effort should
duct stonebe observed during this procedure. Con-
infiltration. hepatic dysfunction who were undergoing elective coronary
than
tion, 5%repair
opsy-proven of deaths satisfy these
of ruptured aorticcriteria,
aneurysms. and only 10% Grade to 20% firmatory tests,pancreatitis/cholecystitis
Postoperative such as transcranial Doppler, electroencephalog-
artery bypass grafting
Encephalopathy withNone eitherGrade normothermic
I-II (>35°C)
III-IV or
ese
s in eligible
uced patients subjects
Hepatocellular
hypothermic actually
A = 5.6 points,(<32°C)
become
injury
B = 7 to CPB.andcan organ
C =cause
Hepatic donors.
postoperative
venous In addi-jaundice
desaturation raphy,(asand auditory evoked potentials, also may be used.
and
Acute viral hepatitis
*Class 9 points, 10 to 15 points. Gilbert’s syndrome/Dubin-Johnson syndrome
mortality was
a significant proportion of(e.g.,
potential organ donors are islost
rect) previously
†
functional
For discussed)
cholestatic impairment
diseases by ofdrug,
primarily hepatic
biliary ischemia,
sinusoidal
cirrhosis),
rmal hepatic proportionate to the impairment in hepatic function and an allowance should be
the bilirubinor virally
endothelial
level dis- mediated
cells Inflammatory bowel syndrome
use
ually of medical made.exclusion
occurred
mechanisms.
y,112 steatosis For these
in both (e.g.,
Inconditions,groups,
addition assignsepsis,
tobut malignancy,
hepatocellular
potential
1 point for level less incurable
dysfunction
a bilirubinanesthetic-induced
than 4 mg/dL, 2
was not hepato-Heart failure
tion) orrisk
uced
gnificant observed.
inability
toxicity,
points
aforto
number obtain
a bilirubin level ofconsent
of commonly
4 to 10 mg/dL, forand donation.
prescribed
6,7 level over
drugs
3 points for a bilirubin
10 mg/dL.In addition to the possible effects of hepatic artery and
Histori-
can cause Intraoperative
hepa-
Blood transfusion
Management
Pulmonary postoperative jaundice
fter abdomi-
organs fromFrom older donors (60 years
hich tocellular injury that mimics JL,old)
either have
hepatitis inferior sur-
or cholestasis
ymptomatic, bleeding portal Pugh RNH,
venous Murray-Lyon
perfusion, IM, Dawson
other et al: Transection
potential of oesophagus
determinants offorhepatic based Delayed Postoperative Jaundice (>3 wk)
erates than
on grafts from younger
after CPBdonors, but if proper selection Organ retrieval is not performed solely at major medical centers.
of oesophageal varices. Br J Surg 60:646-649, 1973. 152-199 Drugs
(1) should
evels liver test
dysfunction abnormalities (Tables
include 66-4
hypotension, andlow66-5 cardiac output ). With the
Blood transfusion
ia are applied,
with syndrome,long-term hypoxemia,graft microembolism
survival reaches or those
macroembolism,of MostPost–intestinal
organ retrievalsbypass statusare performed at community hospitals
8 cytokine and oxygen-free radical formation, and the influence of
ger
igendonors. Table 66-3 Medications Associated with Hemolysis Total parenteral nutrition
vasoactive and anesthetic drugs. Small retrospective studies have
In an attempt
ines (Table to fulfill
shown66-1).
Acetaminophen
116 the need for more organs, organs are
11% to This 30% scoring
mortality system
rates assigned
in CTP class points basedB on
A and patientsTable 67-1 Brainstem Reflexes That Should Be Absent in Brain Death
hg thetransplanted levelsfrom of extended
serum albumin criteria
undergoing nonemergency cardiac surgery.
Cephalosporins
and donors—donors
bilirubin, the INR, the
143-145 who
degree
Although of more
hronic
ade; formsHydralazine
onsidered ascites,
not ideal
deaths and the presence
because
occurred in oftheand grade
underlying
CTP classof Bencephalopathy
demographics
group, significantand strati-
or
morbidity, and renal failure. The diagnosis is made by the laboratory constel-
iated hepatic fied risk in order of severity as class A, B, or C. A number of Pupillary response to light
IgG)
cal conditions particularly
Ibuprofen (e.g.,
and age,in the form(e.g.,
hypertension) of postoperative hemorrhagepro-
orperioperative
subsequent and infec- lation of anemia, indirect hyperbilirubinemia, positive direct anti-
studied 20 studies haveother NSAIDs
used this system to predictdiclofenac, tolmetin) outcome in
tion, was seen in the CTP class A patients. Finally, noncardiac,Corneal globulin
reflextest, low serum haptoglobin, and the presence of
and
rd Cischemia
and were times.
cirrhosisOutcomes
Insulin
thoracic
patients undergoing
surgery may
databe a
for all
a variety
risk
solid
factor
organs
of surgeries.
for postoperative
are not
mortality fragmented erythrocytes and reticulocytosis on the peripheral
f 34 surgical
sted Garrison and coworkers117 retrospectively evaluated out-
stent with
ant from the
studies
Intravenous
in patients
comes in 100
performed
contrast
with media
cirrhosis,
patients
in kidney
although theproven
with histologically
transplantation,
basis for this association
cirrhosis who blood smear.
Oculocephalic Mechanical
reflex (doll’s eyedestruction
response) of erythrocytes can also
rting Penicillin
either and all derivatives 124 (e.g., ampicillin, methicillin)
eratively, nor similar
remains
were or inferior
speculative.
undergoing surgerypost-transplant
predominantly for biliary graft tractquality.
proce- occur from surgically implanted prosthetic heart valves or from
teNonetheless,
of Procainamide Oculovestibular reflex (caloric
intrinsically diseased valves.response)
150
ure or death. dures significant
(cholecystectomy, ethical conflicts surrounding
choledochotomy), as well as for the gas-
eigenpostopera- Ranitidine
troduodenal repair, colon and small bowel resection, and open Multiple blood transfusions can increase levels of uncon-
ition of
is who were
brain
Sodium
death
liverthiopental
in different
biopsy. An overall operative
social and cultural
mortality of 30% and an addi-
settings Gag and cough
jugated bilirubinreflex becauseAapproximately 10% of stored whole
uria,
been
ar an obstacle
carcinoma tional in transplantation.
Postoperative
perioperative morbidity ofIn
9
thewere
Jaundice
30% United noted,States and
with sepsis- blood undergoes hemolysis within 24 hours of transfusion (see
Facial motor response
ern
e testEurope, a consensus
results mediated multiorgan has beensystem reached
failure being among the major the scien-
cause of Chapter 55). Each 0.5-L unit of blood stored in citrate-phosphate- 86
t HHC, and death (87%). When
Postoperative stratified
jaundice to CTP
occurs as aclasses
resultA,ofB,overproduction
or C, mortality and dextrose-adenine (CPDA-1) yields 7.5 g of hemoglobin, which is
Dr Azam’s
was Notes in Anesthesiology
and 76%, 2013
underexcretion of bilirubin, direct hepatocellularCTP
10%, 31%, respectively. Excluding the classifi-
injury, or extra- then converted to approximately 250 mg of bilirubin.151 Multiple
atic patients cation, the authors also 148
performed a multivariate analysis of other
during
must be
d chronic Table 67-2 Immunosuppressive Drugs Used in Solid Organ Transplantation
on.277,278 and Their Side Effects gas emb
Table 68-1 Management of Patients with Cardiac Disease for Laparoscopy
ention or
Mechanism of Action Side Effects
with ca
ed organ.
linked to Inhibition of T-cell interaction Preoperative Evaluation: Echocardiography artery m
immuno- Prednisolone As with all steroids: osteoporosis, an arter
1962 and diabetes mellitus, glaucoma, infections If left ventricular ejection fraction < 30%:
ansplants, Muromonab-CD3 Fever, lymphoproliferative disease,
ogress. In (Orthoclone OKT3) pulmonary edema, anaphylactic Intraoperative monitoring
h as tissue
15-Deoxyspergualin
reaction, neoplasia
Bone marrow suppression,
Intra-arterial line Ane
tor–based
gastrointestinal syndromes, paresthesia Pulmonary artery catheter?
e survival
inhibitors Inhibition of adhesion Transesophageal echocardiography Genera
ne (1979). molecules
Continuous ST-segment analysis? fully an
ith excel- Rabbit/horse antithymocyte Fever, nausea, anaphylactic reaction,
plants.279 globulin higher incidence of cytomegalovirus Gasless laparoscopy?
g tailored and Epstein-Barr virus infection Laparotomy? Genera
Antilymphocyte globulin Fever
dual risk Genera
e a blood Enlimomab Fever, hypertension, chills, nausea, Intraoperative Management
point of
vomiting ventilat
to require
OKT4A Unknown Slow insufflation techniq
an needed Inhibition of cytokine synthesis Low intra-abdominal pressure long lap
immuno- Cyclosporine Nephrotoxicity, hepatotoxicity,
sed doses neurotoxicity, hypertension, Hemodynamic optimization before pneumoperitoneum (preload trolled v
increased hyperlipidemia, hirsutism, tremor, augmentation) 35 and
gingival hyperplasia, diabetes
oxicity. In Patient tilt after insufflation a 15% t
Tacrolimus (FK506) Nephrotoxicity, neurotoxicity,
lantation,
hypertension, hyperlipidemia, Anesthesia: remifentanil, vasodilating anesthetic and drugs (nicardipine, subcuta
id further
hyperglycemia nitroglycerin), cardiotonic agents
ntly com-
Sirolimus (rapamycin) Hyperlipidemia, myelosuppression, rather
munosup- Experienced surgeon
ty (Table
infections with CO
SDZ-RAD (everolimus) Hyperlipidemia, myelosuppression,
infections Postoperative Care mothor
h isolated Inolimomab Headache, leukopenia, thrombocytopenia inflation
all immu- Slow recovery from anesthesia (benefit of clonidine)
men con-
Basiliximab No major adverse effects
of vaso
Daclizumab No major adverse effects
e, therapy
Inhibition of DNA synthesis
necessary,
Azathioprine Myelosuppression, hepatotoxicity,
ent drugs
development of malignancy
e medical
Mycophenolate mofetil Leukopenia, gastrointestinal syndromes
nt immu-
herapy is 87
multiple
t of infec- Dr Azam’s Notes in Anesthesiology 2013
of patients
V 2190 Adult Subspecialty Management Dr Azam’s Notes in Anesthesiology 2013
Intra-abdominal pressure
Pooling of blood Caval Venous Intrathoracic Stimulation of Vasc. resistance

in the legs compression resistance pressure peritoneal receptor? of intraabd. organs
Release of neurohumoral
factor(s) (vasopressin,
catechol …)
Venous return Inotropism?? Systemic vascular

resistance
Cardiac output Arterial pressure
Figure 68-4 Schematic representation of the different mechanisms leading to decreased cardiac output during pneumoperitoneum for laparoscopy.
Systemic vascular resistance was reported to be increased in The increase in systemic vascular resistance is thought to
studies where no decrease in cardiac output was found.73,76 be mediated by mechanical and neurohumoral factors.90 The
Although the normal heart tolerates increases in afterload under return of hemodynamic parameters to baseline values is gradual,
physiologic conditions, the increases in afterload produced by the taking several minutes, suggesting the involvement of neuro-88
presence of a pneumoperitoneum can be deleterious to patients humoral factor(s).68,82,87 Catecholamines, the renin-angiotensin
87
with cardiac
Dr Azam’s Notes disease.
in Anesthesiology 2013 system, and especially vasopressin are all released during the pres-
The increase in systemic vascular resistance is affected ence of the pneumoperitoneum and may contribute to increasing
nagement
to 8.5 L. By term, blood volume increases by up to 45% whereas cardiac output, increased
hemoglobin dissociation
sthesiolo- Table 69-1 Cardiovascular Changes in Pregnancy A state of hyper
he mother increased levels of most c
red cell volume increases by only
Parameter 30%. This differential
Change Amountincrease
(%) Table 69-2 Effect of Pregnancy on Cardiovascular Investigations
unication gen and factor VII are
y team is leads to the “physiologic anemia”
Heart rate
of pregnancy with
Increased 20-30
an average Investigation Findings factors increase to a les
nancy as
principles hemoglobin and hematocrit of 11.6 g/dL and 35.5%, respec- factors has been verified
giotensin tively.
Stroke15 volume
However, oxygen transport is not impaired 20-50
Increased by this relative Chest radiography Apparent cardiomegaly
ist in the bly a protective adaptati
Enlarged left atrium (lateral views)
dy water anemia because
Cardiac output the mother’s body compensates
Increased for it by increased
30-50 acute hemorrhage that
Increased vascular markings
whereas cardiac output, increased Pa2, and a rightward shift in the oxy- state, however, may lead
Contractility ±10 Straightening of left-sided heart border
hemoglobin dissociation curve.Variable leading cause of matern
Postpartum pleural effusion
CentralA venous
state pressure
of hypercoagulabilityUnchanged exists in pregnancy, with unchanged throughout m
increased levels of most coagulation factors (Table 69-3). Fibrino- Electrocardiography Right-axis deviation reduced in the third trim
Pulmonary capillary wedge Unchanged
genpressure
and factor VII are markedly increased, whereas the other Right bundle branch block platelet count increases
factors increase to a lesser extent. This increase in coagulation ST-segment depression of 1 mm on left precordial because of activation of
Systemic
factors hasvascular Decreased
been verified by thromboelastography 1620
and is proba- leads incidence of low platelet
resistance Q waves in lead III
a result of bly a protective adaptation to lessen the risks associated with the
T-wave inversion in leads III, V2, and V3
id uterus, acute hemorrhage
Systemic that occurs Slight
blood pressure at delivery.
decreaseThis hypercoagulable
Midtrimester Small decrease in PR and QT interval (heart rate
demands state, however, may lead to thromboembolism, which remains
10-15 mm Hg, a dependent) Table 69-3 Coagulation Fact
associated leading cause of maternal mortality. The platelet count remains
then rises
Rotation ± 15 degrees (QRS axis)
unchanged throughout most ofDecreased pregnancy, but it may Factor
re signifi- Pulmonary vascular 30 be slightly Echocardiography Trivial tricuspid regurgitation (up to 43%-93% at
plications reduced in
resistance the third trimester with increased activity in vivo. The II
term)
urients. platelet count increases in the postpartum period, probably Pulmonary regurgitation (up to 94% at term)
Pulmonary artery pressure Slight decrease VII
precordial because of activation of hemostasis at the time of delivery. The Increased left atrial size by 12%-14%
incidence
From Birnbachof DJ,
low platelet
Gatt SP, Dattacounts in normal
S (eds): Textbook pregnancy
of Obstetric is approxi-
Anesthesia. New
Increased left ventricle end-diastolic dimensions
VIII, IX, X, XII
York, Churchill Livingstone, 2000, p 34.
by 6%-10% XI
Inconsistent increase in left ventricle thickness
art to
rate Fibrinogen
cy meet Mitral regurgitation (28% at term)
Table 69-3 Coagulation Factors in Pregnancy
cardiovas- Pericardial effusion (40% postpartum) Platelets
Although Factor Change Modified from Gei AF, Hankins GDV: Cardiac disease and pregnancy. Obstet From Birnbach DJ, Gatt SP, Datt
appear
93% at to compensate, collateral routes of venous return develop, including Gynecol Clin North Am 28:465-512, 2001. York, Churchill Livingstone, 200
he second the II paravertebral veins to the azygos vein. Unlike compression Unchanged of
yrm)approxi- the
VII vena cava, compression of the aorta is generally not associated
Increased +++
ases from with maternal symptoms in a healthy parturient but it may be
VIII, IX, X, XII
levels at associated
mensions with decreased uteroplacental perfusion.11Increased Anesthetics
t increase and
XI drugs that cause vasodilation or anesthetic techniques Reduced that
oximately
kness cause sympathectomy (e.g., neuraxial techniques) may exacerbate
Fibrinogen Increased +++
he eighth the impact of aortocaval compression. In the operating room, a
output is small
Plateletspillow or “wedge” should be used to provideStable left uterine
the
tet
more displacement of 15 to 20 degrees. This angle can be increased
From Birnbach DJ, Gatt SP, Datta S (eds): Textbook of Obstetric Anesthesia. New
as 89
0% to 50% York,necessary
Churchillby increasing
Livingstone, 2000,the wedge or tilting the table. Although
p 41.
t rate are Dr tilting the table will also
Azam’s Notes in Anesthesiology 2013accomplish uterine displacement, the
t that the amount of tilt necessary may prove too anxiety provoking to
anesthe-
aths with V 2226 Adult Subspecialty Management
Table 69-4 Values for Renal Function
opharynx deferred for 10 to 12 hours in a parturient who has received pre- Table 69-8 Factors That Differentiate Mild from Severe Preeclampsia*
lications. Parameter
operative LMWH orPregnant Nonpregnant
24 hours for parturients receiving higher
orophar- doses of LMWH (e.g., enoxaparin, 1 mg/kg 242 Mild Severe
Creatinine clearance 140-160 mL/min 90-110 daily).
twice mL/min
ion. Any Systolic arterial pressure <160 mm Hg ≥160 mm Hg
insertion Urea 2.0-4.5 mmol/L 6-7 mmol/L
ing, and Diastolic arterial pressure <110 mm Hg ≥110 mm Hg
Creatinine 25-75 µmol/L 100 µmol/L
e mucosa Urinary protein <5 g/24 hr ≥5 g/24 hr
hould be Uric acid Complicated Obstetric 0.35
0.2 mmol/L Conditions
mmol/L Dipstick + or 2+ Dipstick 3+ or 4+
pregnant pH 7.44 7.40 Urine output >500 mL/24 hr ≤500 mL/24 hr
0 to 7.0) Preeclampsia and Eclampsia
nimized. Bicarbonate 18-22 mmol/L 23-26 mmol/L Headache No Yes
r in the Preeclampsia
From Birnbach complicates
DJ, Gatt SP, Datta up toof8%
S (eds): Textbook of pregnancies.
Obstetric 243
Anesthesia. New It is the Visual disturbances No Yes
most common condition seen by obstetric anesthesiologists in
Epigastric pain No Yes
which an otherwise healthy parturient can become critically ill.
The classic triad of preeclampsia includes hypertension, proteinu- Right upper quadrant abdominal No Yes
ria, and edema. Certain conditions predispose a woman to pre- pain
eclampsia. In order of risk ratio, these conditions include Pulmonary edema No Yes
homozygous angiotensin T-235, chronic renal disease, antiphos-
pholipid syndrome, chronic hypertension, a family history of Cyanosis No Yes
preeclampsia, multiple gestation, nulliparity, maternal age older HELLP syndrome No Yes
than 40 years, diabetes, and African American race.244 Preeclamp-
sia has been defined as hypertension occurring after 20 weeks’ Platelet count >100,000/mm3 <100,000/mm3
gestation or in the early postpartum period and returning to HELLP, hemolysis, elevated liver enzymes, and low platelet count.
normal within 3 months after delivery or onset after 20 weeks’ *Not all features need be present in the same patient.
gestation and at least one of the following245: From Birnbach DJ, Gatt SP, Datta S (eds): Textbook of Obstetric Anesthesia. New
t Proteinuria higher than 300 mg/24 hr

t Oliguria or a serum-plasma creatinine ratio greater than
0.09 mmol/L
t Headaches with hyperreflexia, eclampsia, clonus, or visual lampsia may be associated with abnormal placentation and failure
disturbances of the normal invasion of trophoblast cells, thereby leading to
t Increased liver enzymes, plasma glutathione S-transferase- maladaptation of maternal spiral arteries.248 This aberration can
alpha 1-1, or serum alanine aminotransferase or right result in abnormal villus development and potentially cause pla-
abdominal quadrant pain cental insufficiency. It has recently been proposed that the sec-
t Thrombocytopenia, increased lactate dehydrogenase ondary pathology in preeclampsia is also linked to endothelial
(LDH), hemolysis, disseminated intravascular coagulation dysfunction and excessive activation of coagulation. This abnor-
(DIC) mality is accompanied by high circulating levels of fibronectin 90
t Intrauterine growth retardation and endothelin, increased coagulation and fibrinolysis with
Dr Azam’s Notes in Anesthesiology 2013 increased platelet activation, and platelet consumption.249 Figure
Preeclampsia may be classified as mild or severe according 69-13 compares the balance in the biologic actions of prostacyclin
V 2228 Anesthesia
Adult Subspecialty Management
69in Anesthesiology 2013
Dr Azam’s Notes
for Obstetrics 2227
Vasoconstriction Vasoconstriction and placental abruption. Hepatic impairment may also occur, but
Table 69-9 Comparison of Properties of Hydralazine and Labetalol for
it is usually associated with HELLP syndrome. Liver rupture is a M
Platelet aggregation Platelet aggregation Treatment of Hypertension
Uterine activity Uterine activity known, rare complication of preeclampsia. High levels of uric and pr
Uteroplacental blood flow Uteroplacental blood flow acid, LDH, or aminotransferases can be indicative of severe publish
Drug Hydralazine Labetalol
maternal disease. seizure

Prostacyclin Thromboxane Mode of action Vasodilator α- and β-blocker (1 : 3) withou
HELLP Syndrome
As stated, this Speed
condition consists of hemolysis,
of onset Gradual elevated liver Quick
effect i
enzymes, and low platelets. Its severity ranges from a mild self- cardiac
Endoperoxide
limiting condition to a fulminant process leadingIVtoslowly
Dose 5-10 mg multiorgan 10-20 mg IV slowly intrave
failure. Considerable
Intervaldebate, however, has centered
Repeat afteraround
20 min the Titrate to effect nance
definition, incidence, etiology, and management of this syndrome. of infu
Arachidonic acid
Patients with HELLP
Infusion syndrome
rate may have various
2 mg/hr up tosigns and 20 mg/hr to maximum levels.
symptoms, none of which is diagnostic and20allmg/hr of which may be of 160 mg/hr
Preeclampsia found in patients with severe preeclampsia/eclampsia without levels b
HELLP syndrome. Effect
254 on heart rate
Sibai, noting the lackCompensatory
of consensus regarding No effect should
Vasoconstriction the diagnostic features of HELLP syndrome, tachycardia
recommended for tox
Platelet aggregation the following criteria: hemolysisAnesthesia (defined forby Orthopedic
an abnormal Surgery 2243 70 reflexe
Uterine activity peripheral blood smear and an increased bilirubin level), increased given
Uteroplacental
complication seenblood flow
in elderly patientsVasoconstriction
after orthopedic surgery. liver enzymes
Table 70-1(defined as an aspartate
Gurd’s Diagnosis aminotransferase
of Fat Embolism Syndrome level
Platelet aggregation ≥70 U/L and LDH >600 U/L), and a low platelet count
effects.
In 2004, $69 billion from Medicare was spent on the treatment platelet count
Prostacyclin Uterine activity (<100,000/mm 3 255
).
Major Features (at leastusually
one) returns to normal within 72 hours of deliv-
of hospital-acquired delirium. Delirium is associated
Uteroplacental blood flow
with an ery,no but thrombocytopenia may persist for longer periods. Anest
Assuming
Respiratory other coagulopathy, hemostasis
insufficiency is typically
increased length of hospital stay, poor functional recovery, pro- unlessOnce
not problematic
Cerebral involvement preeclampsia
the platelet is diagnosed,
count decreases the goal of therapy is pre-
below 40,000/ Anesth
gression to dementia, and increased mortality.24,25 Postoperative mm3.256Petechial
The rate of fall in the platelet count is also of clinical sig-
vention and reduction of further complications
rash by taking into detaile
Section V Adult Subspecialty Ma

delirium manifests as attention and awareness Thromboxane
deficits, including
nificance, andFeatures
Minor regional (at anesthesia may be contraindicated if the
least four)
acute confusion, reduced ability to focus, change in cognition, account both maternal and fetal factors. Although the only defini- the co
plateletPyrexia
count has dramatically fallen over a short period. The
irritability, anxiety, paranoia, and hallucinations. Delirium tive cure is delivery, management of maternal hemodynamics and
Tachycardia
evaluat
Endoperoxide
develops acutely, but generally has a fluctuating course over prevention of the development of eclampsia are key to a favorable
Retinal changes Investi
several days (see Chapter 71).26 Some patients manifest a hypoac- Jaundiceoutcome for the mother and infant. There is now international profile
tive form of delirium,Arachidonicconfused acid but quiet and nondisruptive, consensus that magnesium is the treatment of choice for preec-
Renal changes not rec
3–5 <4
which can be difficult to diagnose. The major risk factors for lampsia
70Laboratory to prevent50eclampsia, but the mechanism underlying its
Features pected
60Fat microglobulinemia (required) 4–8
Figure 69-13 Comparison
postoperative deliriumofarethe advanced age, and
normal equilibrium alcohol
actionsuse,
of preopera- salutary effect remains debatable. Although magnesium is a direct Howev
Patients (n=45)(%)
thromboxane and prostacyclin in normal pregnancy with the dysequilibrium Anemia 40

tiveassociated
dementia or cognitive
with preeclampsia. impairment,
(Redrawn psychotropic
from Walsh SW: medica-
Preeclampsia: An
50 smooth muscle relaxant at relatively high concentrations, it does recent
Thrombocytopenia
tions, and inmultiple
imbalance medical comorbid
placental prostacyclin conditions.
and thromboxane production. Perioperative
Am J 40 not significantly
High erythrocyte reduce
30
sedimentation rate systemic blood pressure at the serum admin
Obstet Gynecol 152:335, 1985.)
events that may trigger delirium include hypoxemia, hypoten- 30 concentrations that 20 are efficacious in treating preeclampsia.257 cryopr
From Gurd AR, Wilson >5
RI: The fat embolism syndrome. J Bone Joint Surg Br 56:408-
sion, hypervolemia, abnormal electrolytes, infection, sleep depri- 20 91 contra
416, 1974.
<3 10 >8
vation, pain, and administration of benzodiazepines and 10 Treatment A
anticholinergic
Drpulmonary
Azam’s Notes medications.
in Anesthesiology The mainstay of therapy in preeclampsia is control of hyperten- retenti
capillary wedge pressure, 2013 low plasma colloid and 0 0
31
Aging alters the pharmacokinetics and pharmacodynamics dence Cardiac
of presentation
sion, indices (Table
prevention 70-2).venous
Central
of seizures, Respiratory
and signs
pressure of
delivery also are
the fetus. Hydralazine becaus
tress and cally benign, but some patients still progressed to FES. The fat
major and Dr Azam’s
Anesthesia Notes in Anesthesiology
for Orthopedic Surgery 2245 2013 7
ble 70-1). Table 70-2 Schonfeld Fat Embolism Syndrome Index*
or criteria surgery is inappropriate in a patient with significant ipsilateral Table 70-3 Anesthetic Considerations for Patients with Rheumatoid Arthritis
the diag- Sign
shoulder arthritis. Although the operative site would Score
be com-
rculation Airway Limited TMJ movement
detected
pletely anesthetized,
Petechial rash the patient may complain of painful
5 shoulder
Narrow glottic opening
n trauma movement during
Diffuse alveolar the procedure. The appropriate regional
infiltrates 4 anes-
Gurd and thetic would include the arthritic shoulder; an appropriate anes- Cervical spine Atlantoaxial instability

Hypoxemia PaO2<70 mm Hg, FIO2 100% 3
oplets in thetic might be an interscalene block.
Cardiac Pericarditis
fat would Confusion 1
Cardiac tamponade
ave indi- Rheumatoid Arthritis
Fever >38°C (>100.4°F) 1
correlate Rheumatoid arthritis (RA) is a chronic inflammatory form of Eyes Sjögren’s syndrome
t of acute Heart rate >120 beats/min 1
arthritis, which affects about 1% of adults, with a prevalence two Gastrointestinal Gastric ulcers secondary to ASA, steroids
Respiratory rate >30 1
the rash to three times higher in women than in men. RA is characterized Pulmonary Diffuse interstitial fibrosis
n folds of byFrom
persistent joint synovial
*Score >5 required for diagnosis of fat tissue
embolisminflammation
syndrome. leading to bone
Schonfeld SA, Ploysongsang Y, DiLisio R, et al: Fat embolism prophylaxis with
ES index, erosion, destruction of cartilage, and loss of joint integrity. RA Renal Renal insufficiency secondary to NSAIDs
corticosteroids: A prospective study in high risk patients. Ann Int Med 99:438-443,
1983.is a systemic disease, affecting multiple organ systems. It
heir inci- also
40 A
ASA, acetylsalicylic acid; NSAIDs, nonsteroidal anti-inflammatory drugs; TMJ,
often progresses through multiple exacerbations and remissions, temporomandibular joint.
but 20% to 30% of affected individuals become permanently disa-
bled within 3 years of diagnosis.
The diagnosis of RA is primarily clinical. Patients com- patients and requires pre-planning even in patients receiving
monly present with pain and stiffness in multiple joints. RA is regional anesthesia because of the complexity of their airways
characterized by morning stiffness often lasting more than 1 hour (see later). Synovitis of the temporomandibular joint may signifi-
after initiating activity. Usually the wrists and metacarpophalan- cantly limit mandibular motion and mouth opening in these
geal joints are involved; this distinguishes RA from osteoarthritis, patients. Arthritic damage to the cricoarytenoid joints may result
which often affects distal interphalangeal joints. The symptoms in diminished movement of the vocal cords, resulting in a nar-
may emerge over weeks and months, progressing from one joint rowed glottic opening; this is manifested preoperatively as hoarse-
to multiple joints, and may be accompanied by symptoms of ness and stridor. During laryngoscopy, the vocal cords may
anorexia, fatigue, and weakness. The rheumatoid joints are usually appear erythematous and edematous, and the reduced glottic
boggy, tender to the touch, and warm. Patients may have promi- opening may interfere with passage of the endotracheal tube.41
nent epitrochlear, axillary, and cervical lymph node enlargement. There also is an increased risk of cricoarytenoid dislocation with
Subcutaneous nodules (rheumatoid nodules) may surround traumatic endotracheal intubations.
joints, extensor surfaces, and bony prominences. Arthritis of the cervical spine is common in patients with
No single diagnostic laboratory test confirms the diagnosis RA. Anterior subluxation of C1 on C2 (atlantoaxial subluxation)
92
of RA, but rheumatoid factor, an anti-immunoglobulin antibody, may occur in 40% of patients with RA, with symptoms of progres-
Dr
is Azam’s
elevated Notes
in 90%in Anesthesiology
of patients with 2013 RA. In addition, C-reactive sive neck pain, headaches, and myelopathy (Fig. 70-3). Posterior
general
ment
loss usually continues for the next 24 hours. Tourniquets are the medial leg to the medial malleolus, and the remainder of the
compartment syndrome should occur before administering long-
hat pre- usually inflated to a pressure 100 mm Hg above the patient’s leg below the knee, including Dr theAzam’s Notes in Anesthesiology
foot, is innervated by the 2013
acting sciatic nerve blocks. systolic blood pressure for 1 to 3 hours. Nerve injury after
Tableblock
The ankle 70-4 isAnesthetic Considerations
used for surgical procedures for Patients
on thewith foot approach to the brachial plexus with documentation of a par-
extended tourniquet inflation (>120 minutes) has been attributed
Osteogenesis Imperfecta
hat do not require the use of a thigh to the tourniquet, although an andesthesia or the use Pero-
of a nerve
combined effects of ischemia mechanical trauma. Tablestimulator
70-5 Patientsto locateforthe
Excluded optimal
Single site
Operation for Bilateral Total
96-98 of TKA
ankle-level Esmarch tourniquet may nealbenerve
used.palsy,
Because which theis block of injection.
a recognized complication The brachial plexus is formed from the ventral
Knee Arthroplasty
he syn-
s primarily Airway
an infiltrative block, itRisk of fractures
(incidence
usually isofnot
0.3% ofperformed
the mandible,
to 10%), maybybemaxillary
caused
rami of surface,
by the combination
C5-T1 nerve roots. After these roots pass between the
of
and tourniquet
cervical ischemia
spine and surgical traction. 86
Horlocker and Age ≥ 75 yr
eliciting
is clas- a paresthesia. anterior and middle scalene muscles, they fuse into three trunks
colleagues86 reported a combined tibial and peroneal nerve dys- ASA class III
nts forFive terminal
Bleeding nerves are usually
Platelet blocked
functionabnormalities to provide com-
of 7% of TKA patients associated (superior C5-6, middle
with younger age, the C7, inferior C8-T1). During performance
plete anesthesia to the foot: (1) posterior
patients presence tibial nerve, which
of preoperative of the ISB,
pro- deformities,
flexion and local anesthetic
longer total isActive
injected between
ischemic the(positive
heart disease scalene muscles
stress test)
Cardiac
vides sensation to the plantar surface; Congenital and
(2) saphenous
tourniquet valvular
time. When heart
nerve,prolonged disease;
which at cystic
the level inflations
tourniquet of the cricothyroid
are notch (C6) (Fig. 70-8).
< 40%)
or more Poor ventricular function (LVEF
nnervates the medial malleolus; (3)required,deep peroneal
degenerationdeflating nerve,
of proximal which
aorta for 30 minutes
the tourniquet The of major acute complications
reperfusion and side effects associated
IA and may reduce neural ischemia.
upplies the interspace between the great and second toes; (4) with ISB are respiratory depression, intravascular injection with
Oxygen-dependent pulmonary disease
rticular Eyes Exophthalmos—prone

Pain related onlypositioning
to oftourniquet inflation and
also cardiac
may occur
uperficial saphenous nerve, which supplies the dorsum the seizures arrest,Patients considered at increased risk for morbidity and mortality
pneumothorax, epidural and spinal
cts the the Hyperthermia after 60 minutes, despite the presence of a regional anesthetic that IDDM
oot and second through the Malignant
fifth toes; and
is adequatehyperthermia;
(5) sural nerve,
for the surgery.hydration;
anesthesia,
It has beenpossible
postulated
Horner’s
cooling
that tourniquet
syndrome, hoarseness,
Renal insufficiency and dysphagia. The
5) Pso-supplies the lateral foot andpain
which lateral fifthbytoe
is caused ipsilateral phrenic
(Fig. 70-7).of unmyelinated
the unblocking nerve is blocked
C fibers during Pulmonary inhypertension
all patients undergoing ISB,
Positioning
95 Risk
Mineo and Sharrock reported thatrecession of repeated
the ankle of block
fractures
performed
a neuraxial block. The at addition
resulting in hemidiaphragmatic
of narcotics to spinal paresis.99 Because
Steroid-dependent asthma hemidiaphrag-
he midtarsalPulmonary
periods level with 30 mL of Kyphoscoliosis—restrictive
0.75% bupivacaine
or epidural anesthesia provided lungadisease
may ameliorate matic paresis pain.
tourniquet may result
After in aMorbid
25% obesity
reduction in pulmonary func-
(BMI > 40)
mean tourniquet release, mean arterial blood pressure decreases signifi-
duration of 17 hours of analgesia with safe blood levels of tion, patients with severe respiratory disease may not tolerate an Chronic liver disease
airway
ocal anesthetic.
ly dan-
cantly, partly
Regional anesthesia Fractures; owing to theinjections
intraosseous release of metabolites
ISB withoutfrom thethe ischemic
addition of mechanical A ventilation. An ISB would
Cerebrovascular disease
limb into the circulation and the decrease in peripheral vascular ASA, American Society of Anesthesiologists; BMI, body mass index; IDDM, insulin-
A be contraindicated in patients after pneumonectomy on the
resistance. In patients with known preexisting sciatic neura- dependent diabetes mellitus; LVEF, left ventricular ejection fraction.
contralateral side and for bilateral operative procedures. The
Upper Extremity Surgeries
Table 70-6 Brachial Plexus Anesthesia
Surgery for the upper extremity, from the shoulder to the hand,
can be performed successfully by blocking the brachial plexus at Site of Block Simulated Brachial Plexus Response
everal points until it branches into peripheral nerves (Table Interscalene Roots; trunks Shoulder to hand
70-6). Several methods are used to document the optimal loca-
ion for neural blockade of the brachial plexus, including eliciting Supraclavicular Trunks (middle, inferior) Upper arm to hand
a paresthesia, motor nerve stimulation, ultrasound guidance, and Infraclavicular Lateral cord Forearm flexion
perivascular infiltration. Regional anesthesia for the upper Hand pronation
extremity also can provide postoperative analgesia using long- Posterior cord Wrist extension
acting local anesthetics or continuous catheter techniques. Medial cord Fingers and thumb
Regional anesthesia for shoulder surgery (see Chapters 52
Axillary Median nerve Forearm pronation
and 53) has not gained wide acceptance because of the belief by
Wrist flexion
anesthesiologists and surgeons that it is often inadequate for sur-
Ulnar nerve Finger flexion
gical anesthesia and the concern for postoperative neurologic
Thumb opposition
ymptoms (PONS). Several studies have reported 97% or greater
uccessful surgical anesthesia using the interscalene block (ISB)
Radial nerve Wrist extension A 93

Anesthesia for Orthopedic Surgery 2255 70 ent lung than when air/oxygenDrmixtures are used
Azam’s Notes (24%). Nitrous
in Anesthesiology 2013
oxide also tends to increase pulmonary artery pressures in patients
Table 70-9 Complications of the Prone Position* who have pulmonary hypertension,100 N2O inhibits HPV,101 and
Airway ETT kinking, dislodgment
N2O is70-8
Table contraindicated
Predictors of in patientsEndotracheal
a Difficult with blebs or bullae. For these
Intubation
Upper airway edema reasons N2O is usually avoided during thoracic anesthesia.
Figure 59-23 Facial dyssymmetry (trauma)
Neck AtelectasisHyperextension
develops in the dependent portions of both lungs
or hyperflexion

after induction of anesthesia, as seen in this chest CTblood
Cervical rotation—compromised scanflow
(top). This
to brain Tracheal deviation
atelectasis disappears in the nondependent lung after turning the patient to Temperature
Cervical fractures
the lateralEyes Orbital pressure—central
position but increases in the dependent retinallung
artery occlusion,This is the
(bottom).
supraorbital nerve Small mouth opening (interincisor gap)
lung that will subsequently be used for gas exchange during one-lung
ventilation. (From KaplanCorneal abrasion
J, Slinger P [eds]: Thoracic Anesthesia, 3rd ed. Maintenance of body
Inability to visualize thetemperature
faucial pillarscan
andbe a problem
uvula during tho-
(Mallampati)
Philadelphia, Churchill
Abdomen Livingstone, 2003.) to epidural veins, increased
Pressure transmitted racic surgery
Limited because
neck range of of heat loss from the open hemithorax. This
motion
bleeding isProminent
particularly a problem at the extremes of the age spectrum.
incisors
. In this Upper extremity Brachial plexus stretch—arms out Most of the
Distance body’s
between physiologic
thyroid cartilage functions, including
and mandible <6 cm HPV, are
tracheal Ulnar nerve compression—arms at the side inhibited during hypothermia.
Narrow maxillary arch Increasing the ambient room tem-
sedated
adequately Lowerwith openFlexion
extremity hemithoraces
of hips—occlusion because
of femoralofvein,
twoDVT,physiologic
kinking
he safest
problems. First, paradoxical ventilation
of vascular grafts (also called “pendelluft”)
care in a
erioroccurs
sta- in which gas moves into to the lung in thenerve open
Pressure lateral fibula—peroneal palsyhemithorax Table 59-17 Fluid Management for Pulmonary Resection Surgery
from the lung in thePressure closedonhemithorax
iliac crest—lateral femoral cutaneous nerve
during expiration. Flow Most spinal surgeries require general anesthesia. In
a flexible 1. Total positive fluid balance in the first 24-hour perioperative period
reverses during inspiration. This leads to hypercapnia and hypox-
surgery *See Chapter 36. patient population with preexisting arthritic conditions, trach
DVT, deep vein thrombosis; ETT, endotracheal tube. should not exceed 20 mL/kg.
ments of Second, there is swinging motion of the mediastinum
emia. intubation often
2. For an average poses
adult patient,a crystalloid
challenge (Table 70-8).
administration shouldAwake,
be seda
general fiberoptic
between the hemithoraces during the respiratory cycle that inter- limited to intubation
< 3 L in the first of many of these patients is the sa
24 hours.
disease. Cobb angles of greater than 65 degrees usually cause
feres with cardiac
ery is an significant preload
decreases andvolumes.
in lung causesAlthough
hemodynamic instability.
exercise tolerance approach to general
3. There should be no fluidanesthesia.
administrationThis is space
for third the standard
fluid losses of care
gist Inandthe isearly 1900s, several
an important determinant pioneers, such ofasthethe
of the effects NewofOrleans
severity the during pulmonary resection.
patient with cervical spinal instability who requires posterior
surgeon
t risk for curve Matas, advocated
on respiratory positive-pressure
function, formal pulmonaryventilation
function studies and a 4. Urine output > 0.5 mL/kg/hr is unnecessary.
ht seda- should be of
obtained before surgery. This information guides deci-
bilization. These patients should be intubated first with a flex
5. If increased tissue perfusion is needed postoperatively, it is preferable
primitive form endotracheal ventilation, which had been dem-
ovement sions regarding the extent of surgery permitted at one time and fiberoptic bronchoscope,
to use invasive then positioned
monitoring and inotropes prone
rather than to cause fluidfor surg
onstrated to be safe in animal experiments, for thoracic anesthe-
or cervi- the requirement for postoperative ventilatory support. A vital
sia. Modern sedated but awake (if possible), and assessed for movement
overload.
prepara- capacity methods,
of less thanincorporating
40% of the normal OLV, have
range evolved offrom
is predictive
mbolism. the requirement for postoperative ventilation. The major abnor-
upper and lower extremities before the induction of gen
rior and mality in arterial blood gases is hypoxemia, secondary to ventila- anesthesia.
pproach, tion-perfusion inequalities caused by alveolar hypoventilation. The careful positioning of patients for spinal surgery i
se pelvic Chronic hypoxemia produces elevated pulmonary vascular resist-
d flow to
important shared responsibility of the anesthesiologist
94
Patients surgeon (see Chapter 36). As stated previously, patients at risk

lly posi- spinal cord compression should be positioned under light se
V 2290 Adult Subspecialty Management below 80 to 90 mm Hg. In Early resuscitation
practice, is much
fluid boluses are more
given complex because the risks
alter- Notes
Furthermore, left asso-
ventricularthe pow
thre
ciatedwith
withthe aggressive Dr Azam’s
volume replacement in
(see BoxleftAnesthesiology
72-4), 2013
includ- performan T
nately with anesthetic agents, goal of reaching a normal quantify ventricular
depth of anesthesia without increasing
advantage of being systolic blood pressure.
inexpensive, pared nonallergenic,
readily available, with purely flow-derived of delib
hem
Box 72-5 Goals for Early Resuscitation* port variables first was
noninfectious,
Box 72-4 andRisksefficacious
Associated in restoring total-body
with Aggressive Volume fluid.asThey
markers of perfusi
tors ran
Maintain systolic blood pressure at 80 to 100 mm Hg Late Resuscitation are easyReplacement
to store and administer,
during Early they mix wellinjured
Resuscitation*
patientsmedi-
with infused during resuscitatio
111 patients were monitoredtwo withtrea
a
Maintain hematocrit at 25% to 30%
cations, and they can be rapidly warmed to catheter body temperature.
during the first 48 infused
hours o
Increasedofblood
Disadvantages pressure include their lack of oxygen-
crystalloids
Maintain the prothrombin time and partial thromboplastin Box 72-7 summarizes end points for late resuscitation, and Figure clear lactate in less than 24 hours fluid unan
carryingDecreased
72-9 presents an algorithm capacity,
for management. their Fluid
blood lack administration
of coagulation capability,
viscosity vivors exhibitedand their
significantlymonth
highes
time in normal ranges limitedcomponent.
intravascular
is an integral, mandatory Decreased Thehalf-life.
adequacyMore
hematocrit recent laboratory
of resuscita- tricular power dataoutput
have than nonsurv
transpo
Maintain the platelet count at greater than 50,000 tion should not beimplicated
per high- specific
judgedDecreased
by the presencecrystalloid
of normal solutions
vital as
signs,
clotting factor concentration immunosuppressants
rate, these were the only variables
then 50t
96
power field and of
but by normalization triggers
organ andof cellular apoptosis.
tissue perfusion. The Unlike
role of necrosis,
to lactateapoptosis
clearance andis survival.
receivedTh
the Greater
anesthesiologist-intensivist is transfusion
to recognize requirement
the presence of ventricular power output in surv
Maintain normal serum ionized calcium highly regulated and involves gene modulation and complex immedi
ongoing shock after traumatic hemorrhage
Disruption of and to
electrolyte resuscitate
balance the
pathways of signal transduction. It seems clear that apoptosis is ventricular-arterial coupling and th
crystallo
Maintain core temperature higher than 35°C patient with the appropriate fluid, in the appropriate amount, at function.
an important elementsuppression
Direct immune of reperfusion injury. In a rat model of substan
Maintain function of the pulse oximeter the appropriate time. on arriv
controlled hemorrhage,
Premature animals receiving LR showed an immedi-
reperfusion
Late resuscitation begins once bleeding is definitively con- took as
trolled by surgery,ate increase in theapoptosis intime.
the The
liverprac-
and small intestine after
Prevent an increase in serum lactate Increased
angiography, or risk for hypothermia
passage of
97 Table 72-5 Modalities for Assessment
spontanof S
Prevent acidosis from worsening resuscitation.
titioner’s goal at this time*Most Neither
is to complications
restore normal whole
of blood
perfusion
volume nor arise
to all
resuscitation hypertonic
from increasedsaline
increased thetoamount of apoptosis. delayed
Achieve adequate anesthesia and analgesia organA systems while continuing support
hemorrhage vital
volume functions.
or excessiveHypo- Technique
hemodilution. Shortc
immedi
Hypertonicshock
perfusion caused by hemorrhagic salinetriggers
solutions, with or without
a predictable the addition of
Vital signs Will no
*Fluid administration to limit hypoperfusion is balanced against an
polymerized
cascade of biochemical
undesirable increase in blood pressure and thus bleeding.
eventsdextran
that will(HS cause
or HSD), have been extensively studied
physiologic
Urine output May be
in resuscitation from hemorrhagic shock.98 In theory, HS will diure
draw fluid into the vascular space from the interstitium and renal
71
Box 72-7 Goalsthereby reverse some of the nonhemorrhagic fluid loss caused by
of Late Resuscitation* Systemic acid-base status Confou
as ARDS in experimental models. Based on this physiology, the shock and ischemia. A given amount of HS will thus have an
recommended goals for early resuscitation are expressed in Box
Maintain systolicenhanced ability
blood pressure to restore
higher intravascular
than 100 mm Hg volume when
Lactate compared
clearance Require
72-5, and an algorithm for management is presentedMaintain in Figure withabove

hematocrit an equivalent
individual volume of an
transfusion isotonic solution.
threshold This
Cardiac has made
output Require
72-8. The emphasis in this situation must be on rapidNormalize
diagnosis HS a popular
coagulation status choice for fluid resuscitation under austere condi- arter
and control of ongoing hemorrhage; the anesthesiologist should
Normalize tions.balance
electrolyte HSD is licensed for prehospital use in a number of Euro- techn
attempt to restore vascular volume and provide anesthesia in pean countries and is used for resuscitation by
Normalize body temperature
units
Mixed of the
venous U.S.
oxygenation Difficul
equal measure by moving the patient from a vasoconstricted state military. Multiple studies of otherwise lethal hemorrhage in mark
Restore normal urine output
to a vasodilated one while facilitating hemostasis by maintenance animals have demonstrated improved survivalGastric after tonometry
resuscitation Require
of lower than normal blood pressure. Maximize cardiac output by invasive or noninvasive
with HSD versus either normal saline solution or the components artifa
measurement
of HSD alone. Studies of the efficacy of HSD in trauma
Tissue patients
oxygenation Emergi
Reverse systemichave acidosis 99
been inconclusive ; the most obvious benefit occurred in a
Vulnerable Patient Populations Document subsetlactate
decrease in to normal range patients with bothStroke
of polytraumatized
volume variation
hemorrhage and
Emergi
arter
TBI,
*Fluid administration in whom
should improved
be continued neurologic
until adequate status was demonstrated in95
systemic
perfusion is restored. Acoustic blood flow Investig
Clinical trials of deliberate hypotensive resuscitation have avoided those who received HSD as a resuscitation fluid. Indeed, HS is
Dr Azam’s Notes in of
the application Anesthesiology
this technique2013
to populations perceived to be commonly used as an osmotic agent in the management of TBI
87,91 100
Anesthesia for Trauma 2291 72
PATIENT IN SHOCK
SBP ≤ 90 mm Hg
Traumatic mechanism of injury

Early management
DIAGNOSIS AND PRIMARY SUPPORT AND RESUSCITATION

TREATMENT ABCs
Rule out mechanical factors 967&$-
9-$3,.2'.0 6 9-23! 2(.-
9 0#( "2 ,/.- #$ 9entilation
Control hemorrhage !.0 2.071 ,/+$1
9(0$"2/0$1130$ 9
9Thoracostomy tubes 9 "2 2$
9.-&!.-$1/+(-2(-& 9ABG
9$+4("!(-#$0.0$62$0- +%(6 2.0 9T.6(".+.&7
9-&(.&0 /'("$,!.+(8 2(.- 9T7/$ -#"0.11, 2"'
930&$07 Monitors
92 -# 0#-.-(-4 1(4$
9Arterial line
T$,/$0 230$
9+3(#5 0,$0
9.0"$#'.2 (0!+ -*$2
+3(#2'$0 /7
9 (-2 (- 80-90 mm Hg
9 (-2 (- ≥30%
9 (-2 (- ≤14 sec
No $,.00' &$".-20.++$#
Yes
Late resuscitation
Figure 72-8 Algorithm for the management of early hemorrhagic shock. ABCs, airway, breathing, circulation; ABG, arterial blood gases; CBC, complete blood
count; HCT, hematocrit; PT, prothrombin time; SBP, systolic blood pressure.
96
Dr Azam’s
short-term careNotes in the
based on Anesthesiology 2013
number of units of blood trans- These concerns led to the concept of damage control surgery,
fused.103 One hundred forty-one patients received massive blood which emphasizes rapid control of active hemorrhage.104
ely con- Dr Azam’s Notes in72
Anesthesiology 2013
Anesthesia for Trauma 2301
The prac- Table 72-5 Modalities for Assessment of Systemic Perfusion
n to all dislocation is a medical emergency that must be promptly
. Hypo- Technique Shortcomings Box 72-8 Advantages and Disadvantages of Regional
addressed if the patient is to have a good functional outcome. Anesthesia for Trauma Patients
dictable
Failure to promptly diagnose
Vital signs and reduce
Will not indicate a dislocated hip joint is
occult hypoperfusion
siologic
a
Urine outputsignificant risk factor for avascular necrosis
May be confounded by intoxication, of the femoral head. Advantages
Reduction typically requires a very deep
diuretic therapy, level
circadian of sedation,
variation, or which Allows continued assessment of mental status

may be facilitated by nondepolarizing
renal injury neuromuscular blockade. Increased vascular flow
SystemicFor this status
acid-base reason the Confounded
anesthesiologist is commonly
by respiratory status involved.177
Although it is possible to reduce a dislocated hip in a spontane- Avoidance of airway instrumentation
g Lactate clearance
ously breathing patient Requires
sedatedtime to obtain
with laboratory
fentanyl, result
midazolam, keta- Improved postoperative mental status
old mine,
Cardiac output propofol, or a combination of two or more
Requires placement of a pulmonary agents, an acutely Decreased blood loss
injured patient is at high riskcatheter
artery for aspiration. Any patient who will
or use of noninvasive
Decreased incidence of deep venous thrombosis
be undergoing surgery in the near future (as for an open long-
technology
boneoxygenation
fracture or exploratory Improved postoperative analgesia
Mixed venous Difficult to laparotomy)
obtain, but a veryshould be intubated at
accurate
the time of reduction and markermaintained with appropriate sedation Better pulmonary toilet
and analgesia until reaching the OR. Other patients who may Earlier mobilization
Gastric tonometry Requires time to equilibrate, subject to
require intubation even for uncomplicated reductions include
artifact
those who are inebriated or uncooperative, hemodynamically Disadvantages
Tissue oxygenation
unstable, or sufferingEmerging technology, appears
from pulmonary beneficial
dysfunction. Peripheral nerve function difficult to assess
Unlike acetabular
Stroke volume variation Emergingfractures, fracture
technology, requires anof the pelvic ring Patient refusal common
requires immediate recognition
arterial line and management by the trauma
Requirement for sedation
mic
team. Hemorrhage, even
Acoustic blood flow
exsanguination, is common after a major
Investigational technology, unproven A
pelvic ring fracture and is a leading contributor to early death Hemodynamic instability with placement
after motor vehicle collisions. Bleeding occurs from multiply dis- Longer time to achieve anesthesia
rupted venous beds in the posterior pelvic bowl; if the pelvis as a Not suitable for multiple body regions
whole is unstable, there is no anatomic barrier to continued May wear off before procedure(s) conclude
expansion of this retroperitoneal bleeding. Surgical exploration
by way of the peritoneum is usually unrewarding because the
bleeding vessels are not easily accessed.178 Therapy consists of
supportive volume resuscitation, external fixation of the unstable of universally accepted diagnostic criteria combined with con-
pelvis, and angiography. Intubation is usually undertaken on an comitant pulmonary and cardiovascular dysfunction accounts for
emergency basis in a hypotensive patient, and the anesthesiologist the varying incidence reported in the literature. Most studies
may remain with the patient throughout the initial hours of sta- suggest that clinically significant FES occurs in 3% to 10% of
bilization to manage sedation, analgesia, transport, and fluid patients, although the presence of multiple long-bone fractures is
resuscitation. In the absence of an orthopedic specialist, tempo- associated with a higher incidence. Patients with coexisting lung
rary stabilization and tamponade of some pelvic fractures can be injury are at additional risk for FES. Signs include hypoxia, tachy-
accomplished with use of a specially made pelvic binder, the cardia, mental status changes, and a petechial rash on the upper
pelvic portion of military antishock trousers, or a bed sheet portions of the body, including the axillae, upper arms and shoul-
knotted tightly around the bony pelvis.179 ders, chest, neck, and conjunctivae. FES should be considered
97
Open fractures should be pulse-lavaged and débrided as whenever the alveolar-arterial oxygen gradient deteriorates in
soon as possible after injury to minimize the risk of infectious conjunction with decreased pulmonary compliance and CNS
Dr Azam’s Notes in IfAnesthesiology
complications. ongoing resuscitation 2013or unstable TBI precludes deterioration. Under general anesthesia, the CNS changes will not
HEMORRHAGE
CONTROLLED
RESUSCITATION
COMPLETE?
SBP ≥ 100 mm Hg
HR ≥ 100/min
pH ! 7.40 Yes Finished
Lactate normal
Urine output adequate
HCT ≥ 25%
PT ≤ 14
No
MAXIMIZE CARDIAC OUTPUT

PA catheter
Fluid bolus
Resuscitation complete?
No
Ongoing hemorrhage? Return to early

(Missed injury?) Yes resuscitation
No
Maintain volume status, blood composition, and cardiac output

Consider inotropic therapy
Figure 72-9 Algorithm for the management of late hemorrhagic shock. HCT, hematocrit; HR, heart rate; PT, prothrombin time; PA, pulmonary artery; SBP,
systolic blood pressure.
Monitoring resuscitation with invasive monitors is chang- during positive-pressure ventilation is a reliable predictor of
ing at present to noninvasive approaches that assess the return of decreased intravascular volume.115 98
adequate metabolism, respiration, and oxygen transport in Tissue hypercapnia has been suggested as a universal indi-
Drperipheral
Azam’stissue
Notesbeds. in
OneAnesthesiology
such technique is tissue oxygen moni-
2013 cator of critically reduced perfusion. Measurement of gastric Pco2
toring (skin, subcutaneous tissue, or skeletal muscle). Skeletal by gastric tonometry has been used in trauma patients as an
muscle blood flow decreases early in the course of shock and is indicator of restoration of splanchnic blood flow, and distal gut
Critical Pathway for Treatment of Cerebral Perfusion Pressure in Patients with

Severe Traumatic Brain Injury
General parameters for ALL patients Initial interventions
C)16;)16:@:;741+"! 55/>1;h C:;)*41:0)19>)@*9-);016/)6,+19+<4);76

;9)6:,<+-94-=-4-,);;0-804-*7:;);1+)?1: C&-6;14);-;75)16;)16")CO2 to 35 mm Hg
C--8+; C"97=1,-:<884-5-6;)4O2 to keep
C)16;)16:-9<5:7,1<5);

<64-:: ")O2 !70 mm Hg or SpO2 !94%
8);1-6;0):"-4-=);176: C)16;)1667957;0-951a
C6+7<9)/-<:-7."%!2 monitoring C)16;)160-),7.*-,;778;151A-"")6,516151A-"
C61;1);-&%89780@4)?1s C6:<9-/77,0-),)6,6-+3)41/65-6;
C61;1);-6<;91;176)::776):5-,1+)44y C#-,<+-<66-+-::)9@67?17<::;15<41
)8897891);->1;0.<44+)4791+9-84)+-5-6; C$--:-,);176)4/791;0m
*@,)@:).;-9162<9@
C61;1);-)6;1+76=<4:)6;:.79;0-.19:t
,)@:).;-9162<9@80-6@;7161:
the agent of choice 6:-9;+)516779&C
"5761;79"*rO2 monitor
'0-68);1-6;0):)6<6-?84)16-,
"-4-=);17679;0-9-1:)+0)6/-
165-6;)4:;);<:
B0-+3;0-;7-6:<9-")O2 )6,")CO2
)16;)16"" ! 60 mm Hg are in the desired range
B6:<9-;0);;0-8);1-6;:87:1;1761:67;
4151;16/=-6;14);17679+)<:16/16+9-):-,"
Intracranial
Intracrainal No
hypertension?
≥20
≥ 25mm
mmHgHg or
or**
Yes
*!25 mm Hg after C6:<9-)44161;1)416;-9=-6;176:)9-1684)+-

decompressive C,5161:;-9:-,);176:--)4/791;05
craniectomy C76:1,-99-8-);16/)*9)16%:+)6 )9-.<44@9-57=-
;9-);5-6;.79"
Intracranial
Intracrainal
No
hypertension?
≥20
≥ 20mm
mmHgHg or
or**
Yes
C6:<9-)44161;1)416;-9=-6;176:)9-1684)+-
C6:-9;&)6,,9)16$F
C76:1,-99-8-);16/)*9)16%:+)6
Intracranial
Intracrainal No
hypertension?
≥20
≥ 20mm
mmHgHg or
or**
Figure 72-10 Clinical pathway for the management of severe traumatic brain injury. The goal of therapy is to maintain cerebral perfusion pressure above
60 mm Hg by support of the circulation and control of intracranial pressure. Progressively more intensive therapies are added until this goal is achieved. ABG,
arterial blood gases; BP, blood pressure; CBF, cerebral blood flow; CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; CT, computed tomography; DVT,
deep venous thrombosis; Hct, hematocrit; ICP, intracranial pressure; IVC, intraventricular catheter.
99
Dr Azam’s Notes in Anesthesiology 2013 A

Adult Subspecialty Management forms of bronchospasm, no breath sounds can be auscultated,
pressure ventilation (NIPPV) such as continuous positive airway is mandatory, especially forDr patients
Azam’swith
NotesSTEMI. The most2013
in Anesthesiology recent
pressure (CPAP) has becomeContinued a standard therapy over the past guidelines recommend starting supportive therapy on the scene
several years in the treatment of acute pulmonary edema.135 consisting of morphine (pain control), high-flow oxygen, nitrates
Adult Medical
Recently published recommendations
Emergencies suggest NIPPV for every
Table 73-3 Common Nontraumatic Causes of Acute Shortness of
(if patient is not hypotensive), and oral aspirin, easily memorized
:1574($//,1,6,$/,16(48(16,215$4(,13/$&( Breath in Adults
patient with acute:+2466(40+93(48(16,/$6,2162$
pulmonary edema.5&$n 136,137
The subsequent therapy
CO 62
00* as the well-known “MONA” acronym.138,139 β-Blockers can be con-
Most textbooks on:215,'(44(3($6,1*$%4$,1
prehospital emergency medicine discuss adult
2
should be guided by the patient’s systolic blood pressure (SBP): sidered if the
Exacerbated patient
chronic is tachycardic
obstructive pulmonary and/or
diseasehypertensive. The goal
medical emergencies under the patient’s final diagnosis, such as
is to reduce myocardial oxygen demand while improving oxygen
Asthma
congestive heart failure (CHF)Intracrainal or chronic obstructive pulmonary
t SBP greater than 140 mm Hg: NIPPV plus
Intracranial No
nitrates (nitro- supply. Thepulmonary
Cardiogenic 12-lead ECG
edemais(congestive
a vital component
heart failure)of prehospital care
disease (COPD). This, however, ismmHg
not
hypertension?
how patients present to the
glycerin spray or continuous ≥20
≥ 20mm Hg or
IV infusion; recommended
or**
for ACS because
Noncardiogenic it is edema
pulmonary the only tool that
(inhalational, can reliably identify
sepsis-related)
EMS team on the scene; instead, patients usually present with a
starting dose: 5-20 µg/min)Yes Pneumonia
patients who may benefit from prehospital reperfusion therapy
chief complaint (or lead symptom), such as dyspnea or chest pain. Pulmonary embolism
t SBP 140 to 100 mm Hg: NIPPV plus nitrates plus diuretics (Fig. 73-4). The overarching goal is to limit myocardial ischemia
Most often, adult medical emergencies fall into only three sepa-
:1574($//,1,6,$/,16(48(16,215$4(,13/$&(
Foreign body obstruction
(furosemide):$11,62/

* .*$1' 24+93(4621,&5$/,1(
if signs of systemic fluid retention time to less than 120 minutes (ideally <60 minutes). Early out-of-
rate chief complaints: 24"
&+/24,'($1'
$&(6$6(#)24
dyspnea/respiratory distress, cardiac/circu- Aspiration
t SBP less than$&76(0$1$*(0(16&215,'(4$
0%2/7s
100 mm Hg: hypoperfusion is predominant
latory emergencies,: and altered level of consciousness. Therefore,
2)+93(4621,&5$/,1(
and signs of $,16$,15(4702502/$4,69!
050 /$1d
cardiogenic shock are present. These patients Adapted from Fowlkes TD: Shortness of breath. In National Association of EMS
we will discuss adultkeep medical emergencies in this chapter by their
patient euvolemic Physicians andDifferential
Kuehl AE (eds): Prehospital Systems andPain
Medical Oversight,
require inotropic agents such as5&$n
:215,'(44(3($6,1*$%4$,1 dopamine and dobutamine Table 73-4 Diagnosis of Acute Chest in Adults
respective chief complaint.
:$,16$,15(47052',70 "0 Dubuque, IA, Kendall and Hunt, 2002, p 665.
and a carefully titrated volume challenge.
Acute coronary syndrome (unstable angina, myocardial infarction)
t Pulmonary edema with signs of acute coronary syndrome
Intracranial
Intracrainal No Pulmonary embolism
(ACS): these patients require hypertension?ACS specific management in Gastroesophageal reflux
≥20
≥ 20mm Hg or
mmHg or**
addition to NIPPV plus nitrates.136 Peptic ulcer disease
Yes Gastritis or esophagitis
The treatment goals are to stabilize the patient, improve
$4()7//94(028( Aortic dissection
oxygenation and perfusion, and reduce dyspnea.
:1574($//,1,6,$/,16(48(16,215$4(,13/$&(
64($60(162)
Pericarditis
:215,'(44(3($6,1*$%4$,1 5&$n
:215,'(475(2)26+(45(&21'6,(46+(4$3,(s Pneumonia
Pneumothorax
Cardiac and Circulatory Emergencies Pleurisy
Boerhaave’s syndrome (esophageal rupture)
(&2034(55,8( ,*+'25( 93(48(16,/$6,2162 (&2034(55,8( Pancreatitis
Chest paincraniectomy
and circulatory problems
%$4%,674$6( PaCO (e.g.,
!30 mmsyncope,
Hg 2 hypertension)
laparotomy
therapy 21,624,1*-O Musculoskeletal pain
are encountered frequently in the prehospital
8-DO %4O $1' 24setting (see Chapter
2 2
2
CBF recommended
Figure 72-10, cont’d
100

s procedure be apparent but may be manifested as failure to awaken after
and general
9. For many Box 72-9 Advantages and Disadvantages of General Anesthesia and Prehospital Eme
provide an Anesthesia for Trauma Patients
and analge- Table 73-2 On-Scene Triage Criteria for Major Trauma Necessitating
xibility and Advantages
Transport to Trauma Center Dyspnea/Respiratory D
Speed of onset
of an ortho- Duration—can be maintained as long as needed Mechanism of Injury
nal anesthe-
Allows multiple procedures for multiple injuries Dyspnea is one of the most comm
mbolism, as Extrication time >20 minutes
Greater patient acceptance High-speed crash with:
prehospital care, carrying a signific
Intrusion into passenger compartment >20 cm 18% in adults.128 Each year in the U
aphy (TEE) Allows positive-pressure ventilation
one fracture Speed >40 mph patients with respiratory distress
d marrow.180 Disadvantages Ejection shown in a large Canadian outcom
om this phe- Impairment of global neurologic examination Death of another passenger in same car ALS decreases mortality in these
e inflamma- Requirement for airway instrumentation Rollover shortness of breath is most commo
dysfunction Hemodynamic management more complex Pedestrian or bicyclist hit by motor vehicle spasm or pulmonary edema second
r laboratory Motorcycle crashA>20 mph or with separation of rider from motorcycle
FES). A lack
Increased potential for barotrauma ential diagnoses such as pulmonar
Falls >3 m (9.8 ft) foreign body obstruction must b
Physiologic Criteria
Identifying the correct diagnosis o
Systolic blood pressure <90 mm Hg
Respiratory rate <10 or >29 breaths/min
straightforward as it may seem13
Glasgow Coma Scale score <14 dyspnea can be multifactorial, for
Pregnancy severe COPD and CHF who develo
Anatomic Criteria
Flail chest Patient Evaluation
Two or more proximal long bone fractures The most important aspect of the
Pelvic fracture with acute dyspnea is to identify if th
Penetrating injury to head, neck, torso, or extremities proximal to with imminent respiratory failure a
elbow or knee ment. Physical signs and symptom
Open or depressed skull fracture
condition are cyanosis, tachypnea
Amputation proximal to wrist or ankle
Paralysis
min or >30 breaths/min), stridor, t
Discretion of EMT in full sentences (<5 to 6 words), an
Per discretion of EMT, patients can be declared a major trauma patient. In tory muscles.133 The use of pulse oxi
addition, preexisting conditions of the patient can lead to an upgraded standard of care in diagnosing hyp
status, such as coronary artery disease, congestive heart failure, severe measurement of the severity of resp
COPD, morbid obesity, or bleeding disorders. Irrespective of the underlyin
COPD, chronic obstructive pulmonary disease. piratory distress should receive high
From O’Connor RE: Trauma triage: Concepts in prehospital trauma care. Prehospital a non-rebreathing facemask. Owing
Emerg Care 10:307-310, 2006. focus on the two most common ca
adults: bronchospasm 101due to asthm
edema due to CHF.
Dr Azam’s Notes in Anesthesiology 2013 and avoiding hypoxemia (SpO2 >90%), maintaining an adequate
cerebral perfusion pressure >70 mm Hg with a systolic blood Prehospital Management
hypertension plus acute coronary syndrome and tachycardia Impo
(quic
h STEMI or Table 73-5 Contraindications of Fibrinolytic Therapy in ST-Segment Elevation onset
ommended Myocardial Infarction Table 73-6 Classification of Acute Hypertensive Episodes
ral fibrino- (e.g.,
ften based Absolute Contraindications (open
Hypertensive emergency Also termed hypertensive crisis;
olytic agent Any prior intracranial hemorrhage
hypertension with acute end-organ
traum
ystems now Known structural cerebrovascular lesion (e.g., AVM)
A or t-PA) Known malignant intracranial neoplasm (primary or metastatic) dysfunction
enecteplase Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 ment
hours Hypertensive urgency Hypertensive episode with high risk of 1 am
ouble-bolus
Suspected aortic dissection imminent end-organ damage that has not
the prehos- Active bleeding or bleeding diathesis (excluding menses) is a v
fibrinolytic yet occurred
Significant closed-head trauma or facial trauma within 3 months this t
also carries Relative Contraindications
r disability History of chronic, severe, poorly controlled hypertension
Acute hypertensive episode SBP > 180 mm Hg or DBP > 110 mm Hg awak
cannot be Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or without signs of evolving or imminent suspe
with percu- DBP > 110 mm Hg)* end-organ dysfunction antag
oal of EMS History of prior ischemic stroke < 3 months, dementia, or known
intracranial pathologic process not covered in contraindications Transient hypertension Related to anxiety or primary complaint starti
Traumatic or prolonged (>10 minutes) CPR or major surgery (<3 weeks) effect
Recent (within 2 to 4 weeks) internal bleeding SBP, systolic blood pressure; DBP, diastolic blood pressure.
Adapted
and n
73-7from Chobanian AV, et al: Seventh Report of the Joint
inNational
Adults:Committee
may o
Noncompressible vascular punctures Table Causes of Altered Level of Consciousness AEIOU-TIPS
difficult to
re nonspe- allergic reaction to these agents
A
For streptokinase/anistreplase: prior exposure (<5 days ago) or prior on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
Hypertension 42:1206-1252, 2003. somee
ead ECG in Alcohol and Airway (hypoxia)
he patient’s
Pregnancy
Active peptic ulcer
b
Epilepsy, Electrolytes, Encephalopathy
ed leg and Current use of anticoagulants: the higher the INR, the higher the risk of c
ound, such Insulin—hypoglycemia
bleeding
Opioids/Overdose
a
severity of
e clots and
AVM, arteriovenous malformation; SBP, systolic blood pressure; DBP, diastolic
blood pressure; INR, international normalized ratio. Urea (metabolic) i
g to acutely *Could be an absolute contraindication in low-risk patients with myocardial
Trauma, Tumor
cute right- infarction.
embolism
Adapted from American Heart Association Guidelines for Cardiopulmonary Infection
tachypnea,
Resuscitation and Emergency Cardiovascular Care. Part 8. Stabilization of the A
Psychiatric
Patient with Acute Coronary Syndromes. Circulation 112(24 Suppl):IV-89-110,
ecific find- 2005. Shock, Subarachnoid hemorrhage, Snake bite
Adapted from Wolfe RE, Brown DFM: Coma and depressed level of consciousness. P
In Marx JA (ed): Rosen’s Emergency Medicine. Philadelphia, Mosby, 2006. h
g
y
severe opioid withdrawal symptoms can result. Similarly,102 if l
patients with benzodiazepine overdose (“sleeping pills”) are a
treated aggressively with the antagonist flumazenil, generalized v
years)

Different triage strategies (Simple Triage and Rapid Treat- example, patients with intra-abdominal bleeding requiring emer-
ment-START,
Table CareFlight
73-8 Definitions in Triage,
Disastermodified
MedicineSTART) show compa- gent surgery have the highest transport priority. For disposition
rable results in identifying the severely injured (Table 73-9). of the patients to adequate hospitals, a quick registration and
Triage implies constant reevaluation of victims because condi- documentation stage is necessary.
Level of Prehospital Medical
tions
Termof the victims and of available resources change continu-
Definition Care Possible Examples
ously.174 Patients whose injuries are so grave (i.e., traumatic cardiac
arrests)
Emergencythat their prognosis
Incidentis that
dismal shouldurgent
demands not beaction;
classified as
impact: Individual medicine Patient with bicycle accident,
critical in the setting ofminutes
a largetomass
hours casuality incident (MCI).
Controversies in Prehospital stroke, angina
They are likely to consume large quantities of resources in a futile Emergency and Trauma Care
Mass casualty
resuscitative effort.175 Large number
The motor of casualties
score of the GCS in aandshort period
systolic Triage; increasing level of medical treatment Airplane crash, train collision,
175
blood pressure show good thatassociation
initially exceedwithlocal
severe injury.
logistic supportThe
The EMSdependent
literature is onfull of conflicting opinions and recommen-
resources mass poisoning
emergency physician oncapabilities;
the scene has to guarantee
impact: hours to that the treat-
days dations about what the ideal EMS system and the ideal level of
ment priorities are followed by the EMTs rather than treating prehospital care are. The plethora of differing opinions is likely
Disasterby himself orLarge
patients number of casualties and destroyed
herself. due toTriage; firstdifferences
the vast aid; significant delay
in how EMS Hurricane, earthquake,
untilsystems are organized
infrastructure;
In the first phase, only BLS, such exceeds local response
as opening the airway, professional medical help available usually
around the world and probably also to a lack of reliable evidence tsunami, nuclear disaster
recovery position, tourniquets, and positioning,
capabilities. Supraregional should be done.
(national) from high-quality
forces research. Ininfrastructure
only after temporary the United States, one of the most
was set (e.g., Chernobyl)
Advanced procedures such are as IV access,
needed oxygen
to solve the therapy,
problem;anesthe-
damage important up documents ever written on the current problems in
sia, intubation, and ventilation can be last
and interruption performed
long-termas(weeks
soon to EMS, The Future of Emergency Care: Emergency Medical Services
as
resources are available. With incoming
years) transport capacity, patientsat the Crossroads, was published in 2007 by the Institute of Medi-
are stabilized and transported according to urgency priorities. For cine of the National Academy of Sciences.12 It is the third part of
a comprehensive study on the state of emergency medicine in the
United States that also includes in-hospital emergency medi-
Table 73-9 Triage Groups in Mass Casualty Incidents
Different triage strategies (Simple Triage and Rapid Treat-
cine 176 example,
and pediatric patients
emergency with
care. 177 intra-abdominal bleeding requiring emer-
It is likely that this report
ment-START, CareFlight
With the aid of triage tags or coloredTriage,
flags themodified START) show will
patients are sorted compa- gent surgery
have a similar haveasthe
effect on EMS didhighest
The White transport
Paper pub-priority. For disposition
11
rable results
into four groups: in identifying the severely injured (Table lished in 1966.of
73-9). Here,
the we focus ontothose
patients areas in hospitals,
adequate prehospital care
a quick registration and
Triage implies Minor
Green/minor constant reevaluationWounds,
injuries with of victims becauseengendering
minor fractures condi- the fiercest debate and
documentation where
stage isanesthesiologists
necessary. could,
in our opinion, make the biggest impact.
tions of the victims and of available resources change continu-
no immediate need
ously.174 Patients of treatment;

whose injuries are so grave (i.e., traumatic cardiac
psychological support
arrests) that their prognosis is dismal should not be classified TheasOptimal Level of Prehospital Care:
needed; patients can
critical in the setting of a large mass casuality incident (MCI).
walk
Controversies in Prehospital
BLS Versus ALS or “Scoop-and-Run”
They are likely to
Yellow/delayed consume
Urgent treatment,large
no quantities
Fractures,of resources
joint injuries, in a Versus Emergency and Trauma Care
futile “Stay-and-Play”
175
resuscitative effort. The motor score of the GCS and systolic
vital threat amputation, major
blood loss, burns 175
blood pressure show good association with severe injury. The articles
Numerous The EMShave literature is fullover
been published of conflicting opinions and recommen-
the past decades
emergency
Red/immediatephysician
Immediate on the
vital scene has
threat to guarantee
Respiratory that the
insufficiency, treat-eitherdations
favoring about approach
a minimalistic what the to ideal EMScare,
prehospital system
basi- and the ideal level of
shock, brain trauma,
ment priorities are followed by the burns EMTs withrather
immediate than cally BLS levelprehospital
treating only, or the opposite,
care are.an The
aggressive strategy
plethora of trying
differing opinions is likely
to bring the level of care in an emergency department to the
patients by himself or herself. vital threat, abdominal due to the vast differences in how EMS systems are organized
scene. In our opinion this discussion is misguided. It is unlikely
In the first phase, only BLS, such traumaas opening the airway,
that a country around the world
that currently and probably
employs also to EMS
a paramedic-level a lack of reliable evidence
recovery position,
Black/expectant Dead tourniquets,
or moribund and Respiratory
positioning, arrest,should be system will abandon this system in favor of a BLS-only system orStates, one of the most
done. from high-quality research. In the United
cardiac arrest, head
Advanced procedures such as IV access, oxygen therapy, anesthe- vice versa (seeimportant
Chapter 97).documents ever written
More importantly, on the current problems in
this discussion
injuries with dismal
sia, intubation, and ventilation can prognosis be performed as leads soonaway
as fromEMS,the The
mostFuture
important determinant of
of Emergency the overall
Care: Emergency Medical Services
efficacy and efficiency of any EMS system: the outcome of the
resources are available. With incoming transport capacity, patients at the Crossroads, was published in 2007 by the Institute of Medi-
are stabilized and transported according to urgency priorities. For cine of the National Academy of Sciences.12 It is the third part of 103
a comprehensive study on the state of emergency medicine in the
Dr Azam’s Notes in Anesthesiology 2013 United States that also includes in-hospital emergency medi-
Table 73-9 Triage Groups in Mass Casualty Incidents
cine176 and pediatric emergency care.177 It is likely that this report
Dr Azam’s74
Chemical and Biological Warfare Agents: The Role of the Anesthesiologist 2339
Table 74-1 Physicochemical Properties of Nerve Agents
Properties* Tabun (GA) Sarin (GB) Soman (GD) VX
Molecular weight (daltons) 162.3 140.1 182.18 267.36

Specific gravity at 25°C 1.073 1.0887 1.022 1.0083
Boiling point (°C) 246 147 167 300
Melting point (°C) −49 −56 −80 −20
Vapour Pressure (VP) and VP Vol VP Vol VP Vol VP Vol

Volatility (Vol)†‡ °C (mm Hg) (mg m−3) (mm Hg) (mg m−3) (mm Hg) (mg m−3) (mm Hg) (mg m−3)
0 0.004 38 0.52 4 279 0.044 470.9 — —
10 0.013 119.5 1.07 8 494 0.11 1 135.5 — —
20 0.036 319.8 2.10 16 101 0.27 2 692.1 0.00044 5.85§
25 0.07 611.3 2.9 21 862 0.40 3 921.4 0.0007 10.07
30 0.094 807.4 3.93 29 138 0.61 5 881.4 — —
40 0.23 1912.4 7.1 60 959 — — — —
50 0.56 4512.0 12.3 8 3548 2.60 23 516.0 — —

*At room temperature, GB is a comparatively volatile liquid. GD also is significantly volatile. GA is less volatile. GD may be thickened to increase its persistence. VX is
relatively nonvolatile and is regarded as presenting little vapor hazard.
†Vapor pressure in mm Hg.
ØOheZmbebmrbgf`f−3. Volatility = concentration of saturated vapor at specified temperature. Volatility calculated from PV = nRT.
§Some authorities quote values 0.1 to 1 mg/m−3.
In the equation:
VP × 101325 × MW VP × MW × 16.035
Vol = =
760 × 8.3143 × A A
Å = absolute temperature.
From Baker DJ: Anesthesia in extreme environmental conditions, part 2: Chemical and biologic warfare. In Grande CG (ed): Textbook of Trauma Anesthesia and Critical
Care. St Louis, Mosby-Year Book, 1993, pp 1320-1354.
poisoning. The interaction of OPs with AChE is nonreversible hours. After 5 half-lives, more than 95% of the enzyme AChE has
after a certain time depending on the nerve agent. The formation aged and cannot be reactivated. This has important consequences
of an irreversible complex is known as aging. Each nerve agent on the window of clinical opportunity31 for treatment to try to
has an aging half-life. For GB, this is about 5 hours, whereas for reverse the AChE inhibition (see section on oximes later).
GD, it is only 2 minutes. GA and VX have aging half-lives of 40
Signs and Symptoms of Nerve Agent Poisoning
CH3 The classic signs and symptoms of nerve agent poisoning are
CH3 shown in Table 74-2. Poisoning is caused by the accumulation of
CH3CHO O 104
acetylcholine and not by the OP itself. As a result of stimulation
CH3CHO O P of muscarinic synapses, there is miosis; ciliary body spasm
P 2013 CH3 F causing pain32; glandular hypersecretion, including salivary,
CH F bronchial, and lacrimal; sweating; cardiac effects, including
piratory irritation with coughing, retching, choking, and ventilation is a matter of interest. More recent work in physical
61,62
chest tightness. These symptoms are accompanied by eye trauma has indicated that the “open lung” strategy Dr Azam’s is Notes
of valuein Anesthesiology 2013
irritation and lacrimation. In some cases, death has fol- in the prevention of inflammatory cascades by opening the alveoli
V 2340 Adultlowed exposureManagement
Subspecialty to high concentrations of phosgene without and keeping them open by use of the correct level of positive
the development of toxic pulmonary edema. The reason for end-expiratory pressure. This technique follows the hypothesis
Table 74-2 Symptoms and Signs of Nerve Agent Poisoning by Type of Cholinergic Receptor and Target Organ
this is obscure, but may be related to hypoxia as a result of that repeated opening and closing of alveoli causes kinin release
Receptor intense laryngeal
Target Organ or bronchospasm. Symptoms and Signs through the action of shear forces in the alveolar walls. There may
2. The
Muscarinic immediate choking symptoms are
Iris muscle; ciliary muscle accommodation followed by a latent be ofanpainimportant
Miosis; spasm leading to failure lesson
in the eyes; nausea for theheadache
and vomiting; early management of lungs
period ofConjunctival
2 to 24vessels
hours before the onset Vasodilation
of more and serious
hyperemiadamaged by phosgene exposure, and the manner of emergency
symptoms and signs, including dyspnea, painful cough, and ventilation may be critical. Bag-valve ventilation, which can lead
Nasal glands Rhinorrhea and hyperemia
cyanosis,Bronchial glands
with increasing signs of pulmonary Increased secretion
edema leading to very high inflation pressures and high flow rates, may be
Bronchial muscle Bronchoconstriction; tightness in the chest; expiratory wheezing; dyspnea
to circulatory collapse
Gastrointestinal tractand cardiac arrest. Anorexia; nausea; vomiting;harmful. Emergency
abdominal cramps; diarrhea;ventilation strategies
tenesmus; involuntary that provide controlled
defecation
Sweat glands Increased activity flow rates with the early use of positive end-expiratory pressure
Pathophysiology Salivaryof Toxic Pulmonary Edema
glands Increased activity are more appropriate. These can be provided by the use of small
Phosgene reacts through
Lacrimal glands covalent attack on Lacrimation many substrate automatic gas-powered ventilators (Fig. 74-8).
(not usually marked)
60
groups, including NH2 and SH. Potential cell targets are type I
Heart Bradycardia; occasionally tachycardia
Modern experience of the management of mass casualties
Bladder Frequency; involuntary micturition
and II pneumocytes and alveolar macrophages. Covalent binding with toxic pulmonary edema is limited, but it must be assumed
can be seen as Skeletal
Nicotinic the primary
muscle attack leading to free radicalfatigue;
Weakness; release. that acramps;
fasciculations; considerable proportion
flaccid paralysis (early effectswho survive the acute toxic pul-
on respiratory
muscles may produce dyspnea)
This stage is followed by a secondary attack involving
Autonomic ganglia
released monary edema would develop acute respiratory distress syn-
Pallor; occasional elevation of blood pressure
inflammatory mediators, including prostaglandins (causing drome unless the appropriate measures are taken. A study by
Muscarinic and Central nervous system
vasoconstriction, vasodilation, and platelet Anxiety; disaggregation), Parkhouse and colleagues63 showed
giddiness; restlessness; headache; withdrawal and depression; memory failure;
improved oxygenation,
nicotinic impaired concentration; slurred speech; depression of respiratory and cardiovascular
decreased
centers; Cheyne-Stokes respiration shunt fraction, and decreased mortality in phosgene-
exposed pigs that received a protective compared with a conven-
From Baker DJ: Anesthesia in extreme environmental conditions, Part 2: Chemical and biologic warfare. In Grande CG (ed): Textbook of Trauma Anesthesia and Critical
Care. St Louis, Mosby-Year Book, 1993, pp 1320-1354.
Table 74-3 Properties and Toxic Exposure Levels of Phosgene
tional ventilation strategy.
the Cold War, the clinical evidence base is smaller than that for
Properties Use of
that corresponds Steroids.
to the The usedescribed
signs and symptoms of inhaled and systemic steroids in
previously,
pesticide
Chemicalpoisoning. During
name: carbonyl the early
chloride (COCl2stages of the Cold
), chloroformyl War,
chloride the treatment
there are considerable of toxicwith
differences phosgene exposure
nerve agents. hasisbeen controversial
It also
64
many
Boilingexperimental
point: 8.2°C studies were done on human volunteers likely that for many years, and Diller, a leading authority
different nerve agents have different effects on the on phosgene
exposed to nerve1215
Vapor pressure: agents;
mm these studies have been reviewed by
Hg at 20°C central andpoisoning,
peripheral nervous systems.
believed in 1985 that the case was unproven. More
8
Marrs
Vaporand colleagues.
density: 3.5 × airThe attacks in Japan in 1994 and 1995 also recently, there has been renewed experimental interest in the
have providedslow
Breakdown: important
aqueousinformation
hydrolysis toconcerning
HCl and CO2the signs and
symptoms after sarin release.3,27
subject using chlorine injury, which has produced some encour-
Cardiovascular Effects of Nerve Agents. Critical care 65
Toxic Exposure Levels management aging
of OPresults in pig
pesticide and rat
poisoning hasstudies.
indicatedGunnarsson
short-term and colleagues
1 ppm chronically—chronic
Clinical Evidence from More disease Military Experience. and medium-term
lung Recent found incardiac
a study of 1835,36
changes. pigs subjected
After an initialtotachycar-
140 ppm chlorine for 10
>25Iran-Iraq
The War produced
ppm/min—acute first-hand clinical information about dia (mediated
lung effects minutes thattheinhaled
through anomalousbeclomethasone dipropionate produced
sympathetic nervous
the effects
50-100 and management
ppm/min—initial of nerve response
inflammatory that may24 be
agent poisoning. Iranian
followedsystem)
by and a vagally induced bradycardia, there
higher Pao2 and ventilation-perfusion ratios,may be ven-with less histologic
casualties fromedema
pulmonary nerve agents apparently fell into four broad cate- tricular dysrhythmias, including torsades de pointes and prolon-
damage, than in the control group. In another study, Wang and
gories. Individuals who had
>150 ppm/min—clinically the greatest
significant exposure died
and life-threatening in the edema
pulmonary gation of the Q–T interval. Dysrhythmias have been reported as
colleagues66 exposed 24 pigs to a higher concentration of 400 ppm
field; mask protection by Iranian troops
Lethal exposure in humans—800 ppm for 2 min was severely compro- a poor prognostic sign.
mised by their having to wear beards for religious reasons. Despite for 10 minutes. They found that the inhaled steroid budesonide,
the fact that Iraqi attacks were made against troops having com-
105
promised or poor protection, the number of deaths seems to have Treatment of Nerve Agent Poisoning:
been low. The most severely injured individuals who reached Antidotes and Life Support
Drmedical
Azam’s Notes
care in Anesthesiology
were unconscious 2013 and often in
and unresponsive Atropine. Atropine has long been a mainstay in the manage-
respiratory arrest. The next group who were seriously poisoned ment of OP poisoning.30,34 Its antagonistic action against acetyl-
Chemical and Biological Warfare Agents: The Role of the Anesthesiologist 2347 74
Table 74-4 Antidotes Used in the Treatment of Cyanide Poisoning
Duration of
Antidote Action Route Dose Concurrent Drugs Administration Possible Side Effects
Oxygen Increases Inhalation High flow via mask or 100% Oxygen used as primary ≤24 hr Unlikely—possible in
arterial O2 via mask via ETT antidote in all cases patients with COPD
content, or ETT
potentiates
activity of
other
antidotes
Amyl nitrite Methemoglobin Inhalation Adult: 0.2 mL Oxygen (not 30 sec/min Difficult to achieve
formation simultaneously) effective antidotal
levels without
cardiovascular
collapse
Pediatric: 0.2 mL; may need
repeating
Sodium nitrite Methemoglobin Intravenous Adult: 300 mg (10 mL of Adult: sodium thiosulfate ≥5 min, ≤20 min Methemoglobinemia,
formation injection 30 mg/mL 3%) 25 mL of 500 mg/mL, vasodilation and
(50%) solution and cardiovascular
oxygen collapse
Pediatric: 0.13-0.33 mL/kg of Pediatric: sodium

30 mg/mL (3%) solution (i.e., thiosulfate 1.65 mL/kg
4-10 mg/kg body weight) body weight of
250 mg/mL (25%)

solution (approximately
400 mg/kg body
weight) and oxygen
Dicobalt edetate Binding of Intravenous Adult: 300 mg (20 mL of 50 mL dextrose (500 g/L) 1 min Urticaria, edema of
cyanide ions injection 15 mg/mL (15%) intravenously face and neck, chest
by dicobalt immediately after each pains, dyspnea,
edetate and dose and oxygen hypotension,
by free convulsions
cyanide ions
Pediatric: 4-7.5 mg/kg (0.3-
0.5 mL/kg of 15 mg/mL (15%)
4-DMAP Methemoglobin Intravenous Adult: 3.25 mg/kg Oxygen and sodium 1 min Methemoglobinemia,
formation injection thiosulfate vasodilation and
cardiovascular
collapse, hemolysis,
elevated bilirubin and
iron (this is unlikely to
be relevant to single-
dose exposure)
Pediatric: 3.25 mg/kg
Hydroxocobalamin Binds cyanide Intravenous Adult: 5-10 g 5 g reconstituted in 20 min Reddish discoloration
ions injection 100 mL 0.9% saline; to skin and mucous
oxygen membranes
Pediatric: 70 mg/kg
Sodium thiosulfate Sulfur donor for Intravenous Adult: sodium thiosulfate Oxygen and sodium 10 min Excess administration
endogenous injection 25 mL of 500 mg/mL (50%) nitrite or oxygen and may cause
enzymatic solution and oxygen DMAP hypernatremia
conversion of
cyanide to
thiocyanate
Pediatric: sodium thiosulfate
1.65 mL/kg body weight of
250 mg/mL (25%) solution
(approximately 400 mg/kg
body weight) and oxygen
COPD, chronic obstructive pulmonary disease; ETT, endotracheal tube.
106
Table 74-5 Characteristics of Common Toxins
Source Toxin Action
Bacteria
Bacillus anthracis Anthrax toxin DNA toxin
Staphylococcus aureus Staphylococcal enterotoxin B Enterotoxin
Vibrio cholerae Cholera toxin Enterotoxin
Clostridium botulinum Botulinum toxins Prejunctional decrease in acetylcholine release
Clostridium perfringens Perfringens toxin Necrosis through phospholipase C
Clostridium tetani Tetanus toxin Neurotoxin increase in excitability of motor neurons
Protozoa
Gonyaulax catenella Saxitoxin Depolarization block
Fungi
Fusarium spp. Tricothecenes DNA toxin; hemorrhagic syndrome
Plants
Ricinus communis (castor bean) Ricin DNA toxin; hepatorenal failure
Amphibia
Colombian frog Batrachotoxin Irreversible; Na+ channel blockade; depolarization block
Reptilia
Asian cobra (Naja naja oxiana) Cobra toxin Postsynaptic neurotoxin via phospholipase A2
Taiwan banded krait (Bungarus multicinctus) α-Bungarotoxin Acetylcholine receptor blocker
Fish
Deadly pufferfish Tetrodotoxin Depolarization block
Adapted from Baker DJ: Anesthesia in extreme environmental conditions, Part 2: Chemical and biologic warfare. In Grande CG (ed): Textbook of Trauma Anesthesia and
Critical Care. St Louis, Mosby-Year Book, 1993, pp 1320-1354.)
107
ICU problem. Treatment is supportive, but an antitoxin has been many years and are centrally acting anticholinergic agents. Phen-
Drdeveloped
Azam’s for
Notes in animals.
use in Anesthesiology
83 2013 cyclidine compounds (related to ketamine) and other hallucino-

Table 74-6 Treatment for Patients Exposed to Biological Warfare Agents
Incubation Effects (after Staff

Agent Infective Dose Period Inhalation) Protection Specific Treatment Chemoprophylaxis Vaccine Mortality if Untreated
Bacillus 8000-15,000 1-5 days Mediastinitis, Isolation, Ciprofloxacin 400 mg IV tid; Ciprofloxacin 500 mg PO bid Michigan at 0, Pneumonic, 100%
anthracis spores meningitis, MOF vaccination, doxycycline 200 mg IV once, × 4 wk + vaccinate; 2, 4 wk, 6,
universal then 100 mg IV tid; penicillin doxycycline 100 mg PO 12, 18 mo,
precautions 2 MU IV 2 hourly + bid × 4 wk + vaccinate then
streptomycin 30 mg/kg IM qd annually
Yersinia pestis 100-500 organisms 2-3 days Pneumonia, Isolation, Streptomycin 30 mg/kg IM qd × Doxycycline 100 mg PO bid Greer at 1- Pneumonic, 100%
septicemia, MOF universal 10 days; doxycycline 200 mg × 7 days; tetracycline 3 mo +
precautions IV, then 100 mg IV tid × 14 500 mg PO qd × 7 days 3-6 mo
days (chloramphenicol)
Viral 1-10 organisms 4-21 days Coagulopathy, Isolation, HEPA Ribavirin 30 mg/kg IV once, then NA None 90% (Ebola-Zaire)
hemorrhagic edema, MOF masks, 15 mg/kg IV qd × 4 days, then
fevers universal 7.5 mg/kg IV tid × 6 days
precautions (immunoglobulin)
Viral 10-100 organisms 2-6 days (VEE) Encephalitis, Universal Supportive, anticonvulsants NA Available for 75% (EEE)
encephalitides 7-14 days convulsions, coma, precautions VEE, EEE,
(EEE/WEE) CNS damage and WEE
Francisella 10-50 organisms 2-10 days Pneumonia, pleural Universal Streptomycin 30 mg/kg IV qd × Doxycycline 100 mg PO bid Live 35%
tularensis effusions precautions 10-14 days; gentamicin 3-5 mg/ × 14 days attenuated
kg IV od
Variola 10-100 7-10 days Rash, secondary Isolation, Cidofovir 5 mg/kg IV once every Vaccinia immunoglobulin Wyeth Unvaccinated 30%,
organisms pneumonia universal 2 wk vaccinated 3%
precautions
Burkholderia 1-10 organisms 10-14 days Septicemia, Universal Co-amoxiclav 20 mg/kg IV tid Tetracycline 500 mg PO qd × None Uncertain: >30% if
mallei pneumonia, precautions 14 days septicemic
lymphadenopathy
Coxiella burnetii 1-10 organisms 10-14 days Myalgia, malaise, Barrier nursing Doxycycline 100 mg PO bid × 5-7 Doxycycline 100 mg PO bid Q vax <1%
fever days after exposure × 5 days for 8-12 days
Brucella spp. 10-100 organisms 5-60 days Malaise + cough, Barrier nursing Doxycycline 100 mg PO bid + Doxycycline and rifampicin None <5%
sacroiliitis, rifampicin 900 mg tid PO for for 3 wk
pancytopenia 6 wk
Escherichia 10-100 organisms 1-5 days Vomiting + diarrhea, Barrier nursing Antibiotics not required NA None <5% E. coli O157:H2
renal failure
CNS, central nervous system; EEE, eastern equine encephalitis; HEPA, high-efficiency particulate air filter; MOF, multiple organ failure; NA, not applicable; VEE, Venezuelan equine encephalitis; WEE, western equine encephalitis.
Adapted from White SM: Chemical and biological weapons: Implications for anaesthetic and intensive care. Br J Anaesth 89:306, 2002.
108

y. intervention. The effects of the release agent on the subsequent
minis- V 2420 Adult Subspecialty Management
Table 74-8 Effects of Chemical and Biological Warfare Agents on
hysical
n con-
Somatic Systems Table 78-1 Key Elements of Perioperative Anesthetic Management for thus have a greater degre
Facilitating a Fast-Track Recovery after Elective Ambulatory Surgery of their operation.
surface System Affected Agents
Outpatient surger
Epithelial Vesicants (e.g., sulfur mustard), smallpox, Preoperative Period
may be remarkably low incidenc
ricin Stabilize coexisting diseases (e.g., hypertension, diabetes) and
protec- Studies have shown that
niques encourage prehabilitation exercise program and smoking cessation.
Respiratory
Optimize patient comfort by minimizing anxiety and discomfort.
and return visits to the h
d treat Upper, lower airway Vesicants, phosgene
after ambulatory surgical
d await Respiratory control Nerve agents, ABO Ensure adequate rehydration by replacing fluid deficits.
Use appropriate prophylactic therapies to prevent postoperative sions (and emergency de
lowing system
Gaseous exchange Pulmonary edemagens complications (e.g., nausea, vomiting, pain, ileus). complications.12 Of the
Mechanics of breathing Nerve agents, neurotoxins had the highest, and gyn
Intraoperative Period
ntidote ticipated admissions. Th
Central nervous system Nerve agents, cyanide, neuropeptides, agents Utilize anesthetic techniques that optimize surgical conditions, while
e basic of anesthetic origin (phencyclidines, BZ) ensuring a rapid recovery with minimal side effects.
outpatient surgery is part
Administer local analgesia via peripheral nerve blocks, wound infiltration, and immunocompromise
Peripheral nervous system Nerve agents, neurotoxins (e.g., botulinum,
saxitoxin) and/or instillation. an increase in surgical si
Apply multimodal analgesia and antiemetic prophylaxis (including use of tive antibiotics and prol
forma- Immune system Vesicants, ABO (provocation of immune
glucocorticoid steroids). evidence that the inciden
forma- responses, inflammatory responses, organ
Minimize use of nasogastric tubes and surgical drains, and avoid monary embolus and pn
ed. On failure)
excessive fluid administration. outpatients with obstru
onsider Cardiovascular Nerve agents, ABO
(Table Postoperative Period found to have an increase
iratory Alimentary, renal Nerve agents, toxins, infectious agents
Allow patients who meet discharge criteria to be fast-tracked (i.e., or unanticipated hospita
ABO, agents of biological origin.
A
discharged earlier from recovery units). Minimally invasive
Ensure adequate pain control in the postdischarge period utilizing benefits. For example, wh
nonopioid analgesics to minimize need for opioid-containing analgesics. procedures, the use of mi
Encourage early ambulation and resumption of normal activities of daily reduce overall hospital co
living. benefit relates to the gr
Modified from White PF, Kehlet H, Neal JM, et al: The role of the anesthesiologist in which results in higher
fast-track surgery: From multimodal analgesia to perioperative medical care. turnover times.8 The abil
Anesth Analg 104:1380-1396, 2007. can lead to reduced surg
similar procedures perfor
erative laboratory testing
the patients have a redu
Rationale for Ambulatory Surgery tions. These factors all co
in overall cost for most
Ambulatory surgery can offer a number of advantages for patients, (versus inpatient) setting
health care providers, third-party payers, and even hospitals ized postoperative care (e
(Table 78-2). Most patients actually prefer to have their surgical pain management
109 techn
procedures performed as outpatients because it decreases separa- formed on an outpatient
Dr Azam’s Notes in Anesthesiology 2013 tion from their familiar home environment. Postoperative cognitive blood transfusions o
Table 74-9 Effects of Toxic Agents on Respiration
Respiratory Component Effect Toxic Agent
Central nervous system Depression of respiratory drive and convulsions leading to apnea Nerve agents, cyanide, neuropeptides
Peripheral nervous system Neuromuscular paralysis of respiratory muscles Nerve agents, neurotoxins
Nasopharynx May become blocked by excess secretions Lung-damaging agents, nerve agents
Prodromal rhinitis and rhinorrhea Vesicants
Sneezing Early symptom of mustard
Larynx Irritation, laryngeal spasm Upper respiratory irritant, lung-damaging agents

Riot-control agents, particularly CS and CR (tear gas)
Large airways Blocked by secretions Nerve agents (theoretical)

Blocked by inhaled vomitus Various agents
Sloughing of walls of trachea and main bronchi, produces Nerve agents
“pseudodiphtheritic” membrane, serious cause of large airway
obstruction, leading to bronchopneumonia and death
Small airways Blocked by secretions

Cholinergic innervation affected; bronchospasm (relieved by atropine) Nerve agents
Chemical bronchiolitis, followed by serious bronchospasm Mustard agents
Alveoli Toxic pulmonary edema Various agents, especially lung-damaging agents

(latency 6-24 hr)
Vesicant agents, particularly if inhaled at high
ambient temperature*
*Data from Willems JL: Clinical management of mustard gas casualties. Ann Med Mil Belg 3(Suppl):1-61:47, 51, 1989.
From Baker DJ, Rustick JM: Anesthesia for casualties of chemical warfare agents. In Zaitchuk R, Grande C (eds): U.S. Army Textbook of Military Medicine, part IV, vol I. U.S.
Department of the Army, Office of the Surgeon General Borden Institute, Washington, DC, 1995, pp 833-856.
conduct of general anesthesia are important. Many of the agents case of OP exposure, there may be a possibility of developing the
described earlier affect the condition of the patient and the action intermediate syndrome,96,97 with a reparalysis of the patient110
of anesthetic agents. requiring several days of ventilation. Experience with OP anti-
Dr Azam’s Notes in Anesthesiology 2013 cholinesterases in this area is lacking, although there is consider-
id recov- does not
Usedepend on the availability
of the modern of a hospital
general anesthetics withbed, and patients
an LMA for benzodiazepine
that the numbershould be prescribed
of available to be
hospital taken
beds at hometo
continues indecline
the in
anagement
ear to be Figure 78-2 Preoperative psychological preparation
airway management combined with antiemetic prophylaxis andreduces stress before evening before or in the morning 1 to 2 hours
the future, the growth of ambulatory surgery before surgery or
will Notes
Dr Azam’s lead toinan
Anesthesiology 2013
and up to 1 week after surgery, as measured by the Spielberger state anxiety
npatients nonopioid
score. *analgesic techniques
= P < .05. (Redrawn can achieve
with modification recovery
from times that
Wallace LM:
increased return on investment of the health care dollar.
450,451
e of the compare 78-2favorably
TablePsychological
Benefits with
of MAC as atechniques.
Ambulatory
preparation Surgery
method of reducing Studies
the stresshave dem-J
of surgery. Table 78-5 Use of Anxiolytic-Sedative Drugs for Outpatient Premedication
with cer- onstrated that outpatients undergoing hernia repair and breast
Hum Stress 10:62, 1984. Reprinted with permission of the Helen Dwight Reid
Educational Foundation. Published by Heldref Publications, 1319 Eighteenth Dosage Range Onset (min) Key Points
s.424,431 surgery
Patientwere able toespecially
preference, ambulatechildrenwithinand 30the
minutes
elderly and were dis-
St, Washington, DC 20036-1802. Copyright 1984.)
Lack of dependence on the availability
charged within 60 minutes after general anesthesia.
Greater flexibility in scheduling operations
of hospital beds When tra- Facility Design and Safety
Benzodiazepines
chealpremedication
intubation is in required (e.g., laparoscopic
the outpatient setting (e.g., procedures,
midazolam, 1-2 riskmg
Low morbidity and mortality Midazolam 7.5-15 mg PO 15-30 Large first-pass
factors for aspiration
intravenously [e.g.,
[IV]). 82,83diabetics, morbidly obese, esophageal
Van Vlymen and associates84 found that Ambulatory surgical facilities need to be well-designed
effect to ensure
Lower incidence
dysfunction]), the ofuse
infection
of minimally
premedication
Lower incidence
with a small
of respiratory
doseeffective doses of a short-
of a benzodiazepine
complicationsor sympatholytic (e.g.,
actually efficient delivery 5-7
of mg
surgical services at the lowest possible cost.
ue would acting opioid
improved analgesic
outcome (e.g.,
in remifentanil)
women undergoing needle-localized breast
IM 15-30
The first freestanding outpatient surgical facility
Water soluble,
was built and
Higher volume of patients (greater efficiency) nonirritating
ast-track” esmolol, labetalol)
biopsies without can facilitate
delaying the early recovery process
recovery. Midazolam premedication and
Shorter surgical waiting lists managed by an anesthesiologist, Wallace Reed, to provide surgical
s or com- allow patients
not only to achieve
decreases earlier discharge
preoperative anxietytimes
but after
may ambulatory
also be associ- 1-2 mg IV
Lower117,276,452
overall procedural costs care to patients whose operations1-53
were deemed Rapid onset,
too demanding
nimizing surgery.
ated with a reduction in postoperative pain. 85 excellent
echnique
Less preoperative testing and postoperative medication for a surgeon’s office yet did not require overnight amnesiahospitaliza-
turnover tion.20 Since that time, outpatient surgical facilities have contin-
Anxiolysis
Modified from Snyderand Sedation
DS, Pasternak LR: Facility design and procedural safety. In Diazepam 5-10 mg PO 45-90 Long-acting
anesthe- White Traditionally,
Table PF (ed):Effects
78-12 Ambulatory
ofthe Anesthesia
Intravenous and Surgery.
Anesthetic
most widely andLondon,
used WB Saunders,
Cardiovascular
premedicants Drugs
haveonbeen ued to grow and evolve.21 The prototypical ambulatory metabolites
surgical
1
regional 1997,
the p 61.
Duration of Electroconvulsive Therapy–Induced Seizure Activity
barbiturates and benzodiazepines. These drugs produce dose- units have four basic designs :
Temazepam 15-30 mg PO 15-40 Comparable
hesia can related anxiolysis, sedation, and ultimately, unconsciousness anxiolysis to
Increased No Change Decreased
rding the (see Chapter 26). Barbiturates are not commonly used as pre- midazolam
al proce- medicants inEtomidate
Anesthetic the outpatientMethohexital,*
setting because of residual sedation,
Thiopental,
which makes them less cost beneficial
ketamine, than nonbarbiturate
thiamylal, seda- Triazolam 0.125-0.25 mg PO 15-30 Prominent
t the best Drugs
alfentanil,† 86 Methohexital sedation
far better tive drugs (e.g., midazolam, propofol). and keta-
lorazepam,
†
ocedure- mine have been used for rectal premedicationmidazolam,
remifentanil in children. Lorazepam 1-2 mg PO 45-90 Prolonged
However, side effects of ketamine (e.g., confusion, propofol
vivid dreams) amnestic
mportant are frequentAminophylline,
Cardiovascular unless this drug is combined
Clonidine, esmolol, with midazolam.87
Diltiazem,
effect
the peri- Melatonin hascaffeine
Drugs also been reported to produce sedation
labetalol, and anxi-
lidocaine α2-Adrenergic Agonists
reduced olysis comparable to oral midazolam
dexmedetomidine,when administered for
premedication. 88 Clonidine 0.1-0.3 mg PO 45-60 Prolonged
e.355,356,387 nifedipine,
sedative
perience nicardipine,
effect
tic tech- Benzodiazepines nitroglycerin,
ncidence The amnesic and anxiolytic properties of small doses of benzodi-

trimethaphan, Dexmedetomidine 50-70 µg IM 20-60 Bradycardia
azepines are also useful in the nitroprusside
outpatient setting (Table 78-5). and
e of pro- hypotension
has been *WhenOral diazepam,
compared 0.1methohexital
with saline, mg/kg, given 60 to the
decreases 90 seizure
minutes before
duration of surgery
electroconvulsive to reduce stress hormone levels after day-case surgery.89
was foundtherapy. 50 µg IV
nt surgi- 5-30 Reduced
†
Diazepam
Increases seizure timewas the of most
because commonly effect.
an anesthetic-sparing used benzodiazepine; anesthetic/
of PONV From Ding Z, White PF: Anesthesia for electroconvulsive therapy. Anesth Analg
however, midazolam has become the drug of choice because its analgesic
nesthetic 94:1351, 2002.
shorter elimination half-life and its anesthetic sparing effects and requirements
lack of significant side effects facilitate the recovery process after Modified from White PF: Ambulatory anesthesia and surgery: Past, present, and
ambulatory surgery.90-92 In addition to its well-known anxiolytic
properties, midazolam may be effective in reducing postoperative
future. In White PF (ed): Ambulatory Anesthesia and Surgery. London, WB
Saunders, 1997.
A
111

Ambulatory (Outpatient)
Dr Azam’sAnesthesia 2427
78
Table 78-6 Common Factors Associated with Nausea, Vomiting, and effective dose should be administered after induction of
Retching during the Perioperative Period anesthesia. 141,142
Table 78-7 Criteria Used to Determine Fast-Track Eligibility after airway devices.202 Although supraglot
Ambulatory Anesthesia used in paralyzed patients undergoin
Patient-Related Factors most practitioners in North America
Criteria Score
Phenothiazines tion in these situations to minimize
Age and aspiration
The antiemetic action of phenothiazines also results
Level of Consciousness
from their for patients in the Tre

Gender Awake and oriented 2
Preexisting diseases (e.g., diabetes)
abilityArousable
to block dopamine
with minimal receptors in the chemoreceptor
stimulation 1 trigger Drugs
Anesthetic
143
History of motion sickness or postoperative nausea and vomiting
zone of the brain. Prochlorperazine suppositories are frequently
Responsive only to tactile stimulation 0 Induction of general anesthesia is ty
used for treating
Physical ActivityPONV occurring after discharge. Premedication rapid-acting intravenous anesthetic
Smoking history has replaced the barbiturates for ind
Level of anxiety
with Some
phenothiazines can
Able to move all extremities on command
produce
weakness in movement of the extremities
intraoperative
2
1
hypotension
ambulatory setting because of its f
Intercurrent illness (e.g., viral infection, pancreatic disease)
along Unable
withtosignificant
voluntarily moveresidual sedation after surgery.
the extremities 0 InHowever,
addition,the most popular technique
these Hemodynamic
compounds may produce extrapyramidal effects ranging sia is a combination of a volatile anest
Stability oxide. The extremely low solubility of
Anesthesia-Related Factors 141
from Blood
restlessness
pressure < 15% toof the
oculogyric crisis. Therefore,
baseline MAP value 2 thisvolatile
classanesthetics
of (i.e., sevoflurane
Premedication antiemetic is rarely used for prophylaxis
Blood pressure between 15% and 30% of the baseline MAP value
in 1
the outpatient
to a more rapid recovery from ge
Blood pressure > 30% below the baseline MAP value 0
Opioid analgesics nitrous oxide can produce emetic sy
setting. tance is questionable because nitrous
Respiratory Stability
Induction and maintenance anesthetics
Able to breathe deeply 2 gesic-sparing effects offset its emet
Reversal (antagonist) drugs Anticholinergics
Tachypnea with good cough 1 intravenous anesthesia (TIVA) utiliz
Gastric distention Dyspneic with weak cough 0 fol and remifentanil (or alfentanil) ha
Anticholinergic drugs (e.g., atropine, glycopyrrolate, and scopo-
outside North America owing in lar
Inadequate hydration lamine) have traditionally been used for their antisialagogue
Oxygen Saturation Status
and
target-controlled, computer-based
Residual sympathectomy Maintains value > 90% on room air 2
vagolytic properties. However,
Requires supplemental oxygen (nasal prongs) transdermal scopolamine
1 (TDS),
Studies suggest that TIVA is as effec
ambulatory surgery with the advan
Surgery-Related Factors a centrally
Saturationactive anticholinergic,
< 90% with supplemental oxygen with potent anti–motion 0 sick-
ness.211 When compared with a targe
Operative procedure ness properties
Postoperative Pain hasAssessment
recently been found to be comparable pofol for to
maintenance of anesthesi
Length of surgery both None
droperidol and
or mild discomfort
ondansetron when used 2
for antiemetic
sevoflurane produced similar anesth
Moderate to severe pain controlled with IV analgesics144 1 emergence times and lower drug cos
Blood in the gastrointestinal tract prophylaxis in the
Persistent severe painambulatory setting. Preoperative 0 placement
Forcing oral intake of a TDS patch can
Postoperative Emeticreduce
Symptoms the incidence of severe PONV in both
Barbiturates
Opioid analgesics the early and late postoperative periods. However, when admin-(3 to 6 mg/kg) was th
None or mild nausea with no active vomiting 2 Thiopental
induction drug because of its rapid
Premature ambulation (postural hypotension) isteredTransient
before outpatient gynecologic laparoscopy,
vomiting or retching
Persistent moderate to severe nausea and vomiting
1
0
transdermal
duration of hypnotic action (see Cha
Pain scopolamine
Total score was associated with a higher incidence
14 of
tal adverse
can impair fine motor skills for se
216
Data from Watcha MF, White PF: Postoperative nausea and vomiting: Its etiology,
effectsA score
(including dry score
over 12 with no individual mouth,
less than 1 somnolence, mydriasis,produce
is required for fast-tracking.
can and a “hangover” effect.
with shorter emergence times, but
treatment, and prevention. Anesthesiology 77:162, 1992. dizziness).
MAP, mean arterial pressure.
From White PF, Song D: New criteria for fast-tracking after outpatient anesthesia: motor skills may still require 2 to
dose.217 When compared with thiope
A comparison with the modified Aldrete’s scoring system. Anesth Analg 88:1069,
1999.
Antihistamines ated with a higher incidence of pa
muscle movement, and hiccoughing.
nancy, phase of the menstrual cycle, preoperative hydration Dimenhydrinate and hydroxyzine are antihistaminic compounds ated with a faster emergence from a
status, and postoperative hypotension (due to residual sym- that also act
period. 197
onofthe
Use central
an LMA vomiting
in children with acenter andairway
recent upper vestibular
dencepath-
of PONV than methohexital w
infection was also associated with increased coughing, laryngos- and maintenance of general anesthe
pathectomy, premature ambulation).136 The incidence of emesis is ways pasm,
to prevent PONV. These compounds are particularly useful
and oxygen desaturation.198 When compared with tracheal pared favorably with propofol when
low in infants, gradually increases toward adulthood, and then for the prophylaxis
intubation, insertionand
of thetreatment
LMA causes of motion-induced
minimal emesis inlasting112
cardiovascular procedures longer than 30 m
145
decreases again at advanced age (e.g., the elderly). The phase of outpatients undergoing middle ear and strabismus surgery. A
responses and is better tolerated at lighter levels of anesthesia. The
Dr Azam’s Notes incycle
Anesthesiology 2013 incidence of sore throat is also reduced when an LMA is used as Benzodiazepines
the menstrual may influence the incidence of PONV, with long-acting formulation of dimenhydrinate compared favorably
an alternative to a tracheal tube.199 In the ambulatory setting, Although midazolam (0.2 to 0.4 m
the highest incidence reported during the ovulatory and luteal with droperidol in reducing vomiting for200up to 24 hours without
chamber would have provided an inspired PO2 equivalent to 26% to 28% O2 at 1 ATA.
Ambulatory (Outpatient) Anesthesia 2447 78 Notes in Anesthesiology 2013

Dr Azam’s
Table 78-15 Modified Postanesthesia3Discharge Scoring (PADS) System

of decompression sickness but remained an isolated medical hours of intravenous
Table 80-1 Partial fluid
List replacement
of Conditions for during
Whichtheir hospital
Hyperbaric stay. Has
Oxygen
curiosity Well-hydrated outpatients can be safely discharged home without
Signs until the early 1960s. A few indications, such as support
Been Used
Vital
of oxygenation in hyaline membrane disease of the newborn4 and demonstrating an ability to tolerate oral fluids after surgery.
during open heart surgery were not useful. For other indica- The requirement
2 5,6Within 20% of the preoperative value Gas-bubble diseaseto void before discharge has also been
544
challenged. *Air The inability
embolism 7,83
to void may be caused by pain (which
1 tions, such as carbon monoxide 20%-40%(CO) poisoning,valuearterial gas

of the preoperative
inhibits normal bladder detrusor
*Decompression sickness83,291 function) and opioid analgesics,
embolism, and decompression sickness, hyperbaric oxygen
0 40% of the preoperative value epidural anesthesia, and anticholinergic drugs.47 Patients
spinal orPoisoning
(HBO) proved to be effective, as evidenced by substantial clinical may be discharged earlier7,41,48-50,55
if voiding is not a discharge require-
Ambulation
experience and randomized controlled studies. Indications are *Carbon monoxide
ment. Delaying
Cyanide 41discharge for voiding after spinal or epidural
2 reviewed regularly by the Undersea Steady gait/noand Hyperbaric Medical
dizziness anesthesiaCarbon
with tetrachloride
short-acting local anesthetics is unnecessary in
292,293
Society (Durham, NC). This medical organization publishes an
low-risk patients (e.g., age41 < 70 years; no hernia, rectal, or urologic
1 With assistance Hydrogen sulfide
extensive bibliography with a list of indications for hyperbaric surgery; no history of voiding problems).544 However, appropriate
0 oxygenation that is updated No every 2 to 3 years.7 Laboratory and
ambulation/dizziness
measures Infections
must be in place for 7,99-101 urinary catheterization if the ina-
clinical data support the use of HBO for a select number of
bility to *Clostridial
void persists myonecrosis
after discharge home. The use of ultrasound
Nausea and Vomiting
acute and chronic illnesses (Table 80-1), and anesthesiologists *Other soft tissue necrotizing infections7,97,98,101
bladder monitoring before discharge may reduce voiding prob-
2 Minimal osteomyelitis7,90,294
are often called on to provide care of patients in this unusual lems after*Refractory
discharge.chronic544
*Intracranial abscess7,295
1 environment. Moderate Before leaving the outpatient facility, patients should have
Mucormycosis296,297
0 Interest in the physiologic Severe and medical aspects of their
altitude dressings checked and be given both verbal and written
originated because of mountaineering and high-altitude balloon instructions
Acute regarding
ischemia their postoperative care. Most postopera-
Pain 8 tive symptoms
*Crush (e.g.,
injury pain,
7,298
PONV, dizziness, headache, and myal-
exploits in the 19th century. An understanding of the physiologic
2 response to altitude hypoxia has had wide application, as increas-
Minimal gias) resolve within 24 hours. However, if these symptoms persist,
*Compromised skin flaps 7,299
300
ing numbers of people fly in aircraft, travel from low to high the patient
alti- should
Central be encouraged
retinal artery occlusion, to contact the facility
central retinal regarding
vein occlusion
1 Moderate appropriate follow-up care. All patients should be discharged
tude, and live or work at higher elevations (Table 80-2). Significant Chronic ischemia
0 effort has been devoted to techniques Severe for prophylaxis and treat- from the *Radiation facility
surgical necrosisin thetissue,
(soft company of cystitis,
radiation a responsible
and adult
and shouldosteoradionecrosis)
be aware of the 7recommendations regarding appro-
ment Bleeding
Surgical of these illnesses in recent years.
priate activities
*Ischemic after discharge.
ulcers, includingPatients
diabetic should be warned about
ulcers7,11,301,302
The effects of space travel are mostly due to microgravity,
2 Minimal the potential dangers of operating complex machinery, driving a
radiation, and confinement. Understanding these effects and
car, or Acute
making hypoxia
important decisions for up to 24 hours after
1 development of tools to dealModerate with sick or injured astronauts are *Exceptional blood loss anemia (when transfusion
545
anesthesia. However, when short-acting anestheticdelayed
drugsorare
0 paramount for the medical support Severe of long-range space missions,
7
unavailable)
used for 1- to 2-hour procedures, return of fine motor skills can
such as to Mars. occur in Support of oxygenation during therapeutic lung lavage103,104
less than 4 hours.
From Chung F, Chan VW, Ong D: A postanesthetic discharge scoring system for
home readiness after ambulatory surgery. J Clin Anesth 7:500, 1995. ItThermal
is important
injury to have an efficient mechanism in place for
admitting*Burns
outpatients
7,303-306
to the hospital if the need arises. Most well-
organized outpatient facilities have an unanticipated hospital
Envenomation
Physiologic
analgesic Effects
can provide spinal anesthesia
310,313
of
without Increased
significantly pro- admission rate of less than 1%.11,12 However, transfer rates are
Brown recluse spider bite307,308
longing the time to discharge. Before ambulation, patients higher in ambulatory centers with a larger proportion of neonates,
Gas
receiving Pressure
a central neuraxis block should have normal perianal elderly*Approved (>80 years),by the and ASA physical
Undersea statusMedical
and Hyperbaric III patients.
Society The
as anFed-
appropriate
7
(S4-5) sensation, have the ability to plantarflex the foot, and have erated indication Ambulatory for HBO Surgery
therapy.Association multicenter survey sug-
Increased
proprioception of theBarometric
big toe. Discharge Pressure
criteria after spinal and gested that 70% of all perioperative complications occurred after
epidural anesthesia should include the return of normal sensa- discharge from the ambulatory surgery center.1 This finding
tion, muscle
Some strength,
effects and proprioception,
of altered ambient pressure as well as return of emphasizes
arethesummarized in the importance of providing clear, written discharge 113
sympathetic
Figure 80-2.nervous function. instructions and the availability of a responsible adult to monitor
Dr Azam’s Notes in Anesthesiology 2013 the patient at home. Most practitioners recommend that out-of-
town patients spend their first postoperative night within a rea-
20
bacteria leading to a decrease in dopamine release.
Table 80-3 Units of Pressure
Atmospheres Absolute Absolute Pressure Gauge Pressure Feet of Sea Water Meters of Sea Water
(ATA) (mm Hg) (mm Hg) (fsw) (msw)
1 760 0 0 0
2 1520 760 33 10
3 2280 1520 66 20
6 4560 3800 165 50

Regional Anesthesia in
Table 81-4 Commonly Used Additives and Recommended Doses in Pediatric preclude hospital discharge). Addition of clonidin
Regional Anesthesia unnecessary the placement of a catheter to prolong
pain relief, thus reducing morbidity and costs. How
Recommended
Additive Doses Maximum Doses
ance in neonates is approximately one third that in
to immature elimination pathways51 and several in
Morphine piratory depression in neonates and small infan
Epidural 30 µg/kg 50 µg/kg reported52,53; this additive should be avoided dur
Intrathecal 10 µg/kg 20 µg/kg month of life.
Fentanyl (epidural) 1-1.5 µg/kg 2.5 µg/kg Ketamine, especially S-ketamine, is an intere
owing to its blocking effects on N-methyl--aspa
Sufentanil (epidural) 0.25-0.5 µg/kg 0.75 µg/kg receptors and interaction with Na+ channels in a lo
Clonidine (epidural or along 1-1.5 µg/kg 2 µg/kg like fashion (it shares a binding site with local an
peripheral nerves) administered at a dose of 0.25 to 0.5 mg/kg, keta
the duration of analgesia for many hours48,54 with
Ketamine* (epidural or 0.5 mg/kg 1 mg/kg
occasionally along
adverse effects.
peripheral nerves) Many other agents have been occasionally
vants to local anesthetics.55 Even though some of
*Preservative free-ketamine (preferably preservative-free S-ketamine).
to have analgesic properties (corticosteroids,
114 b
neostigmine, tramadol, midazolam, and biodeg
vacaine/polyester microspheres), they all produ
Regional Anesthesia in Children 2535 81
Table 81-9 Usual Doses and Infusion Regimens for Epidural Anesthesia in Pediatric Patients
Continuous Infusion
Agent Initial Dose (Max. Doses) Repeat Injections
Bupivacaine, levobupivacaine Solution: 0.25% with 5 µg/mL <4 mo: 0.2 mg/kg/hr (0.15 mL/kg/hr 0.1 to 0.3 mL/kg every 6-12 hr of a
(1/200,000) epinephrine of a 0.125% solution or 0.3 mL/kg/ 0.25% or 0.125% solution
Dose: hr of a 0.0625% solution) (according to pain scores)
<20 kg: 0.75 mL/kg 4-18 mo: 0.25 mg/kg/hr (0.2 mL/kg/
20-40 kg: 8-10 mL (or 0.1 mL/year/ hr of a 0.125% solution or 0.4 mL/
number of metameres) kg/hr of a 0.0625% solution)
>40 kg: same as for adults >18 mo: 0.3-0.375 mg/kg/hr
Section VI Pediatric Anesthesia

(0.3 mL/kg/hr of a 0.125% solution
or 0.6 mL/kg/hr of a 0.0625%
solution
Ropivacaine Solution: 0.2% Same age-related infusion rates in 0.1 to 0.3 mL/kg every 6-12 hr of a
Dose: same regimen in mL/kg as for mg/kg/hr as for bupivacaine 0.15% or 0.2% solution (according
bupivacaine (see above) (usual concentration of to pain scores)
ropivacaine: 0.1%, 0.15%, or 0.2%)
Do not infuse for more than 36 hr
in infants < 3 mo
Adjuvants Avoid in infants < 6 mo Select only one additive: Morphine (without preservatives):
Fentanyl (1-2 µg/kg) or sufentanil Fentanyl: 1-2 µg/mL 25-30 µg/kg every 8 hr
(0.1-0.6 µg/kg) or clonidine (1-2 µg/kg) Sufentanil: 0.25-0.5 µg/mL
Morphine: 10 µg/mL
Hydromorphone: 1-3 µg/mL
Clonidine 0.3 at 1 µg/mL of solution
order to avoid buckling, knotting, and lateralization of blockade In mature children understanding the concept of patient-
or erratic migration. Tunneling the catheter reduces the incidence controlled analgesia and willing to use it, patient-controlled epi-
of accidental removal and bacterial contamination.176 Catheters dural analgesia (PCEA) can be an interesting option. A prospective
inserted over a long distance have to be controlled in the same study involving 128 children older than 5 years of age reported a
way as for caudal catheters. 90.1% success rate; PCEA was stopped in 6.1% of children because
The volume of anesthetic solution depends on the upper of adverse effects and only in 3.8% because of inadequate analge-
level of analgesia required for completion of the surgery; around sia.178 The local anesthetic was either 0.0625% or 0.125% bupi- 115
0.1 mL per year of age is necessary to block 1 neuromere.177 Usual vacaine with fentanyl (2 to 10 µg/mL); background infusion rate
volumesNotes
Dr Azam’s of injectate range from 0.52013
in Anesthesiology to 1 mL/kg (up to 20 mL), was less than or equal to 0.2 mL/kg/hr, and 1- to 3-mL bolus
and the upper limit of sensory blockade ranges between T9 and doses were permitted every 15 to 30 minutes with a 0.4-mg/kg/hr
d in adults the overall failure rate ranges from 10% to 25%. Short dura-
Table 81-10 Usual Doses of Local Anesthetics for Spinal Anesthesia in

Neonates and Former Preterm Neonates Younger than 60 Weeks of
Preconceptual Age (up to a Weight of 5 kg)
Dose Volume Duration

n 1 year of
Local Anesthetic (mg/kg) (mL/kg) (min)
ee “Caudal
onsiderably Tetracaine 1% 0.4-1.0 0.04-0.1 60-75
n neonates, Tetracaine 1% with 0.4-1.0 0.04-0.1 90-120
3 mL/kg in epinephrine
adults. The
ge: Half the Bupivacaine 0.5% isobaric 0.5-1.0 0.1-0.2 65-75
noid space or hyperbaric
macokinetic Levobupivacaine 0.5% 1.0 0.2 75-88
anesthetics
Ropivacaine 0.5% 1.08 0.22 51-68
ng children.
Regional Anesthesia in Children 2537 81
Table 81-11 Usual Doses of Local Anesthetics for Spinal Anesthesia in
Children and Adolescents Indications and Contraindications
Local Anesthetic Usual Dose(s)
Indications for brachial plexus blocks include emergency as well
0.5% Isobaric or hyperbaric 5 to 15 kg: 0.4 mg/kg (0.08 mL/kg) as elective surgery of the upper extremity in conscious or anes-
bupivacaine >15 kg: 0.3 mg/kg (0.06 mL/kg) thetized children.202-205 These blocks are particularly useful for
0.5% Isobaric or hyperbaric tetracaine 5 to 15 kg: 0.4 mg/kg (0.08 mL/kg) outpatient surgery and elicit a high degree of patient satisfaction.
>15 kg: 0.3 mg/kg (0.06 mL/kg) Axillary blocks are considered first, especially when the lesions
involve the forearm and the hand, because they are virtually free
0.5% Isobaric levobupivacaine 5 to 15 kg: 0.4 mg/kg (0.08 mL/kg)
of complications. Infraclavicular paracoracoid approaches are
15-40 kg: 0.3 mg/kg (0.06 mL/kg)
Section VI Pediatric
>40 kg: 0.25 mg/kg (0.05 mL/kg)
being increasingly used with the development of ultrasound guid-
ance: The technique is easy and provides complete blockade of
0.5% Isobaric ropivacaine 0.5 mg/kg (max 20 mg) the upper extremity; catheter placement is easier and more com-
fortable than at axillary levels; catheter immobilization and pro-
tection against accidental removal are also easier.
Supraclavicular blocks are recommended when the lesion
(or a tourniquet) is located on the proximal part of the 116 arm,
tion of blockade and lack of residual analgesia are important including the elbow. Peri-subclavian approaches should not be
Dr Azam’s Notes Alternative
limitations: in Anesthesiology
(awake2013
caudal anesthesia) or complemen- used in infants owing to the proximity of the apical pleura, even
Sugammadex is a cyclodextrin whose endoskeleton forms a concerns. Because the anxiety felt by the parents may be trans-
water-soluble complex with the exoskeleton of rocuronium; it was ferred to the child, any practice that reduces anxiety in Dr
the Azam’s
parents Notes in Anesthesiology 2013
specifically designed to antagonize the effects of rocuronium (also may also reduce anxiety in the child. Therefore, the anesthesiolo-
Table 82-4 Commonly Used Muscle Relaxants and Reversal Agents in Pediatrics
Drug Average Intubation Dose (mg/kg) Category Approximate Duration
Muscle Relaxants*
Pancuronium 0.1 Long acting ∼45-60 min
Cisatracurium 0.1 Intermediate acting ∼30 min
Vecuronium 0.1 Intermediate acting ∼30 min
Rocuronium Dose related:

0.3 Short acting ∼15-20 min
0.6 Intermediate acting ∼30-45 min
1.2 Long acting ∼45-75 min
Reversal Agents†
Edrophonium 0.3-1.0 mg/kg + atropine, 0.02 mg/kg
Neostigmine 0.02-0.06 mg/kg + atropine, 0.02 mg/kg
*The response of preterm and term neonates (who may be more sensitive to the drugs) to muscle relaxants varies greatly from patient to patient. Therefore, all doses
should be titrated to response. The recommended intubation doses may be reduced 30% to 50% in the presence of a potent inhaled agent.
†
The dose of reversal agent given to antagonize nondepolarizing neuromuscular blockade should be determined by the degree of residual neuromuscular blockade (i.e.,
the dose should be titrated to clinical effect).
Pediatric Anesthesia 2575
Table 82-5 Fasting Guidelines for Pediatric Patients induction with potent inhaled anesthetics, but only in infants
younger than 6 months.104
Fasting Time (hr)*
Age Milk and Solids Clear Liquids
<6 months 4 2 The Child with an Upper Respiratory

6-36 months 6 3 Tract Infection
>36 months 8 3
A child with a URI is a major concern for the anesthesiologist
*Note that the American Society of Anesthesiologists guideline allows a “light because the anesthetic implications can be quite important.
breakfast” (tea and plain toast) 6 hours before anesthesia; however, it is difficult to
determine what a “light breakfast” is for a child.
Unfortunately, data regarding URIs and the anesthetic implica-
tions are difficult to place in perspective because complications
117
are not particularly common and the definition of what a URI
Dr Azam’s Notes in Anesthesiology 2013 consists of has varied from study to study. The decision whether
Premedication
those who have diminished glycogen stores. Data are inadequate
to eliminate glucose completely because the relevance of the
animal data
Table 82-8 is not
Laryngeal clear
Mask and Patient
Size versus the true
Weight*incidence of hypoglycemia
erapy is not known in all populations of food-restricted children. This
Laryngeal Mask Size Patient Weight
issue is further complicated by the fact that different values are
used
1 to define hypoglycemia, depending on ≤5 the
kg child’s age.
must con- 1.5 Despite limited data, a balanced salt 5-10 solution
kg (e.g., lactated
dy surface Ringer’s
2 solution) should be used for all deficits 10-20 kg and third-space
or calcu- losses.
2.5
If a child is thought to be at risk 20-30 for hypoglycemia,
kg
5%
iday and dextrose in 0.45% normal saline should be administered by “pig-
3 30-50 kg
d directly gyback” infusion at maintenance rates. This minimizes the chance
water is of4 a bolus administration of glucose and satisfies 50-70 kg the concern for
ating this unrecognized

5 hypoglycemia or accidental70-100 hyperglycemia.
kg The
g for chil- routine
6 use of 5% dextrose or 5% dextrose in 0.45%
>100 kg normal saline
am above as the initial replacement for fluid deficit, third-space losses, and
*Manufacturer’s recommendations (LMA North America).
kilogram
d require establish a patent airwayofbefore the airway is secured more defini-
Table 82-9 Calculation Maintenance Fluid Requirements for
mL. This tively with an endotracheal tube or a cricothyrotomy (Table
Pediatric Patients
es, modi- 82-8). In neonates with difficult airways such as those with Gold-
require- enhar,
Weight Treacher-Collins,
(kg) or Pierre Robin
Hourly syndrome,
Fluid awake topi-
Requirements (mL)
al, deficits calization of the airway with lidocaine (1% nebulized to avoid
excessive
<10 doses) followed by placement
4 mL/kg of an LMA is very helpful
by multi- in guiding awake/sedated fiberoptic intubation. A skilled assistant
hours of 11-20can hold the head in proper
who mL + 2 mL/kg
40position for each
and assist with kilogram
the dif- above 10
first hour ficult airway is critical to the success of most of these approaches
>20 60 mL + 1 mL/kg for each kilogram above 20
osses are to a difficult airway. It should be noted that in children the ProSeal
LMA will allow ventilation at significantly higher peak infla-
tion pressures (∼25 cm H2O) than possible with the classic
LMA (∼15 cm H2O); thus, this device may be preferable in a
difficult airway situation, especially since the stomach can be
suctioned.113
If the child should progress to a “cannot ventilate, cannot
intubate” situation, one must immediately establish a surgical
airway. It is vital to properly position the child with a roll of towels 118
under the shoulders to force the larynx anteriorly so that the best
Dr Azam’s
accessNotes
to theinlarynx
Anesthesiology 2013
is provided. It is also important to have a
VI 2604 Pediatric Anesthesia Dr Azam’s Notes in Anesthesiology 2013
Table 83-2 Classification of Congenital Heart Defects
Physiologic Classification Pulmonary Blood Flow Comments
Left-to-right shunts
VSD ↑ Volume-overloaded ventricle
ASD Development of CHF
PDA
AV canal
Right-to-left shunts
Tetralogy of Fallot ↓ Pressure-overloaded ventricle
Pulmonary atresia/VSD Cyanotic
Eisenmenger complex Hypoxemia
Mixing lesions
Transposition/VSD ! Qs
Generally ↓ but variable Qp ! Variable pressure versus volume loaded
Tricuspid atresia Usually cyanotic
Anomalous venous return
Univentricular heart
Obstructive lesions
Interrupted aortic arch Ventricular dysfunction
Critical aortic stenosis Pressure-overloaded ventricle
Critical pulmonic stenosis Ductal dependence
Hypoplastic left heart syndrome
Coarctation of the aorta
Mitral stenosis
Regurgitant lesions
Ebstein’s anomaly Volume-overloaded ventricle
Other secondary causes Development of CHF

! , pulmonary blood flow; Qs
ASD, atrial septal defect; AV canal, atrioventricular canal; CHF, congestive heart failure; PDA, patent ductus arteriosus; Qp ! , systemic blood
flow; VSD, ventricular septal defect.
119
of three pathophysiologic states: ventricular volume overload, for the LV, which is required to increase stroke volume and heart
Drventricular pressure
Azam’s Notes overload, or 2013
in Anesthesiology hypoxemia. Ultimately, these rate to ensure adequate systemic perfusion; and (3) excessive PBF,
pathophysiologic conditions can result in myocardial failure or resulting in progressive elevation in PVR. Volume overload causes
Anesthesia for Pediatric Cardiac Surgery 2611
Table 83-6 Common Perioperative Cardiovascular Medications and Considerations
Cardiac Drug Class Interactions Considerations
Angiotensin-converting enzyme inhibitors Hypotension with induction of general anesthesia Consider withholding AM dose, or reducing dosage, in
hypotensive patients; avoid fixed dose induction
regimens with drugs having a profound vagomimetic
effect
β-Blockers Acute withdrawal can precipitate tachycardia Continue in the perioperative period
and arrhythmias; can potentiate hypotension
with volatile anesthesia; can decrease

response to inotropic agents
Calcium channel blockers May augment the negative inotropic and Continue in the perioperative period
chronotropic effects of volatile anesthesia
Diuretics Hypovolemia/hypokalemia; may augment effect Discontinue preoperatively

of neuromuscular blocking agents
Antiarrhythmics Can be proarrhythmic with inotropes, electrolyte Avoid electrolyte imbalance

disturbances; high catecholaminergic states; Avoid drugs that are proarrhythmic
can interact with other antiarrhythmics and Monitor carefully
precipitate bradycardia
α2-Agonists Reduces perioperative shivering, ischemia, Continue into the perioperative period with appropriate
anesthetic and analgesic requirements monitoring
with reduced repolarization reserve such as congestive cardiac children with heart disease. Typically, MRI is used for segmental
failure or digoxin toxicity can precipitate torsades de pointes. description of cardiac anomalies; evaluation of thoracic aortic
Drugs that may cause torsades in patients with congenital LQTS anomalies; noninvasive detection and quantification of shunts,
are shown in Table 83-7. stenoses, and regurgitations; evaluation of conotruncal malfor-
Laboratory evaluation should include analysis of hemo- mations and complex anomalies; identification of pulmonary and
globin, hematocrit, pulse oximetry, and, in selected patients (e.g., 120
those on diuretics or with renal impairment), serum electrolytes.
An elevated hematocrit in a normovolemic child gives an indica-
indica-
. Levels Dr Azam’s Notes in Anesthesiology 2013
condary
Table 83-7 Drugs That May Cause Torsades de Pointes in Patients with
liberal- Congenital Long QT Syndrome Table 83-8 Monitoring of Organ Systems renders
dren to newborn
Cardiopulmonary System
duction Drug Category Drug Name Esophageal stethoscope provide
ents for Electrocardiogram temperat
Antiarrhythmics Amiodarone
Procainamide Standard seven-lead system, ST-T wave analysis, esophageal Th
g (echo- electrocardiographic lead nary arte
Disopyramide
e means Pulse oximetry mined o
Ibutilide
nd esti- Automated oscillatory blood pressure physiolo
Quinidine
re inva- Sotalol
Capnograph
dren un
graphic Ventilator parameters
Indwelling arterial catheter
univentr
r defin- Antipsychotics Chlorpromazine
pulmona
Central venous pressure catheter
es, such Haloperidol
operatio
Pulmonary artery catheter
o define Thioridazine
pumping
Transthoracic pressure catheter
on. The Mesoridazine
Left or right atrium, pulmonary artery nary ven
quires a Antimicrobials Erythromycin Echocardiography with Doppler color flow imaging output. D
ell-inte- Clarithromycin Epicardial or transesophageal pressure
osed by cular vo
nditions Miscellaneous Cisapride Central Nervous System
Arsenic Peripheral nerve stimulator complian
experi- approach
Methadone Processed electroencephalography
iologist Specialized As
Droperidol
limita- Cerebral blood flow—xenon clearance methodology catheter
Domperidone
gement
Dolasetron Cerebral metabolism—near-infrared spectroscopy, oxygen consumption children
measurements children
Ondansetron
d major Transcranial Doppler
tool in
Glycopyrrolate A
Jugular venous bulb saturations
for child
than 7.0
Temperature eter can
Nasopharyngeal, rectal, esophageal, tympanic latter tec
Renal Function transtho
Foley catheter for trans
is preferred. In older children and adolescents, a 20-gauge cathe-

121
Spe
ter may be substituted. Careful inspection, palpation, and four-
Dr Azam’s Notes in Anesthesiology 2013 extremity noninvasive blood pressure determinations help ensure Intraop
that previous or currently planned operative procedures (e.g., a Of the n
Drfor
Anesthesia Azam’s Notes
Pediatric in Anesthesiology
Cardiac Surgery 26192013 8
Table 83-10 Differences between Adult and Pediatric Cardiopulmonary Bypass
Parameter Adult Pediatric
Hypothermic temperature Rarely below 25-30°C Commonly 15-20°
Use of total circulatory arrest Rare Common
Pump prime
Dilution effects on blood volume 25-33% 150-300%
Additional additives in pediatric primes Blood, albumin
Perfusion pressures 50-80 mm Hg 20-50 mm Hg

Influence of α- vs. pH-stat management strategy Minimal at moderate hypothermia Marked at deep hypothermia
Measured PaCO2 differences 30-45 mm Hg 20-80 mm Hg
Glucose regulation
Hypoglycemia Rare—requires significant hepatic injury Common—reduced hepatic glycogen stores
Hyperglycemia Frequent—generally easily controlled with insulin Less common—rebound hypoglycemia may occur
variable levels of electrolytes, calcium, glucose, and lactate. Elec- The addition of fresh frozen plasma or whole blood (see
trolytes, glucose, and lactate levels may be quite high if the solu- Chapter 55) is an attempt to restore the level of procoagulants,
tion includes large amounts of banked blood or quite low if a which are severely diluted with CPB in infants. For neonates and
minimal amount of banked blood is added. Calcium levels are infants, blood must be added to the priming solution. Most insti-
generally very low in pediatric priming solutions; this may con- tutions use packed red blood cells, but some use whole blood. The
tribute to the rapid slowing of the heart with the initiation of use of whole blood supplements both red blood cells and the
bypass. coagulation factors with a single donor exposure. In fact, low-
The main constituents of the priming solution include volume bypass circuits may enable perfusionists and anesthesi-
crystalloid, banked blood (to maintain a temperature-appropriate ologists to share a single unit of whole blood, thereby limiting the
hematocrit), and colloid. Other supplements that may be added donor exposure to one throughout the entire perioperative 122
to the prime are mannitol, a buffer (sodium bicarbonate or tris- course.
Drhydroxymethylaminomethane
Azam’s Notes in Anesthesiology [THAM]),
2013 and steroids. Many The addition of any blood products will cause a much
damag-
with the
VI
systolic
2634 Pediatric Anesthesia
ccompa- Table 83-12 Sequelae of Pediatric Cardiopulmonary Bypass

o distin- management, drug therapies, and postoperative management. Table 83-13 Comparison of ECMO versus VAD
End-Organ Injury
c injury Despite theseEtiology/Signs
advances patients may still require therapies for
ECMO VAD
hat ulti- both
Renal acute andOrgan
injury chronic heartpreexisting
immaturity, failure that renalare refractory to medical
disease
rs. therapy. Mechanical support in the form of ECMO
Post-cardiopulmonary bypass low CO, use of DHCA or ventricular Bleeding at insertion ++ ++
uring the Renal dysfunction characterized by
assist devices (VADs) may then need to be instituted. Examples reduced GFR and
coupled ATN Sternotomy Not required Required
of conditions that may require support include failure to wean
ncreased from CPB, acute cardiac
Pulmonary injury Endothelial arrest,
injury, malignant
increased arrhythmia, and wors-
capillary leak, Left atrial venting ± −
tal heart complement activation, and leukocyte
ening myocardial function secondary to the underlying congeni- +++ +
rctation, degranulation Blood product use
sis) may tal defect or related to acquired cardiomyopathy. Fortunately,
Pulmonary dysfunction characterized by reduced Number of cannulae for biventricular 2 4
mpairing however, the numbers are small, with less than 2% of post-CPB
compliance, reduced FRC, and increased A-a
patients requiring this intervention.270 Mechanical support can support
dent on gradient
them to thus be used as a treatment option to allow for recovery of ven- Pulmonary support + −
Cerebral injury Loss of autoregulation, suppressed metabolism and
cemia in tricular
after DHCA function, as a blood
cerebral bridge tocellular
flow, transplant,
acidosis,orand
tocerebral
support the heart
Intravenous anticoagulation + ±
hypogly- in those with marginalvasoparesis functional reserve requiring invasive diag-
lycemia- nostics or treatments (e.g., Williams’
CNS dysfunction characterizedsyndrome
by seizures, with
reducedsevere supra- Duration of support Weeks Months
ut states valvar pulmonary or aortic stenosis). As with any therapy,
developmental quotients, choreoathetosis, learning
stopera- disabilities, behavioral abnormalities Emergent support Yes No
contraindications must be excluded before embarking on the use
ntial ino- of a mechanical
A-a, alveolar-arterial; assisttubular
ATN, acute device. These
necrosis; CNS,contraindications
central nervous system;may include Patient mobility − +
res and CO, cardiac output; DHCA, deep hypothermic
extreme prematurity, severe and irreversible
residual capacity; GFR, glomerular filtration rate.
circulatory arrest; FRC, functional
multiorgan failure, A extracorporeal membrane oxygenation; VAD, ventricular assist device.
ECMO,
incurable malignancy, and preexisting neurologic devastation.270
Anesthetic management in the use of ECMO is supportive with use of an ECMO circuit with a membrane oxygenator requires
management limited to assistance in the resuscitative efforts and ongoing intravenous anticoagulation with maintenance of the
hemorrhage associated with the cardiac surgery that was ongoing ACT in the aforementioned range. Apart from the immediate
at the time of conversion to ECMO. Once the patient is on full postoperative phase, patients with VAD systems can be transi-
ECMO support, ventilation is continued but at a slower rate of tioned to oral agents. A two-part therapy is recommended.
ventilation in the order of 10 breaths/min with peak pressure of Antiplatelet therapy includes aspirin or clopidrogel. The second
20 cm H2O with PEEP set at 5 to 10 cm H2O and F2 also part of the therapy will entail the use of anticoagulation with
decreased to about 40%. These settings will aid in the prevention either warfarin (Coumadin) or subcutaneous low-molecular-
of atelectasis with management of CO2 and O2 related to flow weight heparin.270
across the circuit membrane. This is very different from the As previously mentioned these modalities are used as a
patient into whom a VAD is placed. Here the anesthesiologist potential bridge to transplant and, as such, exposure to donor
continues to manage the patient as for routine CPB weaning. antigens is of great importance. In a study by Stiller and associates
123
Obviously differences exist in this scenario. If a systemic VAD is comparing the volume of blood products used, it was shown that
placed, careful attention must be given to the ventricle pumping the volume was less in those treated with a VAD in a period up
AnesthesiaDr
forAzam’s Notes
Pediatric in Anesthesiology
Cardiac Surgery 26452013 83
Table 83-15 Infective Endocarditis Prophylaxis
Single Dose 30-60 min before

Dental Procedure
Situation Drug Adults Children
Oral Amoxicillin 2g 50 mg/kg
Unable to take oral medication Ampicillin or 2 g IM/IV 50 mg/kg IM/IV
Cefazolin/ceftriaxone 1 g IM/IV 50 mg/kg IM/IV
Allergic to penicillins/oral Cephalexin or 2g 50 mg/kg IM/IV

Clindamycin or 600 mg 20 mg/kg IM/IV
Azithromycin/clarithromycin 500 mg 15 mg/kg
Allergic to penicillins/unable to take oral medication Cefazolin/ceftriaxone or 1 g IM/IV 50 mg/kg IM/IV
Clindamycin 600 mg 20 mg/kg
Vancomycin is an alternative for patients who are unable to tolerate a β-lactam or when the infective agent is considered to be methicillin-resistant Staphylococcus
aureus.
threat to patient safety. Usually an MR screening form is part of cardiac surgery will result in a number of patients’ requiring
the evaluation and needs to be discussed with the MR technolo- emergent chest exploration for ongoing hemorrhage or as part of
gist/radiologist. In a majority of patients, the scan can be per- resuscitation to relieve tamponade or for ECMO placement, all
formed as an outpatient procedure. Patients who are younger, of which may take place in the ICU setting. It is obvious that we
uncooperative, or claustrophobic require sedation or general cannot predict which patients will have problematic postopera-
anesthesia. Total intravenous anesthesia can be provided with a tive courses with absolute certainty, but the practitioners who
propofol infusion and a natural airway, avoiding the need for have participated in the operative phase will gain an accurate
scavenging and allowing rapid recovery.338 Anesthesia has been sense of which patients may require possible further exploration
provided with a range of inhalational agents, such as dexmedeto- or surgery. Accordingly, it is best to plan ahead, and it cannot be
midine, ketamine, and midazolam.339 In patients in whom breath stressed enough that even if as a group of practitioners we are
holding is necessary, or there is a potential for airway compro- overprepared, this is the best option to have. This being said,
124it is
mise, general endotracheal anesthesia with positive-pressure ven- imperative that the patient have enough blood and blood prod-
Drtilation
Azam’smay
Notesbeinrequired. Irrespective
Anesthesiology 2013 of technique chosen it is ucts available to perform surgery at any given time. Successful
mandatory to maintain continuous monitoring of heart rate, treatment of these patients is dependent on a team approach to
VI 2658 Pediatric Anesthesia
Table 84-3 Vasoactive and Inotropic Agents in Pediatrics
Drug Effect Dose* Inotropy Chronotropy Vasodilation Vasoconstriction
Epinephrine (Adrenalin) A, B 0.05-2.0
Isoproterenol (Isuprel) B1, B2 0.05-2.0
Dopamine (Inotropin) D 1-3 Renal splanchnic

BA 5-15 /
B, A 15
Milrinone Bolus: 50 Mg/kg over 10-min period

Infusion: 0.375-0.75
Norepinephrine A B 0.05-1.0 sl
Nitroprusside 0.5-10
Arterial venous
Nitroglycerin 1-20
*All infusions are Mg/kg/min.

sl, slight.
require higher doses of dopamine than adults do to produce the of its long half-life and unpredictability, digitalis should be admin-
same effect. In one study, an infusion of 15 Mg/kg/min was istered cautiously to children who have changing levels of serum
required to increase cardiac output above control levels after potassium, calcium, and pH. In these cases, it is more appropriate
cardiac surgery.33 This may reflect the decreased releasable myo- to use rapid-acting, titratable inotropic agents.
cardial stores of norepinephrine in immature ventricles.
Calcium
Isoproterenol When serum ionized calcium levels are below normal, adminis-
Isoproterenol is a pure B-agonist with strong chronotropic effects tration of calcium produces a positive inotropic effect. If the
and is usually well tolerated in children. However, high doses of patient’s ionized calcium levels are normal, less marked inotropic
isoproterenol can cause myocardia ischemia.34 Isoproterenol also effects occur. Low ionized calcium levels most commonly occur
induces vasodilation that is responsive to acute volume in patients with DiGeorge’s syndrome, when large volumes of
administration. citrate-containing blood products are rapid administered, and in
neonates with relatively unstable calcium metabolism. Calcium
Dobutamine also has effects on the cardiac conduction system. Rapid admin-
Dobutamine provides positive inotropy and afterload reduction. istration of calcium can cause severe bradycardia or asystole. This
In children but not in adults it causes tachycardia.35,36 effect may be exaggerated in hypokalemic children or in those
receiving digitalis. The vasomotor effects of calcium are contro- 125
Norepinephrine versial, but most reports show an increase in both SVR and PVR
DrNorepinephrine,
Azam’s Notes aindrug
Anesthesiology 2013
with A- and B-agonist effects, has had a when the drug is administered.43
37
resurgence of use in infants and children. Children with nearly
VI Dr Azam’s Notes in Anesthesiology 2013
2660 Pediatric Anesthesia
Box 84-2 Causes of Severe Hypertension in Children
Renal Adrenogenital disease

Acute glomerulonephritis (e.g., poststreptococcal, Henoch- Cushing’s syndrome
Schönlein purpura)
Hyperaldosteronism
Hemolytic-uremic syndrome
Hyperthyroidism
Chronic glomerulonephritis (all types)
Hyperparathyroidism
Acute and chronic pyelonephritis
Iatrogenic
Congenital malformations (dysplasia, hypoplasia, cystic
Intravascular volume overload
diseases)
Administration of sympathomimetic drugs (e.g., epinephrine,
Tumors (e.g., Wilms’, leukemic infiltrate)
ephedrine)
Post–renal transplantation status; also rejection
Administration of corticosteroid
Oliguric renal failure
Rapid intravenous infusion of methyldopa
Trauma
Miscellaneous
Obstructive uropathy
Immobilization (e.g., fractures, burns, Guillain-Barré syndrome)
After genitourinary surgery
Hypercalcemia (e.g., hypervitaminosis D, metastatic disease,
Blood transfusions in children with azotemia sarcoidosis, some immobilized patients)
Cardiovascular Hypernatremia
Coarctation of the aorta Stevens-Johnson syndrome
Renal artery abnormalities (e.g., stenosis, thrombosis) Increased intracranial pressure (any cause)
Takayasu’s disease Dysautonomia
Endocrine After resuscitation
Pheochromocytoma
Neuroblastoma
Specific Pediatric Diseases

Kawasaki Disease
Kawasaki disease (mucocutaneous lymph node syndrome) occurs Box 84-3 Antihypertensive Medications
primarily in children 4 years of age or older. The disease is divided
into three stages: an acute febrile stage (1 to 2 weeks), a subacute Converting enzyme inhibitors to decrease angiotensin II
phase, and finally, the convalescent stage (typically 6 weeks after Caution in the face of renovascular disease
onset). The cause is uncertain, but it is presumed to be Captopril
infectious. Enalapril
Although the disease affects many organ systems, cardio- Calcium channel blockers, usually type II blockers
vascular involvement is the usual cause of ICU admission. Forty Caution: Myocardial decompensation
percent of patients with this disease have myocarditis, pericardial Nifedipine
effusions, arrhythmias, or any combination of these findings. Nimodipine
Coronary aneurysms, with and without thrombosis, develop in Diuretics, usually as an adjunct
20% of cases. Acute myocardial infarction is responsible for the
B-Adrenergic blockers
death of 3% to 4% of patients.
Caution: Reactive airway disease
Laboratory tests reveal an elevated leukocyte count with a
Propranolol 126
left shift, increased acute-phase reactants, and a platelet count that
Esmolol
is often grossly elevated after the first few weeks of the disease.
A2-Antagonist
DrAnAzam’s
echocardiogram
Notes is required for any child with this
in Anesthesiology 2013presumed
Prazosin
diagnosis.
Treatment includes high-dose aspirin (20 to 25 mg/kg Central A-agonist
Causes of hypoventilation include neuromuscular disease, central bronchopneumonia, asthma, and bronchopulmonary dysplasia
hypoventilation, and structural/anatomic impairment of lung (BPD). Dr Azam’s Notes in Anesthesiology 2013
Table 84-5 Classification of Causes of Neonatal Respiratory Failure
Congenital Abnormalities Developmental Immaturity Specific Neonatal “Stress”
Impaired control of Central nervous system dysgenesis Apnea of prematurity Drug intoxication (note maternal drugs)
ventilation Ondine’s curse Intracranial hemorrhage Sepsis
Central nervous system infections
Seizures
Neuromuscular disorders Congenital myopathies High cervical cord injuries
Structural impairment Thoracic deformities Severe abdominal distention

Lung hypoplasia Pneumothorax or other air leak
Diaphragmatic hernia
Potter’s syndrome
Abdominal malfunction
Gastroschisis
Omphalocele
Airway obstruction Choanal atresia Massive meconium aspiration

Upper airway Pierre Robin syndrome Vocal cord paralysis secondary to
Laryngeal web/cleft myelodysplasia
Congenital tracheal/laryngeal stenosis
Recurrent laryngeal palsy
Hemangioma
Lymphangioma
Lower airway Tracheoesophageal fistula Meconium/blood aspiration
Lobar emphysema
Alveolar disorders Respiratory distress syndrome Bronchopulmonary dysplasia
Cardiovascular disorders Congenital cardiac malformations Persistent pulmonary hypertension

Congestive heart failure (critical coarctation or
aortic stenosis)
Total anomalous pulmonary venous return
127

Adrenergic Receptors
Ahlquist
a b (original definition)
"Classic"
a1 a2 b1 b2 pharmacology
a1A1D a1B a1C a2A a2B a2C b1 b2 b3 Molecular

pharmacology
Gq/11 Gi;Go Gs Gs/Go Gs/Gi Signal

transduction
Activates Inhibits adenylyl cyclase; Stimulates adenylyl cyclase;
phospholipase C Ca2;, K; channels Ca2; channels Effectors
Postsynaptic: Postsynaptic: vasoconstriction Cardiac Smooth muscle Lipolysis

vasoconstriction Presynaptic: vasoconstriction inotropy and relaxation
HR (bronchial, vascular)
and cardiac effects
Figure 12-10 Classification of adrenergic receptors. HR, heart rate.
128

The Autonomic Nervous System 267 12
Table 12-2 Responses Elicited in Effector Organs by Stimulation of Sympathetic and Parasympathetic Nerves
Effector Organ Adrenergic Response Receptor Involved Cholinergic Response Dominant Response (A or C)
Heart
Rate of contraction Increase β1 Decrease C
Force of contraction Increase β1 Decrease C
Blood vessels
Arteries (most) Vasoconstriction α1 A
Skeletal muscle Vasodilation β2 A
Section II Anesthetic Physiology

Veins Vasoconstriction α2 A
Bronchial tree Bronchodilation β2 Bronchoconstriction C
Splenic capsule Contraction α1 A
Uterus Contraction α1 Variable A
Vas deferens Contraction α1 A
Prostatic capsule Contraction α1 A
Gastrointestinal tract Relaxation α2 Contraction C
Eye
Radial muscle, iris Contraction (mydriasis) α1 A
Circular muscle, iris Contraction (miosis) C
Ciliary muscle Relaxation β Contraction C
(accommodation)
Kidney Renin secretion β1 A
Urinary bladder
Detrusor Relaxation β Contraction C
Trigone and sphincter Contraction α1 Relaxation A, C
Ureter Contraction α1 Relaxation A
Insulin release from pancreas Decrease α2 A
Fat cells Lipolysis β1 A
Liver glycogenolysis Increase α1 A
Hair follicles, smooth muscle Contraction α1 A

(piloerection)
Nasal secretion Increase C
Salivary glands Increase secretion α1 Increase secretion C
Sweat glands Increase secretion α1 Increase secretion C
A, adrenergic; C, cholinergic.
From Ruffolo R: Physiology and biochemistry of the peripheral autonomic nervous system. In Wingard L, Brody T, Larner J, et al (eds): Human Pharmacology: Molecular to
Clinical. St. Louis, Mosby–Year Book, 1991, p 77.
129
Dr Azam’s Notes inand

contractility, Anesthesiology
conduction through2013
the AV node. One of the MI; and it can be assessed by changes in the time interval between
two systems normally dominates the organ’s function and thus successive heartbeats (i.e., beat-to-beat or heart rate variability)
minance at Specific Table 12-5 Adrenergic Receptor Differentiation 1

The Autonomic Nervous System 275
Receptor Stimulation Inhibition Table 12-7 Distribution of α- and β-Receptors
edominant Tone Receptor Distribution Response Agonist Antagonist

Alpha
α1 Smooth muscle Constriction Methoxamine Prazosin
rasympathetic
Heart Phenylephrine
rasympathetic α2 Presynaptic Inhibits norepinephrine release Clonidine Yohimbine

Blood vessels Vasoconstriction Dexmedetomidine
rasympathetic (skin, gut, kidney, β1 Heart Inotropy Dobutamine Metoprolol
liver, heart) Chronotropy
mpathetic β2 Smooth muscle Dilation Terbutaline
Gastrointestinal tract Sphincters Relaxation
mpathetic
Genitourinary tract Sphincters
rasympathetic
II 282 Anesthetic Physiology
Metabolic and endocrine
10. There is more than theoretical relevance in the subclassifica- adrenergic receptor kinase. The β-receptor has mechanistic and
Insulin release
rasympathetic tion of receptors35 in that mutations that decrease α2c presynaptic structural similarities with muscarinic but not nicotinic receptors,
effects function and enhance β1-receptor linkage cause adrenergic primarily in the transmembrane sections.
rasympathetic longer duration of action because they are not metabolized by Table
hyperactivity and predispose to CHF.36
12-9 Dose-Dependent Actions of Inotropes β-Receptors have been further divided into β1-, β2-, and
and Chronotropes
Beta Amino acid sequence comparisons indicate that α- β3-subtypes, all of which increase cyclic adenosine monophos-
COMT or MAO. receptors are members of the seven–transmembrane segment phate (cAMP) through adenylate cyclase and the mediation of G
rasympathetic Drug* (Proprietary Usual Infusion
gene superfamily, which uses G protein for signal transduction. A proteins.41 Although β1-receptors were traditionally thought to be
Heart (1) Rate, conduction
core of 175 amino Name) acids constitutes the sevenReceptors
transmembrane isolated to cardiac Rate tissue and β2-receptors were believed to be
mpathetic (cholinergic) Epinephrinecontractility regions and is highly conserved among different family members. restricted to vascular and bronchial smooth muscle, we now know
Blood vessels
Epinephrine is used intravenously in life-threatening circum-
(2) Vasodilation
The plethora ofEpinephrine
receptor subtypes (Adrenalin) β2
remains incompletely 1-2 µg/min
explained, that the β2-receptor population in human cardiac tissue is sub-
although the observation that different signal transductionβ1 + β2 mech- stantial and accounts for 15% of β-receptors in the ventricles and
stances, including the treatment of cardiac arrest,
(skeletal muscle,
circulatory col- 2-10 µg/min
anisms are used suggests finer control and physiologic signifi- 30% to 40% in the atria.42 β2-Receptors may help compensate for
lapse, and anaphylaxis, but it is also commonly
heart, brain) used locally
cance.toIt may be important that there is considerable α1 ≥10 µg/min
variability disease by maintaining
†
response to catecholamine stimulation
limit the spread of local anesthetics or to reduce blood loss.in α-adrenergic when β1-receptors
37
receptor subtypes among species. are 2-10
downregulated
µg; during chronic cate-
12-5). α-Receptor– The (bolus:
Receptors can be presynaptic as well as postsynaptic. Presy- cholamine stimulation and in‡CHF.43 The β2-population is almost
Respiration (?) Respiratory
systemic effects of epinephrine are variable and are related napticto
0.5-1.0 mg )
receptors may act as heteroreceptors or autoreceptors. An unaffected in end-stage congestive cardiomyopathy.44 In addition
the sympathetically center autoreceptor is a presynaptic receptor that reacts with the neuro- to positive inotropic effects, †β2-receptors in the human atria par-
out the body, includ- blood levels. The choice of dosing and the route of administration Norepinephrine
transmitter released from its own nerve terminal α1to, βprovide
1, >>β2 4-12 µg/min
feed- ticipate in regulation of the heart rate. Generation of cAMP in
are determined (2) Bronchodilation
by the indication for use and its urgency. back regulation. (Levophed)
A heteroreceptor is a presynaptic receptor that the human heart appears to be mediated primarily by β2-
ular, bronchial, and
Gastrointestinal tract Epinephrine activates all adrenergic muscle α1, α2, β
receptors: 1, β2,
responds to substances other than the neurotransmitter released receptors, although this may be an artifact related to the lability
and genitourinary (2) Smooth from that specificDopaminenerve terminal.
(Intropin)This regulatory scheme is of β1-receptors.
Dopaminergic 44
0-3 µg/kg/minof β3-receptors to fat cells suggests
Localization
and β3. Potential therapeutic effects of epinephrine include present posi-throughout the nervous system but is particularly impor- a new therapy for obesity. Polymorphism of this β-receptor
drenergic receptors. Genitourinary tract (2) Ureteral and β 3-10 µg/kg/min
tive inotropy, chronotropy, and enhanced conduction in the tant
heartin the sympathetic nervous system. 38
subtype is associated with obesity and the potential for the devel-
etic nervous system uterine muscle Although several presynaptic receptors α
have been identi- opment of >10
diabetes.µg/kg/min
45-47 †
Point mutations in genes encoding β2-
(β1); smooth muscle relaxation in the vasculature and bronchial fied, the α2-receptor may have the greatest clinical import. Pre- receptors are correlated with decreased downregulation of
stimulation of α2-
tree (β2); and(2)vasoconstriction
Metabolic and endocrine Glycogenolysis (α1). With vasoconstriction, aortic
synaptic α2-receptors
Dobutamineregulate(Dobutrex) β1 >> β2, α and β-receptors and
the release of norepinephrine µg/kg/min
nocturnal
2.5-10 asthma.†48,49
lin from pancreatic ATP through a negative-feedback mechanism.39 Activation of
effects diastolic pressure is increased,
(muscle, liver) thereby promoting coronarypresynaptic
flow α2Isoproterenol
-receptors by norepinephrine
(Isuprel) inhibits β1 > βsubsequent 0.5-10 µg/min
1- and α2-receptors
2 Dopamine Receptors
during cardiac arrest, which may be the single most importantof norepinephrine in response to nerve stimulation. A Dopamine exists as an intermediate in the biosynthesis of nor-
(1) Lipolysis release
orally borne neuro- survival.86 Endocrine and metabolic effects
determinant(2)ofGluconeogenesis similar inhibitory
ofto presynapticresponse(Inocor)
Amrinone is produced by attachmentIncrease of cyclic
acetyl- adenosine
epinephrine, and
0.75inmg/kg
addition, over dopamine exerts α- or
exogenous
load
choline cholinergic receptors. In the human brain, β-adrenergic effects (depending on the dose administered). Fur-
rugs. epinephrine (1) include increased levels of glucose, lactate, andligand
Insulin release monophosphate through a period of 2-350 min
freestudies reveal a high density of α2-receptors, particularly thermore, Goldberg and Rajfer demonstrated physiologically
onsible for sympa- fatty acids. (?) Renin release in the cerebral cortex and medulla.40 This latter distributioninhibitionmay of distinct dopamine 5- to type
10-µg/kg/min
1 (DA1) and dopamine type 2 (DA2)
account for the bradycardiac and hypotensive responses to α2- receptors, and infusion
these remain the most important of the five
vascular and bron- Epinephrine may be given intravenously as a bolus agonist
(?) Antidiuretic or bydrugs.
phosphodiesterase
dopamine receptors cloned (Fig. 12-12). DA1 receptors are post-
retion by the kidney, infusion. The usual bolus doses for pressure support begin atβ-Adrenergic
hormone release 2 to *All agents have elimination half-lives of a few synapticexcept
minutes and actamrinone
on renal, mesenteric,
( t 1 , 3.6 splenic, and coronary vas-
Receptors cular smooth muscle to mediate2 vasodilation through stimulation
hours; 5.8 hours in congestive heart failure).
8 µg given intravenously; 0.02 mg/kg or approximately 1.0 Like
(1), Mediated by β1-receptors; (2), mediated by β2-receptors; (?), controversial.
mg the is α-receptor,
† the β-receptor is one of the superfamily of of adenylate cyclase and increased production of cAMP. The
Much higher doses have beenthe used in clinical
mem- practice.
given for cardiovascular collapse, asystole, ventricular fibrillation, proteins that have
brane. These
‡
seven
transmembrane
helices
With anaphylaxis
woven through
or cardiac
domains are arrest.
labeled M
cellular
through
vasodilatory effect tends to be strongest in the renal arteries. It is
M7; for this action, particularly the redistribution of blood flow to the
ervous System electromechanical dissociation, or anaphylactic shock (seeantagonists 87
also have
1
Dataspecific binding sites,
from Hoffman BB,whereas
Lefkowitz agonists are more kidneys,
RJ: Catecholamines andthat dopamine isdrugs.
sympathetic most frequently
In used.
130Additional renal
Chapter 97). The larger dose range is recommended in thesediffusely criti- attached
Goodman to hydrophobic
A, Rall T,membrane-spanning
Nies A, et al (eds): domains Goodman DA and1 receptors
Gilman’slocated in the tubules modulate natriuresis through
the Pharmacological
Inhibition (Fig. 12-11). Basis
The extracellular portion 8th
of the ed.receptor in an the sodium-potassium
ends Pergamon ATPase pump and the sodium-hydrogen
Dr Azam’sand
Notes in cal situations to2013
Anesthesiology maintain myocardial and cerebral perfusion of Therapeutics, New York, Press, 1990, p 187.
amino group. A carboxyl group occupies the intracellular termi- exchanger.50-53 DA2 receptors are presynaptic; they may inhibit
several metabolic
through consequences, including lipolysis
peripheral vasoconstriction. and gly-
High-dose epinephrinenal,(0.1
where phosphorylation occurs. At the cytoplasmic domains, release of norepinephrine and perhaps acetylcholine. There are
there is interaction with G proteins and kinases, including β- also central DA2 receptors that may mediate nausea and vomiting,
II have been synthesized that bind preferentially to one or another pressure. OH NJ
However, it receives
306 Anesthetic Physiology 12% to 15% of cardiac output. This high flow H C
3 CH3 2013
OJCJCH
rate is a reflection of the brain’s high metabolic rate. At rest, the
J
Table 12-11 Muscarinic Anticholinergic Drugs Atropine Glycopyrrolate
brain consumes
This chapter oxygenthe
reviews at effects
an average rate of approximately
of anesthetic drugs and tech- sumed by the
Table brain
13-2 is involved
Factors in Cerebral
Influencing cellular Blood
homeostatic
Flow* activities.
3.5 mL of
niques onoxygen
cerebral perphysiology,
100 Central
g of brain tissue pertheir
in particular, minute. Whole-
effects on cere-Local CBF and CMR within the brain are very heterogeneous, and
brain O2 consumption (50Nervous
J CHgreater
bral blood flow (CBF) andmL/min) represents about 20% of both are approximately four times in gray matter than in
Factor 3
Comment
metabolism. The final section presents N
total-body oxygen utilization. Normal values for CBF, CMR,Heartand
Rate white matter. The cell population of the brain is also heterogene-
J
aDrug
brief discussion Duration System*
of pathophysiologic Antisialagogue
states, including cerebral
J
Chemical/Metabolic/Humoral
other physiologic variables are provided in Table 13-1. ous in its oxygen requirements. Glial cells make up about half the
J
ischemia,
Atropine as well
Approximately as discussion
Short of theofbrain’s
60% Stimulation cerebral
+ energy protection. ++The chapter
consumption is brain’s CMRvolume and require O less energy O neurons2OHdo. intact
CHassumes
J CMR than
influence Besides
flow-
gives greatest emphasis to information that is of immediate rele-
K
J
J J
used to support
Glycopyrrolate Long electrophysiologic
0 function.
++ The depolarization-
+ providing a physically
Anesthetics supportive latticework
metabolism
OJCJCH for the brain,
coupling, the glial
mechanism of
vance to the rationale for use of the anesthetic and intensive
repolarization activity that occurs and is reflected in the EEG cells are important care Temperaturein reuptake of neurotransmitters, in delivery
which is not fully understood
management
Scopolamine of patients
Short with
Sedation intracranial
++ pathology.
requires expenditure of energy for the maintenance and restora- and removal 0/+Chapter 63 of metabolic substrates
Arousal/seizures and wastes, and in blood-
Scopolamine
presents
tion
*The effects the
of ionic clinical
of atropine are management
gradients andwith
limited forthetheof synthesis,
usual these
clinicalpatientsbut in
transport,
doses, detail.
they be Neu-
and
can brain barrier (BBB) function.
rologic inmonitoring,
reuptake
significant including
oftheneurotransmitters.
elderly. Thethe effects of
remainder of the
anesthetics
energy con- on the PaCObrain’s
The 2 substantial demand for substrate must be met
electroencephalogram (EEG) and evoked responses, is reviewed
0, no effect; +, mild effect; ++, moderate effect. by adequate
PaO2 delivery of oxygen and glucose. However, the space
Figure 12-18 Structural formulas of clinically useful antimuscarinic drugs.
in Chapter 46. constraints imposed by the noncompliant cranium and meninges
Table 13-1 Normal Cerebral Physiologic Values requireVasoactive
that blood flow not be excessive. Not surprisingly, there
drugs
are elaborate mechanisms for regulation of CBF. These mecha-
Anesthetics
CBF nisms, which include chemical, myogenic, and neurogenic factors,
Vasodilators
Global 45-55 mL/100 g/min
are listedVasopressors
in Table 13-2.
Regulation of Cerebral
Cortical (mostly gray matter)
75-80 mL/100 g/min
≈20 mL/100 g/min
Subcortical (mostly white matter) Myogenic
Blood Flow
CMRO 2 3-3.5 mL/100 g/min Chemical Regulation ofThe
Autoregulation/MAP Cerebral Blood
autoregulation Flowis fragile,
mechanism
CVR and in many pathologic states CBF is
Anesthetic drugs cause dose-related 1.5-2.1 mm Hg/100 alterations
and reversible g/min/mL in
Several factors, including changes in CMR, Pa
regionally 2, and Pa
pressure 2, cause
passive
many
Cerebralaspects
venous POof 2 cerebral physiology, 32-44including
mm Hg CBF, cerebral alterations in the cerebral biochemical environment that result in
metabolic rate (CMR), and electrophysiologic function (EEG, Rheologic
adjustments in CBF.
Cerebral venous SO2 55%-70%
evoked responses). The effects of anesthetic drugs and techniques Blood viscosity
ICP (supine)
have the potential to adversely affect 8-12 the
mm Hg diseased brain and Cerebral Metabolic Rate
Neurogenic
Increased neuronal activity results in increased local brain metab-
conduct
CBF, cerebralof theflow;
blood neurosurgical
CMRO2, cerebral procedure
metabolic rate and are CVR,
of oxygen; thuscerebral
of clinical
importance
vascular inICP,
resistance; patients with
intracranial neurosurgical disease. However, olism,
pressure. in and this increase
Extracranial in CMR
sympathetic andis associated with
Contribution anda well-matched,
clinical significance poorly
certain instances, the effects of general anesthesia on CBF and parasympathetic pathways defined
CMR can be manipulated to improve both the operative course
Intra-axial pathways
and the clinical outcome of patients with neurologic disorders.
The adult human brain weighs approximately 1350 g and *See text for discussion.
therefore represents about 2% percent of total-body weight. CBF, cerebral blood flow; CMR, cerebral metabolic rate; MAP, mean arterial131
pressure.
However, it receives 12% to 15% of cardiac output. This high flow
rate is a reflection of the brain’s high metabolic rate. At rest, the
of Hypoxemia and Hypercapnia a gap between the estimated P2 and the measured Pa2, another
15 Azam’s Notes in Anesthesiology 2013
or an additional cause Respiratory
of hypoxemia must beDrsought.
Physiology 363
It is also
us sections
Boxwe discussed
15-1 Alveolar Gasventilation,
Equations gas distribution, dependent on sex, age, height, and weight. FRC goes up with
height and age and down with weight and is smaller in women
ratory mechanics that govern distribution, diffusion, Table 15-1 Causes of Hypoxemia
than in men.1,6 The balance of the inward force of the lung and
ary perfusion.
AlveolarAll theseTension
Oxygen components
(PAO ) of lung function
2 the outward force of the chest wall determines the volume. The
e oxygenation of Pblood, PACO 
AO = PIO −and all except
+ PACO
2 1− R 
× FIO ×diffusion can inward force of the lung, or Pa “elastic PaO2 of the elastic
O2 recoil,” consists PaO2
R  fibers of the lung tissue, as well as the contractile forces of airway
2 2 2 2
R  (breathing (breathing (breathing air)
ably affect CO2 elimination. The different mecha- smooth muscles and the surface tension of alveoli. The outward
where PIO is inspired oxygen tension, PACO is alveolar CO air) by
force of the chest wall is exerted at the ribs, joints,
oxygen) with Exercise
and muscles.
d hypoxemia and CO2 equal
2
tension (assumed to
retention, or hypercapnia or 2
arterial PCO ), R is the respiratory
2
It can be asked why any gas volume persists in the lung after
2 Disturbance Rest at Rest (Versus Rest) PaCO2
have been touched
exchange on ininprevious
ratio (normally the range of 0.8paragraphs
to 1.0), and FIObut expiration. There are two good reasons, at the least. One is that if

2
is the inspired oxygen fraction. alveoli collapse during expiration, much moreNormal effort would have
zed in more detail here. Hypoventilation Reduced
to be spent to reopen them again than during a normal breath
No change or Increased
The term within brackets compensates for the larger
s of hypoxemia
O uptakecan
2 than suitably be over
CO elimination
2
classified ascapillary
the alveolar hypoven- with no collapse because less resistance is encountered when further
Q! mismatch,
membranes.impaired diffusion, and right-to-left expanding an alveolar wall in an open lung with a liquid-gas decrease
interphase unit than expanding a collapsed alveolus with a liquid-
rcapnia can A simplified equation can be written without the com-
be caused by hypoventilation, V !A Q ! liquid! interphase. The other Reduced
reason is that theNormal
inspired air mixesNo or minor Normal
pensation term:
with V Q! mismatch
A remaining
the gas in the lung, thereby leveling off the varia-
nd shunt, although in practice PAO = PIO −
hypoventilation
PACO
. 2 is the tion in O2 and CO2 concentrations that occur during the respira- increase or
real importance (Tables 15-1 and R 15-2).
2 2
tory cycle. With just little air in the lung, the gas variations in decrease
alveoli would be much greater, and they would cause a similarly
Alveolar Ventilation
Alveolar ventilation ( V! A ) can be expressed as Shunt
varying Reduced
Pa2 and Pa2 in blood. Reduced
This can indeed No change or
be observed in Normal
ation patients with reduced lung volumes (see later).
further
With increased ventilation, as during exercise, V is raised
is low in proportion to metabolicV! A = f × ( VT − VDSdemand,
) elimina- by increasing both inspiration and expiration so that FRC is decrease
will be inadequate andVTitis tidal
where f is breaths/min, willvolume,
accumulate in the
and VDS is physio- lowered by approximately 0.5 L. However, in the presence of
Diffusion
airway Reduced
obstruction, as in asthma, Normal is slowed
for example, expiration Small to large Normal
d, and other body
logic dead tissues. Hypoventilation is often
space.
entilation that results
Alveolar in acan
ventilation Paalso be above 45 mm Hg
derived from
down so that the
impairment end-expiratory level is elevated instead
lowered.7 This is called air trapping and is a means of reducing
of being decrease A
2
V! CO2 = c × V! A × FACO2 the resistance to gas flow in the narrowed airways (Fig. 15-2).
However, it has to be paid for because the increased level of
where V! CO2 is CO2 elimination, c is a conversion constant, breathing increases the elastic work of breathing.
and FACO2 is the alveolar CO2 concentration. FRC increases with age because of loss of elastic lung tissue,
which lessens the contractile force of the lung and moves the
If V! A is expressed in L/min, V! CO2 in mL/min, and FACO2
balancing point between the outward force of the chest wall and
is replaced by PACO2 in mm Hg, c = 0.863. By rearranging,
the inward force of the lung to higher lung volume. In patients
V! CO2 × 0.863 with chronic obstructive pulmonary disease (COPD), FRC
V! A = .
PACO2 increases faster over the years than in normal subjects because of
an effect of chronic air trapping and more severe loss of elastic
tissue (in particular in emphysema).1
FRC is reduced in lung diseases characterized by fibrosis
of the lung, such as idiopathic fibrosis, pneumoconiosis, and dif-
ferent forms of granulomatosis and vasculitis.7 In extreme cases,
will lower Pa2 and affect consciousness. In respiratory tests of the reduction can be down to 1.5 to 2 L (see Fig. 15-2). Obviously,
ventilatory capacity it is therefore necessary to perform the test pulmonectomy (e.g., for treatment of lung cancer) will also reduce
during rebreathing of expired gas or add CO2 to the respiratory FRC. However, the remaining lung will expand and fill in some 132
gas so that Pa2 is maintained at a normal or nearly normal level. of the space left after resection of lung tissue, sometimes called
Dr
The Azam’s
increase inNotes in Anesthesiology
ventilation is brought about by 2013
an increase in V “compensatory emphysema.”
to approximately two thirds of vital capacity (VC) (see later), or
participate in gas whole capillary distance
The efficiency may becontraction
of cardiac required before the capillary
is estimated by the found only small shunts of 1% to 2%, although log SDQ increased

at theHeart
samefailure
time blood has been fully
12 oxygenated, even in resting conditions. On
! which causes
Q,
following formula :
from 0.77 to 1.13. When F2 was increased to 0.5, an increase Dr Azam’s
in AgeNotes in Anesthesiology 2013
space ventilation Cardiac efficiency = External work Engergy equivalent of It is well known that arterial oxygenation is
lexity of MIGET Box 15-2 Derivation ofoxyge
the Physiologic Dead Space Equation
n consumption increasing age of the patient (see Chap
alFatal myocardum
purposes and The corkscrew motion of the heart for the ejection of blood Box 15-3 Derivation of the Venous Admixture mentioned earlier, formation of atelectasis
depression
ce must rely on FisE ×the = FA ( Vfavorable
VT most T − VDS ) +in
(FIterms
× VDS )of work efficiency based FonE the (“Shunt”) Equation
VT
age in adults, and the sparse number of
CO2 dead space architecture in a normal LV (with the cardiac muscle bundles
ume
By rearranging,
arranged so that a circumferentially oriented middle F A layer is Fsand-
I
studied in the CT scanner during anesth
e in all patients wiched by longitudinally oriented outer -V D In heart failure,
V Tlayers). Ca × Q! T = (Cc ′ × Q! c ) + (Cv × Qs
! ) (1) larger percentage of atelectasis in the tr
VDS FA − FE
poxemia in most =
ventricular dilation reduces cardiac efficiency because it increases patients of other ages do.63 Similarly, shunt
ftward shift of the
wall FA − Fwhich
VT stress, I
in turn increases oxygen consumption.11 ! = Q! T − Qs !
ntributing factor,
hereas a rightward shift Qc (2) in the tested range of 23 to 69 years. In con
t causes
ar function. hypox-
In The If FI = 0, F replaced by P, and PA replaced by Pa, for CO2, be increasing V !A Q! mismatch with age
adelphia, Lippincott- Heart Rate and Force-Frequency Relationship By inserting Equation 2 into Equation 1, ! regions both in awa
!A Q
In isolated cardiac muscle,VDS an CO2 − PECO
Paincrease in2 the frequency of stimu- fusion of low-V
ung disease and
lation induces an increase
=
in the
PaCO2 of contraction. This rela-
force Ca × QT = (Cc × QT − Qs ) + (Cv × Qs)
! ! ! ! they are subsequently anesthetized. Figure
blood flow. Sys- VT
tionship is termed the “treppe” (Treppe means staircase in German) C. C .C V– tionship between shunt, perfusion of low-V
as periarteritis Qs
drugs such as digi- phenomenon
where FE , FA, or
andtheFIforce-frequency
are mixed expired, alveolar,12,13
relationship. andAt between Rearranging, QC of the patient. Thus, the major cause of i
leroderma, and
nerate pressure and 150 andgas
inspired 180concentration,
stimuli per minute, maximal
respectively, andcontractile
VT, VDS, and force
VAis .Ca during anesthesia at ages younger than 50
ary dysfunction ! QT
e intrinsic inotropic
!A Q ! reached
are tidal in an isolated
volume, deadheart muscle
space, and at a fixed
part muscle
of the tidal length.
volumeThus,
to Qs Cc ′ − Ca
d shunt. V an increased frequency incrementally increases inotropy, whereas = at higher ages mismatch (increased log SD
ntybe
perfused alveoli, respectively. A Q! T Cc ′ − Cv
of seen in pul- or
contraction, stimulation at lower frequency decreases contractile force. ingly important. Because the correlation
jection at zero load. However, when the stimulation becomes extremely rapid, the age during anesthesia is almost parallel
muscle shortening in force of contraction decreases. In the clinical context, pacing- where Cc′, Ca, and Cv are oxygen content in pulmonary end-
! awake state, it can be said that anesthesia
of force. Although induced positive inotropic effects may be effective only up to a capillary, arterial, and mixed venous blood, respectively; QT
ed myocytes, Vmax certain heart rate based on the force-frequency relationship. In a ! is capillary flow; and Qs ! is shunt. ventilation and blood flow by as much as 2
is cardiac output; Qc
se complete unload- fully, log SDQ returns to the preanesthesia
ontractile activity of
en attempted with
Internal work
t requiring catheter- External work
ntly the best way to
(Fig. 16-6).7 The End-systolic (ES)
ct measure of the PV relationship
) and muscle length
d noninvasive index End-systolic
tion fraction, which c
Aortic valve
Ejection open
hy, or radionuclide b
Contraction
V ) LVEDV , Relaxation
End-diastolic
volume. a
Mitral d Filling
e opening
xternal and internal

ood under pressure,
e ventricle to change Ventricular volume
ction. Internal work Figure 16-6 Pressure-volume loop. Point a depicts the start of isovolumic
he heart. Wall stress contraction. The aortic valve opens at point b, and ejection of blood follows
of the heart.11 (b→c). The mitral valve opens at d, and ventricular filling ensues. External
work is defined by a, b, c, and d and internal work by e, d, and c. The
oduct of the stroke pressure-volume area is the sum of external and internal work. (From Opie
ring ejection of the LH: Ventricular function. In The Heart. Physiology from Cell to Circulation,
4th ed. Philadelphia, Lippincott-Raven, 2004, pp 355-401.)
A
133

II 434 Anesthetic Physiology
Cirrhosis
Resistance to Hepatic dysfunction

Backward theory intrahepatic blood flow
Vasodilators Hypoalbuminemia
Portal Portal systemic
hypertension Nitric oxide, glucagon,
shunt prostacyclin, activation of K+
channels, cytokines,
endotoxemia, adenosine
Forward theory Peripheral and splanchnic PVBF Plasma

vasodilatation HABF oncotic
Splanchnic AV shunting THBF pressure
GI bleeding
Liver and
intestinal Effective blood volume
lymph flow
Ascites and
edema
Volume receptor stimulation
Ascites and
edema
Neural factors Humoral factors Intrarenal factors

Sympathetic nervous Renin Endothelin
activity Aldosterone Urinary kallikrein
Role of hepatorenal Angiotensin II or PGs
reflex ADH Thromboxane
Refractory to ANF Leukotrienes
PAF
Adenosine
Tubular sodium retention and reduced renal blood flow
Figure 17-13 Schematic of pathways for cirrhosis-induced portal hypertension: the forward and backward theories. Cirrhosis and portal hypertension induce
circulatory changes that decrease effective blood volume. This activates volume receptors and stimulates neurohumoral and intrarenal reflexes, which
decreases renal blood flow and increases renal retention of sodium. ADH, antidiuretic hormone; ANF, atrial natriuretic factor; AV, arteriovenous; HABF, hepatic
arterial blood flow; PAF, platelet-activating factor; PGs, prostaglandins; PVBF, portal venous blood flow; THBF, total hepatic blood flow. (Reprinted with
permission from Mushlin PS, Gelman S: Anesthesia and the liver. In Barash PG, Cullen BF, Stoelting RK [eds]: Clinical Anesthesia, 4th ed. Philadelphia, Lippincott
Williams & Wilkins, 2001, p 1088.)
134

immunoglobulin 2013
A, cholesterol, and various forms of bile salts coagulopathies, the liver continues to make procoagulants.
though
e meas-
bias (in
asonog- Vasoconstrictor Vasodilator Renal Physiology 459 18
output Systems Systems
allows Table 18-2 Dopamine and its Analogs
alitative Systems Promoting
Sympathoadrenal system Vasoconstriction
Prostaglandins and
Renin-angiotensin system Kinins
een the SaltAldosterone
Retention Atrial natriuretic peptide (ANP)
Receptor DA1 DA2 β1 β2 α1
Antidiuretic hormone (ADH) Dopamine +++ ++ ++ ± +++
The Sympathoadrenal Axis
RBF RBF Dobutamine 0 0 +++ ++ ±
Sympathetic effects GFR on the kidney are mediated GFR by circulating
epinephrine and Urine neuronal
flow release of norepinephrine.
Urine flow The renal Dopexamine ++ + ± +++
Basic Principles of Pharmacology 485
0 19
Na excretion Na excretion
cortex has a dense plexus of autonomic nerve fibers derived from Fenoldopam ++++ 0 0 0 0
the T12 to L4 spinal segments via the celiac plexus. The primary doses is less than Vm/3. Clearance of such drugs is generally
at Vm=1 g/min
systems to the 2.00
Figure 18-17 Neurohormonal
stimulus sympathetic renal regulatory systems. GFR, glomerular
response is a decrease in arterial Dobutamine, expressed as a and
dopexamine, constant
fenoldopam (e.g.,are
propofol
all pharmacologic = 1.6ofL/min).
clearanceanalogs
E.R. calculated
Section II Section
filtration rate; Na, sodium; RBF, renal blood flow; ↓, decreased; ↑, increased. dopamine.SomeHowever, dobutamine is devoid of dopaminergic activity; dopexamine
d water
blood(Modified
pressure from sensed
Sladen RN:by baroreceptors
Effect of anesthesia andin the aortic
surgery on renal arch,
function.carotid drugs, such as phenytoin, exhibit saturable pharmacokinet-
has abouticsone(i.e.,
third have
of the such
dopaminergic activity of dopamine; and
low Vm that typical doses exceed the linearfenoldopam is a
renin-
sinus,Critand
Care Clin 3:380, 1987.)
afferent arteriole. Afferent fibers travel via the vagus pure, selective dopamine1-receptor agonist. α1, alpha1-receptor; β1, beta1-receptor;
portion of Fig. 19-6). Clearance of drugs with saturable metabo-
nerve and decrease impulse transmission rate to the mediatingExtraction β2, beta2-receptor; DA1, dopamine1-receptor; DA2, dopamine2-receptor.
1.50
centers in the hypothalamus, which results in increased adrener-
Renal Physiology 465 1.0 18 lism is a function of drug concentration rather than a constant.
ratio
gic nerve activity. The kidney does not have any parasympathetic 0.9 Renal Clearance
Clearance (L/min)
Anesthetic
0.8
yclic innervation.
GMP. Table 18-3 Adenosine Receptor Subtypes and Functions with
0.7 The kidneys clearβdrug
predominantly 1- and fromβplasma
2-adrenergic activity,
by filtration at thesuch
glomeru- as
lar smooth A G protein–coupled phospholipase-C receptor populates dobutamine lus andor direct
isoproterenol,
transport cause into themarked
tubules. increases
Renal bloodin cardiac
flow is
Receptor Agonist Function Ischemic Injury 0.6
. It inhibits 1.00
vascular smooth muscle and the mesangium and responds to α- output inversely
and thus correlated
RBF, but itwith age, as is to
is difficult creatinine
ascertain clearance, which can
their intrarenal
0.5
n, and cel- A1 Outer cortical vasoconstriction Highly protective be predicted from age and
adrenergic stimulation by epinephrine and norepinephrine. It effects. Dopaminergic agonists (Table 18-2) selectively increaseof
weight according to the equation
III Anesthetic
P by phos- 0.4 5
andCockroft and Gault :
α-adrenergic renal vasoconstriction.43
canmediates vasoconstriction induced by a variety of other hor- RBF
also may oppose
Decreased renin release
oxide 0.3 Men:
PhysiologyPharmacology
mones and peptides,
phodieste- including
Inhibition of diuresis angiotensin
and natriuresis II, vasopressin,
0.50 3 0.2 Renin-Angiotensin-Aldosterone System
endothelin,
is rapidly A2a
platelet-activating factor, and leukotrienes.
Juxtamedullary vasodilation
The The
Highly protective Creatinine clearance (mL min )
receptor subunit in the cell membrane is coupled through Gq Renin and Angiotensin (140 − Age [ yr ] × Weight [ kg ])
me proteins (9)
clooxygen- Increased renin release 0.1 = consists of three groups of special-
protein to phospholipase C, which hydrolyzes phosphatidylinosi- The juxtaglomerular apparatus
Section II Anesthetic Ph
72 × Serum creatinine (mg%)

tol biphosphate (PIPPromotion 2) to inositol
of triphosphate
diuresis and natriuresis (IP 3 ) and diacyl- ized tissues. In the afferent arteriole, modified fenestrated endothe-
0.00
glycerol (DAG).A2b In turn,Unknown DAG activates protein kinase, opening lial cellsWomen: produce renin; in the juxtaposed distal tubule, cells of
0 0.5 1 1.5 2
up a calcium channel in the membrane, and IP3 triggers the the macula85%
ine the site
densaof the
actabove.
as chemoreceptors; and in the glomerulus,
A3 Unknown Liver disease/ Potentiates injury
ve NOS release
is of calcium from theenzyme sarcoplasmic orVmendoplasmic reticu- mesangial cells have contractile properties (see Fig. 18-3). Together
Enzyme induction
inhibition
lum. Both
ll amounts mechanisms result in a rapid increase in intracellular these provideEquation
From Fozard JR, Hannon JP: Adenosine receptor ligands: potential as therapeutic
an important 9 shows that age issystem
regulating an independent
for bloodpredictor
pressure,of
agents in asthma and COPD. Pulm Pharmacol Ther 12:111-114, 1999. creatinine clearance. Thus, 46 elderly patients have decreased creati-
calcium, whichFigure
e). Consti- binds 19-8with calmodulin
Corollary to Figure 19-7andshowingthereby activates
the relationship betweensalt, and water homeostasis.
metabolic capacity, clearance,in andsmooth
extractionmuscle
ratio (E.R.).contrac-
Changes in nine clearance, even in the presence of normal serum creatinine
h actsmyosin
as a light-chain kinase, resulting Renin
levels.secretion
Inhaled is stimulated by hypovolemia
decrease renalthat mayflow.be 135
maximum metabolic velocity (Vm) have little effect on drugs with a high anesthetics also blood
asodilation,
tion. The calcium-calmodulin complex simultaneously activates overtof (hemorrhage, diuresis, sodium lossthe or offset
restriction)
extraction ratio, but they cause a nearly proportional decrease in clearance Decreased renal clearance will delay of effectorforcovert
renally
ndothelium A
phospholipase A (Table 18-3).
, resultingActivation
in the of the A
production adenosine
of receptor
vasodilator induces
pros- (positive-pressure ventilation, congestive heart failure, sepsis, or
3 drugs
2 with a low extraction ratio. 1
excreted drugs or their metabolites.
Basic Principles of Pharmacology 505 19

Table 19-2 Site of Action of Sedatives and Hypnotics
Anesthetic GABAA Glycine Neuronal nAChR 5-HT3 AMPA (GluR1-4) NMDA
Barbiturates +++ +/0 −−− −/0 −−− 0
Chloroform +++ +++ −−− Unknown −−− 0
Diethyl ether +++ +++ −−− +++ −−− −−−
Section III Anesthetic Pharmacology

Enflurane +++ +++ −−− +++ −−− −/0
Etomidate +++ +/0 −/0 0 Unknown Unknown
Halothane +++ +++ −−− +++ −−− −/0
Isoflurane +++ +++ −−− +++ −−− −/0
Ketamine +/0 0 −−− +/0 0 −−−
Methoxyflurane +++ +++ −−− +++ Unknown Unknown
Nitrous oxide +++ +/0 Unknown Unknown −/0 −−−
Propofol +++ +++ −/0 0 −/0 −/0
Sevoflurane +++ +++ −−− Unknown Unknown Unknown
Steroidal anesthetics +++ 0 −/0 −/0 0 0
Xenon 0 Unknown Unknown Unknown 0 −−−
AMPA, α-amino-3-hyudroxy-5-methyl-4-isoxazoleproprionate; GABA, γ-aminobutyric acid; 5-HT, 5-hydroxytryptamine; nAChR, nicotinic acetylcholine receptor; NMDA, N-
methyl-D-aspartate; +++, potentiation of the agonist; −−−, inhibition of the agonist; +/0 and −/0, little potentiation or inhibition, except at concentrations well in excess of
the clinical range; 0, no effect at any concentration.
From Krasowski MD, Harrison NL: General anaesthetic actions on ligand-gated ion channels. Cell Mol Life Sci 55:1278-1303, 1999.
136
Efficacy
100
III 540 Anesthetic Pharmacology
Table 21-1 Partition Coefficients at 37°C
Anesthetic Blood-Gas Brain-Blood Liver-Blood Kidney-Blood Muscle-Blood Fat-Blood
Desflurane 0.45 1.3 1.4 1.0 2.0 27
Nitrous oxide 0.47 1.1 0.8 — 1.2 2.3
Sevoflurane 0.65 1.7 1.8 1.2 3.1 48
Isoflurane 1.4 1.6 1.8 1.2 2.9 45
Enflurane 1.8 1.4 2.1 — 1.7 36
Halothane 2.5 1.9 2.1 1.2 3.4 51
Diethyl ether 12 2.0 1.9 0.9 1.3 5
Methoxyflurane 15 1.4 2.0 0.9 1.6 38
Data from references 1 through 8.
Box 29-2 Reported Indications for the Use of Muscle

able quantities of anesthetics are taken up because the solubilities of an anesthetic in the alveoli is transmitted to arterial blood and
Relaxants in the
of anesthetics far Intensive
exceed theCare Unit of oxygen (or nitrogen).
solubility thence to all tissues (especially the central nervous system), devel-
ulation At low inspired concentrations, the balance between delivery opment of an adequate central nervous system anesthetic partial
Facilitate
of anestheticmechanical ventilation
by ventilation and removal of anesthetic by uptake pressure may be delayed in the case of highly blood-soluble agents
upreg- determines the F/F
Facilitation intubationis a simple one. For such as ether and methoxyflurane (Table 21-1).1-8 Indeed, the
ratio. The relationship
of endotracheal
o non- example, if uptake removes a third of the inspired anesthetic delay in development of an anesthetizing cerebral partial pressure
vity to Enable patients to tolerate mechanical ventilation
molecules, F/F equals two thirds; if uptake removes two thirds has contributed to the elimination of such highly blood-soluble
e listed High
of the pulmonary
inspired inflation
molecules, F/Fpressures, e.g., acute respiratoryagents from anesthetic practice. Even the moderate solubility of
equals a third.
ent of distress syndrome isoflurane could slow induction of anesthesia were it not for the
r scald Hyperventilation for increased intracranial pressure use of anesthetic overpressure—that is, we compensate for the
nonde- Anesthetic Uptake Factors uptake of anesthetic by delivering a higher concentration than we
Facilitate therapeutic or diagnostic procedures hope to achieve in the alveoli, perhaps 2% isoflurane to produce
injury
Three factors determine anesthetic uptake: solubility (λ), cardiac an alveolar concentration of 1%.
Tetanus
respect output (Q), and alveolar-to-venous partial pressure difference
Status epilepticus
(P − Pv). 1
Uptake equals the product of these factors: λ × Q × Cardiac Output
uscular (P − Pv)oxygen
Reduce dividedconsumption
by barometric pressure. The effect of altering cardiac output is intuitively obvious. If more
at least Because uptake is the product of these factors rather than blood passes through the lungs, more blood is available to remove
Abolish shivering
omus- a sum, if any factor approaches zero, uptake must approach zero, anesthetic and thereby lower the F/F ratio. To the student of
or even andReduce work
ventilation of breathing
rapidly drives the F/F ratio to 1.0. Thus, if solu-
assium bility is low (as in the case of oxygen), if cardiac output approaches
succi- zero (as in profound myocardial depression or death), or if the
alveolar-to-venous difference becomes inconsequential (as might 1.0 137
Potas- patient may be at risk for a hyperkalemic response is not well
occur after an extraordinarily long course of anesthesia), uptake
rted to defined.be A conservative guideline
wouldtherefore
1. would be to avoid the
Drwould
Azam’sminimal,
Notes inandAnesthesiology
F/F equal2013
rest.434 use of succinylcholine in patients 24 to 48 hours after a thermal
Volatile Anesthetics
Ryanodine
Muscarinic Receptor Phospholipase C cAMP Ca2+ channel
Stimulation + (PLC)
+ +
+ Voltage dependent
Protein Ca2+ channel
Heterotrimeric kinase C Inositol triphosphate
+ (IP3)
G-protein receptor
complex
Regulation of Intracellular Ca2+

actomyosin (ICa2+)
Monomeric
G-protein crossbridge Calmodulin (CaM)
(Rho) formation
Exchange Ca2+/CaM
at the Ga
Rho-associated subunit
kinase (ROK) Myosin light chain Bronchodilation
kinase (MLCK)
ATP ADP
Smooth muscle
protein
Phosphorylated myosin
phosphatase Myosin light chain (pMLC)
light chain
Figure 22-4 Proposed signaling pathways underlying volatile anesthetic (specifically, halothane)-induced bronchodilation or inhibition (or both) of muscarinic
agonist–induced contraction of airway smooth muscle. +, excitatory action of muscarinic receptor agonist; ↑, activation or increase attributable to the volatile
anesthetic; ↓, inhibition or decrease attributable to the volatile anesthetic. Signal transduction along pathway A is supported by work from Warner and
coworkers on a role of halothane in decreasing Ca2+ sensitivity rather than a change in ICa2+ content. (Adapted from Pabelick CM, Prakash YS, Kannan MS, et
al: Effects of halothane on sarcoplasmic reticulum calcium release channels in porcine airway smooth muscle cells. Anesthesiology 95:207, 2001; and Hanazaki
M, Jones KA, Perkins WJ, et al: Halothane increases smooth muscle protein phosphatase in airway smooth muscle. Anesthesiology 94:129, 2001, with
permission.)
110 neurally derived mediator of reflex bronchospasm). Inhaled anes-

Thiopental thetics may remain effective bronchodilators even with severe 138
Isoflurane
100 serotonin- or histamine-induced bronchospasm that is refractory
sistance
Halothane
Dr Azam’s Notes in Anesthesiology 2013 Sevoflurane to β2-adrenoceptor therapy.
90
Desflurane Volatile anesthetic–induced decreases in bronchomotor
)
ity, many 50% to 75%. Because of the potential for halothane-induced hepa- Dr Azam’s Notes in Anesthesiology 2013
III
gh an idi- titis,Anesthetic
640 halothane is not generally recommended for use in adults.
Pharmacology
ependent, In several medical malpractice cases, injury or death as a result
Table 24-1 Anesthetic Properties of Xenon versus Other Anesthetics
which the of the use of halothane has been successfully litigated against
osyncratic anesthesia health care providers. Although there
Xenon are some indica-
Nitrous Oxide Isoflurane Desflurane Sevoflurane
nesthetics, tions for the

Oil-gas partition use of halothane1.9in adults, 1.4
coefficient they must be clearly
90 18.7 53.4
e prodrug evaluated and

Blood-gas partition written in the medical
coefficient 0.14 record
0.47 before each such
1.4 0.42 0.6
. Instead, use.
Minimum alveolar concentration (%) 71 ≈105 1.15 6.0 1.71
eins and
onjugate)
Table 24-2
recovered in the process
Clinical of fractional
Features of Halothane of liquefied air, and coworkers showed that hemodynamic stability was better
distillationHepatitis
ypothesis and after several separation steps, a purity of greater than 99.99% with xenon than with nitrous oxide with respect to maintenance
metabolite can be obtained.
Mild Form The cost of xenon is presently Fulminant about
Form $10.00 of left ventricular systolic function.41 More recently, a randomized
taken up (U.S.) per liter (100 times more expensive than nitrous oxide), multicenter trial was undertaken to compare left ventricular
and it may be1unlikely
Incidence, :5 to enjoy widespread use because
Incidence, of the function in patients without cardiac disease who were undergoing
1 : 10,000
processed expense associated with its extraction from air. If this problem elective surgery under either xenon or isoflurane anesthesia.42
mpatibility could be overcome,
Repeat exposurexenon would be the most
not necessary ideal inhaled
Multiple exposures anes- Xenon did not reduce contractility, whereas isoflurane decreased
ypothesis thetic agent because xenon (minimum alveolar concentration the contractile index, suggesting that xenon provides favorable
[MAC] of 71%) isofmore
Mild elevation ALT,potent
AST than nitrous Markedoxide,elevation
can provide cardiovascular
of ALT, stability in patients without cardiovascular disease.
AST, bilirubin,
e drug or surgical anesthesia in 30% oxygen, is very insoluble (blood-gas Although it is clear that emergence from xenon anesthesia is more
alkaline phosphatase
gnals that partition coefficient of 0.14), and has positive medical and envi- rapid than emergence from desflurane or propofol anesthesia,
signal 2). ronmental effects (Table 24-1). Xenon exhibits
Focal necrosis Massive minimal
hepatic cardio- studies have not found any significant differences in postoperative
necrosis
vascular and hemodynamic side effects, is not known to be cognitive measures in patients exposed to these two agents.43 In
4-12).88 In metabolized
Self-limitedin the liver or kidney, is notMortality
teratogenic, and50%
rate, does a recent study involving ASA III patients undergoing aortic
ne, isoflu- not trigger malignant hyperthermia in susceptible swine. Recent surgery and receiving xenon (n = 20) or remifentanil (n = 19), no
30
immune- evidence suggests both a neuroprotective31Antibodies to halothane-altered

and a cardioprotective advantageprotein
of total intravenous anesthesia over xenon was dem-
32 44
effect after exposure to xenon. Environmental positives are that onstrated. A recent study that included 40 ASA III and IV
antigens
cillin and xenon does not deplete stratospheric ozone or contribute to patients with known coronary artery disease randomized to
global warming
ALT, alanine and the greenhouse
aminotransferase; AST,effect. The unique
aspartate aminotransferase.
A
combina- either xenon (n = 20) or propofol (n = 20) anesthesia, both sup-
tion of analgesia, hypnosis, and lack of cardiovascular depression plemented with remifentanil, showed higher arterial pressure and
in this one agent makes xenon a very attractive choice for patients better left ventricular function, as assessed by echocardiograph
with limited cardiovascular reserve. Xenon has a density of indices, with xenon than with propofol.45 It is certainly 139 too early
5.887 g/L, with nitrous oxide and air having densities of 1.53 and to know whether xenon anesthesia improves clinical outcomes,
1.00Notes
Dr Azam’s g/L, respectively. Because
in Anesthesiology 2013of its greater density, xenon does particularly in high-risk patients, and thus justifies the additional
lead to an increase in pulmonary resistance, which results in an cost associated with its use in clinical anesthesia.
fol alone Uses when arterial
III
nt hyper- 650 Anesthetic Pharmacology
etically to the surface of nitrocellulose Dr membranes. Withinthis
Azam’s Notes Anesthesiology 2013 pre
inhaled halogenat
with this Induction and Maintenance of Anesthesia technique, 42 of 68 (62%) patients with a clinical diagnosis of which may be dir
Box 24-2 Risk
Propofol Factors for
is suitable forAnesthetic-Induced
the induction and Hepatitis
maintenancehalothane
of anesthe- hepatitis
Box 24-3have been foundoftoPostoperative
Investigation test positive forLiver
the Dysfunction associated nephro
ion does sia (Table
Gender 26-3). The induction dose is 1 to 2.5 mg/kg. Physiologic
halothane-induced antibodies. 92
Although this approach provides halogenated anest
ponse to characteristics that best determine the induction important
dose are information
age,
History and about the apparent
physical molecular mass of the
examination
Age
neoantigens reacting with the patients’ antibodies, it is laborious
Propofol lean body mass, and central blood volume.149 Premedication
Obesity with
and time Medications
consuming. It also has the potential disadvantage of Methoxyflurane
matologic, an opiate
Enzyme or a benzodiazepine, or both, markedly reduces
induction the less sensitive than other methods because it
being inherently Methoxyflurane is
150,151 Previous anesthetic exposure
in vitro induction
Prior anesthetic exposure A dose of 1 mg/kg (with premedication)
dose. involves thetoprotein-denaturing conditions of sodium dodecyl nephrotoxicity fro
ns to the 1.75 mg/kg (without premedication) is recommended for induc- Intraoperative
sulfate–polyacrylamide gel course
electrophoresis. This could lead to a lism of methoxyflu
Genetics
decreased Postoperative
level
152 of response course
if a patient’s antibodies were directed the nephrotoxic p
n at least ing anesthesia in patients older than 60 years (see Chapter 71).
against, at least in part, conformational epitopes of the TFA
propofol As notedofearlier,
importance older
developing and model
an animal sickerof(ASA classSeveral
this disease. III to IV) patients
Clinical tests
neoantigens.
anesthetics. Studie
patients develop more exist
profound hypotension, especially
Therewhen propofol is immunochemical an association with
other associations for development A
of this disease. is The Antibody
second screening assay that has been used for
a clear sex difference observed in patients with halothane hepati- detection of antibodies in the sera of patients with a clinical of inorganic fluori
previous
tis. The disease develops in approximately twice as many females diagnosis of halothane hepatitis is based on the more rapid, facile,
rug aller- as males, the reason for which is unclear at present. In addition, and potentially more sensitive enzyme-linked immunosorbent
alone in the vast majority
Table 26-3 Uses of cases of halothane
and Doses hepatitisPropofol
of Intravenous have occurred in assay methodology, in which test antigen is applied directly to the
opofol is middle-aged adults, with relatively few cases reported in prepu- wells of a microtiter plate. TableOne 26-4reported
Recommended Doses ofimmu-
enzyme-linked Barbiturates for Anesthesia Induction volum
Induction
bertal children, of general
102,103 1-2.5 mg/kg IV dose reduced with
and the disease is more common in obese nosorbent assay procedure and Maintenance
uses microsomes from halothane- mass).
ations do
than anesthesia
in nonobese patients. There is currently increasing
no age
evidence to treated rabbits as test antigen. With this approach, investigators tion, w
suggest that the incidence of halothane hepatitis is increased in have demonstrated the presence of the antibodies Inductionin the sera of
ctivity at patients
Maintenance of general 50-150 µg/kg/min IV combined with N O 126 126 Dose Intravenous
intestin
with liver disease unrelated to previous halothane expo- 16 of 24 (67%) and 28 of 39 (72%) patients with a clinical
2
to treat sure. However, because halothane can cause direct hepatotoxicity diagnosis of halothaneDrug
anesthesia or an opiate hepatitis. In another
(mg/kg)*enzyme-linked
†
Onset (sec) Maintenance Infusion barbitu
median and other alternatives exist for the provision of general anesthesia, immunosorbent assay that uses the TFA hapten as test antigen in
isSedation 25-75 µg/kg/min
relatedIVfluoro- the form of TFA–rabbit Thiopental 3-4 10-30 in 50-100 mg every
ntiemetic itcarbonprudent to avoid halothane, as well as the other serum, albumin-positive responses
inhaled anesthetics, in patients10-20
Antiemetic
eved by a dysfunction.
with preexisting
mg IV, can repeat patients
hepaticevery with a clinical diagnosis of halothane hepatitis were
5-10 min 127
10-12 min
Sid
found in two of six (33%) patients and five of six patients
or start infusion of 10 µg/kg/min128 Methohexital 1-1.5 10-30 20-40 mg every 4-7 min
by 10 µg/ (83%). More recently, purified proteins from rat liver have been
used as test antigens in*Adult
the enzyme-linked The eff
ng breast Assays to Detect
N2O, nitrous oxide. Patients Sensitized to and pediatric IVimmunosorbent
doses are roughlyassay.
the same in milligrams per kilogram.
Fluorinated Anesthetics In a study using three†Methohexital
of the purified TFA-protein neoantigens
can be given rectally in pediatric patients as 20-25 mg/kg/dose. studied
The diagnosis of halothane hepatitis has always been one of exclu- (100, 80, and 57 kd), 79% of a group of 24 halothane hepatitis varyin
sion, whereas other potential causes of liver injury, such as hepa- patients tested positive with this assay.129 monar
titis A, hepatitis B, hepatitis C, cytomegalovirus, Epstein-Barr Methohexital is the only IV barbiturate used for induction ference
virus, hepatotoxic drugs, hypotension, and hypoxia, are systemati-
cally ruled out as precipitating causes. One of the important goals Fluoride-Associated that offers a serious challenge to thiopental. With a dose of 1 to
Nephrotoxicity the va
of halothane hepatitis research is the development of an assay 2 mg/kg, induction is swift, and so is emergence. Methohexital testina
capable of detecting sensitized patients who may be at risk for the Evidence suggests thatalso may
inhaled be used may
anesthetics as the hypnotic
induce component to maintain anesthe-
differential compl
development of a hypersensitivity response on re-exposure to effects on renal physiology. sia. Similar to thiopental,
For example, halothane and it isenflurane
not an analgesic. Additional opioids barbitu
halothane or other fluorinated anesthetics, as well as detecting decrease the glomerular filtration rate and renal
or volatile anesthetics are required blood flow, to provide a balanced tech- allergic
patients with the disease (Box 24-3). The assays that have been whereas isoflurane may also decrease the glomerular filtration
nique satisfactory for general anesthesia during surgery. Because
developed measure serum antibodies in halothane hepatitis rate but has minimal effects on renal blood flow. Conversely, the 140 An urt
patients. Two general types of immunochemical assays have been newest inhaled halogenated methohexital
anestheticsishave
cleared more
minimal rapidly
effects on than thiopental, it is supe- lasts a
Drreported
Azam’sforNotes in Anesthesiology 2013
detection of these antibodies. The first is immuno- renal physiology. Nevertheless, despite these physiologic effects, of anesthesia, as accumula-
rior to thiopental for the maintenance hives,
blotting. In this procedure, test antigens are microsomal proteins renal autoregulation protects tion and saturation
the kidney of peripheral
from decreases in blood sites takes longer. For brief anaphy
reactive airway disease. Otherwise healthy trauma victims whose was administered. Etomidate is metabolized 382
Ketamine
Intravenous Drin
in the a liver
1 : 1 primarily
Azam’s
Anesthetics combination
Notes by26ester
withhydrolysis
735in Anesthesiology mor- 2013 m
blood loss is extensive also are candidates for rapid-sequence phinetousing the corresponding
an 8-minute lockout carboxylic acid of
interval etomidate
provided (majorpost-
optimal metab- m
Table 26-5 Physicochemical Characterization of Three 377 Benzodiazepines
anesthesia induction with ketamine. Patients with septic shock impaired by certain
operative population characteristics
or by N-dealkylation.
olite)analgesia for this combination. 179 (e.g., old
The main 383 age),
initial 406 m
metabolite isaninactive.
Alternatively,
Table 26-7
disease states Uses
(e.g., and Doses of Intravenous Benzodiazepines Inductio
also may benefit Diazepamfrom ketamine.
Lorazepam
378
The Midazolam
intrinsic myocardial bolus ofhepatic
Only 0.52% ofcirrhosis),
mg/kg theof drug or
is the
ketamine coadministration
excreted unchanged,
followed ofthe rest being
by a continuous excreted oc
infusion
depressant effect of ketamine may manifest in this situation,
other drugs that as
of 3
canmetabolites
µg/kg/min
impair oxidizing
duringby the capacity
kidney
surgery
(e.g.,
(85%)
and
cimetidine).
1.5 and bile (13%).
µg/kg/min for
406
48 hours Midazola
na
Midazolam
Conjugation is less susceptible to these factors. Midazolam and Diazepam Lorazepam
total knee of m When
Molecular 284.7* 321.2* 362*
however,
weight (D) if trauma or sepsis has caused depletion of catecho- after surgery Etomidate has been has been usedused successfully
for induction and in maintenance
diazepam undergo oxidation reduction or phase I reactions in the
lamine stores before the patient’s arrival in the operating liver. Induction
room. anesthesia
arthroplasty.
The fused imidazole
384 (Table
0.05-0.15 mg/kg26-10).
ring 407of midazolamThe
0.3-0.5 induction
mg/kg
is oxidized rapidly dose
0.1 of etomidate isinductio
mg/kg 0.2
pKa 3.3 (20°) 11.5 (20°)
Use of ketamine in these patients does not obviate the need
6.2 (20°)*
for toThe0.6 mg/kg,
action andthe
ofthan
ketamineit ismethylene
reduced by premedication and with amnesia
an opiate,
by the liver, much
Maintenance more
0.05 rapidly
mg/kg prn 0.1on opiate
mg/kg prntolerance
group of 0.02
the mg/kg hyperalge-
prn
appropriate
Water soluble preoperative
No* preparation,
Almost insoluble includingYes †
restoration of sia
diazepine a benzodiazepine,
ringcombined
of other with its or
benzodiazepines.
1 µg/kg/min
a barbiturate.
direct Thisanalgesic Onset
activity
fast oxidation of has
anesthesia
prompted of action
after a

blood volume. Yes*
Lipid soluble Yes (less so, Yes† accounts for theroutine
increasing greater useinduction
hepatic doseinofofchronic
clearance
of ketamine 0.3 mg/kg
midazolam painofcom- etomidate
states. Ketamine is rapidmay(one Th
for indu
Other cardiac diseaseshowever) that can be well managed withpared withbediazepam.
Sedation*
keta- arm–brain
effective 0.5-1 Lorazepam
inmg circulation)
therepeated is less2and
treatment mg is
affected equivalent
repeated
of cancer by pain,
enzyme to mg
0.25 anesthesia
chronic repeated obtained
peripheral sin
injection
induction and some of the other factors known to alter the cyto- 407
mine anesthesia Highly
are cardiacRelatively
tamponade less
andHighly lipophilic
restrictive pericardi- with0.07
and central anneuropathic
induction
mg/kg IM dose
pain, of thiopental
phantom and or methohexital.
ischemic The 26
limb pain,concurre
lipophilic lipophilic chrome P-450 and other phase
duration of I enzymes. after a single induction dose is linearly m
anesthesia
fibromyalgia,
Cimetidine inhibition complex
of oxidative regional
enzyme pain syndrome,
of function impairs visceral pain, andpatient, m
related tountil
the dose—each 0.1 mg/kg administered
on a few provides about is
581 *Incremental doses given desired degree sedation is obtained.
*Data from Moffet.
theprn, migraine.
clearance
as requiredof 100 These
diazepam,
to keep
234indications
patientbut it has
hypnotic no are
and based
effect on
amnestic. largely
lorazepam.
408 short-term anesthes
pH dependent: pH >4, lipid soluble; pH <4, water soluble.
†
seconds of loss of consciousness. Repeat doses of etomidate ha
Age decreasestrialsandwithsmoking limited clinical
increases application
the clearance or limited
of diazepam, 235
nonrandomizedwith dia
effect on385midazolam
ha
but neithertrials
has a and case studies.
significant There also have been a limited numberpatients r
biotransforma-
tion. Habitual alcohol consumption increases theare ho
Table 26-9 Uses and Doses of Ketamine must of236monitored
be reports
Table 26-10 that indicate
when
Uses and these thedrugs
Doses value ofclearance
of Etomidate multimodal
used for of sedation
pain therapy
to (Fig. 26-
ene glycol, with 2% benzyl alcohol as a preservative. Midazolam midazolam.including Race, because of differences in isoenzymes respon- kg
prevent undesirable ketamine
degrees ofinrespiratory
preventing postoperative
depression. There chronicASA phy
may aff
solution (1 or 5 mg/mL) contains 0.8% sodium chloride and sible for hydroxylations, Inductionproduces
386,387 of general genetic differences 0.2-0.6 mg/kg in IV drug
Induction of general 0.5-2 mg/kg IV be a pain.
slight
237 synergistic
0.01% disodium edetate, with 1% benzyl alcohol as a preservative. metabolism. The high frequency of mutated alleles in Asians in
anesthesia action between midazolam and spinal reductio
re
anesthesia* 4-6 mg/kg IM
The pH is adjusted to 3 with hydrochloric acid and sodium theanesthesia genes codingwith The epidural/caudal
respect to
for CYP2C19 mayventilation. administration
explain the reduced
273
The hepatic of ketamine
use of midazolam inductio (0.5 to et
1 mg/kg) Maintenance
has been of increasingly
general 10 µg/kg/min
reported. IV with N2Othe
Although andefficacy
an opiateof
hydroxide. Midazolam
Maintenance of general is the most lipid soluble of the three
0.5-1 mg/kg IV with N2O 50% in O2 drugs for sedation during
biotransformation of diazepam.
anesthesia
regional and epidural anesthesia requires 0.15 mg/ bl
in vivo, 232
but
anesthesia because of its pH-dependent solubility, it is water
15-45 µg/kg/min IV with N2O 50-70% invigilance O2 The these
metabolitesdoses ofof ketamine
the seems
benzodiazepines tocanbe be
with regard to respiratory function, similar to when (coinduc established,
important. the safety of this pr
soluble as formulated in a buffered30-90 acidicµg/kg/min
medium IV (pH 3.5).
without N2OThe Diazepam technique
forms
these drugs two
Sedation
areadd has
active
given not
and yet
metabolites,received
analgesia
with oxazepam regulatory
and
Limited
opioids.drug’s effects. Midaz- to approval.
desmeth-
periods of The
brief preserva-
sedation because (e
inductio
imidazole ring of midazolam accounts for its stability in solution yldiazepam, which
tive of racemic to and prolongisthe
mixture potentially neurotoxic,
of inhibition whereas
of corticosteroid studies
synthesis
Sedation for longer periods, such which as in have the ICU, also is 388 seen wh (u
and rapid metabolism.
Sedation and analgesia The high lipophilicity
0.2-0.8 mg/kgof all
IVthree
over 2-3 minA olam is biotransformed
accounts to date indicate to preservative-free
hydroxymidazolams, S(+) ketamine may be safe.
for the rapid CNS effect and 2-4 relatively
mg/kg IM large volumes of activity, accomplished
and when N2O,withnitrousbenzodiazepines.
given oxide.
over a longer time can Prolonged
accumulate. infusion
238 results such asget
distribution.233 in accumulation
These metabolites areofrapidly drug and, in theand
conjugated caseexcreted
of midazolam, in the significant Aw
Preemptive/preventive 0.15-0.25 mg/kg IV urine, Sedation
however. The α-hydroxymidazolam has an estimated clini-
concentration of the active metabolite. Reviews have pointed out entation
analgesia cal potencyKetamine
20% to 30% is of
particularly
midazolam.suitable 239 for sedation
It is excreted largely of bypediatric
238,274,275 patients
concerns and advantages of benzodiazepine sedation. The received
Metabolism
*Lower doses are used if adjuvant drugs such as midazolam or thiopental also chief
theare
kidneys undergoing
and can cause procedures
profound sedation outside inofpatients the operating
with room (see
advantages
Chapter240 82).
renal impairment. areprimary
The the amnesia
Pediatric and hemodynamic
patients
hydroxymetabolite have fewer is cleared stability,
adverse and and awa
emergence
given.
Biotransformation
N2O, nitrous oxide. of the benzodiazepines occurs in the liver. The
therapidly
more disadvantage
90 346compared
than midazolam
reactions than adults, with
in healthyand propofol
patients
this feature is themakes
(Table sometimes
26-6). the use longerof keta-dose of 0
two principal pathways involve either hepatic microsomal oxida- Thedissipation metabolites are of effects
less potent when infusions
and normally are terminated.
cleared more rapidly The superi- midazola
tion (N-dealkylation or aliphatic hydroxylation) or glucuronide than midazolam,
ority of one making drug over themthe of little
other concern
has not in patients with
been established; both gence fro
conjugation. The difference in the two pathways is significant normal hepatic and renal function. Lorazepam
drugs should always be titrated downward to maintain sedation 10 minut has five metabo-
because oxidation is susceptible to outside influences and can be lites, but the principal one is conjugated to glucuronide. This
as required. Dosing should not be fixed, but it should be reduced 141 fentanyl
over time to avoid accumulation of parent or metabolites during fol.285 Th
Table 26-6 Pharmacokinetic and Pharmacodynamic Comparison of Midazolam and Its prolonged infusion.
Active Metabolite* ence for
III plete anesthesia. However, midazolam-alfentanil TIVA has not surgery range fro
772 Anesthetic Pharmacology
been found to compare favorably with propofol-alfentanil Dr Azam’s NotesTIVA, through27
in Anesthesiology CPB.
2013 H
even with flumazenil reversal Opioids
359 781
Table 27-2 Pharmacologic Actions of Opioids and Opioid Receptors in The µ-receptors are located in both theofbrainbenzodiazepine
and spinal action. effective and safe
Animal Models 5
cord and mediate TIVA techniques
a variety are especially
of pharmacologic useful when delivery of fentanyl, 25 to 50
effects of opioids.
Endogenous opioid activity is present Actions of
in the cerebral arter-
Further Table
pharmacologic 27-4 Potential
classification Problems
inhaled agents is compromised. By keepingof the Associated
µ-receptor as µwith
1, µthe
2,
Opioid-Induced Rigidity was sufficient to
goals of balanced
es, although exogenously administered opioids were found and µto 3 has been proposed. Perhaps post-translational modifica-
Receptor Agonists Antagonists anesthesia inismind,
tion of99 the µ-receptor
combining modern opioids and other drugs, the pre-CPB pha
the molecular basis of the µ-receptor
System Problem
xert little effect on pial artery diameter in several animal models. subtypes. using
However,infusion
the pumps,
molecular and
identity having
of these an increased
receptors still understanding of children (Fig. 27-
Analgesia
entanyl (100 µg/kg) causes
Supraspinal µ, δ, κ dose-related
Analgesic reductions No effect in CBF and pharmacokinetics,
remains to beHemodynamic
clarified. clinicians can successfully ↑CVP, ↑perform
PAP, ↑ PVR a variety 75 to 100 µg/kg,
CMRO2 inSpinal rats receivingµ, δ,Nκ2O. InAnalgesic the piglet, fentanyl, Hydropathy analysis of the primary structures
No effect alfentanil, of TIVA techniques. Approximate opioid doses and infusion rates of the opioid NK cell function.
that the opioid receptors possess seven↓trans-
Respiratory
receptors indicates Compliance, ↓ FRC, ↓ ventilation
nd sufentanil
Respiratorydecrease
function arteriolar
µ diameter in aNodose-dependent,
Decrease effect membrane fordomains
TIVA are (Fig. listed
27-2), ain Table 27-7.
characteristic structural feature were successfully
100
aloxone-reversible manner.
Gastrointestinal tract µ, κ InDecrease
human volunteers,
transit No effect PET of dem-
the G protein–coupled receptor. The µ-, δ-, and κ-opioid Hypercapnia recep- of fentanyl (tota
nstratedPsychotomimesis
that the CBF changes induced
Increase by fentanyl
tors and the nociceptin receptor share approximately 50% amino
are regionally bolus, 3.4 ± 2.6 µ

κ No effect Hypoxemia
101 acid sequence homology with each other. support under the
eterogeneous.
Feeding µ, δ, κ
The effect of sufentanil on CBF in the dog may
Increase feeding Decrease
feedingbe dose fiedand
SeveralOpioid-Based
single-nucleotide polymorphisms
Miscellaneous (High-Dose
in the human µ-opioid receptor gene.6 The A118G mutation,
have beenOpioid)
identi-
↑ Oxygen consumption ± 7 hours.365 The
me dependent.
Sedation It was reported
µ, κ that sufentanilNo(20
Increase effectµg/kg an
intra- Anesthesia
A-to-G substitution forresults
in exon 1 that Cardiac
in exchange Surgery
of aspar-
↑ Intracranial pressure
individual dose t
enouslyDiuresis
[IV]) producesκ 30% to 40% agine at position 40 for aspartate (N40D), is the most common anesthesia while
Increasedecreases in CBF 5 mutation to 10 leading to a change in the gene product in the human
minutes Hormone
after opioid 102 Opioids can be administered as the primary or sole anesthetic in was recently sho
↑ Fentanyl plasma levels
secretion administration. Another report showed µ-opioid receptors. It was suggested that cancer patients who
hat sufentanilProlactin(10 to 200 µ µg/kg) produces
Increase releasetransient
Decreaseincreaseswere in opioid-based
homozygous anesthetic
for thevenous
CVP, central A118Gpressure; techniques.
variant required High-dose
higher
FRC, functional doses opioid anesthesia associated with a
residual capacity; PAP, pulmonary
CBF that peak 2 minutesµ after drug administration of oral
in the dog.
release wasartery
103morphine introduced
for long-term
pressure; as treatment
PVR, apulmonary
stress-free
of their anesthetic
7
A118Gmethod for cardiac
pain.resistance.
vascular cognitive dysfun
Growth hormone and/or δ Increase release Decrease mutationsurgery
of Modified
the human(also µ-opioid
from see receptor
BaileyChapter
PL, Egan TD,gene reduces
60). However,
Stanley analgesic severalopioid
TH: Intravenous factors have Inartery bypass sur
anesthetics.
n humans, both fentanyl and sufentanil can increase release middle
responses to morphine-6-glucuronide (M6G) but does not sig-
Miller RD (ed): Anesthesia, 5th ed. New York, Churchill Livingstone, 2000, p 291. (10 µg/kg) leads
erebral Neurotransmitter
artery blood flow velocity by about 25%.104 In healthy nificantly affect the respiratory depression induced by M6G.8
release
Furthermore, morphine consumption via intravenous PCA after may be associated
olunteers,Acetylcholine
sufentanil (0.5 µ µg/kg Inhibit
IV) produces no significant total abdominal hysterectomy was significantly greater in women nitive dysfunction
ffect on CBF. 104
Dopamine
Alfentanil δ
50 µg/kg IV), when adminis-
(25 toInhibit homozygous Tablefor27-7 Approximate
the A118G variant Opioid
than inLoading (Bolus)9 Doses, Maintenance Infusion
other patients.
ered to patients receiving isoflurane (0.4% to 0.6%)-N2O anesthe- Rates, isoflurane,
and Additional fentanyl neither
Maintenance increased
Doses nor decreased
for Total Intravenous brain injury
Anesthesia
Alfentanil
117
a, produces minimal reductions in middle
receptors. Four different cDNAs have been isolated as members
cerebral artery flow when compared
Endogenous OpioidLoading with
Peptides awake unanesthetized rats. Induction of ane
Maintenance Additional
elocity.of105the opioid receptor family.2 Three of them correspond to the Dose (µg/kg) Infusion Rate Boluses applied to cardiac
Inpharmcacologically
the dog, alfentanil defined andµ-, δ-,remifentanil decrease
and κ-opioid receptors. Theregional
Enkephalin, β-endorphin, and dynorphin were identified as may be used wit
lood flowfourth byreceptor
40%didto not50%
bind within opioid
the ligands high affinity. endogenous
cortex,withhippocampus, Muscle
agonists
and Alfentanil for the δ-, µ-, and κ-opioid receptors,
Rigidity
25-100 0.5-2 µg/kg/min
respec- 5-10 µg/kg
Later, Other investigato
106 a novel peptide named nociceptin/orphanin FQ was identi- tively. After purification of these peptides from mammalian
audate.fied A PET study in human volunteers showed
as an endogenous agonist of the fourth member of the opioid tissues, cDNAs that Sufentanil
for the precursors 0.25-2of these peptides 0.5-1.5 µg/kg/hr
were cloned. 2.5-10 µg induced with alf
emifentanil induces dose-dependent changes in relative regional Opioids can increase muscle tone and may cause muscle rigidity.
receptor family. 3,4
The characteristics of three opioid receptors cDNA cloning and amino acid determination of proopiomel- adults.85 Continu
Fentanyl 4-20 2-10 µg/kg/hr 25-100 µg
CBF in andareas theinvolved
nociceptin/orphanin FQ receptor are
in pain processing, such listed in Table
as the lateralanocortin
pre- demonstrated
The incidence that cleavage
of rigidityof thisnoted
precursorwith protein
opioid anesthetic techniques have been used to
27-3. produces not only β-endorphin but also several other neuro-
rontal cortex, inferior parietal cortex, and supplementary motor varies greatly because of differences in the dose and speed tanil
Remifentanil 1-2 0.1-1.0 µg/kg/min 0.1-1.0 µg/kg of concentrati
107
rea. In patients scheduled to undergo supratentorial tumor Fromopioid Bailey PL,administration,
Egan TD, Stanley TH: concomitant
Intravenous opioiduse of N2InO,Miller
anesthetics. presence
RD Enthusiasm
or for
Table 27-3 Characteristics of Opioid Receptors
urgery and receiving N2O, remifentanil (1 µg/kg/min), similar (ed):absence Anesthesia,of 5thmuscle
ed. New York,relaxants, and patient
Churchill Livingstone, 2000,age.
p 335.Opioid-induced limited
142 by the am
o fentanyl (2 µg/kg/min), reduced CBF µ and did not significantly δ rigidity is κcharacterized by increased Nociceptin muscle tone that sometimes
Dr Azam’s Notes in Anesthesiology 2013 108
ffect cerebrovascular carbon dioxide reactivity.
Tissue bioassay Guinea pig ileum Mouse vas deferensprogresses to severe stiffness with the potential for serious prob-
Rabbit vas deferens
azocine. times as potent as morphine and is available only in parenteral
orphine, form. After intramuscular injection, the onset of effect is rapid, Dr Azam’s Notes in Anesthesiology 2013
endence.
Table 27-10 Hemodynamic Effects of Agonist-Antagonist Compounds

Compared with Morphine
ne
Pulmonary
Cardiac Blood Artery
uscular Drug Workload Pressure Heart Rate Pressure
io
Morphine ↓ ↓ =↓ =↓
Buprenorphine ↓ ↓ ↓ ?
Butorphanol ↑ =↑ = ↑
Nalbuphine ↓ = =↓ =
Pentazocine ↑ ↑ ↑ ↑
From Zola EM, McLeod DC: Comparative effects of analgesic efficacy of the agonist-
antagonist opioids. Drug Intell Clin Pharm 17:411, 1983.
Intravenous Drug Delivery Systems 845 28
Table 28-6 Manual Infusion Schemes*
Anesthesia Sedation or Analgesia

Maintenance Maintenance
Drug Loading Dose (µg/kg) Infusion (µg/kg/min) Loading Dose (µg/kg) Infusion (µg/kg/min)
Alfentanil 50-150 0.5-3 10-25 0.25-1
Fentanyl 5-15 0.03-0.1 1-3 0.01-0.03

Sufentanil 0.5-5 0.01-0.05 0.1-0.5 0.005-0.01
†
Remifentanil 0.5-1.0 0.1-0.4 0.025-0.1
Ketamine 1500-2500 25-75 500-1000 10-20
Propofol 1000-2000 50-150 250-1000 10-50
Midazolam 50-150 0.25-1.5 25-100 0.25-1
Methohexital 1500-2500 50-150 250-1000 10-50
Dexmedetomidine‡ 0.5-1 over 10 min 0.2-0.7

*After the loading dose, an initially high infusion rate to account for redistribution should be used and then titrated to the lowest infusion rate that will maintain adequate
anesthesia or sedation. When using opiates as part of a nitrous-narcotic technique or for cardiac anesthesia, the dosing scheme listed under anesthesia is used. When the
opiate is combined as part of balanced anesthesia, dosing listed for analgesia is needed.
†
For analgesia or during sedation, an initial loading dose of remifentanil should not be given because its very rapid onset may result in apnea or muscle rigidity. 143
DrConsequently,
Azam’s Notes the accuracy of any model-based
in Anesthesiology 2013 control system plasma concentration of an intravenously administered drug
depends on how well the model represents the process under whose kinetics is described by a two-compartment model. This
III 864 Anesthetic Pharmacology Dr Azam’s Notes in Anesthesiology 2013
Table 29-1 Relationship between Dibucaine Number and Duration of Succinylcholine or Mivacurium Neuromuscular Blockade
Response to Succinylcholine
Type of Butyrylcholinesterase Genotype Incidence Dibucaine Number* or Mivacurium
Homozygous typical E1uE1u Normal 70-80 Normal
Heterozygous atypical E1uE1a 1/480 50-60 Lengthened by 50%-100%
Homozygous atypical E1aE1a 1/3200 20-30 Prolonged to 4-8 hr
III *The dibucaine number indicates the percentage of enzyme inhibited.

868 Anesthetic Pharmacology
Table 29-3 Classification of Nondepolarizing Neuromuscular Blockers According to Duration of Action (Time to T1 = 25% of Control) after Twice the ED95
of butyrylcholinesterase. The variant was found by Kalow and is the development Clinical Durationof cardiac dysrhythmias, principally mani-
43
Genest to respond to dibucaine differentlyLong-Acting than normal butyryl-Intermediate-
fested as sinus bradycardia, junctional Ultrashort-acting
Short-Acting rhythms, and ventricular
cholinesterase
Class of Blocker does. Dibucaine inhibits normal (>50butyrylcholineste-
min) Actingdysrhythmias.
(20-50 min) Clinical studies
(15-20 min) have described
(<10-12these
min) dysrhythmias
rase tocompounds
Steroidal a far greater extent than it inhibits the abnormal enzyme.
Pancuronium under various conditions in the presence of the intense auto-
Vecuronium
This observation led to development of the test for dibucaineRocuronium
Pipecuronium nomic stimulus of tracheal intubation. It is not entirely clear
number. Under standardized test conditions, dibucaine inhibits whether the cardiac irregularities are due to the action of succi-
Benzylisoquinolinium compounds d-Tubocurarine Atracurium Mivacurium
expression of the normal enzyme by about 80% and
Metocurine
the abnormal nylcholine
Cisatracurium alone or to the added presence of extraneous auto-
enzyme by about 20% (Table 29-1). Subsequently, Doxacurium many other nomic stimulation. An in vitro study using the ganglionic
genetic variants of butyrylcholinesterase have been identified, acetylcholine receptor subtype α3β4 expressed in Xenopus laevis
Others
although the dibucaine-resistant variants are the most important. oocytes suggested that at clinically relevant concentrations,
Asymmetrical mixed-onium chlorofumarates 44 Gantacurium
The review
Phenolic ether
by Jensen and Viby-Mogensen can be
Gallamine
consulted for succinylcholine had no effect on the expressed receptors.48 Only
more
Diallyl detailed information
derivative of toxiferine on this topic. Alcuronium at high doses of succinylcholine was inhibition of ganglionic ace-
Although the dibucaine number indicates the genetic tylcholine receptors noted.48 The significance of these findings is
A majority of nondepolarizing neuromuscular blockers are bisquaternary ammonium compounds. d-Tubocurarine, vecuronium, rocuronium, and rapacuronium are mono-
makeup of an individual with respect to butyrylcholinesterase, it difficult to extrapolate into clinical practice because the method
quaternary compounds, and gallamine is a trisquaternary ammonium compound.
does not measure the concentration of the enzyme in plasma, nor used (Xenopus laevis oocyte expression model) does not match
does it indicate the efficiency of the enzyme in hydrolyzing a clinical reality.
substrate such as succinylcholine or mivacurium. Both of the SINUS BRADYCARDIA. The autonomic mechanism
latter
onset or factors
durationareof determined
action (long-,by measuring butyrylcholinesterase
intermediate-, and short-acting 4. involved
When dTc inissinus bradycardia
methylated at theistertiary
stimulation
amineofand
cardiac muscarinic
at the
activity,
drugs) which maydoses
of equipotent be influenced by genotype.
(Table 29-3). receptors in the sinus
hydroxyl groups, node.is This
the result is particularly
metocurine, problematic in
a compound
The molecular biology of butyrylcholinesterase is well individuals with greater with predominantly
potency (by a factor ofvagal tone, such
2 in humans) butasmuch
children
144 who
understood. The amino acid sequence of the enzyme is known, have weakernotganglion-blocking
received atropine. and histamine-releasing
Sinus bradycardia hasproper-
also been noted
Structure-Activity
Dr Azam’s
and Notes in Anesthesiology
the coding errors responsibleRelationships
2013 for most genetic variations have in tiesadults
than dTc
andhas (see Fig.
appears more29-7). Metocurine
commonly contains
after three
a second dose of the
44 49
potency by a factor of 3 to 5. ment only. The drug is distributed very rapidly throughout this
Table 29-4 Dose-Response Relationships of Nondepolarizing Neuromuscular Blocking Drugs in Human Subjects
ED50 (mg/kg) ED90 (mg/kg) ED95 (mg/kg) Reference(s)
Long-Acting
Pancuronium 0.036 (0.022-0.042) 0.056 (0.044-0.070) 0.067 (0.059-0.080) 103, 107
d-Tubocurarine 0.23 (0.16-0.26) 0.41 (0.27-0.45) 0.48 (0.34-0.56) 107
Intermediate-Acting
Rocuronium 0.147 (0.069-0.220) 0.268 (0.200-0.419) 0.305 (0.257-0.521) 103, 108-110
Vecuronium 0.027 (0.015-0.031) 0.042 (0.023-0.055) 0.043 (0.037-0.059) 107
Atracurium 0.12 (0.08-0.15) 0.18 (0.19-0.24) 0.21 (0.13-0.28) 107
Cisatracurium 0.026 (0.015-0.031) — 0.04 (0.032-0.05) 11, 111, 112, 118
Short-Acting
Mivacurium 0.039 (0.027-0.052) — 0.067 (0.045-0.081) 9, 113-115
Ultrashort-Acting
Gantacurium 0.09 — 0.19 106
Data are medians and ranges of reported values. ED50, ED90, and ED95 are the doses of each drug that produce, respectively, a 50%, 90%, and 95% decrease in the force of
contraction or amplitude of the electromyogram of the adductor pollicis muscle after ulnar nerve stimulation.
145

Table 29-6 Guide to Nondepolarizing Relaxant Dosage (mg/kg) with Different Anesthetic Techniques*
Dosage for Relaxation

Supplemental Dose
ED95 under N2O/O2 Dose for Intubation after Intubation N2O Anesthetic Vapors†
Long-Acting
Pancuronium 0.07 0.08-0.12 0.02 0.05 0.03
d-Tubocurarine 0.5 0.5-0.6 0.1 0.3 0.15
Intermediate-Acting
Vecuronium 0.05 0.1-0.2 0.02 0.05 0.03
Atracurium 0.23 0.5-0.6 0.1 0.3 0.15
Cisatracurium 0.05 0.15-0.2 0.02 0.05 0.04
Rocuronium 0.3 0.6-1.0 0.1 0.3 0.15
Short-Acting
Mivacurium 0.08 0.2-0.25 0.05 0.1 0.08
Continuous Infusion Dosage (µg/kg/min) Required to Maintain 90%-95% Twitch Inhibition under N2O/O2 with Intravenous Agents
Mivacurium 3-15
Atracurium 4-12
Cisatracurium 1-2
Vecuronium 0.8-1.0
Rocuronium 9-12
*The suggested dosages provide good intubating conditions under light anesthesia. Satisfactory abdominal relaxation may be achieved at the dosages listed after intuba-
tion without a relaxant or with succinylcholine. This table is intended as a general guide to dosage. Individual relaxant requirements should be confirmed with a peripheral
nerve stimulator.
†
The potentiation of nondepolarizing relaxants by different anesthetic vapors has been reported to vary 20% to 50%. Recent data suggest, however, that this variation may
be much less, particularly in the case of intermediate- and short-acting relaxants. Therefore, for the sake of simplicity, this table assumes a potentiation of 40% in the case
of all volatile anesthetics.
neuromuscular junction, receptor affinity, plasma clearance, and µM/kg) is highly predictive of a drug’s initial rate of onset of effect
the mechanism of neuromuscular blockade (depolarizing versus (at the adductor pollicis).155 A drug’s measured molar potency 146 is
nondepolarizing).101,155,156 The speed of onset is inversely propor- the end result of many contributing factors: the drug’s intrinsic
Drtional
Azam’s toNotes
the potency of nondepolarizing
in Anesthesiology 2013 neuromuscular block- potency (Ce50—the biophase concentration resulting in 50%
101,155
ers. A high ED95 (i.e., low potency) is predictive of rapid twitch depression), the rate of equilibration between plasma and
Anesthetic Pharmacology
Decubitus ulcers bodies to nAChRs have been demonstrated in a rodent model of
Pharmacology of Muscle Relaxants 901Dr 29
Inability to cough
sepsis.450 Thus, myasthenia-like syndromeand Their
is also seen Antagonists
in critically Azam’s Notes in Anesthesiology 2013
Retention of secretions and atelectasis documented in asthmatic patients and those with chronic lung
Box 29-3 Complications of Pulmonary
Muscle Paralysis
infection in the Weakness 445 and in
Intensive Care Unit disease without
Box 29-4 paralysis who received
Causes of Generalized corticosteroids
Neuromuscular
Dysregulation of nicotinic acetylcholine receptors in the Intensive Care Unit
critically ill patients with sepsis who received neither corticoster-
Prolonged paralysis after stopping relaxants
Short-term use oids norCentral nervous system neuromuscular blockers.446 Animal
nondepolarizing
Persistent neuromuscular blockade
Specific, known drug side effects
studies have revealed
Septic that the number
or toxic-metabolic encephalopathyof cytosolic corticosteroid
Critical illness myopathy
receptors is increased in immobilized muscles relative to contra-
Brainstem stroke
Inadequate ventilationCritical
in theillness
eventpolyneuropathy
of ventilator failure or Central447pontine
lateral controls. It seems—at
myelinolysisleast in some patients—that pro-
circuit disconnection Combination of the above
longed immobility may disorders
Anterior horn cell be the key(e.g., risk
amyotrophic
factorlateral
for myopathy in

Unrecognized effects of drug or metabolites sclerosis) 448
Inadequate analgesia and/or sedation
Succinylcholine and metabolic acidosis/hypovolemia corticosteroid-treated patients and that selective muscle atrophy
Peripheral neuropathies
Long-term use 3-Desacetylvecuronium and neuromuscular blockade is a result of changes in glucocorticoid sensitivity.447
Critical illness polyneuropathy
Laudanosine and cerebral excitation
Complications of immobility
Sepsis, immobility, and the catabolism associated with
Guillain-Barré syndrome
negative nitrogen
Porphyria
balance may also result in myopathy.14 Skeletal
Deep venous thrombosis and pulmonary embolism muscle hypoperfusion
Paraneoplasia is noted in patients with severe sepsis
Peripheral nerve injuries despite normal or elevated whole blood oxygen delivery.449 Anti-
Vasculitis
neuromuscular blockers in the ICU are outlined in Box 29-3. In to nAChRs have been demonstrated in a rodent model of
bodies
Decubitus ulcers
the ICU, the duration of mechanical ventilation, sepsis, dysfunc- 450 Nutritional and toxic
sepsis. Thus, myasthenia-like syndrome is also seen in critically
Inability to cough tion of two or more organs, female sex, administration of steroids, Neuromuscular junction disorders
and hypercapnia are known risk factors for the development of Myasthenia gravis
Retention of secretions anddysfunction.
neuromuscular atelectasisSyndromes of weakness in critically Lambert-Eaton myasthenic syndrome
ill patients are relatively common and probably polymorphic in
Pulmonary infection Box 29-4Botulism
origin. In a retrospective study of 92 critically ill patients with Causes of Generalized Neuromuscular Weakness
Dysregulation of nicotinic acetylcholine
clinically receptors
diagnosed weakness, in the Intensive
electromyographic studies indi- Care
Prolonged Unit
neuromuscular junction blockade
cated that acute myopathy (critical illness myopathy) is three Myopathies
Prolonged paralysis after
timesstopping
as common relaxants
as acute axonal neuropathy (critical illness Central nervous system
neuropathy):
Persistent neuromuscular blockade 43% versus 13%, respectively.440 The additional
Cachectic myopathy
health care cost of one case of persistent weakness was estimatedSeptic or toxic-metabolic encephalopathy
to be approximately $67,000.441 Conditions to consider in the Rhabdomyolysis
differential diagnosis of neuromuscular weakness in the ICU areBrainstem stroke
Inflammatory and infectious myopathies
Critical illness polyneuropathy
listed in Box 29-4. CentralMuscular
pontine myelinolysis
dystrophies
Combination of the above Toxic
Critical Illness Myopathy Anterior horn cell disorders (e.g., amyotrophic lateral
Unrecognized effects Lacomis
of drugand orcolleagues
metabolites
442 Acid maltase deficiency
suggested using the term “critical illnesssclerosis)
myopathy” (CIM) instead of the current terms used in the litera- Mitochondrial
Succinylcholine andture,metabolic acidosis/hypovolemia
such as acute quadriplegic myopathy,443 acute (necrotizing) Peripheral neuropathies
Hypokalemia
myopathy
3-Desacetylvecuronium andof neuromuscular
intensive care, thick blockade
filament myopathy, acute corti-
CriticalHypermetabolic
illness polyneuropathy
syndromes with rhabdomyolysis
costeroid myopathy, and critical care myopathy.
Laudanosine and cerebralMostexcitation (e.g., neuroleptic malignant syndrome)
published reports of CIM in the ICU have focusedGuillain-Barré syndrome
on patients with status asthmaticus.444 Affected individuals typi-
cally have been treated with corticosteroids and nondepolarizingPorphyria
From Lacomis D: Critical illness myopathy. Curr Rheumatol Rep
4:403-408, 2002.
neuromuscular blockers. Nevertheless, myopathy has also beenParaneoplasia
Vasculitis
neuromuscular blockers in the ICU are outlined in Box 29-3. In
the ICU, the duration of mechanical ventilation, sepsis, dysfunc- Nutritional and toxic
tion of two or more organs, female sex, administration of steroids, Neuromuscular junction disorders
and hypercapnia are known risk factors for the development of Myasthenia gravis
neuromuscular dysfunction. Syndromes of weakness in critically Lambert-Eaton myasthenic syndrome
ill patients are relatively common and probably polymorphic in
origin. In a retrospective study of 92 critically ill patients with Botulism
clinically diagnosed weakness, electromyographic studies indi- Prolonged neuromuscular junction blockade
cated that acute myopathy (critical illness myopathy) is three Myopathies 147
times as common as acute axonal neuropathy (critical illness Critical illness myopathy
neuropathy): 43% versus 13%, respectively.440 The additional
Dr Azam’s Notes in Anesthesiology 2013 Cachectic myopathy
health care cost of one case of persistent weakness was estimated
441 Rhabdomyolysis
distributed all along the axon of nonmyelinated fibers (Fig. 30-3). Structure of the Axonal Membrane
A classification of peripheral nerves according to fiber size and Dr Azam’s
Pharmacology of Muscle Relaxants and Their Antagonists 29 in Anesthesiology 2013
903 Notes
physiologic properties is presented in Table 30-3.
Box A typical
29-5 peripheral nerve
Recommendations for theconsists of several axon
Use of Neuromuscular bundles,
Blockers Biologic
in the Intensive Care membranes
Unit consist of a molecular lipid bilayer contain-
or Avoid
fascicles. Each axon has its own connective tissue covering,
the use of neuromuscular blockers by:
the ing proteins adsorbed on the surfaces, as well as embedded in or
Administer only when required and to achieve a
endoneurium. Each fascicle of many axons is encased by a second spanning
well-defined goal. the hydrocarbon core (Fig. 30-5). The character of the
Maximal use of analgesics and sedatives
connective tissue layer, the epithelial-like perineurium, andContinually the bilayer is determined
allow recovery by the phospholipids, which have long
from paralysis.
Manipulation of ventilatory parameters and modes
entire nerve is wrapped in a loose outer sheath called the Consider epineu- alternative
hydrophobic fatty acyl tails that lie in the center of the membrane,
therapies:
Minimize the dose of neuromuscular blocker:
rium (Fig. 30-4). To reach the nerve axon, a local anesthetic Avoid as well as
mol- vecuronium by thepatients
in female polar hydrophilic head groups, which are usually
with renal failure.
Use a peripheral nerve stimulator with train-of-four

eculemonitoring.
must traverse four or five layers of connective tissue orUse lipid composed of zwitterionic portions (containing positive and nega-
isoflurane in place of muscle relaxants in patients with
membranous barriers, or both.
Do not administer for more than 2 days continuously.
tive charges) that project into the cytoplasm or the extracellular
severe asthma.
Administer by bolus rather than infusion. Minimize the dose of steroid in patients with asthma.
Table 30-3 Classification

complications. As statedofinPeripheral Nerves
the clinical According
practice to Anatomy,
guidelines for wePhysiology,
emphasize and
thatFunction
all other modalities to improve the clinical situ-
436
sustained neuromuscular blockade in adult critically ill patients, ation must be tried, using neuromuscular blockers only as a last
“Independent of the reasons for using neuromuscular blockers, resort.” Susceptibility to
Fiber Conduction Local Anesthetic
Class Subclass Myelin Diameter (µm) Velocity (msec) Location Function Block
A References
α + 6-22 30-120 Efferent to muscles Motor ++
β + 6-22 30-120 Afferent from skin and Tactile, proprioception ++
1. Griffith HR, Johnson GE: The use of curare in junction: Implications for the anesthesiologist. 27. Bovet D: Some aspects of the relationship between
general anesthesia. Anesthesiology 3:418-420, Anesthesiology 96:202-231, 2002. joints chemical constitution and curare-like activity. Ann
1942. γ + 3-6 15. Machold J, Weise C, Utkin Y, et Efferent
15-35 al: The handedness N Y Acad SciMuscle
to muscle spindles 54:407-437, 1951.
tone ++++
2. Cullen SC: The use of curare for improvement of of the subunit arrangement of the nicotinic acetyl- 28. Szalados JE, Donati F, Bevan DR: Effect of
δ relaxation during
abdominal + inhalation anesthesia:
1-4 choline5-25
receptor from TorpedoAfferent
californica.sensory
Eur J nerves Pain,
d-tubocurarine cold temperature,
pretreatment touch
on succinylcholine +++
Report on 131 cases. Surgery 14:261-266, 1943. Biochem 234:427-430, 1995. twitch augmentation and neuromuscular blockade.
B 3. Beecher HK, Todd DP:+ A study of <3 deaths with 3-15IU, Hong A, Whisenant
16. Willcockson Preganglionic
RP, et al: Ori- sympathetic
Anesth AnalgVarious
71:55-59, autonomic
1990. functions ++
anesthesia and surgery. Ann Surg 140:2-34, 1954. entation of d-tubocurarine in the muscle nicotinic 29. Kopman AF, Klewicka MM, Neuman GG: An alter-
− och kliniska0.3-1.3
C 4. ThesleffsCS: Farmakologiska forsok med 0.7-1.3receptor–binding Postganglionic
acetylcholine site. J Biol Chem sympatheticnate methodVarious autonomic
for estimating functions
the dose-response rela- ++
L.T. I. (O,O-succinylcholine jodid). Nord Med 277:42249-42258, 2002. tionships of neuromuscular blocking drugs. Anesth
dC 1951. −
46:1045-1051, 0.4-1.2 17. Paul 0.1-2.0
M, Kindler CH, Fokt RM, etAfferent sensory
al: The potency of nerves Various
Analg 90:1191-1197, autonomic functions
2000. +
5. Foldes FF, McNall PG, Borrego-Hinojosa JM: Suc- new muscle relaxants on recombinant muscle-type 30. Curran MJ, Donati F, Bevan DR: Onset and recovery
Pain, warm temperature, touch
cinylcholine, a new approach to muscular relaxation acetylcholine receptors. Anesth Analg 94:597-603, of atracurium and suxamethonium-induced neu-
in anaesthesiology. N Engl J Med 247:596-600, 2002. romuscular blockade with simultaneous train-of-
Modified From Bonica JJ: Principles and Practice of Obstetric Anesthesia and Analgesia. Philadelphia, FA Davis, 1967.
1952. 18. Martyn JA: Basic and clinical pharmacology of the four and single twitch stimulation. Br J Anaesth
6. Baird WL, Reid AM: The neuromuscular blocking acetylcholine receptor: Implications for the use of 59:989-994, 1987.
properties of a new steroid compound, pancuro- neuromuscular relaxants. Keio J Med 44:1-8, 1995. 31. Viby-Mogensen J: Correlation of succinylcholine
nium bromide. A pilot study in man. Br J Anaesth 19. Kallen RG, Sheng ZH, Yang J, et al: Primary struc- duration of action with plasma cholinesterase activ-
39:775-780, 1967. ture and expression of a sodium channel character- ity in subjects with the genotypically normal
7. Savage DS, Sleigh T, Carlyle I: The emergence istic of denervated and immature rat skeletal enzyme. Anesthesiology 53:517-520, 1980.
of ORG NC 45, 1-[2 beta,3 alpha,5 alpha,16 muscle. Neuron 4:233-242, 1990. 32. Gissen AJ, Katz RL, Karis JH, Papper EM: Neu-
beta, 17 beta)-3,17-bis(acetyloxy)-2-(1-piperidinyl)- 20. Bowman WC: Prejunctional and postjunctional romuscular block in man during prolonged arterial 148
androstan-16-yl]-1-methylpiperidinium bromide, cholinoceptors at the neuromuscular junction. infusion with succinylcholine. Anesthesiology
Dr Azam’sfromNotes
the pancuronium series. Br J Anaesth 52(Suppl
in Anesthesiology 2013 Anesth Analg 59:935-943, 1980. 27:242-249, 1966.
1):3S-9S, 1980. 21. Prior C, Tian L, Dempster J, Marshall IG: Prejunc- 33. Torda TA, Graham GG, Warwick NR, Donohue P:
of action is almost immediate for all agents after intradermal or intravenous regional anesthesia. If a lower leg tourniquet is used,
subcutaneous administration; however, the duration of anesthesia it should be applied well below the fibular neckNotes
Dr Azam’s to avoid pressure
Table 30-4 Infiltration Anesthesia
Plain Solution Epinephrine-Containing Solution

Drug Concentration (%) Max Dose (mg) Duration (min) Max Dose (mg) Duration (min)
Short Duration
Procaine 1-2 500 20-30 600 30-45
Chloroprocaine 1-2 800 15-30 1000 30
Moderate Duration
Lidocaine 0.5-1 300 30-60 500 120
Mepivacaine 0.5-1 300 45-90 500 120
Prilocaine 0.5-1 350 30-90 550 120
Long Duration
Bupivacaine 0.25-0.5 175 120-240 200 180-240
Ropivacaine 0.2-0.5 200 120-240 250 180-240
149

DrLocal
Azam’s Notes in 929
Anesthetics 30
Anesthesiology 2013
Table 30-8 Spinal Anesthesia*
Usual Glucose Usual

Drug Concentration (%) Usual Volume (mL) Total Dose (mg) Baricity Concentration (%) Duration (min)
Procaine 10.0 1-2 100-200 Hyperbaric 5.0 30-60
Lidocaine 1.5, 5.0 1-2 30-100 Hyperbaric 7.5 30-90
Mepivacaine 4 1-2 40-80 Hyperbaric 9.0 30-90

Tetracaine 0.25-1.0 1-4 5-20 Hyperbaric 5.0 90-200
0.25 2-6 5-20 Hypobaric 90-200
1.0 1-2 5-20 Isobaric 90-200
Dibucaine 0.25 1-2 2.5-5.0 Hyperbaric 5.0 90-200

0.5 1-2 5-10 Isobaric 90-200
0.06 5-20 3-12 Hypobaric 90-200
Bupivacaine 0.5 3-4 15-20 Isobaric 90-200

0.75 2-3 15-20 Hyperbaric 8.25 90-200
Levobupivacaine 0.5 3-4 15-20 Isobaric 90-200

0.75 2-3 15-20 Hyperbaric 90-200
Ropivacaine 0.5 3-4 15-20 Isobaric 90-200

0.75 2-3 15-20 Hyperbaric 90-200
*Dosing refers to a 70-Kg adult. Dosing may be reduced in pregnancy (see Chapter 69) and with advancing age (see Chapter 71). Pediatric dosing is detailed in Chapter 81.
bupivacaine possesses an anesthetic profile similar to that of including tetracaine gel70 and liposomal lidocaine.71 Physical
tetracaine.64 methods to accelerate local anesthetic transit across skin, includ-
The addition of vasoconstrictors may prolong the duration ing iontophoresis, local heating, electroporation, and a variety of
of spinal anesthesia; for example, the addition of 0.2 to 0.3 mg of forms of needle-less pressure injection, may lead to more rapid
epinephrine to lidocaine, tetracaine, or bupivacaine solutions will onset of cutaneous analgesia.72 Synera (originally studied as S-
produce a 50% or greater increase in duration.65,66 The duration Caine) is a formulation of lidocaine and tetracaine that was devel-
of spinal anesthesia produced by tetracaine can also be increased oped with a heating element (activated by opening the package
to a similar extent by adding 1 to 5 mg of phenylephrine. The to initiate an oxygen-dependent exothermic reaction). This for-
addition of epinephrine to bupivacaine or lidocaine may be more mulation has a rapid onset and evokes vasodilatation.73
effective in prolonging the duration of spinal anesthesia in lum- Topical anesthesia through cut skin is commonly used in 150
bosacral segments than in thoracic segments. pediatric emergency departments for liquid application into lac-
erations that require suturing. Historically, this had been provided
or primary
Anesthesia Management
tions, including pulmonary and cardiac events and mortality, and
eferred for
g
aid in decisions regarding the need for further specialized testing Dr Azam’s Notes in Anesthesiology 2013
tances,
briskly the
Table 34-1 American Society of Anesthesiologists Physical
such as pulmonary function tests (PFTs) or noninvasive cardiac Preoperative Evaluat
al depart- Status Classification
stress testing.13 This is frequently not practical, and a report by
basketball
nformation theASA
patient is oftenpatient
sufficient. Table 34-2 Metabolic Equivalents of Functional Capacity advance planning ensures that the necessary equipm
1 Healthy without organic, biochemical, or psychiatric
a potential
distances The pulmonary examination should include auscultation skilled personnel are available.
disease MET Functional Levels of Exercise
atxercise
the time for wheezing and decreased or abnormal breath sounds and nota- Evaluation of the heart, lungs, and skin is necessa
ion.
n Cardiol ASA
tion of2cyanosis
A patient with mild systemic
or clubbing, disease, e.g.,
use of accessory mild asthma
muscles, or well-
and effort 1 Eating, working at a computer, dressing as further focus on the organ systems involved with
reported by the patient. Auscultation of the heart and, w
eoperative of breathing.controlled hypertension. No significant impact on daily activity. 2 Walking down stairs or in your house, cooking
O2/min/kg of Unlikely to have examination
an impact on anesthesia and surgery cated, inspection of the pulses and peripheral and cen
gh level of A basic neurologic to document deficits in 3 Walking 1-2 blocks and assessment for the presence of edema in the extrem
t’s history, mental
ASA 3 status, speech, cranial nerves, gait, and motor
Significant or severe systemic disease that limits normal and sensory
activity, aid in developing a perioperative plan. One should ausc
4 Raking leaves, gardening
anning of function maye.g., be renal
indicated,
failure depending
on dialysis oron the2 surgical
class congestive procedure
heart failure. murmurs, rhythm disturbances, and signs of volume
during
ormidable the and patient’s Significant
history. For selective
impact patients
on daily activity.(e.g., thoseimpact
Probable with deficits
on 5 Climbing 1 flight of stairs, dancing, bicycling Physical findings should focus on examination for third
sion. This
perspective or disease oranesthesia
undergoing neurosurgery), a more extensive or
and surgery 6 Playing golf, carrying clubs heart sounds, rales, jugular venous distention, ascites
se patients
luate often focused neurologic examination is necessary to document spe- megaly, and edema.
ASA 4 Severe disease that is a constant threat to life or requires 7 Playing singles tennis
ntment or cific preexisting abnormalities that may aid in diagnosis or inter- Observing whether the patient can walk up on
uality and intensive therapy, e.g., acute myocardial infarction, respiratory flights of stairs can predict a variety of postoperative
heir usual
important fere with positioning. Establishing a baseline allows comparison 8 Rapidly climbing stairs, jogging slowly
failure requiring mechanical ventilation. Serious limitation of tions, including pulmonary and cardiac events and mor
after the postoperatively for evaluation of new deficits and can aid in 9 Jumping rope slowly, moderate cycling
daily activity. Major impact on anesthesia and surgery aid in decisions regarding the need for further specializ
ing previ- defense of potential malpractice claims of adverse events.
American 10 Swimming quickly, running or jogging briskly such as pulmonary function tests (PFTs) or noninvasiv
ients what ASA Obesity,
5 hypertension,
Moribund patient who and large neck
is equally circumference
likely to (>17
die in the next 24 hours stress testing.13 This is frequently not practical, and a
ndards
.
and inches in men, with >16 inches
or without in women, or >60 cm in anyone)
surgery 11 Skiing cross country, playing full-court basketball
Recent and the patient is often sufficient.
important predict an increased incidence of obstructive sleep apnea (OSA).14 12 Running rapidly for moderate to long distances The pulmonary examination should include au
by multiple
sthesiolo-
ASA 6 Brain-dead organ donor
These same neck measurements also predict difficulty with mask for wheezing and decreased or abnormal breath sounds
From Jette M, Sidney K, Blumchen G: Metabolic equivalents (METs) in exercise
in prepar-
ay evalua- ventilation
“E” added to and intubation.
the classification Intravenous
indicates emergency access
surgery.sites should be testing, exercise prescription, and evaluation of functional capacity. Clin Cardiol tion of cyanosis or clubbing, use of accessory muscles,
he such
es current
as Available from www.asahq.org. 13:555-565, 1990. of breathing.
MET, metabolic equivalent of the task. 1 MET = consumption of 3.5 mL O2/min/kg of
A basic neurologic examination to document d
ogists will body weight. 34
Preoperative Evaluation 1009 mental status, speech, cranial nerves, gait, and motor an
Box 34-1
Box 34-1 Components of the Airway Examination function may be indicated, depending on the surgical p
toring and replacement. Calcium channel blockers (e.g., Not infrequently, patients will have increased BP during the and patient’s history. For selective patients (e.g., those wi
ion of an Box 34-2 Revised Cardiac Risk Index
preoperative visit, even without a history of hypertension. This or disease or undergoing neurosurgery), a more ext
Length ofamlodipine,
the upper incisors
5 to 10 mg daily) can be very effective. Frequently,
tion clinic may be due to anxiety or missing doses of drugs because patients focused neurologic examination is necessary to docum
Mallampati Conditionanxiety
of the increases
teeth BP, and therefore antianxiolytics can be used as High-risk surgery (intraperitoneal, intrathoracic, or
adjunctive therapy. BP should not be often do not take their medications before an appointment or cific preexisting abnormalities that may aid in diagnosi
he mouth Relationship of the upper (maxillary) incisors tolowered too rapidly. Con-
the lower suprainguinal
procedure. This vascular
reading procedures)*
is probably not reflective of their usual fere with positioning. Establishing a baseline allows co
tinuation of antihypertensive treatment preoperatively is
A tongue (mandibular) incisors Ischemic
control.heart disease
Repeating the(by BPany diagnostic criteria)
measurement, especially after the postoperatively for evaluation of new deficits and c
critical.
tire uvula, Ability to protrude or advance the lower (mandibular) incisors administration of anxiolytics
History of congestive heart failure if this is planned, obtaining previ- defense of potential malpractice claims of adverse even
ces, and a in front of the upperHeart
(maxillary) incisors ous readings from either medical records or asking patients what Obesity, hypertension, and large neck circumfer
Ischemic Disease History of cerebrovascular
their “usual” BP measurements disease
are, can be informative. inches in men, >16 inches in women, or >60 cm in
ase of the
Section IV Anesthesia Managem

Interincisor
Theorgoals
intergum (if edentulous)
of preoperative distance
evaluation are to DiabetesInspection of the airway
mellitus requiring may† be the single most important predict an increased incidence of obstructive sleep apne
insulin
on should
Tongue size component of the physical examination from an anesthesiolo- These same neck measurements also predict difficulty w
the neck, Creatinine >2.0 mg/dL
t Identify the risk for heart disease based on risk factors (Fig. gist’s perspective. Without specialized training in airway evalua- ventilation and intubation. Intravenous access sites s
with laryn- Visibility of the uvula
tion and management, including advanced techniques such as
34-2, Box 34-2)
pertinent Presence oftheavy facialthe
hairpresence and severity of heart disease from *This risk factor
fiberoptic is not considered
intubation, a clinical
it is unlikely that predictor in the ACC/AHA
nonanesthesiologists will
Identify 2007 guidelines for perioperative cardiac evaluation for noncardiac
of dental be capable of performing an adequate assessment. See Box 34-1
Compliance of symptoms,
the mandibular space
physical findings, or diagnostic tests surgery. 7
Box 34-1 Components of the Airway Examination
f preexist- † for components of the airway examination.
cuss with Thyromental distance with the headfor
t Determine the need preoperative
in maximum interventions
extension This risk factor has been changed to simply diabetes mellitus in the
All2007
patients shouldforhave thorough cardiac
documentation
t Modify the risk for perioperative adverse events ACC/AHA guidelines perioperative evaluationofforan Length of the upper incisors
echniques Length of the neck airway examination,
noncardiac surgery.7 whether in a preoperative evaluation clinic
or immediately before surgery (see Chapter
CM, et 50). The Mallampati Condition of the teeth
d prepare Thickness or circumference From Lee TH, Marcantonio ER, Mangione al: Derivation and
The basis of ofcardiac
the neckassessment is the history, physical classificationvalidation
prospective is performed by having
of a simple patients
index for openofthe
prediction mouth
cardiac Relationship of the upper (maxillary) incisors to the lo
examina-
identified,
Range ofexamination,
motion of theand
headECG.andRisk
neckfactors for CAD are as important or A of major
risk
widely noncardiac the
and protruding surgery.
tongue Circulation
completely 100:1043-1049, 1999.
forward. A tongue (mandibular) incisors 151
more important than symptoms of ischemia because CAD is not depressor is not used. In class I, the soft palate, fauces, entire uvula, Ability to protrude or advance the lower (mandibular)
diagnosed in 40% of men and 65% of women before an acute increased incidence
and pillars of perioperative
are visualized; in class II,cardiac
the soft events (see Fig.
palate, fauces, and34-2
a in front of the upper (maxillary) incisors
Dr Azam’s Notessyndrome
coronary in Anesthesiology 2013
(unstable angina, acute MI, or sudden death) and portion
Box 34-2). of the uvula; intraditional
However, class III, the softfactors
risk palate are
andimportant
base of thein
Interincisor or intergum (if edentulous) distance
occurs. The traditional risk factors for CAD, such as smoking, uvula;the
assessing andsignificance
in class IV, theofhard palate
chest pain,only. The evaluation
dyspnea, should
or an abnormal
ment
hypertension, age, male gender, hypercholesterolemia, and family ECG. The Revised Cardiac Risk Index (RCRI; Box 34-2) has been
history, are not the same risk factors that are associated with an Dr Azam’s
validated in several studies as the best scoring system to predictNotes in Anesthesiology 2013
+) -),.+" +10$-#

Step 1: Emergency Surgery ' $&+$,%+ .-$)((
* +$)* +-$/ ,.+/ $&&(
Step 2: Active Cardiac Conditions
4(,-& )+)(+1,1(+)' ,.(,-& )+, / + ("$(+ (-&
4 )'* (,- ( 0)(, -&,, ),-*)( ,.+" +1.(-$&
,-$&$2 )+)++ -
4$"($!$(-++#1-#'$,)$-2)++ "+ # +-&)%)+0$-#+*$
/ (-+$.&++- ,1'*-)'-$/ (-+$.&+++#1-#'$)++1+$( 0
4 / + /&/.&+$, , , / + )+
Step 3: Low-Risk Surgery (risk<1%)

4.* +!$$&)+ (),)*$
4-+-)++ ,- +) -),.+" +1
4'.&-)+1
Step 4: Functional Capacity

4)): ≥ ,(0&%!&$"#- +) -),.+" +1
)!,-$+,0$-#).-,1'*-)',
Step 5: Clinical Predictors )&$($&*+ $-)+, +) -),.+" +1

4,# '$# +-$, ,
4)'* (,- )+*+$)+ ,.&+,.+" +1 +) -),.+" +10$-#
4 + +)/,.&+$, , ,-+)% 3&$($&*+ $-)+, )(-+)&)+)(,$ +
4 $ - ,' &&$-., ()($(/,$/ - ,-$("$!$-
(- +' $- +$,%,.+" +1 0$&&#(" '(" ' (-
4 (&$(,.!!$$ (1
≥&$($&*+ $-)+, ,.&+,.+" +1 )(,$ +- ,-$("$!$-0$&&

#(" '(" ' (-
Figure 34-2 Simplified cardiac evaluation for noncardiac surgery. AF, atrial fibrillation; AS, aortic stenosis; HF, heart failure; HR, heart rate; METs, metabolic
equivalents of the task; MI, myocardial infarction; MS, mitral stenosis; NYHA, New York Heart Association; SVT, supraventricular tachycardia; TIA, transient
ischemic attack; VT, ventricular tachycardia. (From Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA 2007 guidelines on perioperative cardiovascular
evaluation and care for noncardiac surgery. J Am Coll Cardiol 50:e159-e241, 2007. Available at http://www.acc.org/qualityandscience/clinical/guidelines/Periop_
/ Accessed September 28, 2007.)
A
152

ng noncardiac Box 34-3 Recommendations for Preoperative Resting

erse events are 12-Lead Electrocardiogram Patients with aspirin Patients with aspirin (75–150 mg/day)+
diabetes, cere- (75–150 mg/day) clopidogrel (75 mg/day)
anced age; and Class I
ures. A preoperative resting 12-lead ECG is recommended for
(pain, pressure, patients with at least one clinical risk factor* who are
pitating factors, Primary Secondary High-risk situations: Low-risk
undergoing vascular surgical procedures
prevention prevention after <6 weeks after MI, PCI, BMS, stroke situations**
rdless of symp-
A preoperative resting 12-lead ECG is recommended for MI, ACS, stent, <12 months after DES
of heart disease stroke, PAD High-risk stents*
patients with known congestive heart failure, peripheral
s. Shortness of
arterial disease, or cerebrovascular disease who are
ent. Dyspnea is
undergoing intermediate-risk surgical procedures
ng, pulmonary
risk factors for Class IIa Intracranial All All
e an investiga- A preoperative resting 12-lead ECG is reasonable in persons Only vital surgery surgery
neurosurgery surgery
cularly likely to with no clinical risk factors who are undergoing vascular
se. One should surgical procedures
Risk of bleeding in
mes of treating closed space***
Class IIb
A preoperative resting 12-lead ECG may be reasonable in
oms suggestive Stop 7 days Operation under Stop clopidogrel
patients with at least one clinical risk factor who are
spnea, need an before operation continuous Maintain aspirin
undergoing intermediate-risk operative procedures
e preoperative as needed treatment
tory of cardio- Class III
1
An abnormal Preoperative and postoperative resting 12-lead ECGs are not *High-risk stents: long (>36 mm), proximal, overlapping, or multiple stent implantation, stents for chronic
diac disease, in indicated for asymptomatic persons undergoing low-risk total occlusions, stents in small vessels or bifurcated lesions.
**Examples of low-risk situations: >3 months after BMS, stroke, uncomplicated MI, PCI without stenting.
7% of individu- surgical procedures
***Risk of bleeding in closed space: intracranial neurosurgery, intra-medullary canal surgery, posterior eye
dditionally, the Class I recommendations: the procedure should be chamber ophthalmic surgery. In these situations, the risk/benefit ratio of upholding vs withdrawing aspirin
ting postopera- performed; class IIa: it is reasonable to perform the must be evaluated for each case individually; in case of aspirin upholding, early postoperative re-institution
mal ECG does is important.
preocedure; class IIb: the procedure may be considered;
class III: the procedure should not be performed because it is
use of advanced Figure 34-3 Algorithm for preoperative management of patients receiving antiplatelet therapy. ACS, acute coronary syndrome; BMS, bare metal
not helpful. drug-eluting stent; MI, myocardial infarction; PAD, peripheral arterial disease; PCI, percutaneous coronary intervention. (From Chassot P-G, Delaba
ased testing are
ies found with A
*Clinical risk factors are listed in Box 34-2.
DR: Perioperative antiplatelet therapy: The case for continuing therapy in patients at risk of myocardial infarction. Br J Anaesth 99:316-328, 2007.
http://bja.oxfordjournals.org.)
ons found only Adapted from Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA
an ambulatory 2007 guidelines on perioperative cardiovascular evaluation and
rmal ECG, but care for noncardiac surgery. J Am Coll Cardiol 50:e159-e241,
2007. Available at http://www.acc.org/qualityandscience/clinical/
d the preopera- guidelines/Periop_Fulltext_2007.pdf/ Accessed September 28,
ose who had a 2007.
CG are impor-
ecially if recent;
ne study found stating “cleared for surgery” are not sufficient to design a safe
vious ECG did anesthetic plan. A letter summarizing the medical problems and 153
eline for com- therapies, along with the results of diagnostic tests, should be
ECG preopera- requested.
frequent orDrthe Azam’sThe Notesgoal in Anesthesiology
is to identify patients with2013heart disease who are
eld lessens. If a at high risk for perioperative cardiac morbidity or mortality or
aortic stenosis,
the intensity every
of murmurs of MVP2 years
and HCM. forSquatting
moderate stenosis,
increases by history, and every
physical 5 tive
examination, endocarditis
or ECG, further evaluation is no by long
40
years for mild stenosis. Patients with aortic
venous return and afterload and therefore increases
Drstenosis
most
Azam’sareNotes
echocardiography at riskin Anesthesiology 2013
or by a cardiologist should be considered (see
murmurs, except those related to MVP and HCM. Asking the Box 34-4).
for sudden death from arrhythmias, heart failure, and myocardial Mitral Stenosis
ed individuals Box 34-4 ACC/AHA Guideline Summary—Echocardiography
ischemia and infarction from concomitant CAD (high incidence) Mitral stenosis is much les
Table 34-3 Descriptions of Murmurs Associated with Cardiac Abnormalities
n concert with in Asymptomatic Patients with Cardiac Murmurs* or a supply-demand mismatch. Patients with aortic sclerosis or usually associated with a hi
Lesion Location Timing Description
operative hos- stenosis need evaluation for CAD regardlessCrescendo-decrescendo,
of other riskradiates factors. occur with aortic valvula
Aortic stenosis Second parasternal interspaces Midsystolic to the carotids; ± S , S ; Valsalva and sustained
function. Those with severe or critical stenosis should handgrip not undergo noncar- normal mitral valve has a
3 4
Class I—There is evidence or general agreement (or both) exercise decrease intensity
that echocardiography is useful in asymptomatic patients diac surgery

Aortic insufficiency(unless
Third andemergency
fourth parasternal and lifesaving)
Holodiastolic without
Decrescendo, blowing,ahigh pitched, radiates when
cardiol- theAustin-Flint
to the carotids; mitralrumblevalve at area
interspaces the apex; squatting, handgrip exercise, and leaning forward increase intensity 2
with the following cardiac murmurs: ogy evaluation and careful consideration of risks or until valve of 1.1 to 1.5 cm , and criti
mine the cause =bZlmheb\fnkfnkl
Mitral stenosis Apex
replacement. Patients with moderate to severeexercise
Mid-diastolic Opening snap; low-pitched rumble radiates to the axilla; squatting and handgrip
aortic stenosis
increase intensity have resting mean transvalvular
en significant <hgmbgnhnlfnkfnkl an Mitral
increased
regurgitation risk
Apex of bleeding (especially from
Holosystolic High pitched,gastrointestinal denotes
blowing, radiates to the axilla; loud
3 S ; standingsevere stenosis. Sy
decreases intensity;
Chapter 60).39 EZm^lrlmheb\fnkfnkl angiodysplasia). The cause appears to be an acquired von Wille- after acute rheumatic feve
squatting and handgrip exercise increase intensity
flow across the FnkfnklZllh\bZm^]pbma^c^\mbhg\eb\dl Mitral valve prolapse Apex

brand syndrome resulting from mechanical Late systolic Crescendo, midsystolic click; Valsalva and standing increase intensity; squatting
disruption of von nancy or illness. Unrecogn
decreases intensity
urmurs occur FnkfnklmaZmkZ]bZm^mhma^g^\dhk[Z\d Willebrand multimers during turbulent blood flow through differential
a intensity; diagnosis
Hypertrophic Apex, lower left sternal border Midsystolic S , single S ; Valsalva and standing increase squatting, passive leg raising, of pu
pregnancy, or @kZ]^,hkehn]^klrlmheb\fnkfnkl A
4 2
narrowed
cardiomyopathy
valve. See the section “von Willebrand’s Disease” for
and handgrip exercise decrease intensity
Preoperative evaluat
ologists often
Class IIa—The weight of evidence or opinion is in favor of patient has a history of dy
urs. In elderly
the usefulness of echocardiography in asymptomatic patients edema, and hemoptysis. Th
e, other abnor-
with the following cardiac murmurs: Table 34-4 Severity of Aortic Stenosis atrial pressure and decrease
anorectic drug
FnkfnklZllh\bZm^]pbmahma^kZ[ghkfZeiarlb\Ze be due to a dilated left a
sease, cardio-
findings on cardiac examination Velocity of Aortic Mean Pressure Valve Area failure and chronically ca
hould be con-
FnkfnklZllh\bZm^]pbmaZgZ[ghkfZe Grade Jet (m/sec) Gradient (mm Hg) (cm2) fibrillation require anticoag
may be useful
electrocardiogram or chest radiograph Tachycardia decreases card
valuation may Mild <3 <25 ≥1.5
will not change Class III—There is evidence or general agreement (or both) and right heart failure may
that echocardiography is not useful in asymptomatic patients Moderate 3-4 25-40 1.0-1.5 S2 suggests pulmonary hy
and require with the following murmurs: Severe 4-4.5 40-50 0.7-1.0 murmur are described in T
ed periopera- @kZ]^+hklh_m^kfb]lrlmheb\fnkfnkl\hglb]^k^] increases HR and BP and m
innocent or functional by an experienced observer Critical >4.5 >50 <0.7
ure in concert should look for rales and
isk of decom- *These are indications for general evaluation but do not necessarily
s are graded need to be performed preoperatively.
r that can be From Bonow, RO, Carabello, BA, Chatterjee, K, et al: ACC/AHA 2006
ard; grade III, guidelines for the management of patients with valvular heart
disease. A report of the American College of Cardiology/American
ith a palpable Heart Association Task Force on Practice Guidelines (Writing
oscope (thrill Committee to Revise the 1998 Guidelines for the Management of
a stethoscope. Patients with Valvular Heart Disease). J Am Coll Cardiol 48:e1,
atable because 2006.
murs and vice
intensity with patient to repeatedly perform a handgrip will increase HR and
lva maneuver afterload (increases BP) and will augment murmurs of mitral
rs and reduces regurgitation and stenosis and aortic insufficiency but decrease
sociated with aortic stenosis and HCM murmurs. All patients with murmurs
ll also increase require an ECG. In patients with significant abnormalities found
tting increases by history, physical examination, or ECG, further evaluation by
creases most echocardiography or by a cardiologist should be considered (see 154
M. Asking the Box 34-4).
Preoperative Evaluation 1017 34
hen aortic Preoperative Evaluation
Box 34-5 Indications for a Pacemaker
) have the “Dyspnea”). Near syncope or syncopal episodes suggest
Medtronic- Box 34-6 Classification of Pulmonary Hypertension
Class I Indications disease. Hypoxia, hypercapnia, vasoconstrictors, and inc
he lowest Lbgnl[kZ]r\Zk]bZpbmalrfimhfl\e^ZkerkêZm^]mhma^ Pulmonary Arterial Hypertension sympathetic tone (even from anxiety) increase pulmonary
(St. Jude, bradycardia (usually with a heart rate <40 beats/min or Primary pulmonary hypertension lar resistance and lead to acute decompensation with righ
alves such frequent sinus pauses) Sporadic failure.
ardial) or LrfimhfZmb\\akhghmkhib\bg\hfi^m^g\^ Familial Patients with pulmonary arterial hypertension have
long-term rate of perioperative morbidity and mortality.57 Mild pulm
<hfie^m^!mabk]&]^`k^^":O[eh\d* Associated with
hypertension rarely affects anesthetic management, but mo
Section IV Anesthesia Management

e duration :]oZg\^]l^\hg]&]^`k^^:O[eh\d![eh\dh_≥2 Collagen vascular disease
to severe disease increases the risk for right heart failure
ter-acting consecutive P waves) Congenital shunts
and symptoms of disease severity include58
in or low- Portal hypertension
LrfimhfZmb\Fh[bmsBhkBBl^\hg]&]^`k^^:O[eh\d
e in con- Human immunodeficiency virus infection
Fh[bmsBBl^\hg]&]^`k^^:O[eh\dpbmaZpb]^g^]JKLhk t Dyspnea at rest
Drugs/toxins
. See the chronic bifascicular block, regardless of symptoms Persistent pulmonary hypertension of the newborn
t Metabolic acidosis
. t Hypoxemia
Class II Indications Pulmonary Venous Hypertension t Right heart failure (peripheral edema, hepatom
Lbgnl[kZ]r\Zk]bZ!a^ZkmkZm^<40 beats/min) with Left-sided heart disease jugular venous distention)
symptoms suggestive of bradycardia but without a clear Extrinsic compression of central pulmonary veins t History of syncope
on in the association between bradycardia and symptoms Pulmonary veno-occlusive disease
Lbgnlgh]^]rl_ng\mbhgpbmang^qieZbg^]lrg\hi^ Physical examination may reveal a split S2 with
icular and Pulmonary Hypertension Related to Lung second component, right ventricular heave, a murmur of
sk of peri- <akhgb\a^ZkmkZm^l<30 beats/min in an awake patient Disease or Hypoxemia pid regurgitation, ascites, hepatomegaly, jugular venous
itself and Class I conditions are those in which permanent pacing is Chronic obstructive pulmonary disease tion, and peripheral edema.
e. Uncon- definitely beneficial and effective, provided that the condition Interstitial lung disease An echocardiogram is the screening test of choice a
high-risk is not due to a transient cause. Class II conditions are those used to estimate pulmonary artery pressure, assess right ve
Sleep-disordered breathing
oned until in which permanent pacing may be indicated but there is lar function, and identify left heart failure and valvular o
Neonatal lung disease genital heart disease.59 Patients with significant finding
trial fibril- conflicting evidence or divergence of opinion (or both).
Chronic exposure to high altitude require right and left heart catheterization, although the n
art block catheterization preoperatively depends on the surgical proc
tive clinic *Controversy exists concerning complete atrioventricular (AV) block Pulmonary Hypertension Caused by Chronic
An ECG, chest radiograph, and echocardiogram are us
without symptoms. The current ACC/AHA guidelines classify Thromboembolic Disease
ocedurest patients with more than mild disease. Findings on the
asymptomatic third-degree AV block with average awake Pulmonary thrombosis or embolism
degree AV ventricular rates of 40 beats/min or greater as a class IIa indication,
include right axis deviation, RBBB, right ventricular hyper
Sickle cell disease and tall R waves in leads V1 and V2. Right atrial hypertrop
c with an although others recommend definite pacemaker placement.
nd-degree From Gregoratos, G, Abrams, J, Epstein, AE, et al: ACC/AHA/NASPE Pulmonary Hypertension from Disorders Directly Affecting “P pulmonale” may be present in severe pulmonary hypert
the Pulmonary Vasculature with peaked P waves most apparent in leads II, III, aVF, a
eater than 2002 guideline update for implantation of cardiac pacemakers and
antiarrhythmia devices: Summary article. A report of the American Schistosomiasis Enlargement of the main pulmonary artery and a globula
ich results shape with loss of the retrosternal air space as a result o
College of Cardiology/American Heart Association Task Force on Sarcoidosis
Two types Practice Guidelines (ACC/AHA/NASPE Committee to Update the ventricular dilation can be seen on the chest radiograph. E
enckebach 1998 Pacemaker Guidelines). Circulation 106:2145-2161, 2002. Available from http://www.who.int/ncd/cvd/pph.html. tors should inquire about a history of OSA, which can also
eart block, cause of pulmonary hypertension.60 A CBC with platelet
rogressive trolytes, BUN, creatinine, and liver function tests (LFTs; m
ccurs and Bundle branch blocks are complete or incomplete and elevated as a result of congestion or the use of bosenta
s from an either right (RBBB) or left (LBBB). They result from aging or needed.
pulmonary arterial hypertension, formerly called primary pulmo- Preoperatively, patients may be treated with diuretic
ck, and is fibrosis of the conducting system, ischemia, pulmonary disease,
nary hypertension, is rare, but other forms are more common coagulants, calcium channel blockers, supplemental o
o a revers- radiation, or cardiomyopathies or can be normal variants. Tradi- and occur with a variety of diseases, including cardiac, pulmo- sildenafil (a phosphodiesterase inhibitor), endothelin re
by a fixed, tionally, LBBB has been considered more ominous and has been nary, liver, thromboembolic, and collagen vascular disease. antagonists (bosentan), and prostanoids (iloprost, epopros
e dropped shown to be associated with CAD and heart failure.46,47 LBBB is Pulmonary hypertension is associated with HIV infection, expo- 155
Some of these agents are given by continuous intravenou
complete strongly associated with CAD, and in a patient with a recent onset sure to anorexics such as fenfluramine, chronic liver disease, espe- sion, and even momentary interruption of therapy can b
waves and DrorAzam’s
no previous
Notes evaluation of LBBB, stress2013
in Anesthesiology testing or cardiology cially if portal hypertension is present, and collagen vascular strophic. All drugs need to be continued preoper
reversible consultation may be warranted. Obtaining a previous ECG for diseases, including scleroderma, SLE, and rheumatoid arthritis. Management of these patients in conjunction with a pulm
if abnormal LFT values are unexpectedly found, further testing count higher than 50,000/mm and an INR less than 1.5, respec-
or referral may be warranted. In patients with elevations in ALT Dr Azam’s Notes
tively. Correction of anemia is controversial but in
mayAnesthesiology
limit renal 2013
dysfunction. Lactulose (30 mL orally every 6 hours for 3 days
Table 34-5 Child-Turcotte-Pugh Classification
before surgery with the last dose given within 12 hours of surgery)
or oral bile salts with intravenous hydration beginning the night
Points (For Each with a Maximum of 15) before surgery may reduce perioperative progression of renal
disease in patients at risk.76 Reduction of ascites preoperatively
Parameter 1 2 3
may decrease the risk of wound dehiscence and improve pulmo-
Ascites Absent Slight Moderate nary function. Sodium restriction (in diet and intravenous solu-
Bilirubin (mg/dL) <2 2-3 >3
tions), diuretics (especially spironolactone, which inhibits
aldosterone), and even paracentesis are useful. If fluid is aspirated,
Albumin (g/dL) >3.5 2.8-3.5 <2.8 it is important to analyze it for infection. Encephalopathy is fre-
Prothrombin time <4 4-6 >6 quently caused by an acute insult such as infection, gastrointesti-
(seconds over control) nal bleeding, hypovolemia, or sedatives. It is important to
determine reversible factors and treat accordingly. Lactulose,
Encephalopathy None Grade 1-2 Grade 3-4
30 mL Leftevery 6 hours
Coronary orally, is first-line therapy. Addressing nutri-
Artery
Class A: <7 points; Class B: 7-9 points; Class C: >9 points. tional deficiencies with enteral or parenteral supplementation
Right Coronary Artery
156

4. Classify cardiomyopathies. Describe management of 60 year old Dr Azam’s Notes in Anesthesiology 2013
male with dilated cardiomyopathy scheduled for laparotomy
ClassiGication of cardiomyopathies on morphologic and hemodynamic basis
Parameter Dilated Restrictive Hypertrophic Obliterative

Morphology Biventricular dilation Decreased ventricular Hypertrophy of left Thickened endocardium
compliance ventricle and usually or mural thrombi
interventricualr septum
Ventricular volume Marked increase Normal to moderate Normal to moderate Moderate decease
increase decrease
Ejection fraction Marked decrease Normal to Moderate Marked increase Normal to moderate
decrease decrease
Ventricular compliance Normal to moderate Marked decrease Marked decrease Marked decrease
decrease
Ventricular filling pressure Marked increase Marked increase Normal to moderate Moderate increase
increase
Stroke volume Marked decrease Normal to moderate Normal to moderate Normal to moderate
decrease increase decrease
Definition
Cardiomyopathies are a heterogeneous group of diseases of the

myocardium associated with mechanical and/or electrical
dysfunction that usually (but not invariably) exhibit inappropriate
ventricular hypertrophy or dilation and are due to a variety of
causes that frequently are genetic.
157

Goldmanʼs Cardiac Risk Index:
i. Age > years 5
Detskyʼs Modified Cardiac Risk Index- 1986
i. Age > 70 years 5
iii. MI > 6 months 5
iii. S3 gallop or ↑ JVP (0-3 cm) 11 iv. Unstable angina 10
v. Pulmonary edema < 1 10
iv. Important aortic stenosis 3 week
vi. Pulmonary edema in the 5
past
v. Rhythm other than sinus, Pac on last preoperative 7 vii. Non sinus rhythm PAC 5
vi. >5 PVC/min at any time before 7 ix. CCVSA class IV 20
x. Critical As 20
vii. PaO2, < 60 or PaCO2 > 50mm Hg, 3 xi. Emergency operation 5
K<3.00 mEq/L or HCO3 < 20 mEq/l xii. Poor general status 5
BUN > 50 or Cr> 3 mg/dl. Abnormal SGOT, signs of chronic Total 120
liver disease, bed ridden from non-cardiac cause
viii Intraperitoneal, Intrathoracic, aortic surgery 3
.
ix. Emergency operation 4 (Assign one point to each of the following variables)
i. High risk type of surgery (intra-peritoneal, intra-thoracic or
suprainguinal vascular procedures.
Total 53 ii. History of IHD (history of MI, positive exercise test, current
complaint of ischemic chest pain or use of nitrate therapy of ECG
with Q waves)
iii. History of CHF
Class II = 1 factor
Leeʼs revised Cardiac Risk Index-- 1999. 158

159

160

Diagrams & Flow Chart Dr Azam’s Notes in Anesthesiology 2013
Reflex Stimuli Receptor Afferents Centre Efferents Response
Baroreceptor Increase BP Carotid Sinus & IX Nerve(carotid Nucleus of Tractus IML Tract Decrease in Blood
Reflex Aortic arch Sinus) & X Nerve Solitarius in pressure, Decreases
(Aortic Arch) Medulla Sympathetic
stimulation, Heart Rate
& SV
Chemoreceptor pH pCO2 & pO2 Carotid & Aortic IX Nerve & X Chemosensitive X Nerve Bradycardia, Increase
Reflex body Nerve area of Medulla Blood pressure &
Hyperventilation
Bain Bridge Reflex Increase filling of Stretch receptor X Nerve Dorsal motor Vagal & Increase in Heart Rate
right atrium in right atrial wall nucleus of vagus sympathetic & Automaticity
fibres
Benzold Jarisch serotonin Pain receptor C X Nerve Respiratory & X Nerve Apnea, Hyperapnea &
reflex Fibre Vasomotor Centre bradycardia, Coronary
Vasodilation &
Hypotension.
Oculo-cardiac Pressure on the Stretch receptor Long & Short Cillary ganglion & Vagal & Reflex Bradycardia
Reflex Eye, Traction on with in extraocular cillary nerve & Gasserian Cardiodepr
the muscles muscles. Opthalmic division ganglion essor fibre
161

Pressure Volume Loop:
Factors that can contribute to perioperative myocardial infarction.
162

Surgical Factors:
Major Intermediate Minor
Emergency Surgery Carotid endarterectomy cataract
Major vessel/surgery Intrathoracic/Peritoneal Superficial surgery

surgery
Surgeries with major Head & Neck Surgery Breast surgery

blood loss or fluid shifts
Open prostatic surgery
Clinical Predictors:
Patient Factors: Cardioplegic solution:
A number of different solutions are described. Most common
Major Intermediate Minor compounds are:
Acute MI (< Previous MI Age > 65 Years • Potassium = 15-40 mEq/l
7days), Recent (7 • Sodium = 100-120 mEq/l
to 30 Days) • Chloride = 110-120 mEq/l
• Calcium = 0.7 mEq/l
Decompensated Pathological Q- Poor functional • Magnesium = 15 mEq/l
CHF Waves state • Glucose = 28 mmol/l
• Bicarbonate = 27 mmol/l
Symptomatic Anginal Class I & II Uncontrolled HTN
arrhythmias St. Thomas hospital solution (supplied in 20ml ampoules):
• MgCl2 6H2O = 16 mmol
Severe Valvular Diabetes
• KCl = 16 mmol
Heart disease.
• Procaine 272.8mg
CRF • Water to 20ml
• This ampoule is added to 1 liter of non-lactated Ringerʼs solution
at 40C and used.
163

Perioperative Myocardial Ischemia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Pathophysiology:
Triggering Stress of Surgery Stress of Surgery. Anesthesia, blood

Surgery & Anesthesia
Factors: Stress of Anesthesia. Stress of Anesthesia. loss & Anemia
• Intubation
• Extubation
• Hypothermia
• Anemia
• Increased blood loss
• Inadequate pain control
Increased Increased
State Inflammatory Hypoxic State
Hypercoagulability
Response
Increased Stress
Increase in ILF, TNF Increased platelet reactivity Increased Cortisol Decreased

Consequence
& creative proteins increased antithrombin 3 Increased catecholamines Oxygen supply
Increased Increased
Coronary Stress HR & BP Decreased
Oxygen Supply
Plaque Rupture Plaque Rupture
Myocardial Infraction
Coronary Artery Thrombosis
164
Perioperative Ischemia
Acute treatments for suspected intraoperative myocardial ischemia

Associated Hemodynamic Finding Therapy Dosage
I Hypertension, tachycardia + Deepen anesthesia Esmolol 2-100 mg, + 50-200

IV β - Blockade Metoprolol 0.5-2.5 mg
Labetalol 2.5 – 10mg
33-330 µg/min +
Ii Normotension, tachycardia + IV Nitroglycerin As above
Assure adequate anesthesia change
anesthetic regimen
IV β- Blockade
III Hypertension, normal heart rate Deepen anesthesia 0-20 mg
nicardipine Nicardipine 1-5 mg, + 1-10 µ
Phenylephrine 25-100 µg
IV. Hypotension, tachycardia + IV α-agonist Nor-epinephrine 2-4 µg
V Hypotension, bradycardia Lighten anesthesia 5-10 mg
IV Ephedrine 4-8 µg
IV Epinephrine 0.3-0.6 mg
IV Atropine As above
IV Nitroglycerin when normotensive
VI. Hypotension, normal heart rate IV α- Agonist As above
IV Epinephrine
alter anesthesia (eg, lighten)
VII. No abnormality IV Nitroglycerin As above
IV Nicardipine As above
165

166

with a second intravenous or subcutaneous
almost equal frequency in each of the three
antithrombotic
Diagrams & Flow agent before Coumadin is
Chart trimesters. In contrast, the incidence of PE is Dr Azam’s Notes in Anesthesiology 2013
discontinued or neutralized.
Table
Drug Site of Route Plasma Excretion Antidote Stop

Action half life Before
procedure
Heparin IIa / Xa IV /SC 1.5 hrs Hepatic Protamine 6 hrs
LMWH Xa SC 4.5 hrs Renal Protamine 12 – 24 hr

(Partial reversal)
Bivalirudin IIa IV 25 min Hepatic None 2- 3 hrs
Argatroban IIa IV 45 min Hepatic None 4 – 6 hrs
Warfarin Vit –k Oral 2 – 4 days Hepatic Vit – k, FFP 2 – 4 days
21
Hypokalemia
167

arterioles in some areas of skin and skeletal muscle are cholinergic. attacks.
Vascular smooth muscle also contains non-innervated cholinergic
Diagrams & Flow Chart
These subdivisions are summarized in Table 7.1.
Sympathetic Parasympathetic
Organ Receptor Effect Receptor Effect
subtype subtype
Heart Pi also P2, t Heart rate M2 J, Heart rate
? also a and f Force of contraction i Force of contraction
DA! t Conduction velocity Slight | conduction velocity
t Automaticity (P 2 )
f Excitability
t Force of contraction
Arteries Pi Coronary vasodilatation Ma Vasodilatation in skin, skeletal
P2 . Vasodilatation (skeletal muscle, pulmonary and
muscle) coronary circulations
Oil, Q-2 Vasoconstriction (coronary,
pulmonary, renal and
splanchnic circulations, skin
and skeletal muscle)
Splanchnic and renal
vasodilatation
Veins ai, also a2 Vasoconstriction
P2 Vasodilatation
Lung P2 Bronchodilatation MS Bronchoconstriction
Inhibition of secretions Stimulation of secretions
Bronchoconstrktion
GI tract 2, P2 Decreased motility M Increased motility
Relaxation of sphincters
Stimulation of secretions
Contraction of sphincters
Inhibition of secretions
Pancreas P2 Increased insulin release
«l,a 2 Decreased insulin release
Kidney P Renin secretion
Liver Glycogenolysis M Glycogen synthesis
P 2 '?ct Gluconeogenesis
Bladder Detrusor relaxation M Detrusor contraction
Sphincter contraction Sphincter relaxation
Uterus Myometrial contraction
P2 Myometrial relaxation
Adipocytes P3 Lipolysis
Eve <*1 Mydriasis (radial muscle M Miosis
contraction) Ciliary muscle contraction for
Ciliary muscle relaxation for near vision
far vision
Platelets Promote platelet aggregation
Sweat glands Mb Sweating
a
Muscarinic receptors are present on vascular smooth muscle, but they are independent of parasympathetic innervation and have little or no
physiological role in the control of vasomotor tone.
^Sympathetic cholinergic fibres supply sweat glands and arterioles in some sites. 168

169

170

171

172

173

174

175

176

177

178

179

180

181

182

183

184

185

186

187

188

189

190

191

192

193

194

195

196

197

198

199

200

201

202

203

204

205

206

207

208

209

210

211

212

213

214

Diagrams & Flow Charts Dr Azam’s Notes in Anesthesiology 2013
215

Diagrams & Flow Charts. Dr Azam’s Notes in Anesthesiology 2013
216

217

218

219

220

221

222

223

224

225

226

227

Diagram & Flow Charts Dr Azam’s Notes in Anesthesiology 2013
228

229

230

231

232

233

234

235

236

237

238

239

240

241

242

243

244

245

246

247

248

249

250

251

252

253

254

255

256

257

Comparative pharmacology of oral Anticoagulants:
Time to Duration after Maintenance

Initial Adult
peak effect discontinuatio adult dose
dose (mg)
(hrs) n (days) (mg)
1 Warfarin 36.72 2-5 15,1st day 10, 2.5-10
second 10,3rd
day
2 Dicumarol 36-48 2-6 200-300 1st 25-200
day
3 18-24 1-2 300, 1st day, 25-200
Phenindione 200 second
day
258

259

Diagram & Flow Charts
Anti-Hypertensive Therapy: In PIH
Drugs Daily Dose Adverse effects & comments
Methyldopa 500 - 3000 mg in safety of mother & fetus (after

( Centrally 2 - 4 divided the first trimester)
acting alpha doses Postural Hypotension,
agonist) drowsiness, fluid retention
Labetalol 200 - 2400 mg in Safety appears equal to

( Alpha & beta 2 - 3 divided methyldopa. Headache, dry
adrenergic doses mouth, tremors, heart block.
blocker) Avoid in bronchial asthma &
CCF
use with caution in Diabetes
Nifedipine 30 - 120 mg in 1 - May inhibit labour; may have

(calcium 4 divided doses synergistic action with MgSO4
channel depending on
blocker) preparation used.
Acute severe hypertension in Pregnancy
Hydralazine 5 - 10 mg IV, if no Tachycardia & increase C.O

onset 10 - 20 response repeat
min at 20 min interval.
Peak 60 min total of 30 mg
DOA - 4 - 6 hrs
Labetalol 10 - 20 mg IV Decreases SVR

Push every 10 - Avoid in Asthmas, CCF heart
20 min max - 300 blocks
mg
NTG 5 - 50 µg/min Increases ICP
260

261

262

263

264

265

266

267

268

269

Post-anesthesia Recovery Score Post-anesthesia Discharge Oxygen Saturation Surgical Bleeding

(Modified Aldrete Score) Scoring System
2 = SpO2 >92% on room air 2 = Minimal: no dressing change
Activity Vital signs (BP and Pulse) required
2 = Moves all extremities 2 = Within 20% of preoperative 1 = Supplemental O2 req. to 1 = Moderate: up to 2 dressing
voluntarily/on command 1 baseline maintain SpO2 >90% changes
= Moves two extremities 1 = 20%–40% of preoperative 0 = SpO2 <92% with O2 0 = Severe: more than 3 dressing
baseline supplementation changes
0 = Unable to move extremities 0 = >40% of preoperative 10 = Total score 10 = Maximum score
baseline
Score >9 required for discharge Score >9 required for discharge
Respiration Activity
2 = Breathes deeply and coughs 2 = Steady gait, no dizziness

freely
1 = Dyspneic, shallow or limited 1 = Requires assistance

breathing
0 = Apneic 0 = Unable to ambulate
Consciousness Pain
2 = Fully awake Acceptable to patient; control

with PO medications
1 = Arousable on calling 2=Yes
0 = Not responding 1 = No
270

Agent MAVC
Nitrous Oxide 105
Halothone 0.75
Isoflurane 1.2
Desflurane 6.0
Sevoflurane 2.0
Enflurane 1.7
271

Maximum Safe Dose (mg/kg)
• Bupivacaine! 2.0
• Levobupivacaine! 2.5-3.0
• Articaine! 7.0
• Lignocaine ! 4.0
with epinephrine! 7.0
• Mepivacaine! 7.0
• Prilocaine! 6.0
• Ropivacaine! 3.0-4.0
Table 3. Safe doses of common LAs
272

Changes in Anemia:
273

16. Halothane Hepatitis Dr Azam’s Notes in Anesthesiology 2013
• Halothane is known to be metabolized by the mixed function !"#$%$&'($)(*+%$"*+,-(.-/+"$"$0#1#"'2

oxidase system in the endoplasmic reticulum of the liver.
• Metabolized by two routes
! Halothane
• Oxidative
• Reductive
• Halothane hepatitis occurs about 2 to 5 days after
anesthesia Genetic and
Reductive Oxidative environment
• Fever, nausea, vomiting followed by jaundice
metabolism metabolism factors
!"#$%&'()*"+,-'.!!
• !"#$%&'()#%*&$"#'+
• Sensitization
Reactive
• Biotransformation of halothane to toxic intermediate
metabolites metabolite
• Sensitization to halothane or its metabolites, or to a new
antigen induced by the reaction of a halothane metabolite
with liver cell macromolecules. Bind to hepatocyte
macromolecules
/$%'-: two forms of liver damage:
• Type I (minor)
• Type II (major) Denaturation and Genetic
1. 012(&3&4',+$%5. A mild relatively common form in which factor
altered antigenicity
serum aminotransferases are raised during the first and
second post-op weeks after receiving halothane.
2. 012(&33&4'"#$%5. A rare form in which massive liver cell
necrosis occur leading to liver failure and even death. Direct Immune-mediated
hepatotoxicity hepatotoxicity
274

! 50
275

Sodium in TURP.
276

277

278

279

280

281

Flow Charts & Diagrams Dr Azam’s Notes in Anesthesiology 2013

For patient with good LV function Esmolol IV 0.5mg/kg over /min 1min 12-‐20min
↑ HR CI in bronchospastic disease 50-‐300µg/kg/min
Labetalol 5-‐20mg 1-‐2min 4-‐8hr

Propanol 1-‐3mg 1-‐2min 4-‐6hr
Ca+2 channel blockers Nicardipine 0.25-‐0.5mg 1-‐5min 3-‐4 hr
Myocardial ischemia ← reGlex Nifedipine (S/L) 10mg 5-‐10min 4h
tachycardia
Mod to severe HTN – most rapid Nitroprusside 0.5-‐10µg/kg/min 30-‐60 sec 1-‐5min
Nitroglycerine 0.5-‐10µg/kg/min 1min 3-‐5min
Sustained control of BP ← Hydralazine 5-‐20mg 5-‐20min 4-‐8hr
delayed onset reGlex tachycardia Phentolamine 1-‐mg 1-‐10min 20-‐40mm
Enalaprilat 0.625-‐1mg 6-‐14min 4-‐6h
ACE Inhibitors Fenoldopam 0.1-‐0.6 µg/kg/min 5 min 5 min
282

Rate
< 60 > 100

60 - 90
Bradycardia
Normal Tachycardia
Narrow Complex Broad Complex

Look at the relation • Atrial ectopics
between P-QRS • Ventricular
premature beat
Each P-wave No relation of P with QRS

followed by P marches through QRS
QRS Complex
CHB
Check PR interval Prolonged
Normal 0.12-0.16 up to 0.20 Sec

First degree AV Heart block
Mobitz type I Heart block
Mobitz type II block
Sinus Bradycardia
283

Tachycardia
Broad Complex
Narrow Complex
Regular Irregular Regular Irregular
• Ventricular tachycardia • Ventricular fibrillation

P(+) P(-) P(+) P(-) • SVT with aberrant
conduction
Sinus
Tachycardia
• (P)SVT • Atrial Flutter • Atrial Fibrillation
• AVNRT/AVRT • MAT
• AF with 2:1 block
284

It is defined as the obstruction to blood flow in aorta by
• Infrarenal! →! Majority of AAA are infrarenal aneurysms.
Flow Charts
application & Diagram.
of clamps (proximal and distal) for the purpose • Suprarenal! →!
Dr Azam’s
Indicated for juxtarenal or inflammatory aneurysms and
of facilitating repair of aorta ! ! ! aorto-iliac occlusive disease with proximal extension. !
• Supra-celiac →! Reconstruction of celiac trunk or mesenteric artery.
!"#$%&'(#)*+*!(',"-.
Aortic Cross-Clamping AoX
Passive ↑ Impedance to Aortic flow

recoil distal
to clamp • Systemic hemodynamic response
↑ catecholamines to aortic cross-clamping. Preload
(other vasoconstrictors) does not necessarily increase.
• If during infra renal AoX the blood
volume shifts into the splanchnic
vasculature, preload does not
increase.
Active ↑ arterial resistance

vasoconstriction
proximal & distal to
clamp
↑ After load
↑ Preload ↑ Coronary Blood Flow
↑ contractility
If Coronary flow & If coronary flow and

contractility increases ↑ CO ! contractility do not 5
increase
285

Flow Charts & Diagram. Dr Azam’s Notes in Anesthesiology 2013
AoX: Continuation Dr Azam’s Notes in Anesthesiology 2013

Aortic Cross-Clamping AoX
Passive ↑ catecholamines (other

recoil distal vasoconstrictors
to clamp
Active venoconstriction proximal

& distal to clamp
!!"#$%&'!()*)(+,-
Shift of blood volume proximally to clamp
↑ Lung blood volume

Inter cranial Shift of blood volume into splanchnic vasculature
blood volume
↑ Venous
↑ Blood volume &
return, preload
flow in muscle
proximal to clamp
!!Venous return,
↑Venous return, Preload (if Preload (if splanchnic
splanchnic venous tone is high) venous tone is low)
286

Aortic Unclamping: Continuation Dr Azam’s Notes in Anesthesiology 2013

AoX
Distal tissue Ischemia “Mediators”

release
Distal Vasodilation
↑ Permeability ( by end of clamping period)
↑ Venous capacitance !!arterial resistance
UNCLAMPING
Pulmonary Edema Systemic effects of UNCLAMPING

“Mediators”
!!"#$%&'()&*!
production
%$+,'&%,)*),#
& washout
↑ Pulmonary vascular resistance
Loss of
Distal shift of Central Hypovolemia intravascular
blood volume
fluid
!!-.+$/0!'.,/'+
!!%&'()&%!1/,2/,
Hypotension 7
287

elow Surgical Factors:
up to 7 to
Major Intermediate Minor
Emergency Surgery Carotid endarterectomy cataract
Major vessel/surgery Intrathoracic/Peritoneal Superficial surgery

surgery
Surgeries with major Head & Neck Surgery Breast surgery

blood loss or fluid shifts
Open prostatic surgery
Years
onal
ed HTN
83
288

Flow Charts Cardiac Reflex. Continuation:
& Diagram. Dr Azam’s
Dr Azam’s Notes
Notes in Anesthesiology2013
Reflex Stimuli Receptor Afferents Centre Efferents Response

Baroreceptor Reflex Increase BP Carotid Sinus & IX Nerve(carotid Nucleus of Tractus IML Tract Decrease in Blood
Aortic arch Sinus) & X Nerve Solitarius in pressure, Decreases
(Aortic Arch) Medulla Sympathetic stimulation,
Heart Rate & SV
Chemoreceptor pH pCO2 & pO2 Carotid & Aortic IX Nerve & X Nerve Chemosensitive X Nerve Bradycardia, Increase
Reflex body area of Medulla Blood pressure &
Hyperventilation
Bain Bridge Reflex Increase filling of Stretch receptor in X Nerve Dorsal motor Vagal & Increase in Heart Rate &
right atrium right atrial wall nucleus of vagus sympathetic Automaticity
fibres
Benzold Jarisch serotonin Pain receptor C X Nerve Respiratory & X Nerve Apnea, Hyperapnea &
reflex Fibre Vasomotor Centre bradycardia, Coronary
Vasodilation &
Hypotension.
Oculo-cardiac Pressure on the Stretch receptor Long & Short cillary Cillary ganglion & Vagal & Reflex Bradycardia
Reflex Eye, Traction on with in extraocular nerve & Opthalmic Gasserian ganglion Cardiodepre
the muscles muscles. division ssor fibre
Cardiac Reflexes:
82

289

Flow Charts & Diagrams. Aortic Unclamping: Continuation Dr Azam’s Notes in Anesthesiology 2013
AoX (Thoracic)
Indications of IABP Contraindications of
IABP
1. Cardiogenic shock 1. Aortic valvular
Myocardial infarction insufficiency
Myocarditis ↑ Aortic ↓ Aortic distal
Shift of
Cardiomyopathy proximal pressure
blood
Pharmacologic pressure (SNP -‐)
volume to
2. Failure to separate from CPB 2. Aortic disease (SNP-)
the brain
Aortic dissection
Aortic aneurysm
3. Stabilization of preoperative 3. Severe peripheral
patient vascular disease
Ventricular septal defect ICP (SNP +)
Mitral regurgitation
4. Stabilization of non-cardiac 4. Severe non-cardiac
surgical preoperative patient systemic disease
5. Procedural support during 5. Massive trauma ↓ Spinal cord
coronary angiography perfusion pressure
6. Bridge to transplantation 6. DNR patients & flow (SNP +)
Spinal cord perfusion pressure

during thoracic aortic occlusion, with
or without SNP
290

FlowBook
Charts
Text & Diagrams Pagina 2 di 8 Dr Azam’s Notes in Anesthesiology 2013
SLUDGE DUMBELS
Salivation Diarrhea
Lacrimation Urinary incontinence
Urinary incontinence Miosis, muscle fasciculations
Diarrhea Bronchorrhea, bronchospasm,
bradycardia
Gastrointestinal Emesis
distress
Emesis Lacrimation
Salivation
Figure 17-1 Schematic diagram showing the distribution of blood flow in the upright lung. In zone 1, alveolar pressure
(PA) exceeds pulmonary artery pressure (Ppa), and no flow occurs because the intra-alveolar vessels are collapsed by the
compressing alveolar pressure. In zone 2, Ppa exceeds PA, but PA exceeds pulmonary ECGvenouschanges
pressure (Ppv). Flow to
due in Hyperkalemia:
zone 2 is determined by the Ppa-PA difference (Ppa - PA) and has been likened to an upstream river waterfall over a dam.
Carbon monoxide Nicotine
Because Ppa increases down zone 2 whereas PA remains constant, perfusion pressure ECG changes
increases, that occur with a raised
and flow steadily K+ concentration are non-specific and
increases down the zone. In zone 3, Ppv exceeds PA, and flow is determined by the Ppa-Ppv difference (Ppa - Ppv),
200 times
which more
is constant affinity
down this portion of 15 to However,
the lung. 50 transmural pressure across may affect
the wall any
of the vessel part of the ECG
increases
down this zone, so the caliber of the vessels increases (resistance decreases), and therefore flow increases. Finally, in
forzone
HB4, pulmonary
than Ointerstitial
2 microgram / ml in
pressure becomes positive and exceeds both Ppv and PA. Consequently, flow in zone 4 is
determined by the Ppa-interstitial pressure difference (Ppa - PISF). (Redrawn with modification from West JB:
smokers
Ventilation/Blood Flow and Gas Exchange, 4th ed. Oxford, Blackwell Scientific, 1970.)
Carboxy Hb, Half life is ½ life of one
In this region, alveolar pressure (PA) then exceeds Ppa and pulmonary venous pressure (Ppv), which
6 hours cigarette
is very negative at this vertical height. Because isthe pressure outside the vessels is greater than the
pressure inside the vessels, the vessels in this region of the lung are collapsed, and no blood flow
30min. (nicotine)
occurs (zone 1, PA > Ppa > Ppv). Because there is no blood flow, no gas exchange is possible, and
ODC - Leftfunctions
the region Shift as alveolar dead
It stimulate
space, or "wasted" ventilation. Little or no zone 1 exists in the
lung under normal conditions,
Absolute decrease in O2 sympatho but
[2] the amount of zone 1 lung may be greatly increased if Ppa is
reduced, as in oligemic shock, or if PA is increased, as in the application of excessively large tidal
content adrenal axis.
volumes or levels of positive end-expiratory pressure (PEEP) during positive-pressure ventilation.
Effects of smoking:
Further down the lung, absolute Ppa becomes positive, and blood flow begins when Ppa exceeds PA
(zone 2, Ppa > PA > Ppv). At this vertical level in the lung, PA exceeds Ppv, and blood flow is
determined by the mean Ppa - PA difference rather than by the more conventional Ppa - Ppv
difference (see later).[3] The zone 2 blood flow-alveolar pressure relationship has the same physical 291
characteristics as a waterfall flowing over a dam. The height of the upstream river (before reaching
the dam) is equivalent to Ppa, and the height of the dam is equivalent to PA. The rate of water flow
Dr Azam’s Notes
over the dam isin Anesthesiology
proportional 2013 between the height of the upstream river and the
to only the difference
dam (Ppa - PA), and it does not matter how far below the dam the downstream riverbed (Ppv) is. This
Magnesium Therapy:
THROMBO ELASTOGRAPHY: Continuation: MgSO4 Loading Dose Maintainance
Regimens
• Zuspan 4 gm over 5 - 10 1 - 2 gm/hr IV

Regimens: min IV
Pritchard 4 gm over 3- 5 5 gm IM every

min IV, 10 gm 4th hour in
IM alternate buttock
Sibai 6 gm over 20 2 gm/hr IV

min IV
Effects of Increasing MgSO4 levels:
Plasma Effects
Normal Hemophilic Thrombocytopenia Fibrinolysis Hypercoagulability Mg
1) Prolonged R 1) Prolonged R 1) ↓ MA 1) Shortened R (mEq/lit)
2) ↓α0 2) ↓α0 2) ↓α0 2) ↑ MA
3) ↓ MA 3) ↓ MA 3) ↓ F 4) Prolonged F 1.5 - 2 Normal plasma level
4 - 8.0 Therapeutic range
5 - 10 ECG changes, (P-Q interval prolonged,

Relationship between BIS & patients Anesthetic status: QRS Complex widens)
BIS Value Patients Status EEG 10 Loss of deep tendon reflex
100 Awake & alert High frequency activity 15 Sinoatrial & atrioventricular block
60 Moderate hypnotic levels Low frequency activity 15 Respiratory arrest
40 Deep Hypnotic level Burst suppression begins 25 Cardiac arrest

delta activity
0 Profound anesthetic state Isoelectric EEG

292

N2O TOXICITY
oxidizes cobalt atom of Vit B12
Deoxythymidine
Homocystine
Decreases Vit B12 availability
Methionine
Synthetase
Methionine Thymidine
Decreases
DNA synthesis
Hematology
Spontaneous Abortion
Congenital Anomalies
• Pernicious anemia
• megaloblastic anemia
(N2O exposer for 24 hrs)
• Splenomegaly
• Agranulocytosis ( N2O Decreases Myeline synthesis
exposer for 4 days)
• Neuropathy - Polyneuropathy
• Subacute spinal cord degeneration - 1.5% of N2O 15 days
• Dementia
• Ataxia
293

N2O Impurities
NH4NO3 -------> 2H2O + N2O
83% at 240 C aqueous solution
If heated further
Nitrogen dioxide (N2O) N2O Nitric Oxide NO
Washed with caustic soda & water Collected in cylinder, French blue cylinder,
To get rid of impurities Pin index: 3,5; 900L
NO2 & NO N2O
C/F:
• Cyanosis (methaemoglobin)
• Respiratory failure / difficulty
• Circulatory arrest
294

Pathophysiology of DIC:
Stimulus
Tissue destruction Endothelial Injury
Tissue factor
Factor XII activation (Intrinsic pathway)
Extrinsic pathway
Thrombin generation
Platelet consumption
Intravascular fibrin deposition
Plasminogen activation
Thrombocytopenia
Thrombosis Clotting factor Bleeding

Plasmin generation
degradation
RBCʼs Tissue Ischemia Fibrinolysis Decreased

Damaged
circulating Decrease O2
blood transport
Fibrin degradation products (inhibit

thrombin & platelet aggregation)
Hemolytic anemia Tissue Hypoxia
ORGAN FAILURE
295

296

Meth-Hemoglobin Concentration % Clinical sign & symptoms
10 to 20 % central cyanosis of trunk & limbs usually

asymptomatic
20 to 45% CNS depression ( headache,

dizziness,fatigue,lethargy, syncope)
45 - 55% Coma, arrhythmia, shock & convulsions
> 70% High risk of Death
297

Flow
S736
Charts
Circulation
& November
Diagrams 2, 2010
!"#$%&'()*+,-&)-$.&),-',/'+0,%)(,1#20 I !"#$%&'()*+,-&)-$.&),-',/'.*%)#)-
32",$-('2//2+&4
5)1-)/)+.-&06')-+#2.*2(')-/0.77.&,#6'%#,&8#,7",&)+'*&.&2
5)1-/)+.-&06')-+#2.*2('%0.&202&'.(82*),-'.-('.11#21.&),-
9:+2**);2'&8#,7",:.-2'!<'.+&);)&6
I
!"#$%&'()%*+,#-,*+%.*
/*&#,'0,1)2#.+3#.45.+%&)'*1)%*6('44'+.#7)0+'+,
=-+#2.*2('+6&,>)-2*?'-2$#,2-(,+#)-2?')-/0.77.&,#6'72().&,#'#202.*2
=-+#2.*2('%0.&202&'.(82*);2-2**'.-('%2#*)*&2-&06'8)18'%0.&202&'+,$-&*
=-+#2.*2('#202.*2',/'%#,+,.1$0.-&'/.+&,#*
@2+#2.*2(A=7%.)#2('/)"#)-,06*)*
B#,&8#,7",&)+AC8#,7",&)+'*&.&2'D)&8')-+,7%02&206'2-(,&820).0)E2('*&2-&F*G
5&2-&'&8#,7",*)*
H6,+.#().0')-/.#+&),-
Figure 1. ACLS Cardiac Arrest Algorithm.
In addition to high-quality CPR, the only rhythm-specific ventions during cardiac arrest may be associated with an
therapy proven to increase survival to hospital discharge is increased rate of ROSC but have not yet been proven to
defibrillation of VF/pulseless VT. Therefore, this intervention increase survival to hospital discharge. Therefore, they are
is included as an integral part of the CPR cycle when the recommended as considerations and should be performed @2.&8
rhythm check reveals VF/pulseless VT. Other ACLS inter- without compromising quality of CPR or timely defibril-
Downloaded from circ.ahajournals.org at VA MED CTR BOISE on October 20, 2010 !"#$%$&'"(#)(*&+,&-./&0(-.+0.12"+3+#1&+,&(45-/&0/)"+0/)(-"6/&2-/7-&-.)+*8+2"2
298

Flow Charts & Diagrams. coronary artery stents. Dr Azam’s Notes in Anesthesiology 2013
Coronary Stents:
Stent thrombosis is classified into:

Bare Metal Stents (BMS) Drug Eluting Stents ( DES) • Acute (with in 24 hours)
• Sub acute ( 24 - 30 days)
• BMS implantation effectively • DES release drugs that inhibit • Late ( 30 - 1 year)
eliminates acute vessel closure. neointimal hyperplasia. • Very late (> 1 year)
• Stent thrombosis rates are • Re-stenosis rates are very low.
reduced by dual antiplatelet • Reason for DES thrombosis is -
therapy with clopidogrel & incomplete endothelialization of the
aspirin. stent.
• Re-stenosis still remains high Factors which increases risk of
( 20 to 25% within 6 months) re-
thrombosis after DES are:
stenosis occurs as a result of
• ACS
neointimal hyperplasia.
• DM
• Renal impairment
Therapy:
• Advanced age
• Patients on BMS insertion dual
• Ejection fraction less that 30 %
antiplatelet should be continued
• Premature discontinuation of
for atleast 4 - 6 weeks with life
antiplatelet
long aspirin.
• Resistance to antiplatelet therapy
Therapy:
• After DES implantation 12 months
dual antiplatelet therapy with
clopidogrel & aspirin and life long
aspirin therapy
299

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!"#$%&'%()*"+",(*$-%./01$02
;%4%56.%('*$0%789%"#,:()*(*"&) 3%4%56.%('*$0%789%"#,:()*(*"&)
<:$+*"=$ >01$)* B&)*")/$%(.,"0")%*@0&/1@&/*%./01$02%

"'%(*%(::%,&.."A:$
?&.*,&)$%./01$02%/)*":% B()%+:&,"-&10$:%()-%(.,"0")%A$%
789%@(.%A$$)% +&)*")/$-%")%*@$%,$0"&,$0(*"=$%
"#,:()*$-%4%5$$6. ,$0"&-C
D$. E& B&)."-$0%A0"-1")1%*@$0(,2
?0&+$$- B()%(.,"0")%A$%
+&)*")/$-C
D$. E& B&)."-$0%A0"-1")1%*@$0(,2
?0&+$$-
300

!"#$%$&'(#)*"+,-&.)*&/0*")/0*1+"20&-131#0-03+&).&/1+"03+4&5"+,&6*7#&0(7+"3#&4+03+4
Discuss the management of Intracrainal HTN or Raised Intra cranial pressure. Continuation: Dr Azam’s Notes in Anesthesiology 2013
d. Neurogenic control:
Causes of
• CBF increases increases with parasympathetic & decreases with sympathetic
raised ICP:
stimulation. HTN
Encephalopathy
Stroke
e. Other factors: Tumor
Infection
• Head down posture - increases CBF
• Hypothermia - decreases CBF decreases cerebral metabolism Metabolic
Encephalopathy Osmolar
Pathophysiology of raised ICP: Disturbance
• Normally, translocation of CSF from intracranial to extracranial Increased
storage sites & hence, into venous blood forms the Complications
of Dialysis ICP Head Injury
mechanism for accommodating increased intracranial volume
- The Munroe - Kelly doctrine.
Post Ischemic
Benign Hypoxia
Methods of reducing ICP:
Intracrainal
1. Diuretics & fluid restriction
HTN Hydrocephalus
• Normovolaemic dehydration can be achieved
with loop diuretic combined with a colloid, this Acute on
would help to reduce the brain water content, Chronic Lung
without causing hypovolaemia Disease
2. Corticosteriods
• ICP due to tumor, abscess & hematoma Principles of Anesthetic management:
3. Hyperventilation 1. Clear airway
4. Reducing of cerebral venous pressure 2. Controlled Ventilation
5. Drugs that increases the cerebrovascular Methods of ICP
3. Adequate oxygenation
resistance Measurement:
4. Production of Hypocarbia
• Thiopentone & Lignocaine • Intraventricular catheter 5. Avoidance of Blood pressure swings
6. Hypothermia • Extradural transducer 6. Avoidance of coughing & straining
7. Reduction of CSF volume • Subdural Bolt 7. Head up
8. Surgical decompression 8. Avoid inadvertent PEEP
9. Use of special methods to reduce ICP
10. Precise management of fluid balance
! 42
!"#"$%&%#'()*(+'%#'(',-)&.)+/+!"
0,%#(+'%#'(',-)&.)+/+()112-+3(/'("12'%45(&"#/*%+'+("+("(678!9()-("(+2::%#(&"4/$#"#'(:5+-,5',&/"3("#:( 301
&2+'(.%('-%"'%:(;/',(/&&%:/"'%(-%<%-*2+/)#(')("=)/:("('-"#+&2-"4(!9(:2%(')(',%(".-2<'(/#'%--2<'/)#()*(
1)-)#"-5(.4)):(*4);(/#("(&5)1"-:/"4(-%$/)#(',"'(/+(#%/',%-(1)44"'%-"4/>%:(#)-(<-%1)#:/'/)#%:(.5(-%12--%#'(
e458 Circulation October 23, 2007 Dr Azam’s Notes in Anesthesiology 2013
Flow Charts & Diagrams
Previous PCI
Balloon Bare-metal Drug-eluting

angioplasty stent stent
<365 days
>365 days
>30-45 days <30-45 days
Time since PCI <14 days >14 days
Delay for elective or Proceed to the Delay for elective or Proceed to the
nonurgent surgery operation room nonurgent surgery operating room
with aspirin with aspirin
!"#$%&'"&($')'*+(,%&-%(
./&*+(,%&-%(
Figure 2. Proposed approach to the management of patients with previous percutaneous coronary intervention (PCI) who require non-
./0%&1'2'*+(0%&",%*+(,%&-%(
cardiac surgery, based on expert opinion.
3%%0(0%&",%*+(,%&-%(
which( is based on expert opinion. Given the reports of late therapy is effective in preventing late thrombosis of the
DES thrombosis and the current recommendations discussed irradiated coronary segment, in 1 study reducing the late
Schematically Drawn Division of the Sciatic Nerve
above, clinicians should remain vigilant even beyond 365 thrombosis rate to 2.5% with 6 months of therapy versus
days after DES placement. The times of 14, 30 to 45, and 365 9.6% with 1 month of dual-antiplatelet therapy. Additional
days for balloon angioplasty, bare-metal stents, andSciatic DES,Nerve benefit was demonstrated with 12 months of dual-antiplatelet
respectively, recommended in Figure 2 are somewhat arbi- therapy (late thrombosis rate of 3.3%).353,354 It is unclear
trary because of a lack of high-quality evidence. when, if ever, antiplatelet therapy can be safely discontinued
Consideration should be given to continuing dual- in these patients.
antiplatelet therapy in the perioperative period for any patient Given the considerations above, antiplatelet therapy should
needing noncardiac surgery that
Common Peroneal falls within the time frame be continued as per the ACC/AHA/SCAI 2005 Guideline
Tibial Nerve
that requires dual-antiplatelet therapy, particularly those who
Nerve Update for Percutaneous Coronary Intervention, with a class
have received DES. In addition, consideration should be IIa recommendation: “It is reasonable that patients undergo-
given to continuing dual-antiplatelet therapy perioperatively ing brachytherapy be given daily chronic clopidogrel 75 mg
beyond the recommended
Superficial Peroneal time frame in any patient at high indefinitely and daily chronic aspirin 75 mg to 325 mg
risk for the Nerve
consequences of stent thrombosis, such as patients Posterior Tibialunless
indefinitely Nerve there is significant risk for bleeding. (Level
in whom previous stent thrombosis has occurred, after left of Evidence: C).”307 Therefore, serious consideration should
main stenting, after multivessel stenting, and after stent be given to continuing dual-antiplatelet therapy in the peri-
placement in the only remaining coronary artery or graft
Deep Peroneal operative period for any patient who has received brachyther-
Nerve Sural Nerve
conduit. Even after thienopyridines have been discontinued, apy for restenosis or in-stent restenosis, particularly those in
302
serious consideration should be given to continuation of whom additional stents (bare-metal or drug-eluting) were
aspirin45%(#2'*$'2(,%&-%(6'-'6%#7(1"&8',9($:"()&*,25%#;(2"88",(0%&",%*+(*,6($')'*+(,%&-%<((45%(2"88",(
antiplatelet therapy perioperatively in any patient with placed at the time of or subsequent to the administration of
Dr Azam’s
previous Notes in of
placement Anesthesiology
a DES. The risk 2013
of stopping antiplate- brachytherapy. The risk of stopping antiplatelet therapy
0%&",%*+(,%&-%(6%#2%,6#(+*$%&*++=(*&"/,6($5%(1')/+*&(5%*67(6'-'6',9(',$"(#/0%&1'2'*+(*,6(6%%0(0%&",%*+(
let therapy should be weighed against the benefit of reduction should be weighed against the benefit of reduction in bleed-
Classification of Inotropes:
Calcium
Sympathomimetics Digitalis Glycoside
Phosphodiesterase inhibitors
• Digoxin • Calcium Chloride
• Amrinone
• Milrinone
Synthetic Natural occurring • Aminophylline
Directly • Nor-adrenaline
Acting • Adrenaline
• Dopamine
• Isoprenaline - β1 and β2
• Dobutamine
• Phenylepherine • Levosimendan (it increases the
sensitivity of the heart to
calcium, thus increasing cardiac
contractility without a rise in
Indirectly intracellular calcium.)
Acting • L-name:
• Ephedrine
• Mephentermine
303

Dopamine Isoprenaline Dobutamine
1) Naturally occurring Synthetic Synthetic derivative of

Catecholamine isoprenaline
2) Site of action -‐ α1, β1 and Only β1 β2 stimulant β1 β2 , α1 (β1 >> β2)
dopaminergic (DA1 DA2) (β1 > β2)
receptors (D>B>α)
3) CVS effects: can cause CVS effects: CVS effects
both relaxation and Stimulates β1 receptors increasing Stimulates β1 à ↑
constriction of vascular H.R, automaticity and contractility myocardial
smooth muscle à ↑ SBP contractility without
Dose dependent Stimulates also β2 receptors hence effect on PVR and H.R.
Causes vasodilatation in vasodilation in skeletal muscle (↓ i.e. inotropic >
renal, mesenteric and PVR), also renal and mesenteric chronotrophic
coronaries vasodilatation à ↓ DBP. β2 and receptors are
Increases contractility SV, Therefore ↓ MAP. Hence (was) used only slightly stimulated
CO (inotropic) hence mild
in complete heart block; cardiac
In high doses stimulates α
failure with valvular disease who vasodilatation effect
à increase PVR à ↓ RBF beneìt with ↑ HR and ↓ venous
(hence raises BP) capacitance ìlling
4) Renal effects RS effects: Renal effects
Improves blood `low to β2 stimulation Does not stimulate
renals by vasodialator Marked bronchodilation renal dopaminergic
effects on kidneys and receptors. Hence no
hence increases RBF, GFR renal vasodilation
and increases Na excretion.
304


B) 2-‐10µg/kg/ml cause β1 Hence useful in bronchial asthma Unlike dopamine it does
stimulation à ↑ cardiac and drug induced not release endogenous
contractility and C.O. i.e. at bronchoconstriction (aerosol form) NE.
doses > 5µg/kg/ml bronchoconstriction due to
stimulates ↑ release of pulmonary embolism
endogenous NE.
C) 10-‐20 µg/kg/ml α and
β1 stimulated, but α
vasoconstriction effect
predominates (renal
perfusion may be lost)
Dosage Dosage Dosage
short-‐half life hence no Infusion 2-‐10 µg/kg/ml
loading dose only infusion µg/kg/ml
Renal dose à 2-‐5µg/kg/ml (1mg in 250ml of `luid gives soln of
Cardiac à 5-‐10 µg/kg/ml 4µg/ml)
Vasopressor à 10-‐20 µg/
kg/ml
Uses Uses Uses
1) Initial agent in 1) To treatment bradycardia or 1) Treatment in low
treatment of shock heart block resistant to atropine cardiac output failure
particularly in
vasodialated state like
septic shock and
hypovolema
2) To protect kidney and 2) To treatment cardiac failures 2) Hypotension 2 to ↓
aid diuresis in oliguric especially with valvular heart M.contractility
patients (renal transplant) disease
305

3) In refractive cardiac 3) To treatment 3) Emergenccy from CP
failure bronchoconstriction -‐ replaced now bypass
by other newer drugs 4) SVR is little effected
and ìlling pressures
Dopamine +
Dobutamine is used to
limit increase in LV
ìlling pressure induced
by dopamine alone.
Side effects Side effects Side effects
Before administration Tachycardia Nausea, headache,
ensure patients has Ventricular arrhythmia angina, palpitation,
adequate B.P and Hypotension arrhythmia, dyspnoea
treatment hypovolemia Isoprenaline used in aerosols to Tachycardia and
Nausea, vomiting, Tachy, treatment B. asthma caused V.dysrythmia are less
arrhythmia, dyspnoea, increased mortality due to common than
angina, headache, 1) ↑ stimulation of β1 race à popamine
vasoconstriction à ↑ SBP V.arrth
Extravasation causes 2) Hypoxia due to V/Q mismatch
sloughing and necrosis in inspite of bronchodilation
tissues, so better given via 3) Toxicity of `luorinated hypo
central line. carbons used in propellants
Contraindication:
Phaeochromocytoma
Arrhythmias
306
Halothane Hepatitis. Continuation:
!"#$%&'("))*#$+,-(."/%$.",*(.*0"$%$%1+#+$23 Pathway for halothane biotransformation:
! H/o allergy Immune ! Halothane

eczema mediated
Reduced hepatic Female sex
perfusion
ss the pathophysiology of hepatorenal Syndrome. What are the measures to prevent it?
Hypoxia Oxidative Reductive 2-bromo-2 chloro 11
Age ! ! difluroethyleenes
Halothane Type 3 hepatorenal syndrome: !
hepatotoxicity
istinct form of acute or subacute renal failure characterized by severe • Coexistent kidney disease and hepatorenal
Pharmacogenetics 1) Trifluroacetic
syndromeacidPatients 1)
with2-chloro-111
Glutathione
constriction, which develops in decompensated cirrhosis or ALF. advanced liver disease frequently have coexistent
2) Bromide ion intrinsic renal trifluroethane
Enzyme dysfunction. 3) Chloride ion 2) 2-chloro-1,1
induction
tion of the hepatorenal syndrome: Multiple
Type exposuresyndrome:
4 hepatorenal to Acute liver failure 1) N-acetyl cysteine
4) Trifluroacetic acid difluroethylene
cirrhosis with rapidly progressive acute renal failure • Morehalothane
than half of patients with ALF develop HRS, although the frequency conjugate
Obesity
cirrhosis with subacute renal failure varies depending on the ALF etiology ethanolamide 3) Bromide ion
cirrhosis with types 1 or 2 HRS superimposed on chronic kidney Preexisting conjugate 4) Fluoride ion
or acute renal injury Minor diagnostic criteria for hepatorenal syndrome
Halothane metabolism hepatic disease
ulminant liver failure with HRSb • Urine volume < 500 mL/24 h
(oxidative or reductive) • Urine sodium <10 mEq/L
gnostic criteria for hepatorenal syndrome • Urine osmolality greater than plasma osmolality
c or acute liver disease with advanced hepatic failure and portal • Urine red blood cells < 50 per high power field Serum
ension • sodium <130 mEq/L
creatinine >1.5 mg/dL, reflecting decreased glomerular infiltration rate
ce of shock, bacterial infection, and current or recent treatment with Pathophysiology of Hepatorenal Syndrome:
toxic drugs; absence of gastrointestinal or renal fluid losses THE HEPATORENAL SYNDROME 819
tained improvement in renal function (decrease in serum creatinine to
mg/dL) after diuretic withdrawal and plasma volume expansion with Progression of liver failure
Central
and portal hypertension
nous albumin (1 g/kg body weight up to a maximum of 100 g) hypovolemia
uria < 500 mg/dL and no evidence of parenchymal renal disease by
sis, or of obstructive uropathy by ultrasonography Increase in arterial Decrease in
vasodilation cardiac output
atorenal syndrome: Reduction in effective Impaired cardiac

HRS the serum creatinine level doubles to greater than 2.5 mg/ dL within 2 weeks. arterial blood volume chronotropic function
atures of type 1 HRS are its rapid progression and high mortality, with a median
only 1 to 2 weeks.
moderate severe extreme
precipitating events in type 1 HRS include bacterial infections, particularly
us bacterial peritonitis; variceal hemorrhage; major surgery; and acute alcoholic Sodium Water retention Hepatorenal
retention Hyponatremia syndrome
51
atorenal syndrome: Fig. 2. Pathophysiology of the hepatorenal syndrome. (From Arroyo V, Terra C, Ginès P. New
HRS, the serum creatinine increases slowly and gradually during several weeks or treatments of hepatorenal syndrome. Semin Liver Dis 2006;26:254–64; with permission.)
th a reciprocal gradual reduction in glomerular infiltration rate (GFR). ! 307
ally occurs without a precipitating factor.
nervous system and stimulation Dr Azam’s hormone
n survival ofDr Azam’s
type 2 HRS is Notes in Anesthesiology
about 6 months, 2013
significantly longer than for type 1 52
of antidiuretic release become
necessary to maintain arterial blood pressure. As the liver disease worsens
Flow Chartsstrategies
& Diagrams Dr Azam’s Notes in Anesthesiology 2013 Dr Azam’s Notes in Anesthesiology 2013
Write the blood conservative in a 20 year
23. Describe oldthe
with female
helpscheduled fordiagram,
of labeled excision of
theangiofibroma
anatomy of lumbar plexus and describe the Dr Azam’s Notes in Anesthesiology 2013
of nose? Continuation: techniques of lumbar plexus block.
ANATOMY: Use of Blood Substitutes: Two types

• The lumbarofplexus is formedare
blood substitutes from the ventral rami of L1–L4 with variable
available:
contributions from T12 and L5.
• The peripheral branches of the lumbar plexus include the iliohypogastric,
ilioinguinal, genitofemoral, lateral femoral cutaneous, femoral, and obturator
Perflurocarbons: nerves. Hb based o2 carriers:
• They are biologically inert volatile fluids • These are based on natural or
• The plexus forms within the body of the psoas
with high dissolving capacity for o2 & CO2
muscle, and the lumbar plexus
recombinant human Hb or bovine Hb
measure was •first presented by
blockDr. Philip
consistently
They transport & deliver O2 by simple D Wood
blocks the three nerves that supply the lower extremity
• produced by purification, encapsulation in
oduced in 1952.physical dissolution(femoral, lateral femoral cutaneous, and obturator nerve.
synthetic phospholid.
Not water soluble
lity of errors in• attaching the gas cylinders to gas • Side effect:
• their O2 carryingPROCEDURE:
capacity depends on athe
Using nerve stimulator • Increased Blood pressure due to
nnections. Its one of the safety system. which
concentration of perflurocarbons increased systemic vasoconstriction
Landmarks.
varies between products. due to scavenging of nitric oxide &
• H+ atoms are The patient
•replaced by is placed in the lateral decubitus position
fluorines with
oxidation thegenerated
which operativeMeth sideHb.up.
m:
• A line is drawn
• One unit of perflurocarbons carry from
3 the top of the posterior• Short
iliac crest down to
intravascular midline.
half life Known as
l cylinders ( used in machines).
times O2 carried by“intercristal
the similar volume of this line is positioned• over
line,” hencetheused
L4 intransverse
emergencyprocess
situation.in most
jecting from the yoke
bloodassembly of gas apparatus and
adults.
tching holes in theFluosol
• body - DA : 20
of the % emulsion of 2
cylinder valve
• The intersection
different compounds. Dose = 20ml/kgof the intercristal line with a line drawn parallel to the spine from
is only one combination of pin &
• Polyfluro-octobromide:holes.
O2 solubility
theDescribe
posterior with is
superior
the iliac
helpspine determines
of labeled the initial
diagram, needle insertion
the anatomy of lumbar point and isand describe the techniques of
plexus Dr Azam’s Notes in Anesthesiolo
ons on the yoke & 7more hole on the gas cylinders.
5 cmlumbar
lateralplexus block.in
from midline Continuation:
most patients.
der of one type to be attached to
Needles a yoke pin indexed for 14 LUMBAR PLEXUS BLOCK
12
• 21-gauge, • The10-cmplexus insulated
should be needle for the majority
stimulated at a depth ofofpatients.
no more 15-cm
than
PROCEDURE needles
2 cm may
be neededbeyond for obese
!"#$%#&'($)*+"#&',-
thepatients.
transverse process.
n cylinder: 28. Fasting guidelines for•neonates
18-gauge, & infants
10-cm insulated Tuohycurrent
needleto
Landmarks.
for0.5
catheter • .$/$0$$1$$$234*+'#'
TheDr patient is placed
Azam’s Notes in the lateral
to
• Decrease the stimulator mA. If placement.
the twitch Catheters
remains evidentside up. A tr
e centre of the outlet valve ofintroduced cylinder at
5 cm an angle of 30°
decubitus .$/$5$$1$$$6"3,78'#
position with the
•anesthetic can proceed. operative
with thebeyond
decreasedneedle tip. injectionline
current, of local
is drawn from the top of the posterior iliac crest pl
e passed through positionStimulation.
Age
number Local1.Anesthetic.
Milk & Solids Liquid • .$/$9$$1$$$:",
down to midline. Known as the “intercristal line,” QH
.$/$;$$1$$$<=$>$)<=$?)<=$@$AB9CD
is• look
ons are located at interval•of
< 6 months
Set12°. 4 hours
the• nerve
In most stimulator
adults, 30
2 hours
initially
to 40 mL at 1.0 to 1.2anesthetic
of local mA,line
this and for a quadriceps
positioned
is sufficient over the L4the
to block muscle
transverse process
twitch (femoral nerve) in most • =$/$5$$1$$$<=$>$E'$?E'$F$GHB9CD
adults. The intersection
as evidence of needle proximity to the lumbar plexus (this of the intercristal Lo
the circumference of a circle
6 - 36 months
of 9/16 6 hours
plexus. inch of radius 3 hours
!
twitch is8usually encountered3 at line with
a depth of 5 to 8 cm from •
a =$/$9$$1$$$<=
line drawn
the skin).parallel to the 56
spine from OR
ve. > 36 months hours hours
Dr Azam’s Notes in Anesthesiology 2013 • Insert the needle with a slight medial angulation to the
the posterior• =$/$;$$1$$$<=$>$)<=$?)<=$FAB9CD
superior iliac spine determines
sagittal plane of the patient.
the
initial needle insertion point and is 5 cm lateral from
• Make small adjustments of the needle tip caudad and 0$/$9$$1$$$6=<
• most
ns in yoke to fit corresponding
guidelines in neonatesholes of cylinder
midline in cephalad if initial
patients (Figurepasses
14-4).fail
Fasting
to contact os. Once
• Breast milk may be given until 4 h preoperatively. bone is contacted (usually the • 0$/$;$$1$$$)*I+7J,7JK#'
transverse process of L4), bring
• Dextrose solutions may bethe
givenneedle back towards the skin, redirecting
until 2 h preoperatively.
! Needles • 5$/$;$$1$$$<=$>$E'$?E'$@$GHB9CD
it caudally to “walk off” the process. 62
eter & 6 mm long except
• Formula for
milk feeds maypin 7 until
be given - which is slightly
6 h preoperatively. These milks contain cow protein and
• $$$A$$$$1$$2#37#7(
are more slowly digested than breast milk.
JDXJHFPLQVXODWHGQHHGOHIRUWKHPDMRULW\
• Babies having continuous feed via jejunal catheters should have these stopped 4 h preoperatively.
Dr Azam’s Notes in Anesthesiology 2013 Figure 14-4. Lumbar plexus block landmarks
s also used when the cylinders are being refilled. This of patients. 15-cm needles may be needed for
rom being filled into the cylinder. obese patients.
JDXJHFPLQVXODWHG7XRK\QHHGOHIRU
catheter placement. Catheters introduced 5 cm
tem one can attache wrong
Clear fluids may cylinder
be taken up to 2 h before if
the the pins
induction on the
of anesthesia.
beyond needle tip. 308
The mandatory fasting period after solid foods should be 6 h.
washers Dror also called

Breast
Azam’s Bodacek
milk can be
Notes
taken up to 4 h seal on the port
before anesthesia.
in Anesthesiology 2013 the pin Stimulation. Set the nerve stimulator initially at 1.0
Oral premedication can be taken with 150 mL of water in adults up to 1 h before anesthesia.
llified and the wrong cylinder will be placed. to 1.2 mA, and look for a quadriceps muscle twitch
Diabetic Ketoacidosis: Continuation Consensus Guidelines
I. Dehydration: Fluids
Pathophysiology of Diabetic Ketoacidosis
(DKA) Management:
Absolute insulin deficiency
or
Determine dehydration status
Stress, infection or insufficient insulin intake
Counter-regulatory hormones
Glucagon Cortisol
Catecholamines Growth Hormone
Lipolysis Glucose utilization Proteolysis Glycogenolysis Severe Mild Cardiogenic

Protein synthesis Hypovolemia dehydration Shock
Gluconeogenic substrates
++
FFA to liver Gluconeogenesis
Ketogenesis Hyperglycemia
Administer 0.9%
Alkali reserve Glucosuria (osmotic diuresis) NaCl (1.0L/hr) Hemodynamic
monitoring &
Acidosis Loss of water and electrolytes
Decreased fluid intake pressors
Lactate Dehydration Hyperosmolarity
Evaluate corrected serum sodium
Impaired renal function
of diabetic ketoacidosis. Copyright # 2006 American Diabetes Association. From Diabetes Care, Vol. 29, 2006;
ith permission from The American Diabetes Association.
Check electrolytes, BUN, venous pH, Serum Serum
Serum Na Normal
ar creatinine
filtration.& glucose
At presentation, the
every 2 - 4 hrly ¤ Increased leukocyte count with left
Nashift
high Na Low
until stable.After resolution of
ic deficits in an individual patient DKA & ¤ Non-specific elevation of serum amylase
ponwhen thepatient is ableand
duration to eat, Initiate SC
severity of ¤ Fever only when infection is present
multi-dose insulin regimen. continue IV
to infusion
which for the1-2
patient
hrs afterwas able to
SC insulin to When Serum glucose reaches
f fluid
ensureand electrolytes,
adequate and levels.
plasma insulin the 200 mg/dl, change to 5 % 0.45% NaCl (250-500 ml/hr) 0.9% NaCl (250-500 ml/hr)
Lookconsumed
fluids for precipitating cause.
before coming to Definition of DKA
Dextrose with 0.45% NaCl at depending on hydration state depending on hydration state
150 - 250 ml/hr
Consumption of fluids with a high- The biochemical criteria for the diagnosis of DKA
nt (juices or sugar containing soft are (4): 309
the hyperglycemia (3).
¤ Hyperglycemia (blood glucose . 11 mmol/L [!200
Diabetic Ketoacidosis: Continuation Dr Azam’s Notes in Anesthesiology 2013
II.Lack of Insulin - Insulin III. Electrolytes - Potassium
Establish adequate renal function

& urine output ( at least 50ml/hr)
Uncomplicated
IV Route
DKA - SC route
If serum K+ is < 3.3 mEq/L, hold insulin

Insulin: Regular Rapid-acting Insulin: & give 40 mEq, K+ per hour (2/3 KCL &
0.1 U/Kg B.wt as 0.3 U/Kg then 0.2 U/Kg 1/3 KPO4) until K > 3.3 mEq/L
IV bolus one hr later
0.1U/kg/hr Rapid-acting If serum K+ > 5.5 mEq/L, but check K+

continuous Insulin: 0.2 U/kg every 2 hour.
insulin infusion every 2 hours
If serum K+ > 3.3 but < 5.5 mEq/L,

give 20 - 30 mEq/L in each liter of IV
If serum glucose does not fall by fluid (2/3 KCL & 1/3 KPO4) to keep
50 - 70 mg/dl in first hour, double serum K+ at 4-5 mEq/L
IV or SC insulin bolus
When serum glucose reaches Check electrolytes, BUN, venous pH,

200mg/dl, reduce regular insulin creatinine & glucose every 2 - 4 hrly until
infusion to 0.05 - 0.1 u/kg/hr IV, or stable.After resolution of DKA & when patient
give rapid-acting insulin at 0.1U/kg When Serum glucose reaches 200 is able to eat, Initiate SC multi-dose insulin
SC every two hrs. Keep serum mg/dl, change to 5 % Dextrose with regimen. continue IV infusion for 1-2 hrs after
glucose between 150-200 mg/dl until 0.45% NaCl at 150 - 250 ml/hr SC insulin to ensure adequate plasma insulin
resolution of DKA levels. Look for precipitating cause.
310

anesthesia.
• VolatileKetoacidosis:
Diabetic anesthetics used today are all fluorinated, their
Continuation Dr cause
F- ions Azam’sintrarenal
Notes invasodilation,
Anesthesiology 2013
metabolism causes renal damage from the release of F- ion inhibits adenylate
Renal effect of the inhalation agents. Continuation: leading to shunting of Drblood
Azam’s flow
Notes from
inorganic fluoride(F-). cyclase activity & prevents
normal action ofisADH on cortical to medullary nephrons & interferes
• The fluoride inducedIV.nephrotoxicity
Acidosis - Assess the need
(high output renalof
Fluoride Bicarbonate
failure)
toxicity is more with methoxyflurane, which 50 to 75%
with countercurrent
This compound A combinesmultiplier mechanism
with glutathione
was noticeable with methoxyflurane. metabolized in liver, & DCT
produces toxicity by 3 mechanism:
in liver
• Enzyme Induction
• Genetic predisposition
Physiological effects: • If preoperative renal dysfunction is present. Glutathione transferase
• Decrease RBF decrease GFR & urine output because of pH > 7.0
• Enflurane causes nephrotoxicity after prolonged administration ( 9.6 Glutathione conjugate
pH < pressure
decrease in blood 6.9 & cardiac output.pH 6.9
MACto 7.0or longer)
hours Impairs ability to concentrate urine
• Sevoflurane is metabolized by liver & also produces fluoride ions &
• Halothane has no effect on autoregulation of renal blood
HFIP (hexafluoroisopropanol) after prolonged exposure. Glutathione peptidase
flow. • When sevoflurane is exposed to sodalime & baralyme it is absorbed
• The adverse can be abolished or decreased by perioperative
and degraded to a variety of compounds (A-E), of which two are Cysteine Conjugate
produced in significant amounts.
hydration.
Dilute NaHCO3 Dilute NaHCO3 No HCO3 Beta lymase
• Compound A - fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl
Polyuria, hypernatremia &
(100 mmol) in 200
Fluoride induced Nephropathy: (50 mmol)
ether in 200
ml NS. Infuse at ml NS. Infuse at Increased Serum osmolality.Thiol reactive
• Compound
• Inorganic fluoride is produced by oxidative dehalogenation B of
- 1,1,1,3,3-pentafluoro-2-(fluoromethoxy)-3-
200ml/hr In addition to fluoride ions
volatile anesthetics. 200ml/hr
methoxypropane
trifluroacetic
acid a by product of volatile anesthetics is alsoFactors
produced.
responsible for formation of compound A:
Covalent Bonds
• Prolonged exposure to sevoflurane with low flow (<2 Liters/min)
• Formation will be more with baralyme compared to sodalime
• Increased temperature
• Increased sevoflurane concentration Nephrotoxicity
Normal Fluoride level is 50 - 60 microm/liter
• Dry sodalime usage
• 50 - 80 microm/ltr - Mild renal injury
• 80 - 120 microm/ltr -37.Moderate
Renal effect ofrenal injury
the inhalation agents. Dr Azam’s Notes in Anesthesiology 2013
• > 120 microm/ltr - Severe injury • Avoid prolonged exposure to sevoflurane with low flows.
• Renal effects are usually secondary to their physiological Fluoride ions produced
• Add water by oxidative
to saodlime metabolism
& use partially exhausted
Fluoride toxicity in Renaleffects
failure:
on the cardiovascular, endocrine & sympathetic causes renal
sodalime injury byformation
to decrease 2 mechanism:
of compound A &
nervous system. nephrotoxicity
• These effects are almost always transient, and renal
parameters return to normal soon after the cessation of
anesthesia.
• Volatile anesthetics used today are all fluorinated, their
F- ion inhibits adenylate F- ions cause intrarenal vasodilation,
metabolism causes renal damage ! from the release of 85
cyclase activity & prevents leading to shunting of blood flow from
! inorganic fluoride(F-). 84
normal action of ADH on cortical to medullary nephrons & interferes
• The fluoride induced Dr
nephrotoxicity (high output renal failure)
Azam’s Notes in Anesthesiology 2013DCT with countercurrent multiplier mechanism
was noticeable with methoxyflurane.
Dr Azam’s Notes in Anesthesiology 2013 effects:

Physiological
• Decrease RBF decrease GFR & urine output because of
decrease in blood pressure & cardiac output. Impairs ability to concentrate urine
• Halothane has no effect on autoregulation of renal blood
flow.
• The adverse can be abolished or decreased by perioperative
hydration.
Polyuria, hypernatremia &
Fluoride induced Nephropathy:
Increased Serum osmolality.
• Inorganic fluoride is produced by oxidative dehalogenation of
volatile anesthetics. In addition to fluoride ions trifluroacetic
acid a by product of volatile anesthetics is also produced.
311

Normal Fluoride level is 50 - 60 microm/liter
efficient at 660 & 940 nm.
• Oximeter interprets as Sao2 of 85%, when the patient is Dr Azam’s Notes in Anesthesiology 2013
hypoxic with the saturation of 40 - 50 %
moglobin to all
o the sum of
g oxygen or
Meth Hb
e concentration
absorption. Type to enter text
Halothane Isoflurane Sevoflurane Desflurane Enflurane
Blood Pressure ↓↓↓ ↓ ↓ ↓ ↓↓
SVR No Change or Potent decreases Potent decreases Potent decreases More than
Very less in SVR in SVR in SVR halothane ↓ in
78
SVR
Contractility ↓ ↓ ↓ Effect on No much effect No much effect No much effect ↓↓

Ca channels
Heart Rate Normal or ↓ ↑ N/↑ ↑↑↑ (if > MAC) ↑
Sympathetic Sensitizes heart ↑↑ N/↑ ↑↑↑ ↑

activity to
catecholamines
Coronary Coronary Steal Causes coronary

Vasodilation vasodilatation
312

42. Guidelines for Management of anesthesia in a patient with coronary stents. Dr Azam’s Notes in Anesthesiology 2013
There are two type of stents:
BMS - Bare Metal Stents DES - Drug Eluting Stents
BMS - Bare Metal Stents: DES - Drug Eluting Stents:

• BMS implantation effectively eliminated acute vessels • DES releases drugs that inhibit neointimal (paclitaxel or
closure, Stent thrombosis rates are reduced Sirolimus) hyperplasia.
dramatically ( currently 1.2%) with the introduction of • They effectively reduces restenosis rates, 6 - 12 months
dual antiplatelet therapy with clopidogrel & aspirin. restenosis rates were low when compared with BMS.
• Restenosis remains high ( 20 - 25% with in 6 months • Studies shows that incidence of stent thrombosis rates high
of BMS) which is slightly lower than that seen with especially late ( > 30 days) and very late (> 1 year) after
PTCA alone. insertion.
• Restenosis seen as a result of Neointimal hyperplasia
( Medial hyper proliferation) in the coronary artery.
Stent Thrombosis after implantation has been classified into:
I. Acute ( within 24 hours) IV. very Late (> 1 year)

II. Subacute( 24 hours - 30 days) III. Late (30 days - 1 year)
• Reasons for DES thrombosis - Incomplete endothelialization of the stent

• Off label use of DES is associated with higher incidence of MI & death
• On label the risk of thrombosis with DES does not outweigh its benefits over BMS in reducing rates of
revascularization
• The ideal duration of antiplatelet therapy is unfortunately still unknown.
• 12 months of dual antiplatelet therapy with clopidogrel & aspirin, life long aspirin therapy after DES implantation.
• With BMS insertion dual antiplatelets should be continued for atleast 4 - 6 weeks with life long aspirin.
! 92

314

Guidelines for Management of anesthesia in a patient with coronary stents. Continuation: Dr Azam’s Notes in Anesthesiology 2013
a in a patient with coronary stents. Continuation: Dr Azam’s Notes in Anesthesiology 2013
osis after DES: Pathophysiology of Acute perioperative Stent thrombosis: Time of Anticipated surgery Preoperative Management
Anesthetic Implications: of patients with BMS
• Regionals or general anesthesia should be weighed.
• Midazolam irreversibly inactivates CYP3A4 and may
therefore prevent clopidogrel activation.
• Fentanyl, alfentanil & propofol are all reversible
inhibitors of CYP3A4. < 6 wks after > 6 weeks after
therapy BMS implantation BMS implantation
• Thienopyridines ( clopidogrel) & dual antiplatelets
therapy are contraindications to neuraxial anesthesia.
h regards to • Aspirin alone is not a contraindication.
s follows: • Those receiving bridging therapy with Glycoprotein IIb/
IIa inhibitors ( Tirofiban & eptifibatide) should have their Urgent
neuraxial block performed 8 hours after discontinuation Elective Continue aspirin
et therapy of these drugs. throughout surgery
• Surgery should be performed only in institutions with 24 if at all possible.
atelet, elective hours cardiology service & door to ballon time should be
less that 90 minutes. Postpone surgery
more than 12
• Restart clopidogrel/ aspirin as soon as possible. until BMS has been
implanted 6 wks. Can clopidogrel &
therapy
aspirin be continued
in the perioperative
period ?
ude “Bridging
IIIa inhibitors
high risk of Consider Bridging
NO
YES Therapy
s. They are
kidney.
mal within 6-8
Can Aspirin be
o the active Proceed continued?
NO
! 94
93
315

Guidelines for Management of anesthesia in a patient with coronary stents. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Perioperative Management of patients with DES
Time of Anticipated surgery
< 12 Months > 12 Months

Can Aspirin be
Urgent continued in the
perioperative Does patient have additional risk
Elective period? factors for stent thrombosis?
• procedural complexities?
Neither • comorbidities?
Can both
clopidogrel /or clopidogrel /or
aspirin can be No
aspirin be
Postpone surgery continued Yes
continued ? Yes NO
until DES has (closed space
been implanted for surgery)
12 months
Consider
Bridging Consider Can Aspirin be
Yes therapy Proceed Bridging
Proceed continued?
therapy &
continue
aspirin Yes NO
Proceed Any procedural
complexities? or
Restart
comorbidities? Restart Proceed
clopidogrel Restart
and aspirin clopidogrel antiplatelet
or Bridging and aspirin or therapy as soon
therapy If Yes Consider Bridging as possible in
Bridging Therapy therapy as post operative
soon as period.
possible in
!
post operative 95
period.
316

Normal AG: 12 ± 2 Sulphate - 1 mEq/L
Total = 23 mEq/L Total = 11 mEq/L
Interpretation of Anion Gap:

• AG - UA - UC = 12 mEq/L
• If albumin is reduced by 50%, anion gap decreases by 4 mEq/L
I. Causes for increased AG II. Causes for Normal AG Metabolic Acidosis:

Metabolic Acidosis: III.Causes for AG Acidosis:
• H - Hyperalimentation fluids (i.e. total parenteral
• M - Methanol nutrition), Hyperchloremic acidosis • Hypoalbuminaemia - Nephrotic
Syndrome, Liver cirrhosis
• U - Uremia • A - Acetazolamide
• D - Diabetic ketoacidosis • R - Renal Tubular Acidosis I,II & VI • Intestinal obstruction
• P - Paraldehyde poisoning • D - Diarrhea • Multiple Myeloma
• I - Intoxication • U - Ureterosigmoidostomy • Lithium toxicity
• L - Lactic acidosis • P - Pancreatic fistulas
• E - Ethanol
• S - Salicylate poisoning
Blood Substitute.Continuation:
Anion Gap. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Urinary Anionic Gap:

Fluosol - DA Polyfluro-octobromide
• If! Normal Anionic Gap Acidosis A 20% emulsion of 2 different 98 Perfluorocompound (radio-opaque)
Its a new
– Urinary AG = (Na + K ) – Cl perfluorocompounds which has oxygen
( Per-requisites: No Ketosis, Carbenicillin) carrying capacity at 370 C of about 40% of
Dr Azam’s Notes
• If UAG is in Anesthesiology
negative 2013
=> GI or Iatrogenic that of red cells.
– Positive UAG (> 20 to 30 mEq/l) = > RTA – (I,II,IV)
– Look at Urine pH: > 6 - Distal ( Type I) RTA Dose: 20 ml/kg It has 2 Advantages:
– Look at Urine pH: <5.5 - Proximal Type II /Type IV O2 is more soluble in perflourocarbon
• Look at Serum K+ • Higher concentration of compound can be
– Hypokalemia - Proximal Type II administered, therefore 100% emulsion with
Hyperkalemia - Aldosterone Deficiency Type IV phospholipids has a sufficiently low viscosity to be
infused without dilution.
ANION GAP: EXPECTED & ACTUAL AG • It may carry as much as oxygen as Hb solution at a
concentration of 7 gm/dl
• Calculated AG = (Na – Cl + HCO3) Side effects: Pulmonary reactions,
• Corrected Expected Anion Gap (S.Proteins /pH)
cytotoxicity, complement activation,
– For every 1gm % increase or decrease of S. Albumin the AG increase
or decrease by 2 mEq/l Vulnerability to O2 toxicity
– E.g.: In Patients with Nephrotic Syndrome / Cirrhosis
S. Albumin 2 gm % so expected AG = 12 – 4 = 8
• In Acidemia State Normal AG decrease by 2 mEq/L
• In Alkalemia State Normal AG increase by 4 mEq/L
317

mmol/Lt). Usually reflects hypotonic state. • State of ECF Volume ( Low, Normal or High)
Flow Charts & Diagrams Neurological Dr Azam’s Notes in Anesthesiology 2013
symptoms
• Fluid management • After using 4:2:1• Formula the amount obtained is Maintenance fluid
Clinical features: in infants is the
Symptoms
Dr Azam’sare most
Notes
important
primarily & critical
neurologic
in Anesthesiology 2013 To calculate deficit the Maintenance fluid is multiplied by number of hours of
as!"smaller volumes involved. •
#$%&'()'*)&+,-(+'./0)1-(,+*$-2''3'456'*789:" fasting
• Normal daily arrest
waterwithconsumption in infant
70 Kg is 10% - 15% of !
Treatment !!"of Cardiac
;+<+,+'./0)1-(,+*$-'='45>'*789:
Lipid emulsion: patient
• Deficit = Maintenance fluid !"#$%&'()*+&,
X number of hours of fasting
o body weight.
c • General symptoms: Headache – (early sign), Weakness, • The deficit is administered in aliquots of 50% in the first hour, 25% in 2nd
A. Start oxygen & secure Airway & CPR - ACLS
apathy, giddiness, fainting, Mental confusion 3rd hour respectively.
Fluid calculation is based on the Holiday Segar Formula:
• GI
It is
symptoms: Anorexia, nausea, vomiting, thirst is
based on energy requirement.
62. Fluid Management
characteristically in Infants.
absent. Replacement requirements: Dr Azam’s Notes in Anesthesiology 2
• 1-
B. Give 10 kgofinfant
IVSkin:
bolus need
Intralipid -about
20%Turgor 100 cal/kg/24
1.5 ml/kg hr ml) -"/,012,
• Loss of skin andover one min (100
elasticity • It can be divided into blood loss-./,012,& third space loss. -!,/,012,
• 10 - 20 kg infant need about 1000 + 50 cal/kg/24 hr
• CVS: Orthostatic hypotension,/ Tachycardia, cold
> 20 kg infantinneed about 1500most
cal +important
20 cal/kg/24 hr •Blood
After Loss:
using 4:2:1 Formula the amount obtained is Maintenance fluid
• management
• Fluid
of extremity .In CCFinfants patient, is aggravation
the & critical
of heart failure Blood
•• To loss is deficit
typically replaced by non-glucose
67()%&4,$(,'8"($+7, containingby crystalloidsof( e.g:
as smaller volumesCerebral
involved.edema, (due to osmotic water shift) calculate
3)%&4,, the Maintenance
05'(&,()%&4,, fluid is multiplied
!)&(',9&+4:(), number hours
3)%&4,9:%;'+$%,,
• Neurological: 3 ml of HRL with each ml of blood)
8"#$9:%;'+$%,
Approximately
• Normal< daily
1ml
C. Continue of water is needed
CPR
water!consumption for is
in infant each
10%calorie
- 15%coma.
of fasting ;+((8$<+<,
expanded: 120 mEq/l seizure, confusion, delusion stupor, • Because their small intravascular volume, neonates & infants are at
• Deficit = Maintenance@.&A,BC,*0DEF,fluid X number of%)#8($'+;,<"%=,
hours of fasting 3)<'(+;'+$%,$9,
body weight. increased risk for electrolyte disturbance ( Hyperglycemia, Hyperkalemia &
awn into • 1 - 10 kg infant requires 100ml/24hr/kg • The deficit is administered in aliquots of 50% in the first hour, 25% >&')(,,in 2nd
etween B/ G%9)(+$(,$9,8"#)('$%+;,HI,.&14=,
Hypocalcemia)
• 10IV -infusion
20 kgofinfant requires 1000 ml + 50 ml/24hr/kg ?:($<)*+7),
e away D. Start
Fluid !"#$%&'"(%)%*+,#
calculation Intralipid
is based 20%
on- 0.25
the ml/kg/min
Holiday (400 ml over
Segar 20 min)
Formula: 3rd J/hour respectively.
G<$'$%+;,<&4+%),+%,&<"*#'$*&'+;,#&'+)%',,
• ' > 20 ?),,+@($<+'(.+,-0/',+8A$,+B'$1CAB$)1')C'$B)()1$@'B-%$1+'),'
kg infant requires 1500 + 20 ml/24hr/kg • Platelets One unit per 10kg & FFP 10-15ml/kg should be given when blood
()<'(+;',>&')(,,
the
It is based on energy requirement. loss exceeds 1-2 blood volumes.
10./0+,()1$@'B-%$1+" PW'Z-(+')C',$B+')C'0%-B*-'E-'B.)A%&'1)('+T@++&'>"6'*789:9.,"
Replacement
• Cryoprecipitate requirements:
is 1U/10 kg.
fatty acid •E.1-
Repeat
kg
Estimatedinfant need
Fluid
bolus every
about 100 cal/kg/24
requirements
3-5 minutes - 4:2:1
up to 3 mL/kg
hr until circulation
Formula:
total dose
uction, D),*A%-2'
• 10 - 20 kgisinfant!"#$%&'(')#*#!+,-".#/01#2$%3',%4#!"5#6#(7,,%8)#!"59
need
restored about
(100 ml 1000
at 5 min + 50
interval X 2 cal/kg/24
times) hr [W'D$1-%'0%-B*-'E-
• It can be divided into "'B.)A%&'1)('+T@++&'4P>'*789:
blood loss & third space loss.
xidation.
• > 20 kg Body
infant Weight
need about 1500 cal + 20 Fluid
cal/kg/24 hr Blood Loss:
6W'F)'0,+<+1('&+*/+%$1-($1N'+1@+0.-%)0-(./"
Third Space Loss:
E),*-%'FGH'I'J>K'%+-1'L)&/'M+$N.(')C'*+1"
• Blood loss is typically replaced by non-glucose containing crystalloids ( e.g
'
First 10 'kg I'6>K'%+-1'L)&/'M+$N.(')C'C+*-%+"
4ml/kg/hr Degree of Blood loss or Tissue Additional fluid requirements
Approximately
F. Continue infusion 1ml of water is stability
until hemodynamic needed for each
is restored. calorie
Increase the rate 3/*%0+1%+2(#(3*024%$"+23*#35#67&3*"+$%)2",#
ml of HRL with each ml of blood)
O+B$,+&'E-'I'4P>'*789:( Trauma
expanded: to 0.5 mL/kg/min if BP declines ( 400 ml over 20 min)
Second 10 kg 2 ml/kg/hr • Because their small
• Hyponatremia intravascular of
is a manifestation volume,
seriousneonates
underlying&disorder
infants are at
-.")&'%,#'Q'J>RN'M$(.'0%-B*-'E-!'45>'*789:( increased
• Requires
Minimal risk for
careful electrolyte
evaluation
(e.g. herniorrhaphy) disturbance (
preoperatively Hyperglycemia,
0 - 2 ml/kg Hyperkalemia &
• 1 - 10 kg infant requires 100ml/24hr/kg
E-'&+S$@$('I'J>'T'>"6'U4P>'V'45>W'I'P>>'*789: Hypocalcemia) +
• Plasma Na > 130 mEq/L – safe for GA.
•A 10 -Subsequent
20 kg infant requires 1000 ml 1 ml/kg/hr
+ 50 ml/24hr/kg
maximum total dose of 8 mL/kg is recommended
QB'PK'E-?%'@)1(-$1B'64P'*78')C'E- "9:( Moderate
• PlasmaOne
• Platelets Na+!""#$%&'&(&)*+
(e.g. should
unit perbe10kg
corrected 2 - 4130
& FFPabove ml/kg
10-15ml/kgmEq/L for elective
should be given when blood
• > 20 kg infant requires 1500 + 20 ml/24hr/kg
surgery.
loss exceeds 1-2 blood volumes.
• The Fluid of choice is controversial: Hartmanʼs Solution, 1/2 Severe
• Risk:(e.g.
• Cryoprecipitate
Bowel resection)
Intraoperative:
is 1U/10cerebral
kg.
4 - 8 ml/kg
edema
Estimated Fluid
Normal salinerequirements - 4:2:1
X)%A*+')C'B-%$1+',+8A$,+&'I' Formula:
I'6Y6'*% • MAC
• Magnitude of perioperative third space loss is proportional to the amount of
• Neonates requires 3-5mg/kg/min of glucose infusion to
Z-(+')C'@),,+@($)1'I'>"6'*789:9., Post operative:
Body Weight
maintain euglycemia ( 40 - 120 mg/dl) Fluid
•
tissue
Third Loss:Agitation
manipulation.
Space
;)'&+S$@$(')C'4>'*789:'U0%-B*-W',+8A$,+B'5>'.,B'C),'@),,+@($)1 ••Confusion
E.g. Burns, trauma, infected tissues, etc.
• Premature requires 5 - 6 mg/kg/min 104
First 10 kg
of glucose infusion.
4ml/kg/hr •Degree of Blood loss
Water intoxication or Tissue
in TURP patient. Additional fluid requirements
Trauma
Second 10 kg
! 2 ml/kg/hr 110
Minimal (e.g. herniorrhaphy) 0 - 2 ml/kg
Subsequent 1 ml/kg/hr 2013
! Moderate (e.g. !""#$%&'&(&)*+ 2 - 4 ml/kg127
• TheDr Azam’s
Fluid Notesisincontroversial:
of choice Anesthesiology 2013
Hartmanʼs Solution, 1/2 Severe (e.g. Bowel resection) 4 - 8 ml/kg
Normal saline
• Neonates requires 3-5mg/kg/min of glucose infusion to • Magnitude of perioperative third space loss is proportional to318
the amount o
maintain euglycemia ( 40 - 120 mg/dl) tissue manipulation.
Dr•Azam’s Notes
Premature in Anesthesiology
requires 2013of glucose infusion.
5 - 6 mg/kg/min • E.g. Burns, trauma, infected tissues, etc.
Indications: •
Flow Charts
• Status & Diagrams
Asthmaticus Dr Azam’s Notes in Anesthesiology 2013
• ARDS
Mechanism & physiologic changes in permissive Hypercapnia
Decrease Tidal Volume ( 4 - 7 ml/kg)

Increase PaCO2
Decrease peak inspiratory
Atelectasis Respiratory Acidosis Hypoxemia
Decreases Mean
airway pressure
To reduce PEEp may be pH may be normalized Corrected by
Hypocalcemia. Continuation: used if airway pressures Dr Azam’s
with sodium bicarbonate or Notes
using in Anesthesiology 2013
Higher
are in acceptable range THAM(tromethamine) FIO2
!"#$%&#'%() Decreases Barotrauma
*$+,-.&)"#/+$,#&#'%)%0#"$/1())) *$.%-3'()
58. Liquid Ventilation / Perfluorocarbons
– !"#$%&#'%()* +"$&)',)-#('* (.* )&/.(0-1-0* '.* '* #-0()',*
– :',)(5#*(.*(11(%'%(/2*%&*G-(/L*+-/)-*%&*I-*0(,5%-06*
-#-12-/)"*%+'%*/-)-..(%'%-.*34*)',)(5#*%+-1'$"6 – T&*I-*'0#(/(.%-1-0*I"*)-/%1',*G-(/6*
• It has been recognized that surface
23+.%-3'4 tension of the
5+#&#'%$+)*$ surfactant deficient
6'-%)73+8 – T&* I-*2(G-/*)'5%(&5.,"*%&*$'%(-/%*1-)-(G(/2*0(2(%',(.*>&%+-1N(.-*)'5.-*
Liquid Ventilation - 2 Forms
lung may be reduced by filling alveoli with certain fluids. For mammals, 0(2(%',*%&U()*'11+"%+#('B*
789*:':,! ;<*#2=#,*>76?*#@AB 78*#,*'#$
to breathe liquid in tidal fashion, for prolonged periods two major – T+-1'$-5%()* 2&',* %&* 1-.%&1-* /-'1* /&1#',* G',5-* N+()+* ',,-G('%-.*
789*:'*2,5)&/'%-*
requirements must be met C*#2=#D*>86E*#@AB 78*#,*'#$* ."#$%&#.L*'G&(0.*+"$-1)',)-#('*=*+"$-1)',)(51('6*
I. A liquid must be Dr Azam’s Notes in Anesthesiology 2013
! used that possess high solubility for oxygen and
cation.
– :'* 1-$,')-#-/%* %+-1'$"* #'"* )'5.-*! )',)(5#*
! • !"#$%&"'&#()$%&%(*+()&,-.#(%$#(".&/!012& >:'B* &G-1,&'0*
107 N+()+*
• !"#$%"&'&%()%*'+,-$%&"$%.-'/!01'
CO2 and $1&05)-.*,-%+',*)-,,*(/V51"*(/*$'%(-/%*N(%+*)(1)5,'%&1"*.+&)PL*+-/)-*:'*
"22.3%"$,*'4"2',536"-4,'!789'.#'
1(")*+,-%.(,/$%2334
work56"/78$..%&'%)*+,%2334 • 345&%(*+()&-*+$%&#"&465&(7&(.7#(%%-)&
dural A ventilator
II. must be +'G-*
F&%+* .&,5%(&/.* used to perform
.&#-* of &H*
in )&/)-/%1'%(&/* breathing
)',)(5#* because
.,'%* >788*of !:;<'
!"#$%&'( Dr Azam’s Notes
)*+,-,)*. Anesthesiology
/*+,-,)*. 2013 (/H5.(&/*.+&5,0*I-*5.-0*V50()(&5.,"6*
(.#"&8!!9&
the high viscous resistance
#2=#,B*I5%*:':, to flow of the liquid medium. The fluid
!*)&/%'(/.*?*%(#-.*#&1-*-,-#-/%',*:'6 • !01'&%()%*',()"&'$.'0=1'%2'>)$'%-$.'
should011"#,234#'&%&, /*.,-,5*++
also be non-absorbable and poor )*+
solvent for surfactant.
• :(;(%$'&,"%+;-7&$'-&<=<%-)&#"& 9??<'
<'#4%0#4-$)$'=)01/3,$+,$#&-$()
iorly, 647"#,234#'&%&,
934$:#() 8*++,-,.*++ )*+ >$<(%(#$#-&?$7&-@<A$.?-&& • ;,-$%&"$,'+%"'3.-+,-$%"&'+,-$%&"$.#''
m•ofLELAND69:;'#
CLARK first identified Perfluorocarbons as a class of & – W"$&)',)-#('*.+&5,0*I-*)&11-)%-0*$1-&$-1'%(G-,"6*
.*++,-,<*++ +*<<,-,+*55 !
compoundsJ F&,5.*0&.-*&H*;88*#2*-,-#-/%',*:'*>(/*K*#,*&H*789*:':,
suitable for liquid breathing. Only recently has a !medical *&1L*;;* – X0-A5'%-*$1-&$-1'%(G-*'..-..#-/%*'/0*'$$1&$1('%-*T=%*(H*1-A5(1-0*(.*
e grade liquid #,*suitable
&H*789*:'*for2,5)&/'%-B*(/*788*#,*
clinical applications&H* of(.&%&/()* .',(/-*&G-1*78*
liquid ventilation -..-/%(',*I-%N--/*-,-)%(G-*.512-1"6*
ves became #(/
available. Per fluro-octyl bromide (perflubron). – Y(%+* G&,'%(,-*'/-.%+-%()* '2-/%.L* 21-'%-1*+"$&%-/.(&/* '/0* #"&)'10(',*
Distance to epidural space:
space J M'(.-.*.-15#*:'*I"*7*#2=0,6 0-$1-..(&/*&))51.6
The over all median distance in normal adult female is 4.7 cm at L3 – L4
PFC are 5:J !D-G-,*H',,.*'H%-1*?8*#(/6 • Liquid ventilation,
– T+-* ')%(&/* allows
&H* #5.),-* liquid to
1-,'U'/%* be I-*
#'"* used to recruit>.#',,-1*
$1&,&/2-0* atelectasis0&.-*lung
ebral level.
!" #$%&%'$()&*$+,-.*&$/0$12"
J F&,5.* 0&.-*depth
H&,,&N-0* and reduce tension at the alveolar lining.
The maximum occursI"* )&/%(/5&5.*
at L3 (/H5.(&/* '%* 7O;* #2=P2=+1*
– L4 inter space. 1-A5(1-0B6
!!" 31%-&,22 H&1*Q*+16
The depth decreases above L3 and below L4 level. • In expiration: The liquid FRC represents an incompressible reservoir
– XG&(0*+"$-1G-/%(,'%(&/L*/&1#&)'$/('*#'(/%-/'/)-6
l of oxygen occupying alveoli that would otherwise collapse and319 allow
!!!" 40-5)(,*.,+2$%+*2$'+$6$()+.&7*&%8,-*.9)+*: !3
J 3=4*:'*.&,5%(&/.*'1-*+"$-1&.#&,'1*'/0*.+&5,0*I-*2(G-/*(/*,'12-*
Epidural space in children: – 34*:'*H&,,&N(/2*1'$(0*%1'/.H5.(&/*&H*)(%1'%-0*I,&&0*$1&05)%.6
)-/%1',*G-(/6
!;" :)<,*,=.-,>,&7*9$'9*2%&0?$&$.7*5%-*-,2@$-).%-7*')2,2" intrapulmonary shunting.
• In children under 6 yrs of age, the epidural space has spongy, – Z&%-/%('%(&/*&H*/-2'%(G-*(/&%1&$()*-HH-)%*&H*I'1I(%51'%-.6
Dr Azam’s Noteslobules
3H*$-1($+-1',*G-(/*(.*5.-0L*:'*2,5)&/'%-*(.*$1-H-11-06 • In inspiration: Tidal volumes of gas purge that reservoir of CO2 and
*
vical A3!J*$2*B*.$>,2*>%-,*2%&0?&,**C*!+*DEA*.9)+*:F3
gelatinous and distinct space. (This is contrast to densely [&/(%&1(/2*N(%+*/-1G-*.%(#5,'%&1*H&1*1-.$&/.-*&H*\[*I,&)P'0-6*
packed fat globules and fibrous strands characteristic of the mature replenish the supply of dissolved O like an efficient bubble
2
Hyponatremia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Flow Charts & Diagrams Dr Azam’s
Dr Notes
Azam’s in Anesthesiology
Notes 2013
59. High Frequency Ventilation - HFV
• Pattern of ventilation in which high RR and small tidal volumes

approximate to or less than patients dead space volume are applied. !"##$ !"%$ !"&$
• It is in general a positive airway pressure technique. ! !! "#$%## %##$&## &##$'&##
• HFV is ventilation at RR > 4 times that of normal with wide range of TV.
()*+,-.//012, 345.10,+.60 345.10,+.60 3720,+.60
Objectives:
1. To provide safe and effective support of CVS functions. 8.9,0:/1.;/7*2, <* =09 <*
2. To provide adequate pulmonary gas exchange. ()*+, ?51@5)02/ ?51@5)02/ ?51@5)02/
3. To treat underlying pulmonary pathologic condition. ;>.1.;/0179/7;9,
Conventional methods consists of artificial ventilatory support with ↑ (7A'63. Oxygen Cascade
B*2/1*))0C B*2/1*))0C B*2/1*))0C
ambient O2 and continuous positive pressure.
D.1*,/1.5E., =09 <* =09
• Oxygen like any other gas, moves down a partial pressure gradient
Physics of gas exchange in HFV: ()*+,F0201./7*2, G205E./7;
from air via the respiratory tract. 3*)02*7C,-205E./7; G79/*2
• In HFV, TV equal to or slightly less than dead space volume at high H:-71./7*2,
• Arterial blood,G.99760
systemic capillariesG.99760
and cells to finallyI;/760
reach the
frequency are used for displacement. But basic exchange depends on G97 mitochondria-"# where it is consumed.
"# "#
agitated mixing and dispersion within alveolar system. This regional gas Definition: The steps by which the partial pressure of oxygen
mixing coupled with augmented molecular diffusion, fresh gas reaches gradually decreases from a high level in the inspired gas to a low
alveoli by combined convention and diffusion. Difference between Various high frequency ventilation:
level in the mitochondria is called oxygen cascade.
• In large airways, convection current is the main mechanism for air
movement, while in terminal airways, movement of air occurs by stream !
dispersion.
• In higher frequency (> 600/mt), coaxial flow occurs i.e., air movement is
bidirectional i.e., movement to alveoli within centre or mainstream and
reverse flow for exit movement occurs at sides / periphery of tube.
• Physics – gas exchange depends on agitated mixing and dispersion
within alveolar system.
Inflation-- active
Expiration—passive "!#$%!&!'()!**+,!
In high frequency (> 600/mt) – bidirectional flow occurs.
Oxygen Cascade:
!"#$%&'("()*+%,%!% "-%.&/01+(/"2% 3/+44)/+%!!% 567!%8%40% %567!%
4$0)'*%.+%"%(0%&90"*%$:30;+1"&%
! 123
<(1043$+/"2%3/+44)/+%=%>67!
?8 @AB%;%B8C?%D%?AB%D%C?%E5&%
<(1043$+/"2%5/+44)/+%F%GH5%;%>"7!
C8 I@AB%F%J@K%B8C?%D%?LB%D%?M%E5&%
! 111
320
!
same size of OD.
point parallel to the longitudinal fibers, an ellipsoidal hole is produced, co
6. ID is&important
Flow Charts Diagrams as it affects the rate of flow of CSF Dr Azam’s Notes in Anesthesiology 2013
Hypernatremia.Continuation:
down the needle, which is related to the CSF to aNotes
Dr Azam’s more round hole2013
in Anesthesiology when
the needle top is at right angles to the fibers.
pressure at the needle tip. With a 26 gauge needle, 17. Because the shape of the needle tip several different typer are available.
it can take 10 to 60 seconds for CSF to appear at
the needle hub. It is seen sooner if the hub is
translucent rather than opaque. It addition the, flow
will be faster if the patient is sitting up rather than in
the lateral decubitus position, as the pressure at the
needle tip is greater.
7. 22 gauge needles can be used without the aid of an
introducer, but thinner needles usually require an
Parts:
introducer which is first inserted into the ligamentum
• Stylet
flavum. • Cannula - Hub &
8. The shape and sharpness of the needle tip affects
the shape and size of the hole produced in the dura.
This hole is not simply the same size as the OD of
the needle.
9. Often there is a flap similar to that of an opened “tin
can” whose lid has not been completely removed.
10. This flap may move back into the hole, partially or
totally preventing CSF escape, even after puncture
with large-bore needles.
TYPES:
! ! 113 134
321

fails and abnormal precursors (porphyrias) are formed in excess.
Flow Charts & Diagrams Dr high
• All porphyrias have Azam’s Notes inactivity.
ALA synthetase Anesthesiology 2013
Classification:
Pathophysiology: !"#$%&'(#)*#+,*&$- .*,%+*)#)&"%&'(#)*#+,*&$-
59& ! !"#$%&$'()*+$,(-".%*$/"( !"#$%&'($%)*'$$%($&+,)+-.)'/& 0).$-),+,'%$'"&#),+,)+-.)'/
-----".%*$/"( 1/)'%2/$%&+,)+-.)'/&3!45 0).$-),+,'%$'"&+),$,&+,)+-.)'/
6%)%7'$/).&",+),+,)+-.)'/
$@ 0-'12#$'2*(%./&3+'&$%#(( 4+"%32*(%./&3+'&$%#(( 8,)+-.)'/&"#$/('/&$/)7/3!45
Acute intermittent porphyria – most serious form of Hepatic

53$&$'2*(6+*"%#237(8-//-*(%./&3+'&$%#! 9+*"%#237(:-//-*(82/%/62/"(( porphyrias
• Autosomal dominant
Increase ALA synthetase Dr Azam’s
and decrease Notes in Anesthesiology
uroporphyrinogen synthetase 201
98. Describe the Anatomy of larynx? Discuss the effect of damage to• recurrent laryngeal nerve
!'+&-(9+*"%#237(4;<(=(476%>-"$2((
vocal cord palsies? • -S/S Acute abdominal pain + Neurotoxicity in females (during
Muscles of Larynx:
menstruation)
• Larynx is the cartilaginous skeletal held together by ligaments ad muscles.
The complete brachial plexus • Neurotoxicity:
MusclesPsychosis (cerebral cortex dysfunction), SIADH,
of Larynx:
• Extends from root of the tongue to the first tracheal ring (C3 to C6)
Hyponatremia (Hypothalamus dysfunction), " Bulbar paralysis
?-8-3-(#-+3%*%@$'( ?6%#&2#-%+/(3-/%*+&$%#(( B:C((
diagram:
8& (Swallowing difficulty and Aspiration – (cranial N), Tachycardia,
$"62$3"-#&A,-2&1( Measurements Male Female orthostatic hypotension, HTN (ANS) pain and paresis (Peripheral
Dr Azam’s Notes in Anesthesiology 2013 nerves),
Length 44 mm 36 mm Extrinsic Muscles:
• Intrinsic
Cutaneous Muscles:
photosensitivity.
Transverse 43 mm 41 mm • Abductors: • Sternothyroid
6'"++7*"/89' !• Posterior cricoarytenoid • Thyrohyoid
!"#$%&'"'()*"$%')&+)',-./&-'0 Diameter
Adductors: • Inferior constrictor
•
! P5.$%#0%&2<7:15#$;&#$/%$;&2$%00<$%@
AP Diameter 36 mm 26 mm Dr•Azam’s
LateralNotes in Anesthesiology 2013
cricoarytenoid • Stylopharyngeus
• Palotopharyngeus
! J%.$%#0%&.#$64#.&1</2</@ • Transverse arytenoid
• Cricothyroid*
! C:541/4.& ?7<46&:#/%$4#7&45&/3%&2#$/<$4%5/&=7116&#024$#/%6&8$1:& • Thyroarytenoid *
• Larynx is made up on 3 unpaired & 3 paired cartilaginous
#&.%5/$#7&F%51<0&1$&2<7:15#$;&#$/%$;&.#/3%/%$&Q&&&I15?4$:#/1$;@&&
structure:
• Relaxors:
• Thyroarytenoid*
! C</120;&7<59&=4120;@ 3 Unpaired 3 paired • Vocalis
• Tensors:
!"##$%$&'"()*+"(,&-."./ Thyroid Cartilage Arytenoid cartilage • Cricothyroid *
Q&&&&C024$#/415&18&9#0/$4.&.15/%5/0&'=$15.31.150/$4./415-
Cricoid cartilage Corniculate cartilage
Q&&&&G<7:15#$;&%:=1740:&'.3%0/&2#45-
Epiglottis Cuneiform Cartilage
Q&&&&R%51<0&#4$&%:=1740:
Q&&&&S1.#7&#5%0/3%/4.&/1T4.4/;&'3493&0245#7&7%F%7-
"-'5*)$'"-' Q&&&&U493&%246<$#7&#5%0/3%04#&
Q&&&&V1/#7&0245#7&#5%0/3%04#&
7#(8"'#$+,
F%#/#(#$<'()#(/8,-'*7'+"7",-(8,-#"'*7'/%#/2'
173 322
5%49+,
NCOP'3%'*4'%*/"%'"$",-(8,(#/'+,7'5#>#-#*$
Describe the Anatomy of larynx? Discuss the effect of damage to recurrent laryngeal nerve Dr Azam’s Dr Azam’s
Notes Notes in Anesthesiology
in Anesthesiology 2013 2013
vocal cord palsies? Continuation:
ynx? Discuss the effect of damage to recurrent laryngeal nerve Nerve Supply:
recurrent laryngeal nerveLigaments:
ation:
! !"#$%&'()!(!
• Branch of
Intrinsic Ligaments:
superior • Supply up toExtrinsic Ligaments:
• Cricovocal membrane • Thyrohyoid membrane
the vocal cord !!!"#$%&'(&!)*&+,-%*).!/! !!!0%1#&&%,2!)*&+,-%*).!/!
thyroid artery
• Quadrangular membrane • Cricotracheal membrane
• Cricothyroid membrane • Hypoepiglottic ligament
• Branch of
• Supplies below !!!!!3,2%&,*)!4&*,15!!!!!!!!!!!
9:2%&,*)!4&*,15!6;(2(&8! ?(2(&!4&*,15! "%,7(&+!4&*,15!
Inferior thyroidof larynx:
Ligaments
Cavities: the vocal cords. 67%,7(&+8!
artery
• Vestibule
• ventricle
• Subglottic "#$$)'%7!)*&+,:! "#$$)'%7!25%! "#$$)'%7!*))!',2&',7'1! "#$$)'%7!*))!
es. *4(<%!)%<%)!(=!<(1*)! 1&'1(25&+('>!;#71)%7! %:1%$2!1&'1(25+&('>! 7#4-)(22'1!&%-'(,!!!
geal 1(&>!
Inlets of Larynx:
stibuli
• It extends from the laryngeal inlet to the lower border of cricoid cartilages.
Folds:
ase of • Aryepiglottic fold - Space between the aryepiglottic fold forms the laryngeal
inlet. !
• Vestibule fold - Space between the vestibule fold is called as Rima Vestibuli
!"#$%&'()!( ! Dr Azam’s Notes in Anesthesiology 2013
• Vocal
Drfold - Space
Azam’s between
Notes the vocal fold2013
in Anesthesiology is called as Rima glottidis
al nerve
• Vallecula: Shallow space present in front of the epiglottis behind the base of
the tongue.
/! !!!0%1#&&%,2!)*&+,-%*).!/!
191
15!6;(2(&8! ?(2(&!4&*,15! "%,7(&+!4&*,15! Lymphatic Drainage:

• Supraglottic lymph vessels: Upper deeper cervical glands
• Subglottic lymph vessels: Pre-tracheal ( lower deep cervical
! glands) 191
'%7!25%! "#$$)'%7!*))!',2&',7'1! "#$$)'%7!*))!
('>!;#71)%7! %:1%$2!1&'1(25+&('>!
Dr Azam’s Notes in 7#4-)(22'1!&%-'(,!!
Anesthesiology 2013!
323
192
CONTROL OF BREATHING. Continuation: Time. Dr Azam’s Notes in Anesthesiology 2013 analgesia
• To promote adequate
• Respiratory rate 10 to 12 breaths per minute - No • To minimize the incidence of postoperative c
Flow Charts & Diagram. Hyperventilation Dr Azam’s Notes• in Anesthesiology
To prevent infections 2013
• Increased E time - prolonged E time for emptying of • Chest physiotherapy & deep breathing exerc
the alveoli. • Consider CPAP - Decreases WOB, Improve
• Continuous administration of Local anesthet
Intraoperative bronchospasm: Identification & Management: opioids via epidural catheter for post operati
To R/O other causes of high Deepen Anesthesia:

airway pressure & • Give 100% oxygen
wheezing: • Inhalation Anesthetic
• ET - Tube Kinking agents if BP is normal.
• Thick secretions • Low BP - Ketamine
• Pulmonary edema
• tension pneumothorax
• Aspiration Pneumonitis Beta2 Agonist:
• Pulmonary edema • Rapid acting albuterol through
• Endobronchial intubation meter dose inhaler directly in
• bucking breathing circuit.
• Aminophylline 0.5mg/kg -
tachyarrhythmias
• Terbutaline S/C 0.25mg every 20
min for 3 doses.
• Epinephrine: 0.1 - 0.5 ml of 1:1000
S/C may be the last resort.
• Steroids: hydrocortisone 4mg/kg
! followed by 3mg/kg.
Control Of Breathing:
! 202
324

Perioperative Myocardial Ischemia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Pathophysiology:
Triggering Stress of Surgery Stress of Surgery. Surgery & Anesthesia Anesthesia, blood
Factors: Stress of Anesthesia. Stress of Anesthesia. loss & Anemia
• Intubation
• Extubation
• Hypothermia
• Anemia
• Increased blood loss
• Inadequate pain control
Increased Increased
State Inflammatory Hypoxic State
Hypercoagulability
Response
Increased Stress
Increase in ILF, TNF Increased platelet reactivity Increased Cortisol Decreased

Consequence
& creative proteins increased antithrombin 3 Increased catecholamines Oxygen supply
Increased Increased
Coronary Stress HR & BP Decreased
Oxygen Supply
Plaque Rupture Plaque Rupture
Myocardial Infraction
Coronary Artery Thrombosis
85
Perioperative Ischemia
Dr Azam’s MI:
Perioperative Notes in Anesthesiology 2013
325

Flow ChartsMyocardial
Perioperative & Diagram.
Ischemia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Acute treatments for suspected intraoperative myocardial ischemia

Associated Hemodynamic Finding Therapy Dosage
I Hypertension, tachycardia + Deepen anesthesia Esmolol 2-100 mg, + 50-200

IV β - Blockade Metoprolol 0.5-2.5 mg
Labetalol 2.5 – 10mg
33-330 µg/min +
Ii Normotension, tachycardia + IV Nitroglycerin As above
Assure adequate anesthesia change
anesthetic regimen
IV β- Blockade
III Hypertension, normal heart rate Deepen anesthesia 0-20 mg
nicardipine Nicardipine 1-5 mg, + 1-10 µ
Phenylephrine 25-100 µg
IV. Hypotension, tachycardia + IV α-agonist Nor-epinephrine 2-4 µg
V Hypotension, bradycardia Lighten anesthesia 5-10 mg
IV Ephedrine 4-8 µg
IV Epinephrine 0.3-0.6 mg
IV Atropine As above
VI. Hypotension, normal heart rate IV α- Agonist As above
IV Epinephrine
alter anesthesia (eg, lighten)
VII. No abnormality IV Nitroglycerin As above
IV Nicardipine As above
87
326

Aortic Stenosis. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Pathophysiology:
Aortic stenosis Calculation of Stenosis:

Gorlinʼs modification of standard hydraulic formula
! (Cardiac output / systolic ejection period) x H.R.

Obstruction to ejection
of blood into the aorta Aortic valve orifice (cm2) = 1 x 44.5 x mean aortic pressure gradient
Where 1 = Aortic orifice constant

Increase in L.V. pressure 44.5 – hydraulic constant Simplified version of Gorlinʼs formula
Aortic valve area = Cardiac out put (lt/min) / Mean aortic pressure
Increased Left ventricular gradient
L.V. Hypertrophy diastolic pressure & Volume
Increase in Increased
LA Pressure Myocardial O2
Demand Normal : Aortic valve area 2.5 – 3.5 cm2
Aortic valve area reduction

• Normal - 2.6 – 3.5 cm2
Pulmonary
Angina Pectoris • Mild - 1.2 – 1.8 cm2
hypertension
• Mod - 0.8 – 1.2 cm2
• Significant - 0.6 – 0.8 cm2
• Critical - < 0.6 cm2
Pulmonary edema Sudden death
RVF
327

• Fibrillation waves in leads V1 or V2 of 1 mm or more.
Anti DNAase
Mitral B. Continuation:
Stenosis.
Flow Charts &Chest
Diagram. Dr Azam’s Notes in Anesthesiology 2013
Cardiograph
Anesthetic Management
• Straightening of left heart border L
Premedication
• Prominence of main pulmonary artery
Mitral Stenosis. Continuation:
• Dilation of upper lobe pulmonary veins •Mitral valve Dr
Anti-anxiety: Stenosis:
Midazolam
Azam’s Notesis thein
benzodiazepine
Anesthesiologymost 2013commonly E
• Kerley B lines
used for anxiolytic. The usual
Grades MVAintra muscular dose is 0.05 to 0.1 s
mg / kg. it is common to administer titrated doses of 1.0 to 2.5 mg •
• Calcification
Pathophysiology: Downward of mitral valves Mild 1.5 –premedication,
2.5 cm2
at a time intravenously. Heavy produces significant •
• Double
to upward disease or shadow
failure. Moderate 1.1 –be1.5 cm2
hypoxemia and oxygen should administered.
• Backward displacement of esophagus by enlarged LA.
! ! • OBSTRUCTION
Elevation of left mainTO LA EMPTYING
bronchus. •Severe
Hypoxemia and hypercarbia 0.6
can– aggravate
1 cm 2 pre-existing pulmonary
Critical
hypertension. Less than 0.6 cm 2 •
! ! • !Calcification
! of mitral valve, best seen on fluoroscopy •
! • Antisialagogue: with less likelihood of increasing heart rate,
! glycopyrrolate is the drug of choice. •
Echocardiogram: This is the most sensitive and specific non invasive •
method for diagnosing and quantifying severity of MS.
'(!,)'')+/!
Mitral Stenosis – hemodynamic goals: •
• Mitral valve severity Symptoms:
Preload Maintain, preload, avoid hypovolemia
• Mitral valve morphology
"!,-.! !!!'"!0)1&! '"!23&00$3&!
"#$%&!
#*! • Dyspnea:
After load The principle symptom
Prevent pulmonary of MS is exertional
vasoconstriction (hypoxia, hypercarbia) D
• Presence of severity of coexisting mitral regurgitation
&'&("%)*+!
dyspnea, largely the results
ionotropes may beof reduced
required for pulmonary
systemic hypotension. C
• Left atrial size and function Contractility RV dysfunction may be a problem with long standing pulmonary
• Pulmonary systolic pressures compliance. C
%6)3*45)!
hypertension.
• Left atrial size and function 4&"+!2$'4!#"2)''"39! • Frank
Ratepulmonary Lowedema. TheAvoid
end of normal. latter may precipitated by
tachycardia D
23&00$3&!<=>!44!6/!
• Pulmonary systolic pressures anyRhythm
condition that increases flow across the stenotic mitral
Maintained B
• Left
&45*')1"%)*+! ventricular size
Mitral and
Stenosis. function
Continuation: valve. Dr Azam’s Notes in Anesthesiology 2013
C
• Right ventricular size and function 2$'4*+"9!&8&4"! • Hemoptysis: This may be due to rupture of thin walled
• Evaluation Acutefor hypertension
rheumatic – Inj. Nitroprusside
involvement of 0.5 – 10
aortic ormicro gram / kg
tricuspid valves. D
per min with monitoring. bronchial veins usually as a consequence of sudden rise in
Pressure Volume Loop:
2$'4*+"39!
Hypotension – Inj phenylephrine 0.2 mg increments. LAP. C
Category Recommended 2$'4*+"39! Not recommended
(&+*$0! Inducing agents Etomidate, Opioids,"3%&39!23&00$3&!
Ketamine • Chest Pain
23&00$3&! A
Benzodiazepines Palpitation
Maintenance Opioids Potent inhalation agents
agents in high concentrations • Systemic embolism; This may be first symptom and may
113
Muscle Succinylcholine, Pancuronium occur even before development of dyspnea. Symptom !
("0#$'"3! 2$'4*+"39!
Dr Azam’s
&+/*3/&4&+%7!Notes
relaxants
in Rocuronium,
Anesthesiology 2013 692&3%&+0)*+! depends on vessel involved: !
Cisatracurium
2&3)("0#$'"3!
&8&4"!
Hypotension Phenylephrine B-Adrenergic against, • Altered consciousness (cerebral vessels) &
Ephedrine, Epinephrine,
3)/6%!!
Dopamine, Dobutamine
Myocardial ischemia and angina pectoris (coronary) D
Right heart Reverse pulmonary(&+%3)#$'"3!*(&3! Systemic hypertension (renal) D
failure vasoconstriction, Dilate '*"8!
'$+/!#*4')"+#&! pulmonary. Vasculature • Pulmonary infection
B
! • Fatigue
!!!!!!:*3;!*,!53&"%6)+/! Postoperative management
• Plain relief: %3)#$02)8!
#*! • Abdominal discomfort due to hepatic congestion D
epidural analgesia >>>> systemic3&/$3/)%"%)*+!
opioids • Edema C
bupivacaine 0.125% - 0.0625% + fentanyl 4-5 µg / ml
• Regional anesthesia in conjunction with other modalities tailored to a
each patients need may prove to offer best outcome for patients.
Patients with decreased pulmonary compliance, increased oxygen 111
cost of breathing, and deteriorating hemodynamics may require
Ventilatory support. 328
Ischemic Heart Disease.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Goldman's CRI -‐ 1977.

Leeʼs revised CRI- 1999. i. Age > years 5
(Assign one point to each of the following variables) ii. MI in previous 6 months 10
i. High risk type of surgery (intra-peritoneal, intra- iii. S3 gallop or ↑ JVP (0-3 cm) 11
thoracic or supra inguinal vascular procedures. iv. Important aortic stenosis 3
ii. History of IHD (history of MI, positive exercise test,
current complaint of ischemic chest pain or use of
nitrate therapy of ECG with Q waves) vi. >5 PVC/min at any time before 7
iii. History of CHF vii. PaO2, < 60 or PaCO2 > 50mm Hg, 3
iv. History of cerebro-vascular disease BUN > 50 or Cr> 3 mg/dl. Abnormal SGOT, signs of chronic liver
v. Insulin therapy for diabetes disease, bed ridden from non-cardiac cause
vi. Preoperative serum creatinine > 2.0 mg/gl viii. Intraperitoneal, Intrathoracic, aortic surgery 3
Class I = 0 factors, ix. Emergency operation 4
Class II = 1 factor Total 53
Class III = 2 factors Class I 0-5 points (low risk)
Class IV = >2 factors Class II 6-12 points (intermediate risk)
High (reported cardiac risk often >5%)
• Emergent major operations, particularly in the elderly.
• Aortic and other major vascular
Peripheral vascular Detsky’s ModiGied CRI -‐ 1986
•
• Anticipated prolonged surgical procedures associated i. Age > 70 years 5
with large fluids shifts and/or blood loss. ii. MI < 6 months 10
Intermediate (risk generally <5%) iii. MI > 6 months 5
• Carotid Endarterectomy iv. Unstable angina 10
• Head and neck v. Pulmonary edema < 1 week 10
• Intraperitoneal and Intrathoracic
• Orthopedic
Prostate vii. Non sinus rhythm PAC 5
•
Low (Cardiac risk generally <1%) viii. CCVSA class III 10
• Endoscopic procedures ix. CCVSA class IV 20
• Superficial procedures x. Critical As 20
• Cataract xi. Emergency operation 5
• Breast
Total 120
329

Flow Charts
Heart& Diagram. Dr Azam’s Notes in Anesthesiology 2013
Ischemic Disease.Continuation: Dr Azam’s Notes in Anesthesiology 2013
47. Endocardial viability ratio. Dr Azam’s Notes in Anesthesiology 2013
Risk of Perioperative re-infarction in patients suffered with recent MI:
• Ratio between diastolic – pressure time index Factors affecting myocardial O2 supply and demand balance.
Duration Since Last MI Re-infarct
(DPTI) Rate
and tension time index (TTI) is called ECG leads! Coronary artery responsible
DECREASE O2 SUPPLY
for ischemia
INCREASE O2 DEMAND
endocardial viability ratio. II, III, aVF! ! RCA
• Normally Decrease coronary blood flow Tachycardia
With in 3 months 30% it is 1 or more. I, avL! ! ! CCA
• Ratio less than 0.7 indicate subendocardial Tachycardia Increase wall tension (↑preload & after
ischemia. V3 – V5! ! LAD
3 - 6 months 15% load )
Hypotension (diastolic)
Sensitivity of leads to monitor Increase myocardial contractility
ischemia
• DPTI ! Measure of blood flow to the left
> 6 months 6%
ventricle
• V3-61%, V5-75%, V4+V5-90%, IIHypertrophy
Increase preload + V5 -80%,!
on. Continuation: • Coronary perfusion
Dr Azam’s pressure
Notes x diastolic time.
in Anesthesiology 2013 Hypocapnia (coronary vasoconstriction) Shivering
• TTI ! Measure of O2 demand.
II + V4+V5-98%
ANESTHETIC MANAGEMENT • Systolic BP and systolic time. MI is defined
•Coronary as persistent ST-THTN
artery spasm changes lasting 60
COMMONLY USED HYPOTENSIVE AGENTS
II)seconds.
DECREASE O2 CONTENT ± Increase metabolic status
. !"#$%!#"&'()#*!"#!&"&'(%+ Mechanism of • Endocardial viability ratio can be useful in AVAILABILITY
Drugs Dosage
• Continue the anti-hypertensives/anti anginal
Advantage
drugs
Disadvantage If only one lead can be displayed,
•Anemia V5 should be used
action evaluating O2 till theand
supply time of surgery
demand balance. Increase stress (surgery)
• 1. Sodium
ACEI is 0.5 on
skipped to 10μg/kg/iv
the day Nitric
of oxide • Myocardial
surgery Rapid onset O2and Cyanide
demand toxicity,
is the ↑ ILP
most importantbecause lead V5 has the greatest sensitivity.
nitroprusside mediated direct determinant
offset Hypoxemia Exercise
of reboundblood
myocardial ↑ pulmonary
HTN, flow. • (75% intraoperatively and 89% during exercise treadmill
s. • Aspirin/clopidogrel - stoppedvasodilator7 days before
shunt to Ocoagulates Decrease O2 release from Hb
abnormal
• Relative contribution 2 requirements testing).
Ticlopidine-stopped
• 2. NTG 14 daysSame
1 to 10 μ/kg/iv before, Rapid onset and Cyanide toxicity, ↑ ILP
of nitric includes. Increase pH
Platelet GPllb/Illa inhibitors:oxide
• nitroglycerine offset rebound HTN, ↑ pulmonary Decrease, DPG
of the • Abciximab - 24 -48 hours • Basal requirement - ! 20%
shunt coagulates abnormal HAEMODYNAMIC
Decrease temp GOALS DURING ANESTHESIA ARE:
tion of each 3. Trimethaphan 1 to 5mg/iv
Eptifibatide & tirofiban -4-8 hours Ganglion • Electrical
Rapid activity
onset and -!Histamine 1% release, Objective is to maintain a favorable myocardial supply -
blockade • Pressure
offset work !-! 64%
↓pseudocholinesterase demand relationship.
imit of the • Warfarin - Should be discontinued 4 - 5• days Volumeprior
work to surgery.
-!
cerebral 15%
compression below 1. Autonomic mediated increases in HR and BP should be
otension • If emergency - CNB can be done if INR < 1.5 MAP 55mmHg
more Vitamin K 10-25 mg im/IV - slowly 12-24 • Myocardium
hours prior normally extracts 65% of O2 in
to surgery. controlled by deep anesthesia or adrenergic blockade and
f duration arterial but while other tissues extract only 25%. excessive reductions in coronary perfusion pressure or
• 4. Esmolol Delay
Heparin: 0.2the
to 5mg/kg/iv
heparinβ-adrenergic
administration Rapid
- 1-2
Therefore
onset
hoursand Cardiac
myocardium aftercannot
thedepress and
compensates for
loading,
procedure. Remove blockade
the catheter after 2-4 offset
hoursinofblood
decrease
bronchospasm
lastflow
heparin dose.more O2
by extracting
arterial oxygen content are to be avoided.
volume by 50-200μg/kg/iv
Re-heparinized onlytabafter from Hb. ofAny increase in myocardial metabolic 2. Diastolic arterial pressure should be generally maintained at
5. Labetalol 20mg 0.5 to2 αhours
and β of
- removal catheter.
↓ probability of Bronchospasm
omplete • LMWH: Risk of 2mgbleeding/spinal
iv, total hematoma
adrenergic
demand must be met by an increase in
are decreased.
adverse effects CNB can be 50mm Hg or above. Higher diastolic pressure may be
coronary blood flow. preferable in patient with high grade coronary occlusion.
performed safely300mg after 12-24blockedhours of administration. Catheter should be
care 6. PGE1 0.1 to 0.65 μg/ Direct Rapid onset, Slow offset, bradycardia 3. Excessive increase in LVEDP (such as those caused by
removed 12 hourskg/iv
after the vasodilation
last LMWHEndocardial
administration.
Viability Ratio = DPTI/TTI
decreases reflex hypotension
• High risk patients - pre-operative NTG infusions tachycardiamayandbe started.
fluid overload) should be avoided because they ↑ L,V. after
• Prophylaxis for venous thromboembolismstable mayCBF be required for some load and can ↓ sub endocardial perfusion. 138
surgeries like major surgery in a patient withNotes

clinical conditions 2013 4. Adequate blood Hb > 9-10 mg/dl and arterial oxygen
7. Nicardipine Begin 5mg/hr Coronary Dr andAzam’srapid onset,in Anesthesiology
Slow off, resists
associated with maxvenous
15mg/hrthromboembolism
peripheral risk or patients
decreases older thantherapy.
reflex antihypotensive 60 ↑ tension (>60mm Hg) should generally be maintained.
years without risk factors, total hip replacement,
vasodilator tachycardiaintracranial
and pulmonary. shunt
neurosurgeries etc. stable CBF
8. Inhalation Titrate by Vasodilation and Provides ↑ ICP, ↑ cerebral edema, ↓

anesthetics inspired conc. myocardial surgical therapy vital organ blood flow
depression 123
330
Dr
siology 2013 Azam’s Notes in Anesthesiology 2013
24. What are the side effects of different irrigation solutions?

Osmolality
Solution Advantages Disadvantages
(MOSM/L)
Distilled water 0.0 Improved visibility Hemolysis, Hemoglobinemia,
Hemoglobinuria Hyponatremia
Glycine (1.5%) 220 Less likelihood of Transurethral Resection Transient postoperative visual syndrome,
syndrome Hyperammonemia Hyperoxaluria
Sorbitol (3.3%) 165 Same as Glycine Hyperglycemia, possible Lactic acidosis

Osmotic diuresis
Mannitol (5%) 275 Isosmolar solution itʼs Not metabolized Osmotic diuresis possibility of acute
intravascular volume expansion.
Normal Saline 308 (ISo) Ionized, cannot be used with cautery
Urea 1% 167 Free passage into extra-

vascular space,↑ Blood urea
Glycine (1.2%) 175 Less likelihood of TURP syndrome Transient visual impairment
(blindness)
Hyperammonemia, Hyperoxaluria
Glucose 2.4 - 5% 139 Sticky

Cytal 178 Expensive
(sorbitol 2.7% + Not easily available
Mannitol (.54%)
331

332

IV Fluids : 0.9% NaCl (NS)
Patient's
Flow Charts Weight :
& Diagram. kg Dr Azam’s Notes in Anesthesiology 2013
tes
Classic Formulas:
Patienteffects
What are the systemic is a :of Glycine?
man WhatHypernatremia
are the manifestation of Hyponatremia? Hyponatremia
Volume of Glycine absorbed Signs and symptoms Serum ECG Changes CNS desired Na+CVSrequirement (mmol) =
Calculate using : Adrogue formula Sodium Total H2O deficit (L) = total body Na +
serum Na+ )
Manifestations
(mEq/L) )
water x ( 1 - serum
>500 ml Visual disturbances, headache 120 Widened QRS Restlessness
Na+ andRate of infusion &
hypotension (cc/hr)
Calculate Fluids Reset =
confusion Bradycardia
>1000 ml IVF Rate : Depressed consciousness, Pain 115 Widened QRs/elevated Nausea and / or Cardiac depression
abdomen St segment semi coma
110 Adrogue Formula:
Ventricular tachycardia/ Seizure and coma CHF
IV Fluids : 0.9% NaCl (NS) fibrillation
>3000 ml Diarrhea (infusate Na+ + infusate K+) - serum Na+
Change in serum Na+ =
What is the strength of sodiumtotal body water + 1
in various
Classic Formulas:
Plasma conc. of Glycine Signs and symptoms
solutions?
Hypernatremia
5-8 mmol/l Hyponatremia
Visual disturbances Infusate Na+ Total Body Water (in li
desired +
Na requirement (mmol) = total bodyInfusate +
water x (desired Na - (mmol/L) Children 0.6 x w
>10 mmol/l Transient
Na + blindness, N&V+
Total H2O deficit (L) = total body serum Na ) 5% NaCl 855 Women 0.5 x w
)
water x ( 1 - Fatal
serum + 3% NaCl (mmol) x 1000
Na requirement 513
>20 mmol/l Men 0.6 x w
Na + Rate of infusion (cc/hr) 0.9% NaCl (NS) 154
= infusate Na+ (mmol/L) x time Elderly Women 0.45 x w
Lactate Ringer's
(hours) 130 Elderly Men 0.5 x w
What is the formula used to calculate change in Serum sodium? 0.45% NaCl (! NS) 77
0.2% NaCl (" NS) 34
Adrogue Formula:
5% Dextrose in water (D5W) 0
(infusate Na+ + infusate K+) - serum Na+
Change in serum Na+ = Insensible water losses = 500 - 1500 cc/day.
total body water + 1
Fever increases insensible water losses by 10% per degree Celsi
cc/day increase per degree Celsius above 37°.
Infusate Na+ Total Body Water (in liters) : Adrogue, HJ; and Madias, NE. Primary Care: Hypernatrem
Infusate (mmol/L) Children 0.6 x weight of Medicine 2000; 342(20):1493-1499.
Adrogue, HJ; and Madias, NE. Primary Care: Hyponatremi
5% NaCl 855 Women 0.5 x weight of Medicine 2000; 342(21):1581-1589.
3% NaCl 513 Men 0.6 x weight DISCLAIMER: All calculations must be confirmed before use. The authors mak
0.9% NaCl (NS) 154 Elderly Women 0.45 x weight information contained herein; and these suggested doses are not a substitute f
MedCalc.com nor any other party involved in the preparation or publication of t
Lactate Ringer's 130 Elderly Men 0.5 x weight special, consequential, or exemplary damages resulting in whole or part from a
this material.
0.45% NaCl (! NS) 77 333
0.2% NaCl (" NS) 34 Copyright © 1999-2012 MedCalc.com

Dr Azam’s Notes in Anesthesiology 2013 Created: Wednesday, January 23, 2002
5% Dextrose in water (D5W) 0 Last Modified: Wednesday, January 27, 2010
The local anesthetics typically have pKa’s greater than 7.4, so less than 50%
of the drug exists inDr
theAzam’s
lipid soluble formininAnesthesiology
Notes normal extracellular2013
fluid.
note that theFlow
MACCharts
values cited above for inhalational anesthetics are
& Diagram.
Additionally, commercial preparations of local anesthetics typically have
or normal adults. Table 5.2 lists MAC values for commonly used inha-
agents. Formula to calculate the sodium deficit?
Table 6.1 Pain fiber types.
• Sodium
MAC value for deficit anesthetic
an inhalational (mEq) = Weight
may beXincreased
Normal TBW X (130 - Current Na)
or decreased Fiber type Local anesthetic sensitivity Size Myelination
• The normal TBW (in liters) is 60% of the lean body weight (in kg) in men,
idual patients by
anda variety
50% ofofthe
factors,
lean as outlined
body weightininTable 5.3: Thus, for a 60 kg woman
women. A + Large Yes
with a plasma sodium of 120 mEq/L, the sodium deficit will be 0.5 × 60 × B ++ Medium Yes
s Oxide (130 - 120) = 300 mEq. C +++ Small No
oxide is a colorless,
• nonpungent
E.g.Because gas with
3% sodium a slightly
chloride sweet
contains odor ofand
513 mEq sodium per liter, the
volume of
is the only inorganic hypertonic
chemical in saline
current needed
use astoan
correct a sodium
anesthetic. Thedeficit of 300 mEq will
be 300/513 = 585 mL. Using a maximum rate of rise of 0.5 mEq/L per hour for
ressure of nitrous oxide atsodium
the plasma room temperature is 745
(to limit the risk PSI. Therefore,encephalopathy),
of a demyelinating it the
s a gas at atmospheric pressure, because
sodium concentration deficit its critical
of 10 mEq/L temperature (theexample should be
in the previous
corrected
ture below which a gas over at least
cannot 20 hours.no
be liquefied, Thus, the maximum
matter how high rate
the of hypertonic fluid
administration will be 585/20 = 29 mL/hour. If isotonic saline is used for sodium
pressure) is in the range of ambient operating room temperatures.
replacement, the replacement volume will be
It is replacement volume
60 3.3ANESTHESIA
L times the STUDENT SURVIVAL GUIDE
s a compressedofliquid. Note that3%
the hypertonic duesaline
to itssolution.
low potency (MAC = 105%).
Table 5.2 Minimum alveolar Table 5.3 Factors affecting MAC.

concentration (MAC) values.
Increased MAC Decreased MAC
Agent MAC
Children (from infancy to adolescence) Premature infants and the elderly
Desflurane 6.0% Hypernatremia Hypothermia
Sevoflurane 2.05% Cocaine or amphetamine intoxication Pregnancy
Isoflurane 1.15% Chronic alcohol use Acute alcohol intoxication
Halothane 0.75% MAO inhibitors Opiates, benzodiazepines, barbiturates, clonidine,
Nitrous Oxide 105% Tricyclic antidepressants dexmedetomidine
administration of 1 MAC of nitrous oxide at atmospheric pressure is not

possible – as this would lead to asphyxia from a lack of oxygen. In practice, the
highest MAC of nitrous oxide that can be delivered on most anesthesia machines
is 0.67 (corresponding to an inspired concentration of 70%).
L Cardiovascular effects: Nitrous oxide depresses myocardial contractility,
but this effect is usually offset by its stimulation of the sympathetic nervous 334
system. Blood pressure and heart rate are generally unchanged by adminis-
tration of nitrous oxide in the absence of surgical stimulation.
20 L
ANESTHESIA STUDENT SURVIVAL GUIDE Bradycardia, owing to a resemblance to acetylcholine and subsequent a
Flow Charts & Diagram.
muscarinic receptors, and malignant hyperthermia (a rare hypermetabo
Table 2.1 Historical dates of note. that
Tablecan
4.3 occur in thedrug
Recommended skeletal
dosages muscle
for commonof susceptible
IV agents.a individuals) are ot
1500 BC The use of opium-like preparations in anesthesia recorded in the Ebers Papyrus
effects of note. Table 4.5Induction
Benzodiazepines b
shows agents
contraindications to the use of succiny
1275 Ether discovered by Spanish chemist Raymundus Lullius Because
Midazolam 1–4ofmg its mechanism
Propofolof
2–2.5action, succinylcholine
mg/kg (induction), cannot be “reve
25–200 mcg/kg/min (infusion)
1540 The synthesis of ether was described by German scientist Valerius Cordus acetylcholinesterase
Diazepam 2.5–10 mg inhibitors. In fact, attempting reversal can actual
Thiopental 3–5 mg/kg
Lorazepam 1–4 mg Etomidate 0.2–0.5 mg/kg

1665 First intravenous injection of an opiate through a quill neuromuscular b
Opioids (Bolus)
blockade prolonged and more intense.
Ketamine 1–2 mg/kg IV, 3–4 mg/kg IM (induction or bolus),
1773 Joseph Priestly introduces nitrous oxide
Morphine 1–5 mg 1–2 mg/kg/h infusion
1842 Crawford W. Long successfully uses ether during neck tumor excision in Jefferson, Georgia Neuromusclular blockersc
1845 Horace Wells publicly demonstrates the use of nitrous oxide in Boston – however, it is
Nondepolarizing
Hydromorphone 0.2–0.5 mg
NMBs Succinylcholine 1–2 mg/kg, 20 mg bolus for laryngospasm
Fentanyl 25–100 mcg
labeled a “failure”
There are several typesRocuronium
Meperidine 25–50 mg
of nondepolarizing
0.6 mg/kg NMBs, with the four in mo
1846 William T.G. Morton shows first successful public demonstration of ether anesthesia at
Massachusetts General Hospital, Boston. mon use being rocuronium, vecuronium, cisatracurium, and pancu
Vecuronium 0.1 mg/kg
Cisatracurium 0.15 mg/kg

1847 James Young Simpson uses Chloroform for labor pain (see Table 4.6). They can be subdivided according to their chemica
Pancuronium 0.1 mg/kg
1853 John Snow administers chloroform to Queen Victoria during childbirth ture
a
Adultinto benzylisoquinoliniums
dosages: Always start at low end of range and(cisatracurium),
titrate up. and steroidals (rocu
1878 William MacEwan introduces oro-tracheal intubation with a flexible brass tube
vecuronium, and pancuronium). NMBs exert their effects by comp
b
Titration ranges for premedication or intraop/post op bolus dosing.
c
1884 Carl Koller discovers local anesthetic properties of cocaine Intubating dosages: Divide by 3 for ED95, divide by 5 for maintenance bolus dosing.
1889 August Bier describes spinal anesthesia for surgery
1894 Anesthetic charts introduced

1905 Long Island Society of Anesthetists founded Table 4.5 Contraindications to succinylcholine use.
1921 Fidel Pagés describes a lumbar approach to epidural anesthesia
1932 First barbiturate, hexobarbital, used clinically Elevated serum potassium levels (!5.5 meq/L)
1941 Robert Miller and Sir Robert Macintosh introduce “Miller” and “Macintosh” blade concepts, History of burn injury
respectively
History of denervation injury
1942 Harold Griffith uses curare for the first time during an appendectomy
Known or suspected myopathy
1956 Michael Johnstone introduces halothane, a halogenated inhalational agent
1960s Fentanyl, ketamine and etomidate synthesized Known or suspected risk for Malignant Hyperthermia
1977 Propofol is synthesized Known pseudocholinesterase deficiency
1970s Pulse oximeter is developed and becomes widely available for use in 1980s
1980s Halothane gradually replaced by enflurane and isoflurane
1983 Archie I.J. Brain introduces Laryngeal Mask Airway (LMA)
1986 ASA House of Delegates passes “Standards for Basic Anesthetic Monitoring” resolution
Table 4.6 Neuromuscular blocking drugs.
1990s Sevoflurane and Desflurane introduced into clinical practice Drug Onset Duration Mode of elimination Important notes/si
2000s Anesthesia Information Management Systems (AIMs) come into widespread use effects
Succinylcholine 30–45 s 5 min Plasma cholinesterase 335 duration in p

Increased
Airway Management with pseudocholineste
DrEveryone
Azam’srotating
Notes in Anesthesiology
through 2013 to learn how to intubate, but it is
anesthesia wants Cisatracurium 2–4 min 30–40 min Hoffman degradation deficiency
more important to learn the way to effectively bag-mask ventilate a patient.
(lipophilic)
Flow
FigureCharts & Diagram.
6.1 Local anesthetic structure.
PHARMACOLOGY 2013
OF ADJUNCT AGENTS 77 L
Table 6.2 Properties of common local anesthetic agents. Table 7.2 Receptor actions of commonly used vasopressors.
Agent Onset of action pKa (36°C) Max dose Duration of Drug Direct Indirect Site of action
(mg/kg)* action (h) Ephedrine + ++ D, E
Amides Lidocaine Rapid 7.8 4.5 (7 with epi) 1–2 Phenylephrine + D
Mepivacaine Moderate 7.7 5 (7 with epi) 1.5–3 Norepinephrine + D, E
Prilocaine Slow 8.0 6 (9 with epi) 1–2 Dopamine ++ + D, E, D (dopamine receptor)
Ropivacaine Slow 8.1 2.5 (3 with epi) 4–8
Bupivacaine Slow 8.1 2.5 (3 with epi) 4–8

Table 7.3 Vasopressor dosing.
Esters 2-Chloroprocaine Very Rapid 9.1 9 (15 with epi) 0.5–1
Ephedrine 2.5–10 mg IV bolus
Procaine Rapid 8.9 7 (10 with epi) 0.75–1
Phenylephrine 40–100 mcg IV bolus or 20–150 mcg/min infusion
Tetracaine Slow 8.4 1.5(2.5 with epi) 3
Norepinephrine 0.01–0.1 mcg/kg/min infusion
Cocaine Rapid
76 ANESTHESIA
L
STUDENT SURVIVAL GUIDE8.7 1.5 0.5
Dopamine 78 L
ANESTHESIA STUDENT
2–20SURVIVAL GUIDEinfusion
mcg/kg/min
* Maximum dose for a single subcutaneous injection.
Table 7.4 Commonly used antiemetics.a

Peak 7.1
Table bloodActions
levels ofoflocal anesthetics
vasoactive are related
receptor sites.to the dose administeredsurgery and anesthesia can cause nausea and vomiting, and consequently there
Ondansetron (Zofran) 4 mg IV, may repeat x 1 (0.1mg/kg up to 4mg in children)
and the rate of absorption of the drug from its site of action. Injection intoare many different Dolasetron drugs available
(Anzemet)
for prevention and treatment.
12.5 mg IV, may repeat × 1
Receptor Receptor site action
a highly vascular area leads to higher blood levels of the drug than placing a Serotonin antagonists are the mainstay 0.5–1
Granisetron (Kytril) of antiemetic
mg IV prophylaxis and
A-1 Glycogenolysis, gluconeogenesis, constricts vascular smooth
similar amount of drug into a less vascular area. The rank order of peak blood muscle, PONV
relaxes GI treatment.
tract These
Promethazine drugs work
(Phenergan) by blocking
12.5–25 mg5HT3 receptor
IV, may repeat ×1 binding.
drugOndansetron is byDroperidol
far the most commonly used serotonin antagonist, but
Dexamethasone (Decadron) 4–8 mg IV, best given early during intraoperative period
A-2
concentrations of local anesthetic
Constricts vascularafter administration
smooth muscle, decreasesofinsulin
the same doseand
secretion ofnorepinephrine b
(Inapsine) 0.625 mg IV, may repeat q 10 min × 3
release
at different sites is shown below: dolasetron and granisetron are also available. Patients at moderate to high risk
a
All dosages for adults unless noted.
B-1 Increases heart rate and contractility, secretion of renin for PONV can be bgiven a prophylactic
Must monitor ECG for 2 h post serotonin
administration.antagonist prior to surgery,
! tracheal ! intercostal ! caudal!gluconeogenesis,

but current guidelines for low risk patients are to treat only those who exhibit
intravenous
B-2 Glycogenolysis, relaxes! sciatic
epidural! brachial plexus vascular! subcutaneous injection
smooth muscle and bronchioles
nausea and vomiting postoperatively. Side effects sometimes include headache,
$-1 Increases renin release, dilates vascular smooth muscle lightheadedness or drowsiness.
Epinephrine and other vasoconstrictors slow the rate of absorption. Droperidol blocks the transmission of dopamine, serotonin, and GABA.
$-2 Constricts smooth muscle, inhibits norepinephrine release Promethazine (Phenergan)
Though an extremelyis aeffective
common secondit line
antiemetic, agentreserved
is typically for treatment
for refractory
Strongly protein-bound local anesthetics (e.g. bupivacaine and ropivacaine)
of nausea and vomiting
nausea andthat has not
vomiting dueresponded
to concernstoabout a serotonin antagonist.
QT prolongation, and the
tend to be more lipid soluble, more potent, and have longer times to onset, longerPromethazine is aconsequent need to monitor the cardiac rhythm of
nonselective antihistamine that may lead to drowsiness, and patients after treatment.
durations of action, and slower absorption from neural tissue (Table 6.2). Droperidol also possesses sedative properties, and was once popular as a
usually administered to patients who have both low blood pressureshould and lowbe used with caution in patients for whom excessive sedation could be
premedication prior to surgery.
heart rate. In addition to having vasopressor effects, ephedrine is also a bron- detrimental (e.g. those with sleepis apnea
Scopolamine or those receiving
an anticholinergic drug which narcotics
is oftenoradministered
other
respiratory depressants).
preoperatively via a transdermal patch (lasts up to 3 days). Patients should be
chodilator, and it can be administered to patients who are in bronchospasm. Dexamethasone counseled to wash their hands
is recommended as after
partthe of removal of a scopolamine
a prophylactic regimen
336 patch, as
Phenylephrine acts on alpha receptors causing increased vascular resistance inadvertent rubbing of the eyes may lead to prolonged
(typically in concert with a serotonin antagonist) for patients at moderate pupillary dilation.
Dr Azam’s Notes in Anesthesiology 2013 Commonly used antiemetics and their dosages are outlined in Table 7.4.
and blood pressure. It has no beta agonist effects and frequently orcauses a for postoperative nausea and vomiting. The exact mechanism
high risk
Physical
pressure factors affecting
medication, mask ventilation
last echocardiogram, can betest.
or stress determined from age and In these patients, the presence or absence of active clinical risk factors
physical
Flow One history
should
Charts as
&then shown in thealist
determine
Diagram. below.functional
patient’s If the likelihood
capacityof(see
a difficult mask
table below). determines the need for further evaluation.
Studies have correlated better perioperative outcome with patients whose
metabolic equivalent (MET) activity was greater than or equal to 4 METs
Factors Affecting Mask Ventilation Clinical Risk Factors for Increased Perioperative Cardiac Risk
(see Table 8.1).
t 1SFTFODFPGBCFBSE
The revised ACC/AHA guidelines (2007) recommend the following )JTUPSZPGIFBSUEJTFBTF .* 2XBWFTPO&$( LOPXO$"%
t #.*! 26 kg/m2
stepwise approach to evaluating a patient’s cardiac status for patients undergoing
t .JTTJOHUFFUI )JTUPSZPGDPNQFOTBUFEPSQSJPSIFBSUGBJMVSF
noncardiac
t "HF! 55 surgery: )JTUPSZPGDFSFCSPWBTDVMBSEJTFBTF
t )JTUPSZPGTOPSJOH
%JBCFUFTNFMMJUVT
Adapted from Langeron, O. Prediction of difficult mask ventilation. Anesthesiology 200; 92:1229. 3FOBMJOTVGGJDJFODZ
# Clinical risk Surgical Risk Action

Table 8.1 Energy requirements for various activities. factors
.&5 &BUJOH HFUUJOHESFTTFE XPSLJOHBUBEFTL
"OZ 1SPDFFEXJUITVSHFSZ
.&54 4IPXFSJOH XBMLJOHEPXOFJHIUTUFQT
.&54 8BMLJOHPOBGMBUTVSGBDFGPSPOFPSUXPCMPDLT 1–2 *OUFSNFEJBUFSJTLTVSHFSZ 1SPDFFEXJUITVSHFSZXJUIIFBSUSBUFDPOUSPM
.&54 3BLJOHMFBWFT XFFEJOHPSQVTIJOHBQPXFSNPXFS
7BTDVMBSTVSHFSZ PS
.&54 8BMLJOHGPVSNJMFTQFSIPVS TPDJBMEBODJOH XBTIJOHDBS
.&54 /JOFIPMFTPGHPMGDBSSZJOHDMVCT IFBWZDBSQFOUSZ VTJOHQVTINPXFS 3+ *OUFSNFEJBUFSJTLTVSHFSZ $POTJEFSDBSEJBDUFTUJOHJGJUXJMMDIBOHFNBOBHFNFOU
.&54 %JHHJOH TQBEJOHTPJM TJOHMFTUFOOJT DBSSZJOHQPVOET
.&54 .PWJOHIFBWZGVSOJUVSF KPHHJOHTMPXMZ SBQJEMZDMJNCJOHTUBJST DBSSZJOHQPVOETVQTUBJST 7BTDVMBSTVSHFSZ $POTJEFSDBSEJBDUFTUJOHJGJUXJMMDIBOHFNBOBHFNFOU
.&54 #JDZDMJOHBUBNPEFSBUFQBDF TBXJOHXPPE TMPXKVNQJOHSPQF
Source: ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for
.&54 #SJTLTXJNNJOH CJDZDMJOHVQIJMM XBMLJOHCSJTLMZVQIJMM KPHHJOHBU.1)
Noncardiac Surgery: Executive Summary. JACC Vol. 50, No. 17, 2007.
.&54 $SPTTDPVOUSZTLJJOH GVMMDPVSUCBTLFUCBMM
.&54 3VOOJOHDPOUJOVPVTMZBU.1)
1VMNPOBSZ
Adapted with permission from Brigham and Women’s Hospital Preoperative Assessment Form.
Postoperative pulmonary complications can prolong the hospital stay by
an average of 1–2 weeks. Therefore, it is important to review patient and
procedure-related risk factors, perform a clinical evaluation, and recommend
risk-reduction strategies to improve patient care and outcome.
Potential patient-related risk factors for perioperative pulmonary complica-
tions include:
L Smoking
L Poor general health status (ASA > 2)
L Old age (>70)
L Obesity
L Chronic obstructive pulmonary disease
L Reactive Airway Disease (Asthma)
Potential procedure-related risk factors include: 337

L Surgery > 3 h
Dr Azam’s Notes in Anesthesiology 2013 L General anesthesia
Figure 9.2 The glottis and epiglottis (Reproduced with permission from Principles of Airway
thy) and increase the risk during certain surgeries. Hepatic disease can also
Management, 3rd ed., Brendan Finucane and Albert Santora, Springer 2003).
Flow
cause Chartscoagulation
abnormal & Diagram.and altered drug pharmacokinetics. Dr Azam’s Notes in Anesthesiology 2013
Table 9.1 Components of the preoperative airway physical examination.

Table 8.2 Risk reduction strategies for pulmonary complications.
Component Nonreassuring finding
Preoperative
Length of upper incisors Relatively long
t 4NPLJOHDFTTBUJPO GPSBUMFBTUXFFLT
Relation of maxillary and mandibular inci- Prominent “overbite” (maxillary incisors anterior to man-
t 5SFBUBJSGMPXPCTUSVDUJPO QBUJFOUTXJUI$01%PSBTUINB
sors during normal jaw closure dibular incisors)
t (JWFBOUJCJPUJDTQPTUQPOFTVSHFSZJOQSFTFODFPGSFTQJSBUPSZJOGFDUJPO Relation of maxillary and mandibular inci- Patient’s mandibular incisors anterior to (in front of) maxillary
sors during voluntary protrusion of the jaw incisors
t &EVDBUFQBUJFOUTBCPVUMVOHFYQBOTJPONBOFVWFST
Inter-incisor distance (mouth opening) <3 cm
Intraoperative
Visibility of uvula Not visible when tongue is protruded with patient in sitting
position (e.g., Mallampati class > II)
t -JNJUTVSHJDBMEVSBUJPOI
Shape of palate Highly arched or narrow
t "WPJEQBODVSPOJVN
Compliance of submandibular space Stiff, indurated, occupied by mass, or non-resilient
t $POTJEFSMBQBSPTDPQJDTVSHJDBMBQQSPBDI
Thyromental distance <3 finger breadths or 6–7 cm
Postoperative
Length of neck Short
t &ODPVSBHFJODFOUJWFTQJSPNFUSZPSEFFQCSFBUIJOHFYFSDJTFT Thickness of neck Thick (neck size > 17 inches)
t *OJUJBUF$1"1 DPOUJOVPVTQPTJUJWFBJSXBZQSFTTVSF
Range of motion of head and neck Patient cannot touch tip of chin to chest or cannot extend neck
t $POTJEFSFQJEVSBMBOBMHFTJBJOUFSDPTUBMOFSWFCMPDLT Reproduced with permission from Caplan RA, Benumof JA, Berry FA (2003) Practice guidelines for
Adapted from STUDENT
Smetana et al. Preoperative pulmonary evaluation. NEJM. Vol 340: 2008. 160 L
ANESTHESIA
the management ofSTUDENT SURVIVAL
the difficult airway: GUIDE
an updated report by the American Society of Anesthesi-
120 ANESTHESIA SURVIVAL GUIDE
ologist’s Task Force on management of the difficult airway. Anesthesiology 98:1269–1277.
L
1 Table10.1 Basic anesthesia machine components.

"QSPTQFDUJWFTUVEZPGQBUJFOUTSFWFBMFEUISFFUJNFTBTNBOZQVMNPOBSZDPNQMJDBUJPOT
BNPOHUIFQBUJFOUTSFDFJWJOHQBODVSPOJVNGSPNSFTJEVBMQBSBMZTJT .FUBOB (81SFPQFSBUJWF
t 4PVSDFPGHBTFT 02, N20 "JS
1VMNPOBSZ&WBMVBUJPO/&+.7PM

Table 12.1 M.S.M.A.I.D.S. mnemonic.
t 'MPXNFUFST
t 7BQPSJ[FST
t 4DBWFOHJOHTZTUFN
M o Machine
Note: the breathing circuit and CO2 absorber are separate from the machine.
S o Suction
Table 10.2 Components of the high and low pressure systems.

M o Monitors
)JHIQSFTTVSFTZTUFN A o Airway
t 1JQFMJOFTBOEDZMJOEFSTGPSUIFHBTFTEFMJWFSFE
t 'BJMTBGFWBMWF
I o IV
t 1SFTTVSFSFHVMBUPS
D o Drugs
t 0YZHFOGMVTIWBMWF
-PXQSFTTVSFTZTUFN S o Special
t 'MPXNFUFST
t 7BQPSJ[FST In preparing a room, most anesthesiologists will use the mnemonic
t 'MPXDPOUSPMWBMWF Our preflight check starts at the beginning of the day with our initial roo
M.S.M.A.I.D.S.
t $IFDLWBMWF
t $PNNPOHBTPVUMFU setup. In preparing a room, most anesthesiologists will use the 338 mnemon
M.S.M.A.I.D.S. (Table 12.1) just as a pilot will use a written checklist to ma

Drfrom
Azam’s Notes
the flow control intoAnesthesiology
valve 2013
the patient. This prevents high pressures (that could
induce barotrauma, or lung damage) from being delivered to the patient. A mod- sure that nothing is missed. The seven individual components of the mnemon
Flow Charts & Diagram.ANESTHETIC TECHNIQUES: GENERAL, SEDATION, MAC L
163
164 L
Dr Azam’s
ANESTHESIA STUDENT SURVIVAL GUIDE Notes in Anesthesiology 2013
Table 12.2 Stages of general anesthesia. Table 12.3 Action sequence of a general anesthetic.
Air plane analogy Anesthesia tasks Important points
Stage 1 – Amnesia Patients should follow commands; Respiration pattern typically regular
Stage 2 – Delirium Period of uninhibited excitation; Patients at risk for laryngospasm; Pupils Preflight check − Operating room setup − M.S.M.A.I.D.S
often divergent; Respirations often irregular − Preoperative patient evaluation − Assessment of medical history
Stage 3 – Surgical anesthesia Target depth for anesthesia during surgery; Respiration pattern typically regular − Preoperative medications − Confirm NPO status
ANESTHETIC TECHNIQUES: REGIONAL L
177 − Obtain informed consent
Stage 4 – Overdosage Patients at risk for hypotension and cardiovascular collapse
− Obtain I.V. access
− Administer appropriate preoperative
ANESTHETIC TECHNIQUES: REGIONAL L
177 medications and/or anxiolysis
Table
use 13.1that Risks
to ensure a patientofisneuraxial anesthesia.
ready for extubation. If a patient is going to be Takeoff − Patient monitoring − Place and confirm appropriate monitors
extubated awake, he/she should be following commands, able to oxygenate and − Induction of anesthesia − Position patient and pad pressure points
− Airway management − Preoxygenate
ventilate
Bleedingwithout assistance,
Table 13.1and able of
Risks to neuraxial
protect his/her airway. The four stages
anesthesia. − Administer induction agent
ofInfection
general anesthesia are outlined in the Table 12.2. − Place endotracheal tube or other advanced
Bleeding
airway device
Nerve injury Infection
Taxi to the Terminal Cruising altitude − Maintenance of anesthesia − Protect patient eyes
Nerve injury − Maintenance of homeostasis − Monitor vital signs and maintain appropriate
The taxi to the
Post-dural terminal
puncture and the post flight check list is analogous to the trip from
headache blood pressure
Post-dural puncture headache
the operating
Failure of blockroom to the post
toFailure
provide anesthesia recovery area (PACU). The anesthesia
adequate − Ensure amnesia and anesthesia
of block to provideanesthesia
adequate anesthesia
provider should be at the head of the bed continuously evaluating the patient and − Monitor blood loss and administer appro-
priate fluids
ready to support the airway if necessary. Once in the PACU, the anesthesiologist
Table
will give13.2
a reportContraindications
to the to neuraxial
turnanesthesia. Landing − Antagonism of neuromuscular − “Reversal” of neuromuscular blockade
13.2 Contraindications toPACUneuraxialnurse and the care of the patient over to
anesthesia. blockade − Turn off anesthetic agents
the PACUcontraindications
Absolute staff. Orders should be written to prepare
Relative for potential postoperative
contraindications − Emergence/extubation − Ensure patient is awake, following
problems,
ute contraindications such as pain, post operative nausea and vomiting,
Relative contraindications hypoxia, and blood commands, protecting airway and can
Patient refusal Bacteremia
pressure and heart rate perturbations (see Chap. 27, Postoperative Care Unit and ventilate and oxygenate adequately prior
Infection in the area of needle puncture Pre-existing neurologic disease (e.g. multiple sclerosis) to extubation
refusal Common Postoperative Problems)Bacteremia (Table 12.3). − Confirm stable vital signs
Elevated intracranial pressure Cardiac disease
n in the area of needle puncture Pre-existing neurologic disease (e.g. multiple sclerosis) Taxi to the terminal − Safe transfer to PACU − Monitor airway
Anesthetic Techniques
Uncontrolled bleeding Abnormal coagulation studies
− PACU orders and discharge − Maintain oxygenation
d intracranial pressure Cardiac disease
Having outlined the basic sequence of a general anesthetic (Table 12.3), we − Confirm stable vital signs
− Write appropriate order to treat pain,
will now turn to the different types
rolled bleeding of anesthetic
Abnormal techniques
coagulation studiesavailable to take a
nausea, vomiting and hyper or hypotension
patient safely through surgery (also see Chap. 13, Regional Anesthesia). Keep − Give report to PACU staff
according
in mind thattothere
the size
is noofabsolutely
the nervecorrect
fiber, technique
myelinationfor and the concentration
any given procedure. of
the local
The type ofanesthetic
anesthesia(also see Chap.will
administered 6, depend
Pharmacology of Local provider,
on the anesthesia Anesthetics).
Differential
surgeon, and blockade (the orderand
patient’s preferences of may
effects
be among
dictated the different
by the type ofnerve
surgerytypes)
ding to theand/or size patient
typicallyofresults
theco-morbidities.
nerve fiber,Some
in sympathetic myelination
blockade areand
(often
surgeries the concentration
accompanied
minimally and in of Monitored Anesthesia Care (MAC)/Anesthesia Sedation
by change
invasive
temperature
cause sensitivity),
the patients little painfollowed by sensory
or psychological blockadeIn(pain,
discomfort. such light
cases,touch),
a sur- and
cal anesthetic (also see Chap. 6, Pharmacology of Local Anesthetics). Monitored Anesthesia Care or MAC is not a technique of anesthesia but 339rather
finally
geon motor
may blockade
request to have(paralysis). A provider
an anesthesia well-placed neuraxial
present anesthetic
to monitor can pro- a descriptive term for an anesthetic service in which an anesthesiologist
the patient
ential blockade
Drand
vide total(the
administer
Azam’s Notes order
sedation
anesthesia of
forwhileeffects among
the procedure
a variety
in Anesthesiology 2013is being
of surgical theperformed.
different
procedures. Thisnerve
is called types) is requested to be present at a surgical or diagnostic procedure to monitor the
Monitored
There Anesthetic
are a number Careof(MAC).
other medications that can be used for both spinal
coagulopathy, it is done to replace coagulation factors and thereby, restore hemo-
Flow Charts STUDENT
192 ANESTHESIA
L
& Diagram.
SURVIVAL GUIDE 194 ANESTHESIA STUDENT SURVIVAL GUIDE Dr Azam’s Notes in Anesthesiology 2013
stasis. In autoimmune or dilutional thrombocytopenia, transfusion of platelets
L
may at least partly correct these conditions and allow thrombosis to occur nor-
Table 13.3 Summary of upper extremity nerve blocks. mally.
Table 13.4In cases of platelet
Summary of lowerinactivity
extremitydue nerve to disease
blocks. or medications (e.g., NSAIDs),
a small amount
Type of nerve
of plateletsAnatomical
Indications
(one unit land-
ratherAverage
than 6 pooled
Potential
units) can serve as a
Type of nerve Indications Anatomical land- Average Potential complications
block marks needle depth catalyst and initiate platelet
block marksthrombus formation andcomplications
needle depth achieve the first steps of
hemostasis.
Femoral
Finally, long
Anterior thigh;
after surgery, or in protracted
1 cm lateral to palpation 3–5 cm
illnesses or recuperation,
Intravascular injection;
Interscalene Shoulder; Between middle 1–2 cm Hemi-diaphragmatic
upper arm and anterior scalene paralysis; Horner’s it is often necessary
knee; medialto give of RBC when
femoral artery alonga critical anemic missthreshold
obturator and is met.
aspect of lower leg the inguinal ligament lateral femoral cutane-
muscles at the level of Syndrome; epidural spread; As the length of procedure and blood loss increase,
(saphenous nerve)
replacement of blood
ous nerves
C6 (cricoid cartilage) intravascular injection; ulnar
nerve sparing
products may
Lumbar plexus
be needed. Besides the clinical
Hip; anterior thigh; 5 cm lateral from 6–8 cm
volume criteria listed above in
Epidural spread;
Supraclavicular Upper and Between the middle 2–3 cm Pneumothorax (1%

Table 14.3, the
(Psoas) knee;hematocrit
medial the(HCT) is another clinical datum
spinous process intravascularused for assessing
injection;
aspect of lower leg (midline) at the level of retroperitoneal hema-
lower arm; and anterior scalene incidence); intravascular red blood cell volume (RBCV) and anemia indirectly. toma;
(saphenous nerve) iliac crest
HCT is really a surrogate
needle trauma
hand muscles, 1 cm above injection
measurement for RBCV, which is impossible to measure practically.
to kidney
the clavicle
Infraclavicular Lower arm; 2–3 cm caudad from the 6–8 cm Pneumothorax (much lower
As a case begins, one can calculate a patient’s allowable blood
Sciatic (posterior Posterior thigh; Posterior superior iliac 5–7 cm Intravascular injection; loss (ABL)
approach) below the knee spine (PSIS); sacral hia- nerve injury
hand midpoint of the clavicle than with supraclavicular); by using thesurgery formula
(exceptbelow tus;in Fig.trochanter.
greater 14.2. This gives the anesthesiologist a guide
intravascular injection to know how muchnerve
saphenous bloodA line
lossbisecting
can the occur prior to starting a blood transfusion
distribution) midpoint of the PSIS
Axillary Lower arm; 4–6 cm Intravascular injection; pro-
(Fig. 14.3). and greater trochanter
hand longed set-up time; miss the
206 L
ANESTHESIA STUDENT SURVIVAL GUIDE musculocutaneous nerve Serial HCT readings (plus thewith
to intersect clinical
a line criteria used to assess volume status,
drawn from greater tro-
see Table 14.3) are the basis for choosing
chanter to sacral hiatus
to transfuse blood cells. By practical
Table 14.4 Example fluid replacement calculation.
convention,
Sciatic (lateral onethegram
Below knee of Between
Hb isvastus equivalent
lateralis 6–8tocm 3 HCT percentage
Intravascular injection,points. For
example, if a patient has a Hb of 10 g/dl, the HCT will be approximately
approach) surgery (except and biceps femoris nerve injury, will miss 30.
linePatient
and marked.
and procedure:The block needle is inserted 1–2 cm lateral to the femoral artery saphenous nerve muscles, contact femur, posterior thigh
Furthermore, each unit ofthenPRBC in an adult is expected to pain)
raise the HCT by
pulse.
An 80 The
kg male desired motora 1-h
patient undergoes response is aat quadriceps
tonsillectomy twitch.
8:00 am after being made NPOFemoral
at midnight.nerve PNB
distribution) change needle (tourniquet
angle approx. 45°
canBlood
be used
Loss: for surgery involving the knee, anterior thigh, and medial portion
of Estimated
the lower bloodleg.
loss isSince the
ultimately 250femoral
ml nerve is located in close proximity to the
femoral artery,
Crystalloid careful
vs. colloid choice: aspiration is important to avoid intravascular injection
of Crystalloid
local anesthetic
is adequate, no(Figure 13.9).
colloid needed for this small volume blood loss. Lactated Ringers is optimal Ultrasonography
Allowable Blood Loss (ABL) Formula
though saline could be used.
The use of ultrasound in regional anesthesia has increased in popularity over
Replacement:
Sciatic Nerve Block EBV isx done,
the past few years. As more research (HCTini!al – HCTmay
ultrasound final)ultimately
/ HCTinitalprove to
(Calculated from the four parts of Table 14.3.)
The sacral plexus is formed from the ventral rami of L4–S3 nerve roots. The be safer, faster, and more effective than the paresthesia or neurostimulation
Total crystalloid administered is: techniques. Ultrasound emits
where high-frequency
HCT sound waves, which are reflected
patient is placed in the lateral position with the operative side up. The operative final = lowest acceptable hematocrit
120 ml (maintenance for the 1 h duration)
back when they encounter different types of tissue. Different tissues have
leg+960
is flexed at the knee, while the nonoperative leg remains straight. A line is
ml (for the NPO deficit)
different degrees
Figure 14.2 of echogenicity
Allowable Blood Lossand thus
(ABL) reflect the sound waves at different
Formula.
drawn
+750 ml between the
(for the blood loss)greater trochanter and the posterior superior iliac spine.
speeds. The resulting image provides varying shades that helps distinguish the
A second line can beloss,
±250 ml (for the third space drawn from
estimated the greater trochanter to the sacral hiatus.
at 2 ml/kg/h)
tissue types.
A =2080
thirdofline
NS or LRisover
drawn from theperiod.
the 2 h perioperative mid-point of the first line, intersecting the
Nerves can be seen as round, oval, or triangular shaped structures and can
second line. This is
Postoperative maintenance: the point of needle entry. The needle is inserted perpendic- be hyperechoic (light) or hypoechoic (dark). For example, nerves visualized
ular
Maytobe all planes
120 ml per hourwith the desired
with adjustments motor
made based response
on vital of output.
signs and urine plantar or dorsiflexion above the diaphragm tend to be hypoechoic, while those below the diaphragm
of the foot. A sciatic nerve block can be used for surgery below the knee 340
(with the exception of the medial portion of the lower leg innervated by a
Dr Azam’s
ColloidsNotes inunder
may even Anesthesiology 2013
some circumstances draw interstitial fluid back into
the intravascular space.
214 L
ANESTHESIA STUDENT SURVIVAL GUIDE
Estimated Blood Volume (EBV) Formula
EBV = weight (kg) x average blood volume
Note: Avg. blood volume in adult male = 75 ml/kg

Avg. blood volume in adult female = 65 ml/kg
Figure 14.3 Estimated Blood Volume (EBV) Formula.
Table 16.1 Common intraoperative problems and differential diagnoses.

3 points. If such a predicted increase does not occur, one should be concerned
Problem Differential diagnosis Remarks
about ongoing blood loss, hemolysis, or hemodilution with excess IV fluids.
HCT is drawn
Hypoxemia from oxygen
Low inspired venipuncture,
(FiO2) peripheral or central
Always start byvenous
increasingline,
the FiOor2, and then continue to look for other causes.
arterial line. One must interpret HCT carefully, because dilution from crystal- or muscle relaxants, which decrease respiratory drive and
Hypoventilation May be from opioids, benzodiazepines,
muscle strength. If a patient is being ventilated, consider increasing respiratory rate or tidal volumes.
loid or colloid may cause significant variation in HCT even without any sig-
Disconnection of breathing circuit The most common cause of serious hypoxemic accidents.
nificant blood loss.
Atelectasis Often a result of positive pressure ventilation, intubation and/or hypoventilaton. Consider
Decisions about giving platelets and plasma or plasma derivatives are based,
alveolar recruitment maneuvers.
in a similar way, on both clinical criteria and lab values. Diagnostic lab studies
Bronchospasm Consider administering albuterol
such as coagulation panels (PT, PTT, INR, platelet counts), and more specific
Mucus plugging Perform suction and alveolar recruitment maneuvers.
studies such as specific factor levels, may be used in more challenging cases such
Right-mainstem bronchial intubation Maximum depth for tracheal tubes measured at teeth: females 21 cm; males 23 cm. May
as hepatic transplantation (high volume fluid turnover), or in the setting of end-
visualize with bronchoscope or auscultate with stethoscope.
stage liver disease (because of the confounding factor of pre-existing coagu-
Pulmonary thromboembolism (PE) This may be diagnosed by a sudden drop in end-tidal CO2, and hypoxemia that does not improve
lopathy). Patients with known hemophilia or platelet withabnormalities may also by tachycardia and hypotension.
100% FiO2. Often accompanied
warrant more specialized studies
Pulmonary edema of coagulation in the perioperative period.
May be from fluid overload, diastolic or systolic dysfunction, or myocardial infarction.
Venous air embolism Also causes drop in end-tidal CO2, and an increase in end-tidal N2.
Using CVP and
Hypotension
PA Catheters for Volume Assessment
Hypovolemia Common causes include blood loss or dehydration from preoperative fasting.
If surgical bloodRelative
loss isanesthetic
expected to exceed one liter, placement
overdose
of a CVP should
Minimal or a decrease in surgical stimulation can lead to relative anesthetic overdose and hypotension.
be a consideration. The insertion of these lines is discussed in Chap. 15. Inser-
Vasodilatation from medication Opioids, sedatives, and most anesthetics reduce central sympathetic outflow and cause
tion of a CVP line allows convenient monitoring of vasodilatation.
right atrial Virtually
(RA) pressure,
every anesthetic induction or heavy sedation will be accompanied by this
central venous oxygen saturation (CvO2), and serial HCT-alltreated
finding. Usually of which are
with phenylephrine, 40–100 mcg.
useful to assess Low
volume
cardiacstatus
output and RBCV (see Table Many 14.2). anesthetics decrease cardiac output. Other causes include congestive heart failure,
The use of pulmonary artery (PA) catheters is much less common
myocardial infarction, orthan the
tamponade.
use of CVP catheters. They nevertheless are useful at assessing volume status(CO = HR × SV), leading to hypotension.
Severe bradycardia This may cause low cardiac output
more precisely Severe

than tachycardia
a CVP can. PA catheters alsoIfallow
or arrhythmias sampling
atrial fibrillation of mixed
or flutter becomes too fast, hypotension may result.
venous (SvO2) blood, which is a more accurate means of assessing total-body 341
oxygen delivery than is CvO2. PA catheters also allow one to manage fluids
Pneumothorax Uncommon, but may spontaneously arise during positive pressure ventilation.
Anaphylactic reaction Most commonly from reaction to muscle relaxants or antibiotics. Give epinephrine to treat.
Sepsis Sudden decreases in blood pressure may result from sepsis.
Hypertension Pain from surgical stimulus Always consider “light” or insufficient anesthesia.
Essential hypertension These patients may be adequately anesthetized, but still markedly hypertensive.
Tourniquet pain A tourniquet can produce a hard, recalcitrant kind of hypertension called “cuff hypertension.”
Light anesthesia Check for empty vaporizers or medication infusors
Hypervolemia Fluid overload from intravenous fluid or blood products; may lead to pulmonary edema and
congestive heart failure in patients with heart disease.
Failure to Kinked endotracheal tube Most likely during ENT or thoracic surgery.
ventilate
Biting on endotracheal tube May occur during “light” anesthesia or emergence; Can cause negative pressure pulmonary edema.
Disconnection of endotracheal tube from The most common cause.
circuit or adapter
Complete endotracheal tube obstruction Can occur rapidly in infants/children whose ETT are narrow (especially when no humidification is
from mucus or tissue used). Suction or replace tube.
Hole in endotracheal tube or a punctured cuff Most often during laser airway surgery or tracheostomy. Both surgeries also have risk of airway fire!
High airway Bronchospasm (1) deepen anesthesia, (2) consider neuromuscular blockade, (3) administer beta-agonists,
pressures inhaled or intravenous corticosteroids, theophylline or epinephrine
Kinked endotracheal tube May require the use of an armored (metal spring reinforced) tube to prevent kinking.
Biting on endotracheal tube Consider placing a bite block or mouth gag.
Mucus plugging Common in patients with COPD, asthma and cystic fibrosis. This may require replacement of the ETT.
Stacking or auto-PEEP of mechanical breaths Occurs when the expiratory phase isn’t long enough to allow exhalation. Decrease the respiratory rate.
Dynamic airway obstruction May be from an airway tumor or mediastinal mass, especially after change in patient position.
248 L
(continued)
Table 16.2 Intraoperative hypoxemia: corrective actions.

1. Assure 100% FiO2 delivery
2. Hand ventilate to assess compliance and chest excursion
3. Look for any disconnection: circuit, endotracheal tube, connectors

4. Check expired gases for ETCO2
5. Inform the surgical team and operating room nurse if severe

6. Examine the capnograph waveform
7. Inspect the endotracheal tube and circuit for kinking, biting, obstruction
8. Inspect the endotracheal tube for excessively deep insertion (should be 21 cm in females, 23 cm in males)
9. Suction the endotracheal tracheal tube to remove secretions and assess patency or obstruction
10. Perform direct laryngoscopy to verify tube placement in the trachea
11. Apply recruitment maneuvers to open up alveoli 342

it is reflected on an oximeter reading by the decrease in SaO . This is important
Table 16.1 (continued)

Problem Differential diagnosis Remarks
Obesity or chest wall rigidity May be difficult to manage. High opioid dose can cause a “rigid chest syndrome.”
Acute Respiratory Distress Syndrome (ARDS) A common cause of high mean pressures, especially in the ICU.
Hypocarbia Hyperventilation May see in anxious (awake) or mechanically hyperventilated (anesthetized) patients.
Leak of CO2 in sampling tubing This may also cause an abnormality in the capnograph waveform or envelope.
Massive pulmonary embolus Can impair gas exchange, manifesting as a sudden drop in expired CO2.
Hypothermia Most evident in severe hypothermia as during cardiopulmonary bypass.
Cardiac Arrest Impaired circulation and CO2 elimination.
Hypercarbia Hypoventilation Often from opioids, residual neuromuscular blockade, or low respiratory rate/ventilator tidal volumes.
CO2 insufflation during laparoscopy May need to increase minute ventilation to overcome hypercarbia.
Malignant hyperthermia Uncoupling of calcium metabolism in mitochondria from a rare (1:15,000) genetic defect in the
ryanodine receptor of the calcium channel
Hyperthermia Metabolic rate increases 15% for every degree centigrade.
Hypothermia Convective, conductive, radiative, Convective losses are the #1 cause of heat loss in the OR (skin to air). Heat loss also occurs from
evaporative losses wet drapes and sheets, exposed skin or body cavities, non-heated breathing circuits.
Anesthetic effects on hypothalamus Anesthetics cause impaired central thermoregulation due to effects on the hypothalamus.
Administration of unwarmed fluid or blood Fluids should be warmed by an FDA-approved device.
products
Massive blood loss Difficult to keep patients warm after t 1 blood volume has been lost.
Hyperthermia Excessive warming Use the air-warming blanket at a room-temperature setting to cool the patient.
Fever from sepsis or transfusion reaction Give acetaminophen or ibuprofen in addition to a cooling blanket.
Stroke Sudden extreme hyperthermia (>105°F) may be from a stroke to the hypothalamus.
Neuroleptic malignant syndrome Uncommon side effect of antipsychotic medications (chlorpromazine, haloperidol, olanzepine).
Malignant hyperthermia (1) stop anesthetic, (2) give iv dantrolene, (3) call for help (see Appendix B, Malignant Hyperthermia)
343

270 L
FlowPHYSIOLOGY
Charts &AND
Diagrams
ANESTHESIA FOR NEUROLOGIC, ENT, AND OPHTHALMOLOGIC SURGERY L
289
by the specific mechanism
Dr of ischemia
Azam’s Notesasinshown in Table 17.4:
Anesthesiology 2013
Tableagents
these 17.3 may Ischemic cardiac disease.
be beneficial in the management of patients with increased Table 17.4 Etiology of Ischemia and Treatments.
ICP or used to facilitate surgical exposure
Disease Definitionin the “tight,” swollen brain.
Etiology Treatments
Other
Coronary agents
artery disease commonly usedNarrowing
in balanced anesthesia
of coronary arteries from include opioids and
atherosclerosis
benzodiazepines.
Ischemic heart disease Generally speaking, these
Myocardial agents
O2 demand have
not met minimal
by coronary bloodimpact
flow on Hypotension – phenylephrine
CMR or CBF
Acute coronary and are
syndrome commonly used
/ myocardial asincludes
Term that part ofanyaofbalanced anesthetic.
the life threatening conditions
Hypoxia – increase the FiO2
ischemia below which represent acute myocardial ischemia Tachycardia – E-blockers
Angina pectoris
Neurosurgical Procedures:Myocardial ischemia with chest discomfort
Anesthetic Management Vasospasm – nitroglycerin
Stable angina Exercise induced chronic angina pectoris
General Goals Anemia – transfusion
Unstable angina Myocardial ischemia at rest or with minimal exertion
The goals for the management of a neurosurgical patient are similar across Thrombosis – heparin
Variant angina Discomfort from coronary artery vasospasm
the spectrum of patient disease. Attainment of these goals relies on a thorough Hypovolemia – fluid administration
Non-ST-segment elevation myocardial Myocardial ischemia from a partially occlusive coronary
appreciation of basic neurophysiology,
infarction (NSTEMI) thrombus understanding of the effects of indi- Figure 19.4 Mild to moderate variable decelerations with pushing during the second stage of
labor. (From Datta, S. Anesthetic and Obstetric Management of High-risk Pregnancy. Springer,
vidual anesthetic agents infarc-
on brainMyocardial
function, and from
clear perioperative communi-
ST-segment elevation myocardial ischemia a totally occlusive coronary
Cardiopulmonary
2004. Used with permission). Bypass (CPB)
cation with the neurosurgical team.
tion (STEMI) thrombus
A basic cardiopulmonary bypass circuit (see Fig. 17.3) consis
also
Keyindicated
Features ofin patients with unstable angina or Non ST Segment Elevation Table
a Neuroanesthetic
drainage
19.2 Apgarby gravity
score. via a cannula in the right atrium. Certai
MI (NSTEMI) who are in shock, and in STEMI. Coronary artery bypass graft require cannulation 0 Points
of the1superior
Point
vena cava and the inferior ve
2 Points
(1) Neuroprotection
surgery is used for patients with >50% stenosis of the left main coronary artery rately in order to enhance surgical exposure to the heart. The ve
(a) optimization of CBF/CMR balance Appearance completely blue extremities blue Pink
and patients with two and three vessel disease who have either reduced left ven- Pulse drains into absent a venous reservoir. <100 bpm The blood>100 is bpm
then passed thro
(b) control of ICP
tricular contractile function or diabetes.
(c) temperature regulation (avoid hyperthermia) genator no(membrane
Grimace or bubble),
response to stimulation temperature
grimaces when stimulated pullsregulator, and acti
away when stimulated
Activity none some flexion moving actively
(2) Provision of optimal operating conditions, including neuromonitoring and “relaxed” brain (roller or centrifugal) back to the patient via an arterial filter in
Valvular Disease Respiration none weak good
(3) Maintenance of normal glucose and electrolyte balance
Common causes for mitral stenosis (MS) are rheumatic fever and congenital
The heart is cooled and arrested with a cardioplegia solution
stenosis. It can lead to pulmonary edema and left ventricular failure. Mild MS in potassium concentration. Cardioplegia is given antegrade in
(4) Prompt emergence from anesthesia to facilitate neurologic assessment
is a valve area of d2 cm2 and critical MS is d1 cm2. Treatment is medical ther-represent root, uteroplacental
or retrograde through that
insufficiency, the is,coronary
insufficientsinus. Of note,
fetal oxygen deliverythe pr
Craniotomy
apy, balloon mitral valvuloplasty, open mitral commissurotomy, or mitral valveduring of the uterine contraction. Variable
extracorporeal decelerations
circuit often containsare typically due to umbilical
albumin, mannitol,
PreoperativeDuring
replacement. Considerations cord compression and
anesthesia it is important to maintain sinus rhythm (atrial depending on surgeon preference. have a variable relationship to uterine contraction.
kick provides
Questions to40%
ask atof the
ventricular
beginning filling),
of anpreload, stroke
evaluation volume, and low/normal
include: During CPB, theThe ventilator is turned off. It is common to ru
Neonatal Evaluation: Apgar Score
heart rate (to allow time for filling). Avoid drops in SVR and prevent increases in
L Why is the surgery being done? of the
Once benzodiazepine, narcotic,
fetus has been delivered, and Score
the Apgar muscle relaxant,
(Table 19.2) canorbeto give
used to th
PVR by preventing hypoxia, hypercarbia, and acidosis.
L Is the targeted pathology related to tumor, neurovascular malformation (aneu-
evaluate its well-being. Named after Virginia Apgar (an anesthesiologist
344 who
Mitral regurgitation (MR) can be caused by myxomatous mitral valve dis-developed the system in the 1950’s), the score is made up of five criteria each
Dr easerysm/AVM),
Azam’s Notesinin
resulting traumatic brain injury
Anesthesiology
prolapse, ruptured 2013 with
chordae, intractable
or flail intracranial
segments hyperten-
of the mitral valve.on a scale of 0–2. The five scores are then summed to provide a single total
sion, or intracranial hemorrhage (epidural, subdural, intracerebral)?
that enter the spinal cord at T10-L1. As labor progresses to second stage, it is
326 ANESTHESIA
puncture STUDENT
headache. SURVIVAL GUIDE
It also has non-procedure-related
Dr Azam’s Notes inrisks such as hypoten-
L
increasingly
Flow accompanied
Charts by somatic pain, which reaches the spinal cord via
& Diagrams Anesthesiology 2013
pudental afferents (S2–S4). Fig. 19.5 depicts pain pathways in the parturient.
Endocrine and Metabolic System
sion, motor blockade, CNS toxicity, urinary retention particularly after anorec-
tal surgery, and pruritis if an opioid is used within epidural infusion.
Obesity is associated with hyperlipidemia, hypertension, insulin resistance, and
pro-inflammatory and pro-thrombotic states. Extra adipose tissue releases sev- Table 20.1 The level of epidural catheter placement for pain management after abdom-
Classification of obesity.
eral products inal surgery is either low thoracic or lumbar, depending on the incision site. For
10 including nonsteroidal fatty acids (NSFA), cytokines, plasmino-
T 11 upper abdominal surgeries, aBMI low thoracic or upper lumbar (T6–L1)
gen activator inhibitor (PAI)-1, interleukin-6, and adiponectin. These products Obesity class Health catheter
risk is
12
are responsible
L 1 for metabolic complications and are associated with higher risk appropriate, and for pelvic and lower abdominal surgeries mid- to low-lumbar
Class I (overweight)
(L2–L5) epidural catheter may 25–30
provide better coverage (TableLow20.2).
of coronary artery disease. Treatment should be targeted toward weight reduc-
tion. Figure 20.1 depicts common systemic manifestations of obesity. Class II (obese) PCA (patient-controlled analgesia)
30–35 as an analgesic option with morphine,
Moderate
hydromorphone, or fentanyl is easier to achieve, can provide pain medication
Class III (severely obese) 35–40 High
upon patient’s demand, and does not involve a special procedure. However,
Neurological 2 and Psychological Problems
S 3 Class IV (morbidly
PCA mayobese)
prevent the patient>40 from taking deep breaths, may Very
delayhigh
ambulation,
Body image 4 may be severely distorted in people with obesity, and obese
people may be discriminated against in school and workplace. Depression is
and can cause respiratory depression and somnolence.
common and it is important to be sensitive to these issues. Carpal tunnel and
Figure 19.5 Pain pathways for the first and second stages of labor. (From Datta, S. Obstetric
other superficial nerve compression are also more common in obese people,
and special attention is necessary during positioning these patients inBMI the has itsTable limitation and catheter
may not be anlevel
accurate way ofpainassessing
control. obe
Anesthesia Handbook, 4th ed. Springer, 2006).
20.2 Epidural placement for postoperative
body builders.
Type of surgery Usual incision Epidural catheter placement
There are two spleen,

Liver, pancreas, types of obesity:
stomach “central-android”
Chevron or upper midline Low thoracic type, which is
common in men and “peripheral-gynecoid” type more common in w
Kidney and ureter Oblique flank Upper lumbar
Colorectal Low midline Upper lumbar
The formerBladder,
is also known
uterus surgery as apple-shape obesity
Low transverse or low midline and the latter is k
Low lumbar
as pear-shape
Hernia obesity. It is important Inguinal to measureLowabdominal
lumbar circumfere
Hemorrhoid Anorectal Caudal
addition to BMI. Central obesity (waist measurement more than 40 in. fo
and more than 35 in. for women) is associated with the respirator
cardiac co-morbidities. Waist-to-hip ratio (WHR) >0.95 for men and >0
women has been shown to confer higher risk of complications.
Physiologic Changes Associated with Obesity

Figure 20.1 Systemic manifestations of obesity. CO = cardiac output; CHF = congestive heart
failure; DM = diabetes mellitus; CAD = coronary artery disease; HTN = hypertension. Cardiovascular System
Obesity is an independent risk factor for cardiovascular disease. Since ad
tissue needs perfusion, total blood volume and stroke volume 345will incre
Dr Azam’s Notes in Anesthesiology 2013 perfuse additional body fat. Cardiac output (C.O.) increases by 0.1 L/m
each 1 kg addition in body weight.
routinely when
thirst and the ambulatory surgery
renal response is performed
to antidiuretic in the setting
hormone (ADH)of(Table
the full sup-
23.1).
342
FlowANESTHESIA
Charts STUDENT SURVIVAL GUIDE
& Diagrams port services of an inpatient hospital. In Dr Azam’s
contrast, Notes
even basicinproblems,
Anesthesiology
such as 2013
L
and disadvantages (Table 21.2). Ideally, one would prefer an isotonic fluid that
the need for postoperative bladder catheterization, may not be easily handled
does not cause hemolysis when intravascularly absorbed, is transparent, non-
electrolytic, Table 23.1 Renal changes in the elderly.
in the office-based practice.
Table 21.1inexpensive and nontoxic.
Spinal pain segments Sinceforthis
theis genitourinary
not possible, a number of
system.
other solutions have been employed and it is critical that the anesthesiologist Specific preoperative issues to consider for ambulatory surgery patients include:
Organ Sympathetics Pain pathways Decrease in renal blood flow
be aware of the type of solution being used and its associated potential periop-
erative
Kidney complications. T8-L1 T10-L1 1. Is the nature of theDecline
surgical procedure
in glomerular filtrationcompatible
rate with same-day discharge?
TURP syndrome is a phenomenon
Ureter T10-L2
that can be caused by intravascular
T10-L2 2. Do patient characteristics
Decline in ADH orresponse
co-morbid conditions (see Table 24.1) predis-
absorption of irrigation fluid into the venous sinuses of the distended bladder
Bladder T11-L2 T11-L2 (bladder dome) pose the patient to complications
Decrease that might require hospital admission?
in total body water
when the pressure of the irrigating fluid exceeds venous pressure. The TURP
S2–4 (bladder neck) Decreased ability to conserve sodium
syndrome is defined as a constellation of signs and symptoms that reflect rapid Indeed, even the simplest procedure done on a physiologically complex patient
Prostate
absorption of irrigating solution, T11-L2 T11-L2S2–4
leading to respiratory distress from volume Diminished urine concentrating ability
overload,
Penis dilution of serum electrolytes and proteins, and resultant cardiopul-
L1 and L2 S2–4
may require hospital admission and overnight observation. Table 24.1 provides
Decline in renin-aldosterone levels
monary
Scrotum changes (Table 21.3). Central nervous system manifestations inS2–4 the representative criteria used to decide whether the patient might be an appro-
Decreased thirst perception
awake patient include nausea, agitation, confusion, visual changes, seizures, and
Testes T10-L2 T10-L1 priate candidate for ambulatory surgery. Table 24.2 presents surgery- and pro-
even coma. These effects are most likely secondary to hyponatremia leading
cedure-related factors one might consider in deciding whether the proposed
This
Tableinnervation is important
21.2 Commonly when
used irrigating one is administering anesthesia for stone
solutions. Table 24.1 Patient selection factors for ambulatory surgery.
extractions. The
Irrigating solution bladder holds 400–500
Relative osmolality Advantages cc of fluid and
Disadvantages receives its innervation
t $BSFHJWFSBWBJMBCMFGPSUSBOTQPSUIPNFBOEQPTUPQFSBUJWFFWBMVBUJPO
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(Table hemoglobinemia,
21.1).
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The blood supply to the kidneys is via a single renal artery, which originates
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incidence diuresis
Mannitol Isosmolar Not metabolized Osmotic dieresis, may cause
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383
Patient Positioning intravascular volume expansion
There are multiple patient positions utilized in urological surgery and the
anesthesiologist must be aware that there are physiological changesTable that 24.2 Procedure-related considerations for ambulatory surgery.
Table 21.3 Symptoms of TURP Syndrome.
accompany these positions.
t %VSBUJPOPGTVSHFSZ OPBCTPMVUFDVUPGG
The lithotomy position

Cardiovascular (Fig. 21.1) is most commonly
Neurologic Other used for cystoscopies,
transuretheral
Hypertension
resection ofConfusion/disorientation
prostate or bladder tumor (TURP or TURBT),
Hemolysis t *OUSBPQFSBUJWFGMVJETIJGUTBOECMFFEJOH
or
Arrhythmias Seizures Hyponatremia
ureteroscopies. Placement in
Congestive heart failure
this position for greater than
Unresponsive
two hours may beta risk
Hyperglycinemia
3JTLPGTFSJPVTQPTUPQFSBUJWFDPNQMJDBUJPOT CMFFEJOH JOGFDUJPO BJSXBZDPNQSPNJTF
factor foredema
Pulmonary development of Visual sensory
problemsneuropathies
or blindness or rhabdomyolysis
Hyperammonemia secondary
t &YUFOUPGQPTUPQFSBUJWFQBJOBOEBOBMHFTJDOFFET
toHypoxemia
compartment syndrome. This position increases upward displacement of
t /FFEGPSJOUSBWFOPVTNFEJDBUJPOTPSJOBCJMJUZUPUPMFSBUFPSBMJOUBLF
Myocardial ischemia
intra-abdominal contents, decreasing pulmonary compliance, forced residual
capacity and vital capacity, and increasing atelectasis. Elevating the legs also
increases venous return, cardiac output, and arterial blood pressure, but these
changes may not have clinically significant manifestations. 346
Placing the patient in the kidney rest position (also called the lateral Table 24.3 Common ambulatory procedures.
flexed position) is preferred for better access during renal surgery. Often an
dation. Table 24.5 shows unique aspects of OOR anesthesia practice.
measured since the last bleeding episode. A healthy patient generally needs no
preoperative testing and “routine” tests such as complete blood count, chem-
istry panel and chest X-ray should never be ordered without a clear idea of
Table
why the24.3 Common
test results willambulatory in the anesthetic planning and perioperative Table 24.5 Unique aspects of Out-of-OR-anesthesia.
be useful procedures.
management of the patient in question.
t -PDBMMFTJPOSFNPWBM DZTU NFMBOPNB CSFBTUCJPQTZQBSU NBTUFDUPNZ
-JNJUFEBOFTUIFTJBSPMFJOQBUJFOUTFMFDUJPOBOEQSFPQFSBUJWFPQUJNJ[BUJPO
t Certain procedures simply cannot be performed on an outpatient basis; 6OGBNJMJBSQSPDFEVSFTBOEQSPDFEVSBMJTUT
0SUIPQFEJDQSPDFEVSFTOPUJOWPMWJOHNBKPSGSBDUVSFT
this is primarily due to the need for continuous postoperative monitor- 3FNPUFMPDBUJPOTXJUIMJNJUFEFRVJQNFOUBWBJMBCJMJUZ
t #BTJD&/5QSPDFEVSFT TJOVTUPOTJMMFDUPNZUZNQBOPQMBTUZ DPDIMFBSTVSHFSZ TJOHMFMPCFUIZSPJEFDUPNZ
ing (e.g. measurement of gastric drainage, placement of drains for bleeding,

t -JNJUFEQMBTUJDTQSPDFEVSFT CMFQIBSPQMBTUZ TDBSSFWJTJPO
&OIBODFESPMFPGOPOBOFTUIFTJBTVQQPSUTUBGG
and need for frequent electrolyte studies), ongoing interventions (intravenous
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(SFBUFSQPUFOUJBMGPSNJTDPNNVOJDBUJPO
medications for pain, fluid resuscitation, and complex dressing changes), or
t 0QIUIBMNPMPHJDQSPDFEVSFT FYDMVEJOHWJUSFDUPNZBOEFOVDMFBUJPO
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inability to eat, drink, or urinate. Examples are listed in Table 24.4.
t -JNJUFE(:/QSPDFEVSFT IZTUFSPTDPQZ %$%& DPOFCJPQTZ UVCBMMJHBUJPO
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Table 24.4 Procedure exclusions for outpatient management. Table 24.6 Anesthetic options for GI endoscopy procedures.
procedure is appropriate for the ambulatory setting. Table 24.3 lists common
t 3FRVJSFTESBJOPSOBTPHBTUSJDESBJOBHFUVCFUPCFQMBDFE Option A:
ambulatory procedures. However, no procedure is always done in an outpatient

P )ZTUFSFDUPNZ CPXFMSFTFDUJPO OFDLEJTTFDUJPO /BTBMDBOOVMBPYZHFOo-
basis. Even the simplest procedure (e.g. cataract removal) done on a physiologi-
t 0SBMNFEJDBUJPOTJOBEFRVBUFGPSQPTUPQFSBUJWFQBJODPOUSPM .JEB[PMBN oNH
*71
cally
Pcomplex patient may require hospital admission and overnight observa-
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tion.
t .BZSFRVJSFQPTUPQFSBUJWFCMBEEFSDBUIFUFSJ[BUJPO JOEVDUJPO
Preoperative testing is a controversial topic that
P 7FOUSBMIFSOJBSFQBJS CMBEEFSUVNPSSFTFDUJPO VSFUFSBMTUFOU requires good judgment.
Comment:-PXMJLFMJIPPEPGBQOFB MJNJUFEIFNPEZOBNJDFGGFDUT NPEFTUBOBMHFTJB BOEQPTTJCMFLFUBNJOF
Patients are best evaluated in a preoperative clinic setting
t 'SFRVFOUMZSFRVJSFTJOUSBPQFSBUJWFPSQPTUPQFSBUJWFUSBOTGVTJPO
well in advance of the
TJEFFGGFDUT
planned procedure. Advance assessment allows problem identification and

P )ZTUFSFDUPNZ 03*'GFNVS
Option B:
implementation of optimization strategies that may facilitate handling of med- /BTBMDBOOVMBPYZHFOo-
t &YQFDUBUJPOPGQPTUPQFSBUJWFFMFDUSPMZUFTIJGUT
ically complex patients in the outpatient setting. 1SPQPGPMJOGVTJPO oNDHLHNJO
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Generally, patients planned for same-day discharge should not have active $POTJEFSBEEJUJPOPGGFOUBOZMoNDHGPSIJHIMZTUJNVMBUJOHQSPDFEVSFT
t 3FRVJSFTIPVSMZQBUJFOUBTTFTTNFOU
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If such medical co-morbidities are present, regardless of anesthetic or surgical
Option C:
approach, the risk of peri-operative exacerbation of underlying medical conditions
is real. The challenges and dangers intrinsic to the management of sick patients in 1SFPYZHFOBUFXJUI0 WJBGBDFNBTL 2
a stand-alone ambulatory surgery center or office-based practice, in many cases, %FMJWFSIJHI'J0 WJB.BQMFTPODJSDVJUBUUBDIFEUPQBUJFOUXJUIMVCSJDBUFEOBTBMUSVNQFU
2
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UP DISPOJD PQJPJE PS CFO[PEJB[FQJOF VTFST PS QBUJFOUT VOEFSHPJOH QBJOGVM QSPDFEVSFT XJUI IJHI BOFTUIFUJD
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347
hemodynamic profile. Ketamine does not suppress respiration but may also be
Dr Azam’s Notes in Anesthesiology 2013 associated with unpleasant psychedelic side effects in a subset of patients.
Several possible anesthetic approaches are outlined in Table 24.6, although
404 ANESTHESIA
receptors STUDENT
respond toSURVIVAL GUIDE
the destructive mediators of thermal, mechanical, and The opioids are a diverse classification of mediation that typically provide anal-
chemical stimuli.&The
Flow Charts chemical stimuli include potassium, serotonin, bradyki-
Diagrams gesic effect via actions on the µ, G, and Dr Azam’s Notes in The
N opioid receptors. Anesthesiology
receptors are 2013
nin, histamine, prostaglandins, leukotrienes, or substance P, which may lead to General
most abundant Pain
in the Definitions
dorsal horn of the spinal cord and also in the dorsal root
activation or sensitization of the polymodal nociceptors. When
ganglion anddiscussing
peripheral acute
nerves.and chronic
Various pain, and
natural it is important to have a basic battery
synthetic formulations
Table 25.3
Following Trauma
transduction, blood protocol.
the nociceptor signal is translated into an electrical Table
definitions
and routes 25.4 Massive
to express
of delivery exist forthe transfusion
type
these and description
medications, protocol.
includingof pain
oral,aintravenous,
patient is experiencin
signal which allows for transmission of the stimuli via the peripheral nerves. buccal, transdermal, and intrathecal. The most common oral agents are listed
Peripheral nerves are typically classified by their primary function (motor or sen-
t 0OFHÀVOJUT UIFO in Table t26.3.5IBXVOJUT''1BOEVOJU$SZPQSFDJQJUBUF
The major side effects of opioids include constipation, nausea,
General Pain Types
sory), diameter and speed of conduction velocity (see Table 26.1). Pain pathways vomiting,tpruritus, sedation, and respiratory depression.
$SPTTNBUDIVOJUT13#$BOEVOJU1MBUFMFUT
t 0QPTJG
are typically mediated through A delta and C fibers via the dorsal root ganglion Some of the major challenges surrounding opioids include those of toler-
o transmitted
Male t %FMJWFSUP03
Nociceptive pain Normal, acute pain perception evoked by short-lasting noxious stimuli in intact
and then through one of three major ascending nociceptive pathways ance, physical dependence, withdrawal,
– Cooler #1:4 units PRBC
and addiction.
tissue, in the absence of peripheral orTolerance is defined
central sensitization.
(spinothalmic, spinoreticular, orbearing
o Obviously non-child age
spinomesencephalic) as shown in Fig. 26.1. as a fixed dose of an
– Cooler
Inflammatory
opioid providing
#2:2 units PRBC
pain
less FFP injury but with no neural injury. lead to
analgesia
+ 3 unitstissue
Pain following
over time that may
Modulation of pain
t $POUJOVFXJUI0OFH (suppression or worsening of a painful stimulus) escalating doses of narcotics
– Bucket: to achieve the same pain relief.
Neuropathic pain Cryoprecipitate + Platelets
Pathophysiologic state of pain after neural injury resulting in peripheral and
occurs either peripherally at the receptor, at the level of the spinal cord or in Physical dependence is a central physiologic state which is manifest by abruptly
reorganization
t $POUJOVFUPSFQMFOJTIDPPMFSTCVDLFUVOUJMUPMEUPTUPQ
stopping opioid medications which then results in a withdrawal state. Opioid
withdrawal presents with irritability, anxiety, insomnia, diaphoresis, yawning,
Table 26.1 Classification of peripheral nerves.
rhinorrhea,
Abnormaland lacrimation. As timeDefinitions
Pain Descriptor progresses, the symptoms may include
Fiber Diameter Conduction fevers, chills, myalgias, abdominal cramping, diarrhea, and tachycardia.
class (µm) Myelin velocity (m/s) Innervation Function
Opioid withdrawal is self-limiting Theand can typically
of pain by alast 3–7 that
days.
Table 25.4 Massive transfusion protocol. Orthopedic Allodynia Surgery
As opposed to physical
perception
dependence, addiction
stimulus
is defined
is not normally painful
by opioid use
A alpha 12–20 +++ 75–120 Afferent to skeletal Motor and reflexes
muscle Notresulting
all trauma is
Hyperalgesia
orthopedic, and not all orthopedic procedures
use of result
The enhanced perception of pain by a normally painful stimulus
in physical, psychological, or social dysfunction and continued
t 5IBXVOJUT''1BOEVOJU$SZPQSFDJQJUBUF Dysesthesia Abnormal sensations experienced in the absence of stimulation
A beta 5–12 +++ 30–75 Afferent from cutaneous Vibration, light trauma. Heredespite
the opioid we shall focus on
the overlying theBehaviors
issues. special challenges
that are mostin care of the rou
indicative
mechanoreceptors touch and pressure Paresthesia An abnormal sensation (e.g. burning, pricking, tickling, or tingling)
t $SPTTNBUDIVOJUT13#$BOEVOJU1MBUFMFUT scheduled, elective orthopedic patient.
A gamma 3–6 ++ 12–35 Efferent to muscle Muscle tone
t %FMJWFSUP03 spindles
A delta– Cooler
1–5 #1:4 units
++ PRBC
5–30 Afferent pain and “Fast”, sharp,
Choice of Acute Versus Chronic Pain
Table 26.3 Common oral opioid pharmacodynamics and dosing.
Anesthetic
thermoreceptors intense, lancinating
– Cooler #2:2 units PRBC + 3 units FFP The clinical definition of acuteEquianalgesic
versus chronic pain is determined
oral Initial Dosing in a tempo
Orthopedic
pain, touch and
Opioids procedures
Half-life lend themselves
Duration (h) to
doses (mg) a wide variety
dose of
(mg) interval
fashion with an arbitrary timeframe of 3–6 months defining the cutoff po
regional
(h) techni
– Bucket: Cryoprecipitate + Platelets temperature
B <3 + 3–15 Preganglionic sympa- Autonomic function many ofbetween
Codeine which 3acute
are detailed
versus in Chap.
3–4 chronic. 80 13. The question
30–60 that
4 patients frequ
t $POUJOVFUPSFQMFOJTIDPPMFSTCVDLFUVOUJMUPMEUPTUPQ
thetic efferent
ask is “Are blocks
Acute2–3
Hydromorphone better
pain and
can2–3
be saferas
defined 2than general
a noxious anesthesia?”
stimulus
2–4 caused Unfortunately
4 by injury or abnorm
C 0.2–1.5 − 0.4–2.0 Afferent pain and “Slow”, dull,
thermoreceptors burning, achy pain, answer is far fromofclear.
Hydrocodone
functioning 1–3
visceraA or
3–6
good general Itanesthetic
10
musculature. 5–7.5
is always
is usually noted 4–6
better
following than a
posttrauma
Oxycodone 2–3 3–6 7 5–10 6
touch, pressure,
regional postoperative,
anesthetic. obstetrical,
Does and acuteanesthesia
regional medical illnesses
reduce (i.e. myocardial infarction
patient morbidit
temperature, Methadone 15–30 4–6 10–20 20 6–8
improve nephrolithiasis). It is typically classified as somatic or visceral in nature. Soma
postganglionic Morphinepatient2–3.5
satisfaction?
3–4 10 10–30 3–4
pain is caused by the activation of nociceptors in the skin, subcutaneous tissu
Orthopedic Surgery
autonomic
The answer 6–12
Propoxypene is an unequivocal
3–6 “it depends.” Patients
43–45 100 with
6 less pain are
Tramadol 6–7 3–6 40 50 4–6
Not all trauma is orthopedic, and not all orthopedic proceduresously morefrom
result satisfied, but again a poorly functioning block (or regional/epid
catheter) will increase pain and aggravation, as well as patient and surgeon
rauma. Here we shall focus on the special challenges in care ofsatisfaction. the routine, Ultrasound-guided catheter techniques are revolutionizing 348 am
scheduled, elective orthopedic patient. latory orthopedic procedures in some hospitals, while others are abando
434 L
POSTOPERATIVE ANESTHESIA CARE UNIT (PACU) AND COMMON POSTOPERATIVE PROBLEMS L
433
Table 27.3 Suggested medical therapies for hypertension.

Table 27.5 Common causes of postoperative bradycardia.
Mild to moderate hypertension t #FUBCMPDLFST MBCFUBMPM FTNPMPM NFUPQSPMPM

Medications t /FPTUJHNJOF FESPQIPOJVN
t $BMDJVNDIBOOFMCMPDLFST OJDBSEJQJOF
t 1IFOZMFQISJOF OPSFQJOFQISJOF
t /JUSPQBTUF t 0QJPJET
t )ZESBMB[JOF t 4VDDJOZMDIPMJOF
Severe or refractory hypertension t *7BOUJIZQFSUFOTJWFJOGVTJPOT t #FUBCMPDLFST
(consider intra-arterial BP monitoring) − Nicardipine t -PDBMBOFTUIFUJDT
− Nitroglycerine t (BOHMJPOJDCMPDLFST
− Nitroprusside t )JHITQJOBMFQJEVSBMBOFTUIFTJB
Physical causes t $BSPUJETJOVTNBTTBHF
Table 27.4 Causes of postoperative tachycardia. t 7BMTBMWBNBOFVWFS
t (BHHJOH
Noxious stimuli t 1BJO BOYJFUZ t 3FDUBMFYBN
t &OEPUSBDIFBMUVCF t *ODSFBTFEPDVMBSQSFTTVSF
t %JTUFOEFECMBEEFS
t %JTUFOEFECMBEEFS
Physiologic derangements t "DJEPTJT t 4UJNVMBUJPOPGQIBSZOY
t )ZQPYFNJB
t )ZQPUFOTJPOBOEIZQPWPMFNJB Metabolic derangements
t 4FWFSFBDJEFNJB
t )ZQPHMZDFNJB t )ZQPYFNJB
POSTOPERATIVE ANESTHESIA CARE UNIT (PACU) AND COMMON POSTOPERATIVE PROBLEMS L
435
t *ODSFBTFEJOUSBDSBOJBMQSFTTVSF
t .ZPDBSEJBMJTDIFNJB
Medications t #FUBBESFOFSHJDWBTPQSFTTPST
ischemia include CHF, valvular disease, low ejection fraction, smoking history,
t %PQBNJOF
Table 27.6 Causes of postoperative mental status changes.
t %PCVUBNJOF anemia, hypertension, and emergency surgery. Causes may include tachycardia
t #SPODIPEJMBUPST
(decreasesHypoxemia
time in diastole, leading to coronary hypoperfusion), hypotension,
Anesthetics t ,FUBNJOF
t *TPGMVSBOF and hypoxemia. Clinical signs are angina, ECG changes, and dysrhythmias.
Metabolic derangements
Work-up and treatment includes treating underlying causes (pain control, fluid
Cerebral hypoperfusion
includes treating the underlying cause, fluid bolus, draining the bladder, andbolus,
pain and anxiolysis), oxygen, aspirin, nitroglycerine, beta blockade, and mor-
control. Symptomatic treatment may be necessary to allow offending medications Extremes
phine. Cardiac of age (e.g. troponin levels) should also be checked.
enzymes
to wear off. Cardiac arrhythmias are also common causes of tachycardia. If atrial Emotionally significant operations
Postoperative
fibrillation occurs, consider beta blockade, calcium channel blockers, and poten-
Presence ofNeurologic and Other Complications
intraoperative recall
tially cardioversion if the patient becomes hemodynamically unstable. The most common cause of delayed awakening is residual anesthetic, sedative,
The most common causes of postoperative bradycardia are increased Scopolamine or atropine
or analgesic. Less common causes include hypothermia, metabolic derange-
parasympathetic flow or decreased sympathetic output, which may addition-
ments, andSubstance abuse
stroke. Management includes treating underlying causes (e.g. apply
ally manifest as hypotension concomitant with the bradycardia. In cases of sus-
Pain, nausea, pruritus
a forced air warming blanket, correct metabolic disturbances) or medication
pected increased parasympathetic output, consider muscarinic blocking agents
reversal. Naloxone reverses opioid effects, although the patient may need
such as atropine and glycopyrrolate. In cases of decreased sympathetic output,
beta-mimetic agents such as ephedrine are useful. Table 27.5 outlines therepeated
most doses if the half-life of the opioid is longer than naloxone. Flumazenil
common causes of postoperative bradycardia. reverses benzodiazepine effects.
349
Myocardial ischemia should always be part of differential diagnosisproviding
Anothersupplemental oxygen,isbenzodiazepines,
common complication altered mental statusarm
andrestraints,
emergence and phys-
in patients with hemodynamic compromise. Risk factors for myocardial ostigmine
delirium.if reaction isfactors
Exacerbating related
are to in Table 27.6.or atropine (central anticholin-
scopolamine
listed
Emergence delirium usually resolves in 10–15 min. Management includes
ergic syndrome).
Characteristic!! ! Type of Fluid
Most Physiological ! ! ! RL
Rich in Na!! ! ! ! NS,DNS
Rich in K! ! ! ! ! Isolyte P,M
Correct Acidosis ! ! ! RL, Isolyte-P
Corrects Alkalosis! ! ! Isolyte G
Avoided in Liver Failure! ! RL, Isolyte G
Cautious use in RF! ! ! RL, Isolyte P,G,E
Glucose Free! ! ! ! NS,RL
Sodium Free! ! ! ! Dextrose 5% 10%!
Potassium Free! ! ! NS, DNS, Dextrose
350

Rapid Assessment of Airway: FUN - M - MAPing with MOANS, RODS, BANGS, Assessment of risk factors for aspiration
& difficulties for removal of airway maintenance device.
Assessment Test
Face Unusual or deformed facies, any obvious abnormality in face, beard, Syndrome - Pierre-robin Syndrome,
klippel-Feil, Goldenhar and Fetal Alcohol.
Upper Incisors Absent, Loose Protruding
Nose Nasal Patency
MMAP”ing Mallampati Class III & IV.
Measurements: 3-3-1;
•Thyromental span = < 3 fingers breath, Mouth Opening = < 3, Jaw Protrusion = < 1 cm or upper lip bite
test.
A-O extension ( in absence of C-Spine precautions), Inability to adequately to flex & extend the atlanto-
occipital joint.
Pathology in the mouth & Upper airway. Swellings in and around the airway H/O snoring & stridor.
MOANS (Specific for BMV) Mask Seal, Obesity/Obstruction, Age > 55, No teeth, Stiff lungs
RODS (Specific for Restricted mouth opening, Obstruction in upper airway, Disrupted upper airway e.g trauma, intra-oral burns,
supraglottic devices) Stiff lungs (Poor compliance)
BANG (specific for surgical Bleeding tendency, Agitated patient, Neck scarring and flexion deformity, Growth or vascular abnormalities
airway) in the region of the surgical airway
Factors for higher risk of NPO status & Full stomach, GE Reflex, Pregnancy, Obesity Hiatus Hernia, presence of Ryleʼs tube.
aspiration.
Difficulties during and after Any cause encountered as above

removal of airway
maintenance device.
351

352

shaped airway tube is wide enough to accommodate a size 8 ET and short enough
Diagrams for placement of the ET cuff below DrtheAzam’s Notes
vocal cords. The LMAin Anesthesiology
Fastrach was intended2013
for blind endotracheal intubation but also can be used with a fiberoptic bronchoscope,
lighted stylets, or the Flexible Airway Scope; it is available in sizes 3 to 5 and comes
Bainʼs Circuit: with a specially designed, reusable, wire-reinforced LMA Fastrach ET (Fig. 9).
Intubating LMA:
Classic LMA:
Fig. 8. Laryngeal mask airway LMA FasTrach. LMA ET Tube is placed in the airway tube. The
tip of the ET tube protrudes under the epiglottic elevating bar. (Courtesy of LMA North
America, Inc; with permission.)
Supraglottic Airway Devices 311

iGel:
Fig. 19. i-gel supraglottic airway device. (Courtesy of i-gel Intersurgical Ltd, Wokingham, 353
Berkshire, UK; with permission.)

Pulse Oximeter Graph:

Aladin Cassette:
How it works Benefits
In the S/5 ADU,
anesthetic agent Easier to handle
control consists • The Aladin Cassette can
of two parts: the
electronic control
Prof. A. K. Seth
any position.
• Weighing only 2 to 3 kg
mechanism in can be easily carried an
the anesthesia
machine and the Automatic record keeping
separate Aladin agent cassettes. • Electronic control of de
provides agent setting
Agent Prof.
concentration Simple
A. K. Sethi’s isdiaphragm
adjusted by
EORCAPS-2011 regulating
pressure the amount
regulator: keeping and fresh gas f
TEC 6 VAPORISER
Tec 6 Vaporizer:
of fresh gas flowing through the cassette. A throttle valve
regulates how much fresh gas flows to the agent chamber. TEC 6 VAPOR
• Gas usage data provide
Part of the fresh gas bypasses the cassette, so the more savings analysis.
#$#%&'()*+%,%-%)'
fresh gas allowed to pass through the chamber, the greater
IJ&,5&'(:)
.$./(0(1% Both flows are electronically ;measured
Enhanced safety
the concentration. .5'F5'+&,-:4'+,()%&/+&'=KB+LKBM
2$3(00%/%)'(&,+2/%445/%+
to control the throttle valve. • During the daily system
6/&)4751%/
,:E%/+:5'F5'+&'+OLPQ-()+0,:ER+S
a check on the Aladin C
Each Aladin Cassette is magnetically coded for its specific mechanism.
89$8%4(4':/
agent. This allows the S/5 ADU to recognize which agent
; 6(,'()*+8%4(4'&)'G
8! ! 7 8 ( '
8!$!)7+8%4(4':/ • S/5 ADU agent control is
cassette is inserted. ; 25-F()*+%00%1'+()4(*)(0(1&)'G
Virtually maintenance-fre
• H-Heating element
; pressur-
The agent vaporizes freely in the cassette without 6<%+:5'F5'+7%1/%&4%4+E('<+V(/+:
• The Aladin Cassette is v
;• O-Orifice ization or
3%40,5/&)%+<%&'%7+':+=>?@+()+&+4%&,%7+1<&-A%/B+&7C54'4+AD+# heating. The cassette has a temperature measuring
;• P-Differential sensor at the rear where the temperature of the agent is
@&//(%/+*&4+0,:E+/%4'/(1'%7+AD+.B4:+'<&'+F/G+(4+F/:F:/'(:)&,+':+0,:E • The S/5 ADU electrical c
Pressure Transducer
;• R1-Resistor measured. The pressure inside the cassette is measured
2/+4%)4%7+AD+2$E<(1<+/%&7C4'4+89+4:+'<&'+0,:E+:0+7%4+H+1&//(%/+*&4+0,:E the S/5 ADU’s intuitive s
;• R2-2nd from the cassette flow before entering the cassette. The
@:)'/:,+7(&,+&7C54'4+8!B&)7+'<54+'<%+:5'F5'+1:)1%)'/&'(:)
Resistor
fresh gas content (O2 and N2O/Air) is taken into account to 354
help achieve greater accuracy.
Dr Azam’s Notes in Anesthesiology 2013 !"!
Bourdon Gauge:
Low Pressure Aneroid Gauge:
Pressure Regulator:
Oxygen failure safety device:
355

Oxygen Flush: Ruben Non-breathing valve:
• Ruben Non rebreathing valve

• Inspiration: 0.8 cm of H2O Inspiratory resistance
• Expiration: 1 cm of water expiratory resistance
AMBU BAG:
Flow will be 35-75 L/min.

Pressure of 45 to 55 psi.
Ruben Non Rebreathing valve:
356

Venturi Mask:
Bernoulliʼs Principle:
Parts:
357

problem has been

,59,61,63,73,76,77
Reservoir Bag:
aluminum foil with
backing, and plastic
nd adhesive on the
le from electronics,
ead foil (commonly
r in appearance, but
ay.
been evaluated for
tubes with various
ection of the inflat-
hese metal tapes do
tent, brief, or unfo-
portion of the tube
however, against the
copper (1-mm foil;
minum (no. 425 or
St. Paul, MN) tapes
direct Nd:YAG laser
An Emergency Care
the 3M aluminum
KTP:Nd:YAG, but it
est power setting of
Figure 77-8 Cuff wrapping technique. If a wrapped endotracheal tube is the
M Corp, Electrical
ignition protection
Cuff wrapping
chosen method for laser protection,technique
the technique for wrapping is crucial in
ensuring protection from ignition and foil-induced mucosal abrasions. It is
und that metallized often helpful first to paint the tube sparingly with a medical adhesive, such
orth, TX) was more as benzoin or Mastisol. The end of the tape should be cut with a scalpel to
ed red rubber tube, approximately 60 degrees. Wrapping is begun by aligning the cut end of the
tape with the junction of the tube and the proximal end of the cuff and is
13 seconds for the done in a spiral with a 30% to 50% overlap between layers. Wrapping should
at although the met- include the inflation tube for the cuff and should be continued until just short
likely to abrade the Link 25 System:
of the pilot balloon, with care taken not to wrinkle the tape at any point. Functional Analysis of Mapleson E Circuit:
O2 lasers, not against
to an endotracheal
uld be wiped with facturer recommends this product only for use with CO2 lasers.
e with adhesion and The shield material adds almost 2 mm to the diameter of the
tincture of benzoin. endotracheal tube. Similar to the nonapproved tapes, Laser Guard
of about 60 degrees, can be applied only to the shaft of the tube and provides no pro-
proximal end of the tection for the cuff.
ped in a spiral, with The FDA also has approved the use of an integral laser-
uff pilot tube. Wrin- resistant coating in the manufacture of endotracheal tubes. The
he tracheal mucosa. commercially available Xomed Laser shield tube (Medtronic
eas of exposed tape Xomed, Jacksonville, FL) is fabricated from silicone with an outer
g the wrapped tube layer of finely divided aluminum powder in silicone; the alu-
ess before tracheal minized layer extends over the inflatable cuff. This tube is speci-
fied for use only with CO2 lasers, a beam power density of less
the medical litera- than 4900 W/cm2, and an F2 of less than 25%.
roval because their Although more resistant to far-infrared radiation than
ans who devise a PVC or red rubber tubing,79,80 the Laser Shield nonetheless burns
incur some product vigorously when ignited in vitro,63 producing friable silica dust.
should injury occur, It also may ignite under typical surgical conditions, failing the
ommercial products ECRI flammability test.78 In at least one case, an airway fire
involving this tube occurred,56 resulting in serious injury attrib-
ic Xomed Merocel uted to an intraluminal fire caused by laser penetration of the cuff;
roved endotracheal the laser power settings were within specified limits, but the res-
nated to a synthetic piratory gas mixture included an excessive F2 and nitrous oxide.
acheal tube and kept A newer version, the Laser Shield II, is approved for use with CO2
ction against CO2, or KTP lasers. The construction of this version includes a sili-
lasers.78 The manu- cone-based tube that is smoothly wrapped by a coated aluminum
358

Jackson Rees Circuit: Waters To & Fro:
Circle System:
Components of the circle system include:

a) Soda lime canister,
b) Unidirectional valves,
c) Fresh gas entry,
d) Y-piece.
e) Reservoir bag.
f) Relief valve,
g) Low resistance interconnecting tubing.
359

Capnogram: Clinical Application:

I. Elevated Base Line:
Seen in:
• Rebreathing
• Incomplete expiratory valve
III. Absence of Plateau:
IV. Slanting & prolongation of the • Exhausted absorbant
expiratory upstroke: • Insufficient fresh gas flow.
• Deliberate addition of FGF.
II. Elevated base & low rounded peak:
Seen in:
• Obstruction to the ET-tube
Seen in: • Airway obstruction - E.g. COPD,
• Contamination of the expired sample gas bronchospasm
by FGF by placing the sampling unit near • Acute Asthma
the fresh gas inlet.
• Too high rate of sampling. Seen in:
• Too low rates of sampling with a side stream.
360

VI. Elevated EtCO2 with good plateau:

V. Low end tidal CO2 with good alveolar
plateau:
Seen in:
• Hyperventilation Seen in:
• Increase in dead space ventilation • Hypoventilation
• Decrease temperature • Increased metabolism
• Increased muscle relaxation • Increased temperature
• Increased depth of anesthesia • Shivering & convulsions
• Decreased blood flow: • Excess of catecholamines
• Decreased CO
• PE
XI. Cardiogenic Oscillations: Release of Tourniquet/

Unclamping of a major
muscle.
Exponential decrease in
EtCO2: Sudden
hypotension, Circulatory
arrest & PE
Small air embolus.

361

VII. Spontaneous respiratory efforts during
mechanical ventilation:
VIII. Curare cleft/Notch
IX. Return of spontaneous ventilation:
X. Circuit leak during Positive pressure ventilation:
362

TEC 5 Vaporizer:
Waters To & Fro:
363

Notes in Anesthesiology Dr. Azam's.... : Flow Charts, Diagrams & Important Tables

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Notes in Anesthesiology Dr. Azam's.... : Flow Charts, Diagrams & Important Tables

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Dr. Azam’s....

Flow Charts, Diagrams

To Mohammed Shafiulla, my father, my oxygen, companion, and best friend; for

Dr Azam’s Notes in Anesthesiology 2013

A NOTE TO THE READER

Dr Azam’s Notes in Anesthesiology 2013

860+930(.'6/2)7(2(-0':(*);'<=3'3-.'<>3?' Right lung Left lung

@(504/)A+7'3BB4(B30+/-'3-.'360+930+/-'' Apical posterior

Upper lobe Posterior 22

Millers: Page # 1842

Mapleson Other Names Configuration1 Spontaneous Controlled Comments

C Waters' to-and-fro 2 x minute 2–2½ x minute

E Ayre's T-piece 2–3 x minute 3 x minute Exhalation tubing should provide a

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Vocal Cord palsy

Intra Cranial: Lesions in the neck:

Dr Azam’s Notes in Anesthesiology 2013

Five Causes of Hypoxemia (↓ PaO2):

Five Causes of Hypoxemia (↓ PaO2):

Hypoventilation: Low inspired Oxygen:

Dr Azam’s Notes in Anesthesiology 2013

3) Marked 35-­‐49 30-­‐44 < 60 > 50

Cohen Blocker Arndt Blocker Fuji Uniblocker

Section V Adult Subspecialty Management

Center channel 1.6 mm ID 1.4 mm ID 2.0 mm ID

ETT, single endotracheal tube; ID, internal diameter.

Table 59-9 Options for Lung Isolation

Options Advantages Disadvantages

Double-lumen tube Quickest to place successfully Size selection more difficult

Univent tube Same as BBs Same as for BBs

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Specific Test - PFT

Single Breath N2 elimination Test

Dr Azamʼs Notes in Anesthesia

Oral Anti-Hypertensive Drugs - Classification

Post gangalionic blockers:

Dr Azam’s Notes in Anesthesiology 2013

Indications Drugs Dose Onset Duration

Labetalol 5-­‐20mg 1-­‐2min 4-­‐8hr

Dr Azam’s Notes in Anesthesiology 2013

i. Age > years 5

ii. MI in previous 6 months 10

iii. S3 gallop or ↑ JVP (0-­‐3 cm) 11

iv. Important aortic stenosis 3

v. Rhythm other than sinus, Pac on last preoperative 7

vi. >5 PVC/min at any time before 7

vii. PaO2, < 60 or PaCO2 > 50mm Hg, 3

ix. Emergency operation 4

Class I 0-5 points (low risk)

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Risk Stratification Procedure Examples

* Combined incidence of cardiac death and nonfatal myocardial infarction.

Advantages: Classification of SGA(Supraglottic Airway):

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Flow rates & percentages:

The purpose of the preoperative

Noxious stimuli t 1BJO BOYJFUZ

The pre-operative respiratory care:

3) Marked 35-‐49 30-‐44 < 60 > 50

Labetalol 5-‐20mg 1-‐2min 4-‐8hr

iii. S3 gallop or ↑ JVP (0-‐3 cm) 11

?-8-3-(#-+3%%@$'( ?6%#&2#-%+/(3-/%+&$%#(( B:C((

3) Marked 35-‐49 30-‐44 < 60 > 50

iii. S3 gallop or ↑ JVP (0-‐3 cm) 11