You are on page 1of 128

Big Blue Review (7.15.

V. Fib/Pulseless V. tach

Please Shock, Everybody Shock, And Lets Make Patients Betters o

o Shock 360 J monophasic, 120 J - 200 J (default) biphasic resume
CPR (100/min) immediately x 5 cycles then check rhythm
o Epinephrine or Vasopressin
o Shock o
Amiodarone 300 mg IV/IO, then additional 150 mg o
Lidocaine 1-1.5 mg/kg, max dose 3 mg/kg o
Magnesium 12 g IV/IO o
Procainamide 100 mg IV
o Buffers bicarbonate 1 mEq/Kg

Synchronized Cardioversion

50 J A flutter, SVT
100 J A. fibrillation
Direct current (DC) cardioversion is NOT useful and NOT indicated in an
unstable patient with Multifocal atrial tachycardia

Drugs given OETT NAVEL


Neonatal Resuscitation
Epinephrine, 0.1 ml/kg of 1:10,000 soln for asystole or spontaneous HR < 60
Naloxone, 0.01 mg/kg IV or 0.2 mg/kg IM if opioids given to mother within last 4
hours of labor
Sodium bicarbonate, 2 mEq/kg, only for severe metabolic acidosis
Calcium gluconate 60 mg/kg only with documented neonatal hypocalcemia or
Calcium chloride 20 mg/kg
Atropine 0.02 mg/kg
Glucose only for hypoglycemia, 2 ml/kg 20% glucose
Dopamine at 5 mcg/kg/min to support BP
Surfactant via ETT to premature neonates with respiratory depression syndrome
Appearance (Color)

Blue or pale

Grimace (reflex
irritability in response
to catheter in nose)
Activity (muscle tone)


Body pink,
extremities blue
< 100

All pink

Some flexion

Active motion

> 100



Slow, irregular

Good, crying

Correct depth of ETT = 6 cm + weight in kg

ACLS steronal compression depth of 1-2.5 cm (0.5-1 inch) at rate of at least
100/min; only perform finger sweep IF object is VISIBLE!

Atrial Fibrillation
Acute therapy = identify and treat associated factors i.e. hypotension, hypovolemia,
or anemia:
o D/C countershock with synchronous mode: 50-100 Joules o DO
NOT shock in setting of digitalis toxicity
o Digitalis loading dose = 1 mg and daily dose 0.125-0.375 mg day o
Verapamil, propranolol
o Pacing is effective for atrial flutter
o Rate control with digitalis, verapamil, propranolol o Maintain SR
with quinidine or disopyramide
o AVOID lidocaine increases A-V conductance accelerated
ventricular response
Digitalis o Inhibits Na+-K+ ATPase prolonged A-V conductance, (+) inotropy,
automaticity o T = 2 days
o Concern for CPB due to hypokalemia causing toxicity
o Withdrawal of propranolol acute MI and death o Toxicity = N/V,
AV block, ventricular arrhythmias, VF Treat arrhythmias with
lidocaine, phenytoin, K+
Predisposition to toxicity:
WPW Syndrome

Impulses conduct through accessory pathway resulting in EKG: short P-R interval,
wide QRS complex, delta wave

Management for NARROW complex SVT = most common dysrhythmia in WPW o

Vagal maneuvers o Adenosine
o Esmolol, procainamide, verapamil, propranolol o Overdrive
(transvenous pacing) o Cardioversion

Management of WPW & A. fib o Procainamide if stable VSS prolongs refractory

period of accessory pathways o Cardioversion if unstable!!
o AVOID -blockers, Ca2+ blockers, digitalis, adenosine when in
A.fib increases accessoary pathway and risk degenerationg into V.

Anesthetic goals:
o AVOID sympathetic stimulation, i.e. pain, hypovolemia, ketamine,
pancuronium o AVOID Digoxin!! enhances cardiac conduction via
accessory pathways o Atropine is OKAY!



A = Anterior ethmoidal nerve (mandibular, V1)

sensory anterior 1/3 of septum and lateral wall

B = Sphenopalatine nerves (maxillary branch, V2) posterior

2/3 of septum and the lateral wall. **MUST CN V2 BLOCK FOR

Palatine nerves (V) sensation hard & soft palate

Lingual nerve (V3) sensation anterior 2/3 tongue

Facial nerve (VII) taste anterior 2/3 tongue

Glossopharyngeal (IX)
Innervation hypopharynx & pharynx (tonsils, base of tongue, epiglottis,
vallecula), omohyoid
Controls gag reflex
Taste & sensation posterior 1/3 tongue
BLOCK: posterior to angle of mandible, used for pain of malignant tongue base
Complications of block: o Ipsilateral VC paralysis, tachycardia from vagus (X)
block. CN X exits w/CN IX o Ipsilateral tongue paralysis. CN XI exits with CN IX.
Vagus (X) - sensation of airway inferior to epiglottis
Superior Laryngeal Nerve - sensation & motor of larynx
External br = motor to cricothyroid muscle VC tensor (closes VC), sensory
anterior subglottic mucosa
Internal br = sensory above the VC (+ false VC, laryngeal & buccal surfaces of
epiglottis), pierces thyrohyoid membrane
BLOCK: inferior to greater cornu of hyoid bone will block laryngospasm
(caused by external br due to cricothyroid muscle tensing VC)
Recurrent (Inferior) Laryngeal Nerve - sensation below VC & motor of all intrinsic
laryngeal muscles, except cricothyroid (external br of superior laryngeal n.)
Runs in groove b/t trachea & esophagus
Bilateral injury ADDuction of VC to midline position (due to unopposed
cricothyroid tension), severe respiratory obstruction
BLOCK: transtracheal approach through cricothyroid membrane
Hypoglossal (XII)
Innervation hypopharynx & motor to tongue
Not necessary to block for oral or nasal intubation!
Awake Nasal Intubation Blocks: (1) RLN, (2) CN V, (3) Superior laryngeal nerve
Awake Oral Intubation Blocks: (1) glossopharyngeal (CN IX), (2) RLN, (3) Superior
laryngeal nerve

Blood supply
Superior laryngeal artery branch of superior thyroid artery off of external
Inferior laryngeal artery br of inferior thyroid artery off of thyrocervical trunk
of subclavian **Injuries**
Unilateral paralysis of superior laryngeal nerve subtle clinical findings, b/c
external branch only innervates cricothyroid muscle
Bilateral paralysis of superior laryngeal nerve hoarse voice, risk aspiration
Unilateral paralysis of recurrent laryngeal nerve paralysis of ipsilateral vocal
cord, paramedian position loss of voice quality
Acute bilateral recurrent laryngeal nerve injury midline, nearly closed vocal
cords, stridor with inspiration, risk aspiration
Bilateral vagus nerve injury flaccid, mid positioned vocal cords
Type I pneumocytes: flat, form tight junctions, prevent albumin passage
Type II pneumocytes: round, contain lamellar bodies which contain surfactant;
resistant to O2 toxicity; produce type I pneumocytes
Blood-Gas Interface
Ficks law of diffusion: amount of gas that moves across a sheet of tissue is
proportional to the area of the sheet, but inversely proportional to its thickness
Path of alveolar gas = layer of surfactant alveolar epithelium interstitium
pulmonary capillary basement membrane endothelium plasma RBC
Combitube Avoid in patients with intact gag reflex, esophageal pathology or h/o
substance ingestion
Orotracheal intubation

Persistent detection of CO2 by a capnograph is the best confirmation of tracheal

intubation, but it cannot exclude endobronchial intubation.
Earliest manifestation of endobronchial intubations => peak inspiratory pressure
Clues of endobronchial intubation unilateral bs, unexpected hypoxia, unable to
palpate ETT cuff, decreased breathing bag compliance (high peak pressure)

Supraglottic vs. Subglottic jetting

Supraglottic jetting causing more splattering of secretions and debris.
CO2 analysis is inaccurate in both settings
Ball-valve effect 2nd to partially obstructing airway lesion is more likely with
supraglottic jetting
Subglottic jetting can effectively bypass an airway lesion, can produce hyperoxia
& normocarbia
Risk of PTX is higher in subglottic jetting
Eye protection during laser surgery
CO2 laser DOES NOT require special glasses. Okay to use glass or plastic eye
Special glasses required for: argon, Ruby, Nd:YAG


Blood Transfusions
How should emergency transfusion needs by met before crossmatched blood is
o Type specific or Type O Rh
o Type O Rh + cells for males or postmenopausal females can be given o
Uncrossmatched blood

If multiple units of Group O WHOLE blood (contains anti-A & anti-B) have been
transfused to Group A or B blood one should NOT switch back to the patients
blood type
FFP and blood need to be ABO compatible
Platelets (just preferred) & cryoprecipitate DO NOT need ABO compatibility

Direct Coombs Test = Direct Antiglobulin Test

Used to detect antibodies or complement proteins that are bound to the
surface of RBC
Blood sample is taken and RBCs are washed (removing patient's plasma) and then
incubated with antihuman globulin. If this produces agglutination of RBCs, the direct
Coombs test is positive, a visual indication that antibodies (and/or complement
proteins) are bound to the surface of red blood cells.
Performed when suspect hemolytic transfusion reaction
Indirect Coombs Test
Used in prenatal testing and in testing blood prior to a blood transfusion (type &
Detects antibodies against RBCs that are present unbound in the
patient's serum.
Serum is extracted from the blood, and incubated with RBCs of known antigenicity. If
agglutination occurs, the indirect Coombs test is positive
Type & Screen = Indirect Coombs test
Purpose is to detect in the patients serum the presence of the antibodies that are
most commonly associated with non-ABO hemolytic reactions
Patients serum is mixed with panel of red cells of known antigenic composition
Can determine ABO & Rh type, cannot determine Rh sensitization
Type & Crossmatch = mimics the transfusion
Trial mix of recipient blood and donor blood
Detects (1) ABO incompatibilities, (2) naturally occurring antibodies, Rh antibodies,
(3) less common antibodies (Kell, Kidd, Duffy)
1/100 has antibodies other than anti-A or anti-B
1/1000 has an unexpected antibody detected at cross-match
Blood Bank Practices
All blood is tested
o Hep B (1: 60,000) o Hep C (1:100,000) o HIV-1/2 (1:500,000) o
HTLV-1/2 (1:650,000) o
Syphillis - unlikely transmitted (FFP,
RBCs, cryo) b/c cannot survive 4 C o
NOT tested for CMV (most
common infection) or Hep A

All can be transmitted in platelets b/c stored at room temp

CPDA-1 preservative is added, contains:

o Citrate as the anticoagulant (binds Ca2+)
o Phosphate buffer o Dextrose red cell energy source o Adenosine
precursor for ATP synthesis
CPDA-1 blood stored for 35 days (CPD 21 days, Adsol 42 days) Blood stored
at 4C, frozen up to 10 years

Changes in stored blood

2,3 DPG Left shift Hgb curve promotes tissue hypoxia
pH (6.7) due to elevated CO2 right shift Hgb curve
platelets & factors V, VIII
Platelet storage

Stored at 22 C to optimize function for ONLY 5 days

pH due to platelet metabolism
Concern for bacterial growth


T 1.5 days
Max amount 20 ml/kg (1.5 liters)
DOES NOT interfere with crossmatching of blood or affect coagulation at 20 ml/kg
o Transient elevation serum amylase o Anaphylactoid rections o
Coagulopathy dose-related due to procoagulants, quality and
number of platelets

Degraded to glucose
Delays systemic absorption of local anesthetics
o Can interfere with cross-matching of blood (rouleaux formation) o
Decreases platelet adhesiveness
o Allergic rxns histamine release Promit (Dextran-1) decreases life
threatening anaphylactoid reactions by 100 fold. Blocks receptors and
decreases histamine release
o Interfere with coagulation
o Pulmonary edema by direct toxic effect on capillaries
T = 20 days
Made from fractionated pooled human plasma HEATED kills VIRUSES

(1) ACUTE Hemolytic Transfusion Reaction = Intravascular o

Risk is 1/1000 from
type-specific blood (1/10,000 from type & screen)
o Intravascular hemolysis occurs when antibody-coated RBCs are destroyed by
the activation of the complement system
o Awake patient fever, chills, pain at site or flank pain, nausea, hypotension,
hemoglobinuria, coagulopathy o
Under GA elevated temp, hypotension,
hemobloinuria, coagulopathy, tachycardia
o 3 most important sequelae = shock, DIC, acute renal failure o Treatment

STOP transfusion!
Treat hypotension - IV fluids, Dopamine, other blood
Establish diagnosis repeat clerical check, Direct Coombs, repeat type &
cross, serum haptoglobin
Treat renal vascular ischemia IV fluids, mannitol, UOP > 1 ml/kg/hr, if no
response give furosemide, low-dose dopamine
Evaluate and treat DIC plt count, PTT, fibrinogen
(2) Allergic-Urticarial-Pruritic
2nd most common
If hives are the only sign, DO NOT stop transfusion
(3) Febrile NON-hemolytic
One of the most common
Temperature rise (> 1 degree C)
Give antipyretics & diphenhydramine, stop infusion to r/o hemolytic rxn
Effectively treated with leukocyte-poor saline washing blood
(4) DELAYED Hemolytic Reaction = Extravascular
Occurs in those who have compatible cross-matched, but over 4-21 days the
transfused RBCs are destroyed via phagocytosis by macrophages in the
reticuloendothelial system
Involves antigens and antibodies that do not bind
(5) Non-cardiogenic pulmonary edema = TRALI
Due to transfusion of anti-leukocytic or anti-HLA antibodies that interact with
patients WBCs aggregate in pulmonary circulation damage to alveolar/capillary
membrane triggers
Rx is similar to ARDS
Resolves 12-48 hrs with supportive care
(6) Anaphylactic Reactions
Typically is IgA-deficient patients with anti-IgA antibodies who receive IgA
containing blood
IgA deficient patients need thoroughly washed pRBCs, deglycerolized frozen red cells,
or IgA free blood units
Massive Transfusion = 10 units/ 24 hrs
Most common problem is dilutional thrombocytopenia
o Hyperkalemia

Other problems:

Post-op metabolic alkalosis from citrate & lactate bicarb conversion o

Hypothermia o
Citrate intoxication hypocalcemia prolonged
QT, hypotension o
Decreases in fibrinogen, factor V & VIII

vWF Disease
Most common hereditary bleeding disorder, 1% of population
Autosomal dominant
Hallmark: prolonged BT, vWF levels & factor VIII activity, NORMAL PT, PTT
platelet #

Treatment vWF:
DDAVP 1st line for type 1 and 2A, Avoid in 2B
thrombocytopenia o Cryoprecipitate contains vWF and factor VIII,
given for urgent correction o
Factor VIII concentrate also
contains vWF
Some patients are not responsive to DDAVP, emergent rx requires cryoprecipitate

Hemophilia A

Most common hemophilia, X-linked recessive (1/5000 males)

Low factor VIII, normal platelet count
Prolonged PTT
Rx: cryoprecipitate or factor VIII concentrate (need 30% of factor VIII for
Ideally, factor VIII levels should be raised to 100% before ELECTIVE surgery

Hemophilia B
X-linked recessive, low factor IX
Vitamin K Deficiency
Vit K required for hepatic synthesis of factors II, VII, IX, X, protein C & S
Factor VII depleted first elevation in PT, with prolonged deficiency, the PTT will
also increase. Normal platelet count
Can de seen in those on TPN without vitamin K supplementation & newborns with
a sterile gut at birth
No bleeding: urgent rx is best accomplished by IM or IV Vitamin K
(1-5 mg) improvement within 8 hours. Give slowly, can cause
hypotension o
Bleeding: vitamin K 10 mg IV + FFP
Sickle Cell Anemia
0.2% black population, inherited d/o of -chain, valine substituted for glutamic acid
Predominant Hgb in 2-mo infant is Hgb F, protects infant from sickle cell
Always concern for excessive blood transfusions hemochromatosis

Hb SS patients have the following:

o Right shift Hgb-curve from 2,3 DPG
levels o
P50 = 49 mmHg (compared to
27 mmHg) o
Resting PaO2 70-90
Mortality from cardiac and/or renal failure, severe infection, stroke, intracerebral
hemorrhage TLC, VC and high risk of pneumococcal pneumonia


Therapy Triva
Factor IV (Ca2+) and VIII are not synthesized by the liver
Most sensitive test is PT (PeT = extrinsic pathway) b/c Factor VII t = 4-6 hrs
PTT (PiTT = intrinsic pathway) tests factors VIII, IX
3 leading causes of transfusion-related death (1) ABO incompatibility, (2) TRALI, (3)
5% of patient who receive heparin for 5 days will develop HIT clinical si/sx due to
thrombosis and thromboembolism, than to thrombocytopenia
Cryoprecipitate = source of factor VIII, XIII, vWF, fibrinogen, no need for ABO

Decreases MAC
Treatment: hypertonic saline (3%), d/c once Na+ rises to 120 mEq/l and give NS
Fick Equation to calculate cardiac output (Q)
SvO2 = SaO2%



Q =
CaO2 CvO2 x 10

x Hgb/dL x 1.34 ml O2/g Hgb

Pacemaker Codes
Anti-bradycardia functions
A = atrium
V = ventricle

A = atrium
V = ventricle

Response to
T = triggered
I = inhibited


P = pacing
S = shock

P = simple pro
M = multiple
D = dual A & V
D = dual A & V
D = Dual T & I
C =
D= P&S
O = none
O = none
O = none
R = rate adaptive
O = none
O = none
*if patients HR is above the rate at which the pacer is set, then edrophonium or a
Valsalva maneuver slows the HR and tests the normal pacemaker function. Use of
a magnet tests only the ability of pacemaker to convert into a fixed rate, asynchronous
Pacemaker Indications:
3rd degree (complete) heart block
Asymptomatic Mobitz type II (dropped QRS, 2:1, 3:1, 4:1)
Symptomatic bradycardia
Symptomatic bifascicular block
Orthotopic heart transplantation
Hypertrophic and dilated cardiomyopathy
Long QT syndrome

Fixed rate = Asynchronous modes: VOO,

Pacemaker paces, but
does not sense!
May compete with the intrinsic rhythm R on T phenomenon , V. tach, V. fib, A.
Use of magnet with MOST pacemaker reverts it to this mode
Mode occurs when pacemaker battery is LOW
Demand = Synchronous modes: pacemaker senses the atrial impulse (P wave),
ventricular impulse (R
wave), or both. Pacemaker is either triggered (fires) or inhibited by
the sensed signal o
AAI, AAT (older types) = atrial demand or
synchronous pacemakers
Intact A-V conduction system is utilized to achieve ventricular depolarization
Useful for sinus node dysfunction i.e. sinus block, sick sinus syndrome, sinus arrest

VVI, VVT = ventricular demand or synchronous pacemakers

Characterized by no A-V synchrony
Indicated in the setting of AV node dysfunction or supraventricular
VVI commonly used for Mobitz type II

VAT, VDD, DVI, DDD = Dual chamber demand or synchronous pacemakers

Dual pacing ensures coordinated AV synchronous depolarization.

VDD: used for AV block with normal atrial rate
AAI: used for normal AV conduction with atrial bradycardia
DVI: used for AV block with atrial bradycardia

Factors Affecting Pacemaker Threshold

Increase threshold (more difficult to
Sleep, rest
Toxic doses procainamide

Decrease threshold (very sensitive to


Increase threshold (harder to capture) = acute hypoK+,

respiratory alkalosis Decrease threshold (sensitive to
capture) = hyperK+, acidosis

Other Pacemake Facts

Decrease > 10% of paced rate = battery failure
VVI Pacemaker

Indicated in the setting of AV node dysfunction or supraventricular

Used for Mobitz type II


May be inhibited by myopotentials administration of sux,

electrocautery, or post-op shivering. If occurs, place magnet to
convert to VOO mode to eliminated further inhibition

AICDs or ICDs = Automatic implantable cardioverterdefibrillators Indications:

o Survival of sudden death episodes
o Sustained VT o
Syncope due to VT
o Arrhythmias not amenable to ablation
Anesthetic management in presence of an ICD:
o Should be deactivated with a magnet, others require programmed
deactivation pre-op if electrocautery will be used. Back up VVI or VOO pacing
can remain active. o Magnet placement can lead to unpredictable
reprogramming or discharge o
Avoid MRI
o Avoid lithotripsy, unless it has been deactivated
Fontan Procedure = RA appendage to Pulmonary Artery
Performed to treated congential cardiac defects with low pulmonary artery blood flow
pulmonary atresia & stenosis, tricuspid atresia
Also usd to increase pulmonary blood flow when it is necessary to convert RV to a
systemic ventricle hypoplastic left heart syndrome
Cardiac Transplantation
Transplanted heart is denervated, with absence of vagal tone HR 90-100, no
response to atropine
Norepinephrine normally slows HR due to reflex bradycardia via baroreceptor &
vagus nerve, but actually see HR from beta-1 effects on SA node
Sympathetic responses to laryngoscopy & intubation are ABSENT
Baroreceptor reflexes are not seen no HR during or after a Valsalva
Changes in cardiac output are achieved by changes in stroke volume, not HR
Heart is responsive to sympathomimetic amines isoproterenol, epinephrine,
dopamine, dobutamine

Frank-Starling Curve
Relates LV filling pressure to LV work o LV
filling pressure (x-axis) = LVEDV, LVEDP,
LA pressure, PAOP, CVP o LV work (Y-axis) =
LV stroke volume or stroke index, CO, CI, arterial
blood pressure



Extracorporeal circuit is in SERIES with the systemic circulation

Basic Circuit

Circuit must be primed with fluid

devoid of bubbles, 2 L balanced salt
solution +/- colloid, 20 cc 20%
mannitol for renal protection,
heparin, bicarbonate, K+
Onset of bypass, hemodilution
decreases the Hct to 22-25%.

(1) Venous Reservoir

Receives blood from 1 or 2 venous
cannulas in the R atrium or SVC & IVC
Blood flows to the reservoir by
gravity drainage
Driving force is directly proportional
to the difference in height b/t patient
and reservoir
Inversely proportional to the
resistance of the cannulas & tubing
Entrainment of air /large bubble
airlock that prevents blood flow
Fluid level is critical if empty, air
can enter the main pump fatal air
Low level alarm is often present
40 micrometers, prevents systemic emobli

(2) Oxygenator
2 types o (1) Bubble oxygenator cheaper, easier to use, lower priming volume o
(2) Membrane oxygenator less RBC damage, best for long cases

Gas-permeable silicone membrane that allows blood to equilibrate

with the gas
Volatile anesthetic is often added at the oxygenator gas inlet
Arterial O2 is inversely related to the thickness of the blood film in contact with
the membrane
Arterial CO2 tension is dependent on total gas flow (i.e. gas flow if want to
CO2 level)
(3) Heat Exchanger
Blood from the oxygenator enters the heat exchanger, either cooled or warmed via
Gas solubility as blood temperature requires a built in filter to catch any
bubbles that may form during rewarming
(4) Main Pump
Roller Pump:


Located after the oxygenator o

Produce flow by compressing large-bore
tubing in the pumping chamber o Prevents excessive red cell trauma o
Continuous nonpulsatile flow directly proportional to # of
Centrifugal Pumps:
o Located between venous reservoir & oxygenator
o Blood flow is pressure-sensitive and must be monitored by an
electromagnetic flowmeter
distal pressure will flow must pump speed

(5) Arterial Filter

In-line, arterial filter (40 micrometers) is mandatory to prevent systemic emboli
Once filtered, blood returns via cannula into the ascending aorta
Inflow pressure is measured before the filter
(6) Accessory Pumps & Devices
Cardiotomy Suction:
o Aspirates blood from the field accessory pump filter venous
reservoir o
Excessive use of cell-saver suction (instead of cardiotomy
suction) depletes CPB circuit volume. Returned to a separate reservoir.
Left Ventricular Vent:
o Blood reaccumulates in the L.V. from residual pulmonary flow from the
bronchial arteries (intercostal arteries, thebesian vessels, aortic regurgitation)
o Distention of the L.V. compromises myocardial preservation and requires
decompression (venting) via a catheter inserted through the right superior
pulmonary vein, into the left atrium , through the MV and into the LV
o LV venting accessory pump filter venous reservoir
Systemic Hypothermia
Core body temp reduced to 20-320C
Metabolic O2 requirements per 100C reduction or 8% /0C

Potassium Cardioplegia
extracellular K+ reduces transmembrane potential (less negative inside)
interferences with Na+ current during depolarization Na+ channels eventually
become inactivated and heart is arrested in diastole **
o K+ = 15-40 mEq/L (keep < 50 mEq/L b/c risk paradoxic energy & high K
load) o
Na+ = 100-120 mEq/L o
Cl2- = 110-120 mEq/L o
= 15 mEq/L
o Glucose = 28 mmol/L (can use glutamate, aspartate)
o Bicarbonate = 27 mmol/L
May not reach areas distal to high-grade stenosis give retrograde via coronary
Reperfusion of myocardium can be associated with extensive cell injury, rapid
accumulation of intracellular calcium and irreversible cellular necrosis o
Oxygen-derived free radicals may play a role o Free radical scavengers,
mannitol therapy, may help



Hormonal & Humoral Responses
Increase in stress hormones = catecholamines, cortisol, arginine vasopressin,
angiotensin partly from hypothermia and exclusion of the pulmonary circulation
where many are broken down
Contact of blood with CPB system complement activation via Hageman factor
Coagulation cascade, platelets, plasminogen and kallikrein are all activated
Alters and depletes glycoprotein receptors on platelets platelet dysfunction
Altered Pharmacokinetics
Opioids bind CPB components
Except for propofol, continuous infusion of a drug during CPB causes progressively
higher blood levels 2/2 reduced hepatic & renal perfusion (reduced elimination)
and hypothermia (reduced metabolism)
-1 acid glycoprotein increases after CPB affects drug binding post-op
High Aortic Line Pressure o
Occlusion of the line by a kink or clamp o
Cannula too small for flow o Improper positioning of the cannula
Low venous return o
Occlusion of the venous line
o Bleeding o
Aortic dissection
Hypotension o Pump problems, malfunction o Low venous return o Low SVR (low
Hct or vasodilator)
Hypertension o Excessive flow
o Inadequate anesthesia
Risk factors for higher M&M
Pre-op CHF
L main stenosis
Unstable angina
Failed angioplasty
Need for re-operation
DDx for Elevated PAP while on-pump
Inadequate ventricular venting
Malposiiton aortic cannula unilateral facial flushing
Malposition venous cannla facial/scleral edema or poor blood return to bypass
Failure to Wean off CPB Treatments
(a) Epinephrine - direct agonist at 1 & 2 > 1
Indications: hypotension, LV failure, bronchospasm
Side effects: HTN, arrhythmias, myocardial ischemia, hyperglycemia
Low dose (0.01 0.05 mcg/kg/min) = 2 > 1 bronchodilation (2) , vasodilation
(2); HR (1), myocardial contractility (1), CO (1)


High dose (0.03 0.15 mcg/kg/min) = 1 SVR ( SV) , reduce splanchnic &
renal blood flow

(b) Dopamine - direct & indirect agonist at DA1, 1, and 1 receptors

Immediate precursor of norepinephrine (NE), it is a neurotransmitter in the basal
ganglia and chemoreceptor trigger zone
Indications: mild hypotension, oliguria
Side effects: HTN, tachycardia, arrhythmias, myocardial ischemia
Unique in ability to increase myocardial contractility, only modest increase in HR o
0.5 - 5 mcg/kg/min = DA1 dilation of renal arterioles, promotes diuresis o
5 - 10 mcg/kg/min = 1 myocardial contractility, HR, CO
o 10 - 20 mcg/kg/min = 1 SVR
o At all doses, mediates indirect release of norepinephrine from pre-synaptic
sites tachycardia
(c) Dobutamine direct synthetic catecholamine at 1 > 2, 1
Indications: cardiogenic shock/CHF with high afterload and low CO. Will reduce
pulmonary vascular resistance and improve right heart function
Unique ability to increase CO without maked increases in HR or MAP
Side effects: systemic hypotension (2), myocardial O2 consumption,
Dose: 1-15 mcg/kg/min
Other Cardiac Drugs to KNOW
Isoproterenol - 1 & 2 agonist
Indications: heart block and when no alpha agonists are needed. Often the drug of
choice in heart transplants. Reduces PVR
Dose: 0.02-0.15 mcg/kg/min
Vasopressin - Direct smooth muscle V-1 receptors
Coronary, pulmonary and cerebral vasculatures are not affected
Useful alternative to catecholamines that do not function well in profound acidemia
Known procoagulant
Amrinone & Milrinone
Selective phosphodiesterase type III inhibitors contractility & C.O. without
(HR) o
Inhibits breakdown of cAMP and hence work downstream of beta
receptors prolongs the contractility and vasodilation hence the term
inodilators (arterial & venodilator)
o In cardiac cells see Ca++ ; in smooth muscles Ca++
NO alteration in myocardial O2 consumption b/c they decrease afterload and do
not HR Synergistic approach with addition of -agonist
Milrinone Dosage : load 50 mcg/kg over 10 mins, infusion rate 0.4 - 0.8 g/kg/min
Mechanism: blocks the Na+, K+ ATPase to cause less Na+ egression. Therefore
Ca++ and contractility, independent of adrenergic stimulation prolongs A-V
conductance, (+) inotropy, muscle automaticity
Elimination: renal renal failure is the biggest cause of toxicity!


Toxic level: > 2 ng/ml

Si/Sx toxicity: ventricular arrhythmias
Should not be used in WPW b/c can cause V. Fib

Causes of digoxin toxicity o

Renal failure o
Hypokalemia (< 2.5) o
Hypothyroid o
Hypomagnesemia o Hypercalcemia
o Acidosis

Treatment of ventricular dysrhythmias while taking digoxin:

o Lidocaine (increases AV conductance)
o Phenytoin o Potassium o AVOID bretylium & D/C

Used to treat WPW & supraventricular tachycardia narrow complex
Raidly metabolized such that it is not influenced by liver or renal function
Effects enhanced by Dipyridamole asystole occurs if given standard dose
Methylxanthines Caffeine, Theophylline and Amrinone are antagonists of
adenosine increase drug dose
Side effects bronchospasm, dyspnea, HA, flushing, neck or throat discomfort
Contraindictions 2nd or 3rd degree AV block & SA nodal dysfunction risk asystole
Chemical structure similar to thyroxine casues hypo- or hyperthyroidism
Action - prolongs duration of action potential of both atrial & ventricular muscle
without altering resting membrane potential depresses SA and AV node function
Treatment of choice for:
Recurrent supraventricular & ventricular tachydysrhythmias
WPW increases refractory period of accessory pathway
Side effect Atropine-resistant bradycadia & hypotension during general
anesthesia due to anti-adrenergic effect Rx with isoproterenol or temporary pacing
Mech inhibits serine proteases plasmin, kallikrein, trypsin
Most common side effect = anaphylactic reactions in redo cardiac surgery 100%
renally excreted!
Beta Blocker Side Effects
Beta Agonist Effects

Vascular SM relaxation - hypotension

Uterine relaxation
Blunt catecholamine reponse to

Bronchodilation hypoglycemia

Renin secretion
Excessive myocardial depression, AV block

Rebound tachycardia with abrupt Glycogenolysis discontinuation insulin
secretion = hyperglycemia
Pulmonary edema
Mucopolysaccharide produced by mast cells, activates anti-thrombin III
inactivates factors II (thrombin), IX, X, XII


100 U = 1 mg
T heparin = 1-3 hours, re-dose with 100 U/kg q 2 hrs, t is temperature & dose
Inactivated by liver & kidneys, t prolonged in hepatorenal syndrome
T is dose and temperature dependent
Side effects: hemorrhage, alopecia, osteoporosis, thrombocytopenia
Neutralized by protamine 1mg /1 mg heparin inactive complex without
anticoagulant activity
If hx anaphylactic protamine rxn, reverse heparin with hexadimethrine or omit
reversal & wait

Highly positive charged base that binds and effectively inactivates heparin (highly
negative charged acid) heparin complexes are removed by reticuloendothelial
Dose protamine based on the amount of heparin initially required to produce that
desired ACT given in a ratio of 1-1.3 mg of protamine/100 U of heparin
Protamine given in excess has anti-coagulant activity (1/100th that of heparin)
Adverse effects:
o Myocardial depression
o Histamine release vasodilatation, flushing, severe pulmonary HTN from
systemic hypotension, pulmonary vasoconstriction, edema, bronchospasm
o Anaphylactic or anaphylactoid reactions o Patients allergic to fish may be at
higher risk
o Most severe, type II reaction mediated by elevated complement &
thromboxane A2 severe hypotension from R heart failure requiring reinitiation of CPB.
Intra-Aortic Balloon Pump
Acute cardiac failure refractory to pharmacologic intervention
Low-output states after CPB
Hypotension and low CI (<1.8) with high wedge pressure (>25 mmHg) despite
Cardiogenic shock 2/2 myocardial ischemia
Bridge to cardiac transplant
Percutaneous insertion into common femoral artery high in descending thoracic
Inflation is triggered from the R wave on the EKG and occurs during diastole,
immediately following closure of the aortic valve just after dicrotic notch
Balloon deflation occurs during isovolemic contraction (late diastole) just
prior to opening of the aortic valve.
Hemodynamic effects
afterload, MVO2 and myocardial work SV & C.O.
intra-aortic diastolic pressure by 70% with balloon inflation coronary
blood flow
R shift of Starling curve


Loss of distal pulses, bleeding, infection (20% overall risk)

inflation during ventricular systole impedes CO
Aortic regurgitation
Aortic aneurysm
Severe aortoiliac or femoral disease precluding insertion
Myocardial Oxygen Consumption Determined by 3 Factors
1. HR - HR results in greatest increase in myocardial O2 consumption
2. Wall tension directly related to end-diastilic pressure or volume (preload) and SVR
Myocardial work is much less with volume work (preload) vs. pressure
3. Contractile state
Coronary Artery Anatomy
Blood flow is 250 ml/min = 80 mL/100g/min = 5% cardiac output
Heart extracts 80% of oxygen from each unit of blood must increase flow to
compensate for increased demand
flow by hypoxia, CO2, H+, lactate, prostaglandins, adenosine, vagal tone dilates

85% incidence
forms PDA
inferior wall LV
SA/AV nodes
Bundle of His

Posterior LV
Inferior LV
muscle of MV

Leads II, III, aVF


Lateral wall
15% incidence
forms PDA
inferior wall LV


**at risk of
injury during
MV replacement
Leads V5, V6, aVL

Anterior wall LV

Anterior papillary
muscles MV
Leads V1 V4

Coronary artery ischemia

ST segment changes are not seen until several events have occurred:
o Increase in LVEDV-LVEDP
o Regional wall motion
o Decreased EF o ST
ST depression = subendocardium 1 mm
ST elevation +/- Q wave (> 40 msec or 1 small box) transmural/epicardial 2 mm
Flat ST depression = digitalis toxicity
J point = point in ST segment where slope changes, meaure ST change 80 msec from
J point
Management of Respiratory Gases


Solubility of a gas increases (CO2) with hypothermia partial pressure (CO2) of

the gas decreases as blood temperature drop
Most significant for arterial CO2 tension b/c of its effect on arterial pH and cerebral
blood flow o temp results in no change in NaHCO3, but a PaCO2 pH
(alkalotic) o At 37oC pH = 7.40, PaCO2 = 40 mmHg 25oC pH = 7.60, PaCO2 = 23
mmHg o
Blood samples are heated to 37oC in blood gas analyzers before gas
tensions are measured
pH-stat management = blood gas tensions are temperature-corrected and goal of
maintaining CO2 tension of 40 mmHg and pH of 7.40 during hypothermia.
o May require adding CO2 to the oxygenator gas inflow to correct for lower
partial CO2 pressure 2/2 increased solubility in solution (during hypothermia)
total blood CO2 content
o Cerebral blood flow becomes more dependent on CO2 tension and MAP than
on oxygen consumption
-stat management = uncorrected gas tensions during hypothermia (sample
warmed to 37oC and not corrected). No attempt is made to correct partial pressures
of O2 & CO2 for differences in temperature.

Bleeding Post-CPB

Surgical re-exploration if 500 ml/hr x 2 hours from chest tubes

Normal ACT < 120, PT < 15 secs, PTT < 35 secs

Vocabulary to Know
Pulsus paradoxus = defined as inspiratory fall in SBP > 10 mmHg cardiac
Pulsus parvus = diminished pulse wave aortic stenosis
Pulsus tardus = delayed upstroke aortic stenosis
Pulsus alternans = alternating smaller and larger pulse waves severe LV
Bisferiens pulse = 2 systolic peaks aortic regurgiation
Adrenergic Reception Up & Down Regulation
# receptors is inversely proportional to the ambient concentration of
Increased adrenergic activity myocardial post-synaptic 1 receptors
down regulate
Calcium-induced inotropism is not impaired because 2 receptor numbers remain
relatively intact, can account for 40% of inotropism of the failing heart
Tachyphylaxis to infused catecholamines is from acute down-regulation of receptor
numbers Seen with chronic use of -agonists (terbutaline or isoproterenol).
Reversible with termination.
Reduction in number or sensitivity of -receptors in HTN patients w/elevated
Down regulation is the explanation for the lack of correlation b/t catecholamine levels
and BP elevation in those with pheochromocytoma
Chronic treatment with non-selective -blockade causes 100% increase in # of receptors propranolol withdrawal syndrome tachycardia, sweating,
tremor and general malaise


IHSS: Idiopathic Hypertrophic Subaortic

Si/Sx: SAD Syncope,
Angina, Dyspnea
Frequently see
mitral regurgitation!
preload avoid hypovolemia and nitroglycerin
afterload phenylephrine is treatment for hypotension
myocardial contractility increases in contractility result in C.O. Beta-blockers
are cornerstone of management. Use Halothane!

Ketamine b/c increase in sympathetic tone, even though a direct myocardial
Ca2+ channel blockers b/c decrease afterload
Digitalis or isoproterenol b/c of increase outflow obstruction Isoflurane
Treat A. fibrillation with cardioversion, not digitalis

Aortic Stenosis
If occurs with rheumatic fever, mitral valve is also affected
Si/Sx: SAD Syncope, Angina (without CAD), Dyspnea life expectancy < 5 years
Compensatory concentric increase in thickness of LV wall (minimal change in LV
size). As becomes more severe, LV becomes dilated and myocardial contractility
HD significant disease = valvular pressure gradient > 50 mmHg
LV filling if very dependent on atrial contraction maintain sinus rhythm
Mitral Regurgitation/Aortic Regurgitation
Large V wave = mitral regurgitation
PDA occlusion posterior papillary muscle rupture acute MR
Achieve small increase in HR and decreases in SVR o Digitalis decrease size of LV
and lessens regurgitation, helps control A. fib o Nitroprusside decreases afterload
reduces pulmonary edema o Atropine beneficial o Isoflurane decrease in SVR and
increase in HR o Isoproterenol decrease in SVR and increase in HR
Mitral Stenosis
Exclusively in rheumatic fever pathophysiologic changes proximal & distal to
abnormal valve
Women > men, latency period 20-40 years
LV is protected, thus rarely see LV dysfunction
PCWP transudation of fluid into pulmonary interstitial space lower pulmonary
compliance & increases WOB
Patients are more susceptible to ventilatory depressant effects of sedative drugs
Increases in central blood volume ie. Trendelenburg position can precipitate R
heart failure
Wide Complex Tachycardia
Could be paroxysmal supraventricular tachycardia with aberrant accessory pathway
If HD unatble cardioversion
If HD stable consider amiodarone (150 mg IV) or procainamide


Pulmonary Artery Rupture

Hallmark: hemoptysis
Risk factors: hypothermia, old age, anticoagulation, PA catheter migration
Not risk factor: PA atheromas


1 = normal
= factor deficiency
3 = hypofibrinogenemia
4 = fibrinolysis
5 = hypercoagulable

Primary Idiopathic Pulmonary Hypertension

Normal PAS = 18-25 mmHg/PAD 6-10 mmHg, PAPmean 12-16 mmhg
Hallmark: hypoxia, PVR, PAP, RV pressure
Mainstain medical therapy o
Anti-coagulation to reduce PE o antagonists phentolamine, prazosin o -agoinsts isoproterentol, terbutaline o
direct-acting vasodilators hydralazine, SNP, nitroglycerin o
Sildenafil, a
selective inhibitor of cGMP specific phosphodiesterase type 5 o Epoprostenol gtt (a
synthetic prostacyclin, PGI2) = Flolan **side effect plt fx**

30% of patients respond favorably to acute vasodilator therapy.

Only those patients whose PAPmean > 10 mm Hg to less than 40 mm Hg with
an unchanged or increased cardiac output when challenged with adenosine,
epoprostenol, or nitric oxide are considered vasoreactive



Of these, only of the patients are responsive to calcium channel blockers in the long
term o
Ca channel blockers used: nifedipine 30-240 mg/day or diltiazem 120-900
mg/day Increases in PVR
Decreases in PVR
Metabolic acidosis
Metabolic alkalosis o Hypoxia
Sympathetic stimulation o
Nitroglycerin *best b/c least systemic effects o
Atelectasis o HCT
Low lung volumes due to compressed vessel from extra-alveolar vessels
High lung volumes b/c alveolar capillaries are compressed
N 2O
High airway pressures/PEEP

* PVR indirectly related to C.O.

pulmonary vessels

C.O. = PVR due to recruitment & distention of

Due to: (1) magnesium-containing antacids, (2) severe burns, (3) DKA, (4) EtOH
withdrawal, (5) prolonged respiratory alkalosis, (6) TPN
Often a serious and unrecognized complication of TPN that can contribute
to post-op muscle weakness and respiratory failure
Low PO4 reduces ATP reduce 2,3 DPG Left shift oxy-Hgb curve
unloading O2
Hyponatremia = Na+ < 135 mEq/L
Na+ < 120 = cerebral edema confusion, restlessness, drowsiness, seizure, coma
Na+ < 100 = V. tach, V. fib
Treatment: water restriction, loop diuretics, 3% NS if severe
Dose Na+ needed: i.e. 100 kg patient, Na+ 105 mEq/L, How much Na+ to
bring up to 120?
Dose Na+ = (wt in kg)(0.6) x (desired Na+ level current Na+)
(100 kg)(0.6) x (120 105) = 900 mEq
Give 3% NS (no faster than 100 ml/hr, once Na+ reaches 120, further treatment is
water restriction and diuretics
Metabolic Alkalosis


Chloride sensitive:
o Vomiting hypokalemic,
hypochloremic metabolic
alkalosis. K+ is lost in
emesis & urine in exchange
for trying to retain H+.
Alkalosis due to H+ loss in
emesis and volume
o Volume contraction o
Chloride resistant:
o Cushings o

Metabolic Acidosis = HCO3- < 22 mEq/L

Respiratory compensation: PCO2 PCO2 equals the last two digits of the pH
Hyperventilation compensation is never complete b/c the ability to
hyperventilate is limited
Anion gap = Na+ (Cl + HCO3-); normal 4-12 mEq
Correct for low albumin add 3 to anion gap for every 1 g/dL of albumin; i.e.
albumin = 1.5, must add 4.5 to anion gap

Anion Gap
Diabetic ketoacidosis, alcoholic ketosis, starvation
Paraldehyde (anti-convulsant)
Lactic acidosis/Lactate (rhabdomyolysis)
Ethylene glycol/Ethanol

Non-anion Gap (hyperchloremic)

Hyperalimentation/Hypoaldosteronism Acids
RTA waste HCO3-, retain ClDiarrhea
Ureterointestinal Anastomosis
Pancreatic fistula
Sparing K+ diuretics
+ Carbonic anhydrase inhibition

*calculate osmolal gap = 2(Na+) + BUN/2.8 +

gluc/18 if > 10 methanol or ethylene glycol
ingestion (also see oxalate crystals in urine)
Acid-base effects of chronic diarrhea
HCO3- is lost, leaving unopposed H+ and Cl- ion excess in a decreased circulating
blood volume = hyperchloremic metabolic acidosis
Large amounts of Na+, K+ are lost as well
Reciprocal rise in Cl- that approximates the drop in HCO3-, if not, then have a mixed


Diabetes Mellitus
Diagnosis: fasting glucose > 140 mg/dL or random glucose > 126 mg/dL
DKA = diabetic ketoacidosis o insulin activity promotes amino acid buildup and
lipolysis with the release of free fatty acids free fatty acids converted into
ketone bodies in the liver acetoacetate & hydroxybutyrate anion-gap
metabolic acidosis
o Profoundly depleted of K+, yet serum levels are not often low b/c of the
acidosis o Treatment: treat hypovolemia from osmotic diuresis,
hypokalemia, start NS gtt
10 U/hr regular insulin or 0.1 U/kg/hr
As glucose moves intracellularly, so does K+
Monitor K+, glucose, serum ketones, UOP hourly
Avoid LR since liver converts lactate to bicarbonate, use NS
Once glucose reaches 250 mg/dL, start D5W
Give bicarbonate if pH is < 7.1 or base excess is > -7 caution b/c
bicarbonate can cause alkalosis with intracellular shift of K+

Lactic acidosis = lactate > 6 mmol/L, absence of urine & plasma ketones
Alcoholic ketoacidosis = recent EtOH history, +/- glucose, -hydroxybutyrate
>> acetoacetate
Hyperosmolar hyperglycemia non-ketotic coma (HHNKC) o Three
components are involved:
(1) Insulin deficiency: liver insulin levels are high enough to permit the
metabolism of free fatty acids, generally dont develop ketosis
(2) Renal deficiency-insufficiency: impairs the ability to excrete glucose and
to hyperosmolarity
(3) Thirst deficiency: either b/c of a stroke or CNS depressant

Brain volume is reduced as free water attempts to equilibrate from a

high concentration in the brain to a low concentration contributes to
coma, MS changes, seizures
Characteristics: hyperglycemia, hyperosmolarity, non-ketosis
Plasma glucose > 600 mg/dL
Osmolality > 300-350 mOsm/L
pH > 7.3
Absent or minimal ketones in urine or serum
Severe hyperglycemia causes a factitious hyponatremia o Treatment:
Fluid resuscitation 6-8 L
Insulin in small doses, dont aggressively treat b/c free water can move
too quickly from the blood to the brain causing cerebral edema
Follow K+, moves into cells with insulin administration hypokalemia

Hypoglycemia = < 50 mg/dL o

Some patients are unable to counter
hypoglycemia by secreting glucagon or epinephrine
(counter-regulatory failure) o
Systemic si/sx are due to
catecholamine discharge diaphoresis, tachycardia, nervousness



Maternal Diabetes o
Hyperglycemia in the mothers leads
to hyperglycemia in the fetus!
o Causes a state of chronic hyperinsulinemia and increased glycogen
synthesis, lipogenesis, protein synthesis macrosomia
o At birth, can see neonatal hypoglycemia from chronic hyperinsulinemia o
Other associated problems:
Respiratory distress syndrome 2/2 to inhibitory effects of
hyperinsulinemia upon surfactant production
Congenital abnormalities

Anesthetic Considerations
Those with HTN have 50% chance of co-existing diabetic autonomic
o Orthostatic hypotension: > 30 mmHg SBP with upright position o
Painless MI: most frequent cause of death in long term diabetic o
Lack of HR variability
o Reduced HR response to atropine and propranolol
o Neurogenic bladder o
Lack of sweating o Impotence o Gastroparesis
Renal dysfunction manifested first by proteinuria, then elevated serum creatinine
Chronic hyperglycemia can lead to glycosylation of tissue protein and limitedmobility joint syndrome check TMJ, cervical spine mobility
o give dose of total morning insulin as NPH o start D5W gtt at 1.5
o Insulin units/hr = plasma glucose
o 1 unit insulin lowers plasma glucose 30 mg/dL
Those requiring NPH or protamine zinc insulin have higher risk of protamine
sulfate allergic reaction
Large volumes of LR given can rise glucose levels for 24-48 hrs post-op

1 hour
2 hour
4 hour

3 hour peak

6 hour duration

6 hour peak

24 hour
24 hour

12 hour

Thyroid gland secretes: triiodothyronine (T3), thyroxine (T4), calcitonin
Dietary iodine is absorbed by the GI tract thyroid gland oxidized back into
iodine bound to tyrosine triiodothyronine (T3) & thyroxine (T4)
Causes: Graves disease, toxic multinodular goiter, thyroiditis, TSH secreting
pituitary tumor, functioning thyroid adenomas, overdosage of thyroid
replacement hormone
Medical treatment:


Propylthiouracil or methimazole to inhibit hormone synthesis, takes 68 weeks o Propranolol rx adrenergic overactivity & peripheral
conversion of T4 to T3 o Sodium iodide + propranolol lead to
euthyroidism within 10 days
Elective surgical procedures should be postponed until euthyroid
Emergency surgery, use esmolol gtt to control hyperdynamic circulation
Thiopental is best b/c is possesses some antithyroid activity at high doses
Patients can be chronically hypovolemic and vasodilated prone to hypotension
Display accelerated drug biotransformation & may be more prone to halothane
hepatitis and kidney toxicity from enflurane
NMB agents should be given cautiously; thyrotoxicosis is associated with
myopathies & myasthenia gravis
Hyperthyroidism DOES NOT increase MAC

Thyroid storm hyperpyrexia, tachycardia, altered MS (delirium, coma, agitation) and

hypotension, CHF, dysrhythmias
Not associated with muscle rigidity, elevated CK or acidosis
Pharmacologic therapy: (1) propranolol, (2) propylthiouracil and (3)
sodium iodide; (4) cortisol b/c of increased utilization, (5) glucose (for
increased metabolism)
Clinical Manifestations
Causes: Hashimotos thyroiditis, thyroidectomy, radioactive iodine, antithyroid
meds, iodine deficiency, autoimmune d/o o
Most common cause is
treatment of hyperthyroidism
Lethargy, hypotension, bradycardia, CHF, gastroparesis, hypoglycemia,
hypothermia, hypoventilation, hyponatremia, poor mentation, depression
Myxedema coma:
o Extreme, severe hypothyroidism hypothermia, hyponatremia,
hypoventilation, CHF o More common in elderly, precipitated by
infection, surgery or trauma
o Treat with IV levothyroxine sodium & hydrocortisone for potential coexisting adrenal gland suppression
Dx: low free T4 level
Treatment: 1-thyroxine (Synthroid) with t = 7 days
Anesthetic considerations:
o More prone to hypotension from low C.O., blunted baroreceptor reflexes,
decreased volume ketamine for induction
o Avoid volatile anesthetics when possible b/c sensitivity of myocardium to
depression o
Pancuronium is vagolytic mild sympathetic effect
Principal regulator of Ca2+ homeostasis bone resorption, limits renal
excretion and indirectly enhances GI absorption via Vitamin D
serum phosphate by increasing renal excretion
Net effect = hypercalcemia & hypophosphatemia
Unbound ionized calcium is the most physiologically important


Hallmark: serum Ca2+ > 5.5 meq/L (normal 4.5-5.5 meq/L)
Primary hyperparathyroidism: parathyroid adenoma, carcinoma, hyperplasia
Secondary hyperparathyroidism: adaptive response to hypocalcemia 2/2 to
renal failure or intestinal malabsorption syndromes
Parathyroid hormone-related peptide secreted by a carcinoma (hepatoma,
bronchogenic) is the most common cause of humoral hypercalcemia of
Effects of Hyperparathyroidism:
o short QT & prolonged PR intervals
o Hyperchloremic metabolic acidosis, polyuria, dehydration, polydipsia,
renal stones, renal failure
o Ileus, N/V, PUD, pancreatitis o Skeletal muscle weakness,
o MS changes
Treatment: maintain UOP, hydrate, give Mithramycin in severe cases
Due to hypocalcemia (< 4.5 meq/L) NM irritability (+) Chvosteks sign
(painful twitch of facial muscles after tapping facial nerve) or Trousseaus sign
(carpopedal spasm after inflation of TQ above SBP x 3 mins)
Hallmark: neuromuscular irritability (tetany) and laryngospasm,
prolonged QT interval
Treatment Calcium chloride
Avoid using 5% albumin solutions which might bind and lower ionized calcium
*HYPERCALCEMIA* = Level > 12 mg/dL
Si/Sx: HTN, dysrhythmias, shortened QT interval, kidney stones, seizure, N/V,
weakness, depression, personality changes, psychosis
Caution with administration of digitalis b/c some may exhibit extreme digitalis
Rx: 1st line Furosemide & fluid hydration with NS o
Other options
calcitonin, mithramycin, corticosteroid
Adrenal cortex secretes 2 classes of steroids, (1) corticosteroids (glucocorticoids
& mineralocorticoids) and the androgens
Glucocorticoid = cortisol = use hydrocortisone for replacement o
for anti-inflammatory and immunosuppressive effects, but also have
mineralocorticoid activity (Na+ retention)
Mineralocorticoid = aldosterone = use fludrocortisone for replacement
50 mg prednisone = 7.5 mg dexamethasone = 200 mg hydrocortisone


Anterior Pituitary Adrenal Cortex

Zona Glomerulosa mineralocorticoid Aldosterone
Zona Fasciculata
Zona Reticularis


Aldosterone enhances Na+-K+ ATPase activity; also enhances H+ secretion
via K+-H+ ATPase HTN, hypokalemic ametabolic alkalosis
A mineralocorticoid steroid, produced in the zona glomerulosa
Acts on the distal tubules and collecting ducts to conserve Na+, secrete K+,
water retention
Its activity is reduced in Addison's disease and increased
in Conn syndrome
Aldosterone is stimulated by several factors:
o plasma concentration of Angiotensin III, a metabolite of Angiotensin II



plasma angiotensin II, ACTH, or K+ levels, which are present in proportion

to plasma Na+ deficiencies.
K + levels are the most sensitive stimulator
Stretch receptors located in the atria of the heart. BP release aldosterone,
Na+ reabsorption from the urine, sweat and the gut


Primary aldosteronism: due to adenoma, bilateral hyperplasia, carcinoma
Secondary aldosteronism: CHF, hepatic cirrhosis, nephrotic syndrome
Si/Sx: HTN, hypokalemia,muscle weakness, metabolic alkalosis hypocalcemia
Treatment: K+ sparking diuretics spironolactone (competes with aldosterone),
amiloride or triamterene (act independently of aldosterone)
Unilateral adrenalectomy, DM, heparin therapy can cause isolated
hypoaldosteronism hyperkalemia, hyponatremia, acidosis, hypotension,
Give fludrocortisone
Excess of corticosteroids = Cushings syndrome o HTN, hypokalemic alkalosis
(aldosterone effects), volume overloaded o
Hyperglycemia, hyperNa+ o
Diabetes o Osteoporosis and easy bruising o
Skeletal muscle
weakness o
o Buffalo hump, moon facies, hirsutism, menstrual changes
Treat pre-op with K+ supplementation & spironolactone, adrenalectomy requires IV
hydrocortisone succinate 100mg
Primary adrenal insufficiency (Addisons disease)
leads to mineralocorticoid & glucocorticoid deficiency
Clinical manifestations due to aldosterone deficiency (hyponatremia, hypovolemia,
hypotension, hyperkalemia, metabolic acidosis) and cortisol deficiency (weakness,
fatigue, hypoglycemia, hypotension, wt loss)
Secondary adrenal insufficiency due to inadequate ACTH secretion by the pituitary
Acute adrenal insufficiency (Addisonian crisis) is triggered in steroid-dependent
patients who do not get increased doses during periods of stress circulatory
collapse, fever, hypoglycemia, depressed mentation
Embryonic neural crest (chromaffin tissue)
90% HTN, 90% in adrenal medulla, 90% benign
5% autosomal dominant o MEN IIA = medullary carcinoma of thyroid and
hyperparathyroidism o
MEN IIB = medullary carcinoma of thyroid and
neuromas of oral mucosa o
Von Hippel-Lindau disease = hemangiomas of NS
(retina or cerebellum)
Hallmark: paroxysmal HA, diaphoresis, tachycardia in setting of HTN o
Other: orthostatic hypotension, N/V, hyperglycemia, hypovolemia, weight loss,
tremulousness, palpitations


o Rarely CHF, cardiomyopathy

Death due to cardiac conditions e.g. MI, CHF or intracranial bleed
Dx: 24 hr-urine & serum catecholamines --> metanephrine or normetanephrine
are more reliable than VMA

Anesthetic Considerations for Pheochromocytoma

Decrease in RBC mass & plasma volume = severe chronic hypovolemia
Adequate adrenergic blockade with phenoxybenzamine (nonselective, longacting, -antagonist)
Propranolol give alpha blocker, before beta-blocker
Treat HTN intra-op: phentolamine (nonselective, short-acting, -antagonist),
nitroprusside, or nicardipine
After tumor removal/ vein ligation expansion of intravascular space
AVOID drugs/techniques that stimulate the sympathetic NS (ephedrine, ketamine,
hypoventilation) potentiate the dysrhythmic effects of catecholamines, inhibit
parasympathetic NS (e.g. pancuronium), or release histamine (e.g. atracurium,
MSO4) may precipitate HTN
ANP = Atrial natriuretic peptide
Activation/stretching of atrial stretch receptors (hypervolemia, CHF)
sympathetic outflow release ANP systemic vasodilation, Na+ retention,
inhibition of renin and aldosterone release
BMI = weight (kg) BMI 22-25: normal
(Height [meters])2 BMI 28-30: overweight
BMI 30-35: obesity
BMI >35: morbid obesity
Clinical Manifestations
Elevated O2 demand, CO2 production, and alveolar ventilation due to elevated
metabolic rate that is proportional to body weight
Respiratory: Hypoxia due to the following o
Restrictive lung disease
Vital Capacity < 75% predicted
FEV1 & FVC are reduced FEV1/FVC unchanged
closing capacity & reduced FRC
RV normal
ERV (20%)
Dead space is NOT CHANGED! o
Maximal reduction in blood
oxygenation in obese patients occurs 2-3 days post-op. Takes 7-10 days
for reductions in FRC, VC, and FEV1 to normalize
o C.O. by 100mL/min/kg of adipose tissue perfused
o Increased workload by the heart SV, no change HR HTN, LVH o
Elevations in pulmonary blood flow and pulmonary artery vasoconstriction
from persistent hypoxia pulmonary HTN and cor pulmonale
Metabolic, Renal, Hepatic:
o Insulin resistance, high cholesterol, triglycerides, and LFTs
o Halothane hepatitis is associated with obesity from increased metabolism


Risk for aspiration pneumonia from GERD, HH, delayed gastric emptying o
Hyperacidic gastric fluid (pH < 2..5) o High gastric volume (> 25

Pickwickian Syndrome = Obesity-hypoventilation syndrome

Characterized by hypercapnia, hypoxemia, pulmonary HTN, cyanosis-induced
polycythemia, right-sided heart failure, and somnolence
Alveolar hypoventilation from blunted respiratory drive
OSA is associated with increased peri-operative complications: HTN, hypoxia,
dysrhythmias, MI, pulmonary edema, stroke
Pharmacologic considerations
Lipophilic drugs (thiopental, benzodiazepines, lidocaine) o volume of
distribution o Lower drug serum concentration
o Longer elimination t , but similar clearance rates
Higher pseudocholinesterase levels (activity linearly with weight) require
larger doses of SCh (based on TBW)
Variable duration and recovery from NMB. Cisatracurium is ideal
Action of fat soluble volatile agents is not prolonged in obesity
Halothane - deposition fat tissues/prolonged recovery
Propofol dose based on IBW, volume distribution/clearance
Fentanyl/Sufentanil dose based on TBW, t , excessive Vd
Remifentanil dose based on IBW, similar to non-obese patients, best to use!
Carcinoid Tumors
Eterochromaffin tumors , > 70% originate in intestine 50% in appendix
Hormones released by non-metastatic tumors reach liver by portal vein inactivate
Once metastases reach liver, released hormones reach systemic circulation
carcinoid syndrome cutaneous flushing, bronchospasm, profuse diarrhea,
dramatic swings in BP and supraventricular dysrhythmias
Clinical Manifestations
R-sided heart failure due to valvular and myocardial plaque formation o Lung
metabolism of serotonin prevents involvement of the L-heart
Diagnosis: detection of serotonin metabolites in the urine (5-hydroxyindoleacetic
acid) or elevated plasma levels of chromogranin A
Treatment: surgery, somatostatin inhibitory peptide, release of vasoactive
Anesthetic Considerations
Avoid histamine-releasing drugs morphine, atracurium
Consider use of anti-serotonin agent, methysergide; somatostatin analog
HTN deepen anesthetic & give IV somatostatin or labetalol
Bronchospasm IV somatostatin or nebulized iprotropium
IV fluid boluses and IV somatostatin



Anterior Pituitary, part of the adenohypophysis

Regulated by hypothalamic peptides (releasing hormones) that are transported to
the adenohypophysis by a capillary portal system
Under negative feedback control by the products of their target organs
i.e. increase in circulating thyroid hormone inhibits the secretion of TRH and TSH
Hormones Produced by Anterior Pituitary
ACTH = adrenocorticotropic hormone stimulates adrenal cortex to secrete
(mineralocorticoid production is not dependent on ACTH)
TSH = thyroid-stimulating hormone accelerates synthesis & release of thyroxine
GH = growth hormone tissue growth, protein synthesis, fatty acid mobilization o
Excess growth before epiphyses are closed = gigantism o
After epiphyses
are closed = acromegaly
FSH & LH normal testosterone production and spermatogenesis, cyclic ovarian
Prolactin support breast development. Dopamine receptor
antagonists PRL secretion
MSH: melanocyte stimulating hormone
Airway resulting from acromegaly are important!
o Mandible increases in thickness & length o
Tongue & epiglottis enlarged
o Pharyngeal tissue overgrowth leads to soft tissue upper airway obstruction o
Glottic and subglottic narrowing o Enlarged vocal cords o
turbinate enlargement
Other important findings in acromegalies: o
o Increased risk of CAD o Increased V/Q mismatching o
from inhibition of insulin o
Osteoporosis/skeletal muscle weakness o
Peripheral neuropathy
o polypoid laryngeal masses (very uncommon)
Posterior Pituitary, part of the neurohypophysis, includes the pituitary stalk &
median eminence
All hormones are made in the hypothalamus and transported along hypothalamic
neuronal axons for storage in the posterior pituitary

ADH = Vasopressin o
Hormones formed in the supraoptic (ADH) neuron o
Most important stimulus are osmoreceptors in the hypothalamus (i.e. 295
mOsm/L) o
Also stimulated by peripheral vascular stretch receptors, reduced
intravascular volume, painful stimulation, and PEEP
Oxytocin o Hormones formed in the paraventricular (oxytocin) neurons o Acts on
areolar myoepithelial cells, part of milk letdown reflex, enhances uterine activity

Diabetes Insipidus (DI)

Hallmark: high UOP, poorly concentrated urine (s.g. < 1.005) , low UrineOsm < 150
mOsm/kg hypovolemia & hyperNa+

Central DI
Mechanism: absence of ADH due to posterior pituitary destruction


Dx: h/o polydipsia, polyuria (> 6L/day), absence of hyperglycemia, urine osmolality
< plasma osmolality o
Confirmed by increase in urine osmolality following
administration of exogenous ADH (desmopressin)
o Desmopressin hormone replacement intranasal or oral o Vasopressin (5U
SC q4 h)
o Chlorpropamide- an oral hypoglycemia agent, promotes renal response to
ADH or to desmopressin
o Carbamazepine enhances response to ADH o
Clofibrate increases
ADH release

Nephrogenic DI
Mechanism: failure of renal tubules to respond to ADH o Can be congenital or 2nd
to drugs: amphotericin B, lithium, demeclocycline, mannitol
Dx: failure to produce a hypertonic urine following exogenous ADH
Treatment: correct underlying disorder o Low salt, low protein diet o NSAIDS
o Thiazide diuretic (HCTZ) results in hypovolemia induced Na-H2O
reabsorption, thus less H2O delivery to ADH sites
o Amiloride for induced DI

Diagnosis: HypoNa+ < 130 mEq/L, PlasmaOsm < 270 mOsm/kg, Urine [Na+] >
20 mEqlL
Hallmark: inappropriate natriuresis
Main clinical difference between cerebral salt wasting & SIADH CSWS leads to a
relative or overt hypovolemia, whereas SIADH is consistent with a normal to
hypervolemic patient
o Restrict fluid intake
o Demeclocycline to antagonizes effects of ADH on renal tubules o Normal
saline gtt 100-400 mEq/day o If acute symptoms (coma, confusion) can give
3% hypertonic NS
o Do not exceed > 8 mEq/ 24hr central pontine myelinolysis = sudden
para or quadraparesis, dysphagia, dysarthria, double vision and LOC. Lockedin syndrome where cognitive function is intact, but all muscles are paralyzed,
except eye blinking.

Hypophysectomy = removal of pituitary gland

Performed for acromegaly, Cushings disease or cancer
Most common post-op problem is central DI (lack of ADH)
Treatment: D5 NS & ADH infusion

Most result from too high current density

Mapleson Circuits
A Dog Can Bite type A is best for spontaneous ventilation o
ml/kg/min FGF to maintain normocarbia

Requires 200


Dead Babies Cant Assist type

D is best for controlled ventilation o
Requires 70 ml/kg to maintain
Bain Circuit = Mapleson D
Advantages: (1) better heat
conservation & humidification, (2)
better scavenging b/c pressure relief
valve located near reservoir bag
Disadvantges: (1) high flows with
spontaneous ventilation (200 ml/kg),
(2) high resistance to breathing, (3)
unrecognized kinking/disconnect of
inner tube
FGF = 70 ml/kg during controlled, 200300 ml/kg during spontaneous
Mapleson E (Ayres T-piece)
Minimal dead space, no valve, and
very little resistance
The expiratory limb is the reservoir
Minimum FGF = 3 x patients MV

Mapleson F = Jackson Reese modification

of Mapleson D
An Ayres T piece with a reservoir bag and an adjustable pressure limiting (overflow)
valve on the distal end of the reservoir bag
Minimum FGF = 2 x patients minute ventilation
Commonly used for controlled ventilation during procedures and for transport. Is
popular for pediatrics
Disadvantages: (1) need for high FGF, (2) lack of humidification, and (3) possibility of
high airway pressures
Circle System vs. Mapleson Circuits
Advantages of circle system: (1) greater preservation of anesthetic gases, (2)
conservation of airway heat & humidity, (3) more reliable scavenging
Advantages of Mapleson: (1) lightweight, (2) allows more rapid adjustments of
inspired gas concentration, however variable control of anesthetic depth

Soda Lime: (1) CO2 + H20 H2CO3

(2) H2CO3 + 2NaOH Na2CO3 + 2H20 + Heat
(3) Na2CO3 + Ca(OH)2 CaCO3 + 2NaOH

Most common, absorbs up to 23L CO2 /100g absorbent

95% Calcium hydroxide Ca(OH)2
5% Sodium hydroxide NaOH primary component for CO2 absorptive property
1% Potassium hydroxide KOH
Hardness due to addition of silica. Hardness diminishes amount of dust


Efficiency of absorption varies inversely with the hardness

The drier soda lime, the more likely it will absorb & degrade volatile anesthetics
can cause delayed induction or emergence
Specific H2O content is required for optimal activity b/c CO2 & Ca(OH)2 rxn is

Baralyme: (1) Ba(OH)2 + 8H2O + CO2 BaCO3 + 9H2O + Heat

(2) 9H2O + 9CO2 9H2CO3
(3) 9H2CO3 + 9Ca(OH)2 9CaCO3 + 18 H2O + Heat

80% Calcium hydroxide Ca(OH)2

20% barium hydroxide Ba(OH)2
15% less efficient than soda lime
Contains H2O, performs better in a dry climate than soda lime (requires H2O)
Desflurane can be broken down to CO by dry barium hydroxide lime to such a
degree that it is capable of causing clinically significant CO poisoning

PA & Central Venous Catheter Waves

a wave = atrial contraction o Large a wave = atrial
contraction against a closed tricuspid valve; heart block
nodal rhythms, tricuspid or pulmonary stenosis
o Loss of a wave = a. fibrillation

c wave = coincides with onset of ventricular systole , due

to tricuspid valve closure

x descent = starts with atrial relaxation, continues as RV contracts during systole

pulling floor of atrium downward o exaggerated in constrictive pericarditis

y descent = when tricuspid opens early in diastole, blood in RA flows passively into
RV, RA pressure falls again, making a 2nd trough o abolished in cardiac tamponade o
exaggerated in constrictive pericarditis
v wave = filling of RA during systole o Large v wave = mitral regurgitation or
tricuspid regurgitation

Catheters & Air Embolism

Aspirate PA or multi-orifice catheter before any other maneuver
The Risk of Electrocution
Leakage current is present in all electrical equipment due to capacitive coupling,
induction between internal electrical components, or defective insulation
MICROSHOCK: Max leakage in OR = 10 A, induces VF at 50 A
MACROSHOCK: Line isolation monitor alarms at 2-5 mA, induces VF at 100
Protection from Electrical shock
OR power supply can be isolated from ground by an isolation transformer. Its
secondary wiring is not grounded and provides 2 live ungrounded voltage
lines for OR equipment
Line isolation monitor measures the potential for current flow from the isolated
power supply to ground


With monitors set at 2 or 5 mA, no warning given if leakage currents in the

microshock range
An alarm is activated if an unacceptable high current flow to ground becomes
possible, but power is not interrupted unless a ground-leakage circuit breaker is also
Line isolation monitor alarms when grounding occurs in OR or when max current
could cause excess of 2-5 mA.
While the line isolation monitor warns of the existence of a single fault (b/t a
power line and ground), 2 faults are required for a shock to occur
If the alarm is activated, the last piece of equipment that was plugged in is suspect
and should be removed
Protective Factors to reduce risk shock: o
Less danger if the catheter is
floating free in the ventricle, not lodged in the wall o Less danger if the catheter tip
is in the atrium
o A pressure transducer prevents current proximal to the transducer from
flowing down the catheter
o An electrically conductive catheter filled with saline is safer than a
nonconductive catheter
o Duration of contact the shorter the better o DC is safer than AC
o Higher frequency has less tissue penetration
o Area exposed to current = current density larger the current density, the

Surgical Diathermy
Malfunction of the grounding pad may result from disconnection from the
electrosurgical unit, inadequate patient contact, or insufficient conductive
gel. In these situations, the current will find another place to exit (eg, EKG
pads or metal parts of the OR table), and result in a burn
To avoid pacemaker malfunction, place the grounding pad as close to the surgical
field and as far away from the heart as practical
Fires and Explosions
Probability of ignition depends on:
o PVC OETT tubes >> red rubber OETT
o Wattage of the laser beam o
Duration of
exposure o
Gas mixture in the ETT
Prevention: ETT can be wrapped with copper, aluminium or use a specialty tube;
run lowest flow O2 and substitute air for nitrous oxide
Thermal Injury &
o Thermal injury from direct exposure to the flame
o Inhalation of smoke causes chemical burn acute respiratory failure:
bronchospasm, intra-alveolar hemorrhage, edema, loss of surfactant
o PVC ETT release HCl when burned severe pneumonitis o Red
rubber ETT releases carbon monoxide

Response to Airway Fires



1. Disconnect O2 source at the Y-piece and remove burning objects from the
2. Irrigate the site with water if fire is still smoldering
3. Ventilate the patient by mask or reintubate the trachea and ventilate with low
4. Evaluate the extent of injury by (rigid) bronchoscopy & laryngoscopy
5. Reintubate or perform a tracheostomy
6. Monitor with oximetry, ABG, CXR x 24 hours
7. Use ventilatory support, steroids, antibiotics as needed
Sources of Medical Gases
Wall outlets supply oxygen, nitrous oxide, air at a pressure of 50-55 psi
Outlets and supply hoses to the machine are diameter indexed
Critical temperature is the temperature above which a substance cannot be liquified
regardless of the pressure that is placed on it.
Critical temperature = - 119C (gaseous state at room temp)
E-cylinder, green = 2000 psi = 660L
i.e. Pt is being transported on nasal cannula at 4 L/min from an E-cylinder with gauge
pressure 1200 psi. How many hours will O2 last?
P1/V1 = P2/V2 o 2000 psi/660 L =
1200 psi/ X X = 400L 100 mins
Nitrous Oxide
Critical temperature = 36.5C kept liquified without refrigeration
E-cylinder, Blue = 750 psi = 1500L
NIOSH: < 25 ppm N2O alone or < 0.5 ppm with other agents
Energy is consumed in the conversion of a liquid to a gas (latent heat of
vaporization), the liquid N2O cools drop in temperature lower vapor pressure and
lower cylinder pressure
The only reliable way to determine residual volume of N 2O is to weigh the
When all liquid N2O has evaporated, pressure in the cylinder falls rapidly
starting at 400 L

Color (U.S.)

Carbon Dioxide


70 F Service

State in

E Cylinder
Capacity (L)



Nitrous Oxide
Humidity - decreases likelihood of static discharges, a relative humidity of at least 50% is



Pressure regulator reduces the E- cylinder pressures to < 50 psi, attached via
pin index safety system
Hospital's medical gas delivery system connects to the machine via the diameter
index safety system. B/c the pipeline gases are supplied b/t 45-55 psi, some
machines have 2nd stage regulator that reduces O2 to 16 psi.
Pressure relief valve o
Pressure controlled via pilot tubing that
communicates w/ventilator bellows chamber. As pressure in bellows during
inspiratory phase, pressure is transmitted via tubing to close pressure-relief valve,
thus gas tight patient circuit
o Pressure relief valve is then opened during expiration release of excess gas
from pt circuit into scavenging system after bellows is fully expanded
o If valve sticks in closed position high pressures within circle system
Scavenging system reservoir bag expands w/expiration & collapses with inspiration. If
pressure relief valve closes/stuck direct communication b/t circuit & scavenging
system part of tidal volume delivered directly to scavenging circuit patient
If oxygen pressure falls < 25 psi, a fail-safe valve closes, supply of gases other
than O2 are shut off and an alarm is sounded! Must have an O2 analyzer is needed in
the inspiratory flow limb
The oxygen flush valve provides a high flow (35-75
L/min) of oxygen
Variable-orifice flowmeters are calibrate for specific gases and depend on:
viscosity at low laminar
flows o
density at high
turbulent flows o
drop in
pressure across flowmeter o
shape of float
Length of the tube makes no difference to accuracy!!!
Flowmeters need to be checked with both negative & positive leak tests!
1. Large temperature fluctuations cause flowmeter inaccuracy
2. Low barometric pressure (high altitude) inaccuracies at high flow (b/c
change in density)
3. The greater the flow, the more error in actual flow delivered
4. Float must be properly aligned
Peak inspiratory pressure (PIP) is the highest circuit pressure generated
during an inspiratory cycle and provides an indication of dynamic
Plateau pressure (PP) is the pressure measured during an inspiratory pause
(a time of no gas flow) and mirrors static compliance
Increased PIP & PP

Increased PIP, no change PP


tidal volume,
pulmonary compliance
pulmonary edema
pleural effusion
abdominal packing
peritoneal gas
tension pneumothorax

inspiratory gas flow rate,

airway resistance
kinked endotracheal tub
foreign body aspiration
airway compression
herniated ETT cuff

Vaporization requires energy (the heat of vaporization), supplied as a loss of heat
from the liquid. As vaporization continues, liquid temperature drops and vapor
pressure decreases unless heat is readily available to enter the system
Decreased ambient pressure does not affect the [agent] delivered, but decreases the
partial pressure of the agent. At altitude, must increase the concentration control
dial to attain the desired anesthetic partial pressure
1 mL of liquid anesthetic = 200 mL of anesthetic vapor
Vapor Output (L/min) = CG x VP
vapor output
total gas flow

CG = carrier gas flow rate

[Anesthetic] =

VP = vapor pressure
BP = barometric pressure

Example: How does the vaporizer deliver the agent? O2 flow rate 2 L/min, if all of it
passes via the vaporizer, what will be the concentration of sevoflurane (VP = 150
mmHg) at the machine outlet?
vapor output = 2 L/min x 150 mmHg = 0.49 L/min
(760 150) mmHg





[sevoflurane] = 0.49 L/min =





The % of an anesthetic delivered increases with increasing vapor pressure

If halothane (VP=240 mmHg) is used in an enflurane (VP=175 mmHg) vaporizer, the
delivered concentration will be higher. Worst situation would be Ether (VP =450
mmHg) in a methoxyflurane (VP = 22 mmHg) vaporizer
Factors that Influence Vaporizer Output
1. Flow Rate o
Output of all variable-bypass vaporizers is less than the dial
setting at low flows (<250 ml/min) b/c of the relatively high density of
volatile agents. Insufficient turbulence is generated to upwardly advance the


At extremely high flow rates, 15 L/min, the output is less than the dial setting
b/c of incomplete mixing and saturation in the chamber decreased output
2. Temperature o Vapor pressure is affected only by temperature and not by
ambient pressure o At 20C VP of isoflurane is 238 mmHg, at 35C is it 450
mmHg (nearly double) o Vaporizers are made with metals having high
specific heat and high thermal conductivity to minimize heat loss.

3. Intermittent Back-Pressure o
Intermittent back pressure (pumping
effect) transmitted to the vaporizing chamber, associated with PPV or O 2
flush, could increase vapor output
o Pumping effect is increased by rapid RR, high PIP due to retrograde pressure
transmission from the patient circuit to the vaporizer during the inspiratory
phase of PPV

4. Carrier Gas Composition o

Most vaporizers are calibrated using oxygen
o When carrier gas is switched from 100% O2 to 100% N2O, there is a rapid
transient decrease in vapor output followed by a slow increase to a new
steady state.
o Decrease in output parallels the proportional decrease in viscosity of the
carrier gas (N2O is less viscous than O2) such that insufficient pressure is
generated at low flow rates in the chamber to upwardly advance the
o Addition of nitrous oxide reduces vapor output by 20% less than the dial
Desflurane Tec 6
Made b/c of desfluranes high vapor pressure (664 mmHg at 20C, nearly 1 atm)
Desflurane has a heat of vaporization close to that of other agents.
Supplying desflurane in higher concentrations would cause excessive cooling of the
Ohmeda Tec 6 is electrically heated to 39C & pressurized at 1500
mmHg (2 atm)
A pressure-regulating valve downstream from the shutoff valve down regulates
the pressure to 74 mmHg at a fresh gas flow rate of 10L/min
Will alarm at agent level below 60 ml, and shut-off valve is closed at 20 ml
Operator controls desflurane output by adjusting the concentration control valve, a
variable restrictor
Vaporizer controls release of the gas with variable resistance controlled automatically
by a differential pressure transducer
A pressure-regulating valve downstream from the shutoff valve down regulates
the pressure to 74 mmHg at a fresh gas flow rate of 10L/min
Requires manual adjustments of the concentration control dial at altitudes to
maintain a constant partial pressure of anesthetic o At high altitudes, the volume
% will represent an absolute decrease in the partial pressure of desflurane; in
contrast with a contemporary variable-bypass vaporizer which delivers a constant
partial pressure
o To compensate for the reduction in partial pressure at altitude, the Tec 6
rotary valve must be advanced to maintain the required partial pressure.



There a 2 distinct circuits within the ventilator that are separated by the
bellows wall: external high-pressure oxygen circuit that powers the
ventilator and an internal extension of the anesthesia breathing circuit.
Oxygen is consumed to power the ventilator at rate at least equal to minute
ventilation. Thus, if oxygen fresh gas flow is 2L/min and a ventilator is delivering
6L/min to the circuit, a total of at least 8L/min of oxygen is being consumed
Disconnect Monitoring
4 basic types of disconnect monitors, none are very sensitive to small leaks:
1. Pressure alarms are trigger if present pressure is not reached. Low
pressure monitor alarms if a critical airway pressure is not reached. It will
be the 1st to alarm when a disconnect occurs!
2. Respiratory volume alarms are triggered if present volume, rate, or
direction are not met
3. CO2 alarm or capnography is one of the most important signs of
4. Others: SaO2 monitor, esophageal stethoscope, and TcO2
Safety Features
An audible oxygen alarm is fitted in the oxygen supply line of the high-pressure
system This does not relate to a disconnect!
"Fail-safe" valve in the high-pressure system of the nitrous oxide supply line opens
only when oxygen pressure in the high-pressure system is above 25 psi.
As oxygen supply pressure (not flow) decreases < 30 psi, the supply of gases,
other than oxygen is shut off and the alarm sounds. This does not prevent the
delivery of hypoxic gas mixtures (normal oxygen line pressure alone will keep the
other gas line open). If the machine does not have a proportioning system, a hypoxic
gas mixture can be delivered
Flow control knobs will not allow a fraction of inspired oxygen (FiO 2) of less than 25%
to be set
Check valves prevent transfilling of gas cylinders or flow of gas from cylinders into
the central supply line. Allows empty gas cylinder to be exchanged for a full one
during opertion of machine.
Oxygen Analyzers
General anesthesia should never be administered without an oxygen analyzer
2 sensors are available: galvanic cell (a fuel cell) and the polarographic cell
(Clark electrode - O2 reacts with the electrodes, a current is generated that is
proportional to the oxygen partial pressure in the sample gas)
Negative Pressure Check Test
Checks for leaks between the common gas outlet and the regulators
Detects smaller leaks than the low pressure test
Machine must be turned OFF and flowmeter valves OPEN!
A bulb is placed on the common gas outlet, negative pressure is generated by
collapsing the bulb x 20 secs. If it remains collapsed, there is no leak b/t the
regulator, flowmeters, vaporizers and common gas outlet
DOES NOT test the CO2 absorber, breathing bag or circuit.
I:E Ratios 1:2 ratio produces LESS depression in C.O. than 1:1 ratio b/c it allows more time
for filling during expiratory phase.


Hole in Bellows
Ventilator is named by the direction of the bellows during exhalation
In a time cycled ventilator, a hole in an ascending bellows (like on HMC Narkomeds)
can lead to alveolar hyperventilation and barotraumas as ventilator driving gas is
forced into the circuit for the length of the inspiratory phase (when bellows
In a volume cycled ventilator, the driving gas volume will never exceed the tidal
volume even if driving gas leaks through the bellows to the patient, alveolar
hyperventilation will not occur.
If the bellows driving gas is 100% O2, will see increase in O2 analyzer.
Laminar Flow
Occurs when gas flows down parallel sided tubes at a rate less than critical velocity
Resistance to gas flow is directly proportional to viscosity of the gas
Flow = P 4

Flow = P/ R

Turbulent Flow
Occurs when Reynolds number > 2000

R= 8L
P 4

Reynolds number = (V) (r)


Orifice flow is a special case of turbulent gas flow where the diameter of the tube is
considerably larger than its length (e.g. larynx)
Flow through a tube increases radius2
Occurs when flow exceeds critical velocity
Resistance to gas flow is directly proportional to density of the gas
substituting helium for nitrogen will decrease the density of the gas mixture and
decrease the resistance!!
High flows through a rotameter will be influenced by increasing altitude (low
barometric pressure) b/c density (not viscosity) is decreased at high altitudes and
high gas flows, rotameter will be greater than expect, but accurate at low flows
(laminar flow not affected by altitude due to dependence on viscosity)

Pulse Oximetry
Depend on pulsatile waveform poor reading during cardiac arrest,
hypovolemia, hypothermia, vasoconstriction or bypass, hypotension < MAP
More sensitive to movement artifact during low-pulse-amplitude state
Earlobe is the LEAST sensitive area to pulse signal loss
Carboxyhemoglobin at high levels of CO, SpO2 overestimates true SaO2 b/c it is
reading a mixture of O2HB and Hb
Methemoglobin at MetHb increases, SpO2 = 85%, regardless of the ture level of
Indigo carmine produces the smallest changes compared to methylene blue or
indocyanine green
Pulse oximetry is NOT possible in deeply pigmented patient b/c of a failure
of LED light transmission


Electrocautery low SpO2 from interference cause by radio frequency emissions at

the probe
Moton artifact, nailpolsih, and ambient light cause inaccurate readings

Bacterial Contamination of Machine

Post-op pulmonary infection is NOT reduced by sterile disposable circuits
Inclusion of bacterial filter has no effect on incidence of infection
Volatile agents have NO bactericidal or bacteriostatic effects
Shifts in humidity & temperature are MOST important for killing bacteria
High O2 & metallic ions are lethal to bacteria
EYE & Intraocular Pressure

Normal range 12-20 mmHg

Volatile & most IV anesthetics decrease IOP. o
extraocular muscles, (3) pupillary constriction

Succinylcholine IOP o
Mechanism drug induced cycloplegia can still
see IOP when intraocular muscles are cut
o Occurs if given by single bolus, infusion, or IM injection
o Pre-treatment w/non-depolarizing drugs reduces, but doesnt reliably
eliminate the
Peaks 2-4 mins after
o Causes sustained contraction, rather than paralysis may affect the forced
duction test used to estimate any restriction in movement of the extraocular

Causes IOP o
Coughing & vomiting cause greatest increase IOP, up
to 35-50 mmHg o
Respiratory acidosis/ hypercarbia by inducing choroidal
vasodilation o
Hypoxia by inducing choroidal vasodilation
o Ketamine IOP changes are controversial, does cause blepharospasm and
nystagmus o
N2O in presence of intraocular air will IOP

(1) lower BP, (2) relaxation of


A malalignment of the visual axes, congenital or infantile due to an innervation

Phenylephrine produces mydriasis and hemostasis, but can cause systemic HTN
caution use
Cyclopentolate produces mydriasis without HTN
High rate N/V post-op either due to altered visual perception or an oculoemtic reflex.
Malignant hyperthermia occurs more frequently
Causes sustained contraction, rather than paralysis may affect the forced
duction test used to estimate any restriction in movement of the extraocular

Oculocardiac reflex o Produced by traction on extraocular muscle, pressure on eye,

orbital hematoma, ocular trauma, or eye pain, can occur with an empty globe or an
awake patient!!



Afferent limb = Trigeminal nerve (V1) relayed to Ciliary ganglion

Gasserian ganglion sensory nucleus of 4th ventricle
Efferent limb = Vagus nerve o Hypercarbia
threshold to elicit OCR
EKG bradycardia, junctional rhythm, ectopic atrial rhythm,
bigeminy, PVCs, v. tach, v. fib o
Increase depth of anesthesia
Make sure you are ventilating adequately
Infiltrate lidocaine into recti muscles o
Retrobulbar block
Atropine IM is NOT useful in preventing reflex

Intraocular Gas Expansion

Sulfur hexafluoride is an inert gas that is less soluble than nitrogen or nitrous
Used to facilitate reattachment of retina o To prevent changes in
size of gas bubble, give 100% O2 15 mins before injection o
anesthesized within 10 days of use, DO NOT use N2O
If using nitrous oxide, discontinue at least 15 minutes prior to the injection
of air or sulfur hexafluoride. If anesthetized within 10 days, AVOID N 2O
Ophthalmic drugs
Echothiophate is an irreversible cholinesterase inhibitor used to treat
glaucoma topical application leads to reduction in plasma cholinesterase
activity. Prolongs succinylcholine duration, usually does not exceed 20-30
o Inhibition last for 3-7 weeks after discontinuation of Echothiophate
Epinephrine eye drops HTN, tachycardia, ventricular dysrhythmias (potentiated
by halothane) Timolol, a non-selective -blocker, reduces IOP by aqueous
humor production.
Rarely associated with atropine-resistant bradycardia, hypotension or
Acetazolamide acts by inhibiting carbonic anhydrase o Carbonic anhydrase is
important in the synthesis of aqueous, in the kidney it converts CO2 & H2O H2CO3
HCO3- + H+ HCO3- (reabsorbed), H+ (secreted) causing reabsorption of
Na+ & H2O
o Results in more alkaline urine & hyperchloremic metabolic acidosis
Atropine has no significant effect upon IOP, either in open or closed glaucoma
Retrobulbar Block
Blocks sensation to the eye by ophthalmic branch of CN V (trigeminal) and ciliary
nerves (conjunctiva, cornea and uvea)
Motor to the eye from CN III, IV, VI
DOES NOT BLOCK maxillary branch of CN V2!!
Success => anesthesia, akinesia, abolishment of the oculocephalic reflex,
temporary blindness
(i.e. blocked eye DOES NOT move during head
turning) o
Akinesia by blockade of CN III,
o CN III of the levator muscle which opens the eye is blocked eye closes,
levator is dead


Facial nerve (CN VII) supplies motor to orbicularis oculi in eyelid allows
squinting need to block to place lid speculum.
Hemorrhage (most common), globe perforation, optic
nerve atrophy o
Block oculocardiac reflex o Acute
neurogenic pulmonary edema o
Seizures from injection in
ophthalmic artery
Post-retrobulbar apnea syndrome due to injection of LA into the optic nerve sheath with
spread into the
CSF unconsciousness without seizure, apnea within 7-20 mins, resolves with in an

PaO2 = 102-Age i.e. 72 yo estimated PaO2 = 102-72/3 = 78 mmHg
LaPlaces Law: T =
P r / 2h
1 mmHg = 1.36 cm H2O
SVR = MAP-CVP x 80
Na deficit = wt in Kg x 0.6 x (140- desired Na+)

PVR = PAPmean -PAOP x 80


HCO3 deficit = wt in Kg x 0.2 x change HCO3

Plasma osmolality (mosm/kg) = 2 [Na+] + BUN + glucose = 280 290 mOsm/L
EKG Morphologies
Hyperkalemia prolonged or absent PR interval, absent P wave, wide QRS, ST
elevation, peaked T waves sine wave
Hypokalemia prolonged PR & QT intervals, ST depression, flat T wave, U wave
Hypercalcemia prolonged PR interval, wide QRS, short QT interval
Hypocalcemia & HypoMg prolong QT interval
TBW 60% of total body wt (kg) 2/3 intracullular (40%)
1/3 extraculluar (20%) (4%) plasma
Important Drugs
-2 agonist = dexmedetomidine, -methyl-dopa (a
false NT) -2 antagonist = atipamezole -blocker =
-1 antagonist = phentolamine, prazosin, phenoxybenzamine
Guanethidine = depletes granular norepinephrine
Glycoprotein IIb/IIIa antagonists = abciximab, tirofiban, eptifibatide
When given with heparin & ASA further reduction of ischemic events in non-ST
elevation MI


Clopidogrel (Plavix ), Ticlopidine = irreversible blockade of the adenosine

diphosphate (ADP) receptor on platelet cell membranes inhibits platelet aggregation
by blocking activation of the glycoprotein IIb/IIIa pathway.
Ticlopidine, increase risk of thrombotic thrombocytopenic purpura (TTP) and
Burn Patients
Parkland Formula (fluid for first 24 hours) = 4 x patient's weight in kg x


First half is delivered in the first 8 hours, and the remaining half is delivered in the
remaining 16 hours.
The "Rule of 9's" is as follows: Head and each arm = 9%
Back and chest each = 18%
Each leg = 18%
Perineum = 1%
Relative resistance to nondepolarizing relaxants b/c of (1) altered protein binding, (2)
proliferation of NMJ and (3) extrajunctional ACh receptors
Decreased serum albumin after injury
alpha1-acid glycoprotein (AAG) free fraction of NMB is reduced due binding
with AAG
Increased vascular permeability due to decreased capillary integrity, however Vd of
NMB agents is unchanged
Discharge Criteria
Orientation to person, place, and time
Stable vital signs for 30-60 mins
Ability to ambulate unassisted
Absence of significant pain or bleeding
Ability to tolerate oral fluids may not be mandatory in all patients
Ability to void - may not be mandatory in all patients

CSF drain and AAA surgery

Paraplegia is a complication of aortic surgery, up to 40% with descending thoracic
CSF drainage is used to improve spinal cord perfusion during TAA repair
Spinal cord perfusion = MAP CSF pressure (or CVP), which ever is greater
Spinal cord blood flow is autoregulated b/t 50-125 mmHg, but lost during hypercarbia
or hypoxia
Drainage of CSF is important b/c CSF pressure increases 10-15 mmHg with x-clamp
Common causes of death: MI, pulmonary edema, renal failure
Major complications related to TURP:
o Hemorrhage o TURP syndrome
o Bladder perforation hypotension, vagal
mediated bradycardia, N/V, shoulder pain o
Hypothermia large volumes of room temp
solutions o


DIC release of thromboplastins from prostate; DO

NOT use aminocaproic acid b/c risk of fatal
o Dilutional thrombocytopenia o
(1) 20 ml/min absorbed via venous
(2) autotransfusion from
lithotomy position
o Ammonia toxicity causes production of false neurotransmitters and
suppression of NE and dopamine release encephalopathy
o Glycine toxicity - transient blindness

TURP Syndrome
Hypoosmolality is the main culprit contributing to CNS serum [Na+] & Osmolality
Can present intra-op or post-op (15 mins to 24 hours post-op)
Si/Sx: HA, restlessness, confusion, cyanosis, dyspnea, arrhythmias, hypotension,
seizures from fluid overload, water intoxication, irrigating solute toxicity, HTN or with
reflex bradycardia
Hypotonic non-electrolyte irrigating solutions:
o Glycine 1.5%
o Sorbitol 2.7% & mannitol 0.54% o
Distilled water massive hemolysis
Absorption of irrigation depends on (1) duration AND (2) height (pressure) of fluid (<
40 cm)
Most last < 1 hour, 20 mL/min is absorbed (1.2 liters)
Hypothermia can result from cold irrigation fluid coagulopathy, delayed awakening
o CNS: < 120 meq/L confusion, irritability, restlessness due to cerebral
edema (edema stops when [Na+] > 130 meq/L) or acute hypoosmolality b/c
BBB is permeable to free water, impermeable to Na.
Seizure Rx: Magnesium (negative effective on NMDA receptor)

Cardiac: < 105 meq/L widened QRS, ST elevation

< 100 mEq/L acute intravascular hemolysis, V tach or V Fib

Mortality comes from either CNS or cardiac complications

Hyperglycinemia transient blindness, NMDA receptor activity o

Hyperammonemia from degradation of glycine, must treat with L-arginine
which acts in the liver to release of ammonia and increase conversion to urea
Glycine is a known inhibitory
neurotransmitter o Glycine toxicity N/V,
HA, weakness
o Administer NS (hypertonic compared to plasma); need to give 3% NS if
patient is seizing or [Na+] < 120, once > 120, change to NS
o Brain edema stops once [Na+] > 130 meq/l o Must correct [Na+] over
48 hours to prevent brain shrinkage = CENTRAL PONTINE
MYELINOLYSIS (demyelination in the CNS ) quadriplegia. No
faster than 2 meq/hr
o +/- Diuretics (Lasix) b/c can lose Na+ o
Fluid restriction


PMMA = Polymethymethacrylate
Hypotension due to microembolization
Femoral shaft venting hypotension by intrafemoral pressure = microembolization
Partial hardening strengths PMMA by decreasing porosity and hypotension associated
with it
Fat Embolism Syndrome
Si/Sx: fever, tachycardia, tachypnea
ABG hypoxemia, widened A-a gradient
Blood lipidemia, anemia, platelet aggregation, thrombocytopenia, prolonged PT, PTT
CV tachycardia and hypotension, EKG with right heart strain
CNS cerebral edema = confusion, obtundation, coma
Renal lipuria
Respiratory increased Vd/Vt, widen A-a gradient
Skin petechial hemorrhage on anterior chest, neck, axilla and conjunctiva
Creatinine clearance (GFR estimation) = [(140-age) x lean body weight]
(72 x Creatinine)
** Multiply by 0.85 in females

Normal Cr Cl men = 95-145 ml/min, women 85 -125 ml/min

Most accurate method available for clinically assessing overall renal function
(really GFR)

Oliguria Pre-renal or Renal Causes?

FENa = UNa+ / PNa+ x 100
UCr /

**if > 2% suspect ATN

Urine [Na+]
% Fractional excretion
Urine Osm

< 0.5 ml/kg/hr
< 20 meq/L
< 1%

< 0.5 ml/kg/hr
> 40 meq/L
> 2%

> 400
> 20

300 mOsm/L
< 20

Chronic Renal Failure Uremia ( GFR < 25 ml/min)

Neurologic: peripheral & autonomic neuropathy, encephalopathy
Cardiac: fluid overload, CHF, HTN, arrhythmia, accelerated atherosclerosis,
Pulmonary: hyperventilation, edema, effusion
GI: anorexia, N/V, delayed gastric emptying, hyperacidity, ulcerations, ileus
Metabolic/Electrolytes o Acidosis b/c cannot excrete H+ ions o
hyperMg2+, hyperPO4 o
HypoNa+, hypoCa2+, hypoalbuminemia


Anemia due to low erythropoietin production & uremic toxins that
marrow function o R shift oxy-Hbg curve due to 2,3 DPG o
dysfunction sepsis is major cause of death, high incidence of Hep B
Coagulopathy: platelet dysfunction, check PT & PTT
Endocrine o Hyperglycemia resistance to insulin
o Hyperparathyroidism b/c cannot excrete phosphate elevated levels of PTH
Skeletal: osteodystrophy (= dystrophic growth of the bone)
hyperpigmentation, ecchymosis, pruritus
Infection: Sepsis is the major
cause of death!
o 20-50% are infected with Hepatitis B

Indications for dialysis

Ingestion of drugs
vOlume overload
Dexamethonium and gallium are 100% renal excretion avoid in renal failure
Failure of Analgesia
Amines (narcotic, local anesthetics): RNH3+ RNH2 + H+
Acidic environment more charged (RNH3+) and less lipophilic less effect
MRI Contraindications
No ferromagnetic objection scissors, pens, keys
No pacemakers, cochlear implants, or aneurysm clips
Relatively contraindicated IUD, recent endovascular stent, sternotomy wires before 8
NO ZINC batteries, only use lithium
Pressure manometers will not work in the presence of a high magnetic field, but NIBP
Effects of Hypothermia (MEMORIZE)
J point elevation, VF (280C)
Coagulopathy and immunosupression

Glucose levels due to (1) fall in
insulin, (2) rise in Epi-Norepi, (3) rise
in cortisol
Hct & viscosity
H+ ions = acidosis
Left shift hemoglobin
K+ ions
More sensitive to NMB agents

Intravascular volume & BP due to (1)
cold suppresses ADH
metabolic O2 consumption
CMRO2 => 6% per 0C
Flat EEG at 25 0C
platelet count & function due to
MAC => 7% per 0C
P aO2 due to more V/Q mismatch


FRC, more atelectasis

hypoxic pulmonary

Heat Loss
40% radiation = form of electromagnetic energy
30% convection = wind chill
29% evaporation
1% conduction = direct skin contact
Hyperbaric Oxygen Therapy
Pulmonary formation superoxides, hydrogen peroxide, hydroxyl radicals retrosternal
chest pain/burning, coughing, fibrosis. Oxygen toxicity is PaO 2 and duration dependent
CNS - CBF, see at 2 ATM tonic/clonic seizure activity
CV HTN, bradycardia

Indications with Carboxyhemoglobin

Carboxyhemoglobin >30%
Pregnancy with levels > 15%
Signs of cardiac ischemia or arrhythmias
Hx of CAD with levels > 20%
No improvement in symptoms after 6 hours on 100% O2
1 ATM, 1.1% isoflurane = 3 ATM, 0.33% isoflurane
Falsely high flowmeter readings due to change in density

Liver Physiology
Dual blood supply, 70% portal vein & 30% hepatic artery (supplies most of oxygenated
blood, 55%)
Blood flow determined by perfusion pressure splanchnic vascular resistance
What decreases hepatic blood flow?
o All volatile anesthetics decrease hepatic blood flow by hepatic pressure
pressure, reduce BP and increase hepatic vascular resistance by releasing
o Close surgical site is to liver, greater the reductions in hepatic blood flow o
o Hypoxia & hypocarbia o
CHILD Classification: bilirubin, albumin, ascites, encephalopathy, prothrombin time
Albumin t = 23 days acute liver dysfunction will not decrease albumin level.
Pseudocholinesterase t = 14 days
All factors, except Factor VIII, are produced in the liver
Increase in unconjugated bilirubin results from liver parenchymal disease vs. increases in
conjugated bilirubin is due to biliary tract obstruction
Immediate post-op concerns should address hypoglycemia. Can occur b/c of insufficient
insulin degradation by the liver, impaired glucose formation, or glycogen depletion
What is malignant hyperthermia?
Earliest signs masseter spasm, tachycardia, hypercarbia & concomitant
respiratory acidosis
(most sensitive) myoglinemia, myoglobinuria, arrhythmias, elevated CK, hyperK+,
Muscle rigidity is not consistently present


Ventricular fibrillation can follow onset within minutes and is most common cause of
< 50% of patients with trismus (masseter spasm) & sux develop malignant
hyperthermia. Best to cancel an elective case, if not able to cancel, then administer nontriggering agent

What is the pathophysiology of MH?

See uncontrolled intracellular Ca2+ in skeletal muscle from SR removes inhibition of
troponin muscle contraction
May be related somehow to the ryanodine Ryr1
Treatment of MH?
Stop triggering agent! Call for help!
Hyperventilate with 100% O2
Administer Na bicarbonate 1-2 mEq/kg IV to treat acidosis
Give dantrolene 2.5 mg/kg, maximum 10 mg/kg
Cooling measures
Treat severe hyperkalemia with dextrose, 25-50g IV, regular insulin, 10-20 U IV
Consider invasive monitoring with A-line, central line
Diuresis with mannitol or lasix to prevent ARF from myoglobinuria
AVOID Calcium channel blockers with dantrolene hyperkalemia
Binds to Ryr1 receptor calcium channel and inhibits Ca2+ ion release from the SR
intracellular dissociation of excitation-contraction coupling.
2.5 mg/kg q 5mins until episode is terminated, maximum 10 mg/kg
initial control, give 1 mg/kg IV q 6 hrs x 24-48 hrs to prevent relapse Side effects:


Muscle weakness respiratory insufficiency or aspiration

pneumonia o
Phlebitis in small peripheral veins; should be given
via central line
AVOID with Ca2+ channel blockers
hyperK+ CV collapse
Which patients are at risk for MH?
Trismus (masseter spasm) after succinylcholine - < 50% incidence of MH
Duchennes muscular dystrophy
Central-core disease
Osteogenesis imperfecta
King-Denborough syndrome young boys with short stature, MR, cryptorchidism,
kyphoscoliosis, pectus deformity, slanted eyes, webbed neck, winged scapula
Operations associated with higher risk orthopedic cases, ptosis or strabismus
surgery, ENT (cleft palate repair, T & A, dental)
Intolerance to caffeine-containing foods
History of unexplained fevers or muscular cramps
What type of hereditary pattern does MH follow?
Autosomal dominance with variable penetrance in 50% of families
chromosome 17, 19
Midwest has highest incidence
Supportive Diagnostic Lab Tests
Elevated serum creatine phosphokinase (CK)
Myoglobin in serum and urine
Elevated serum K+, Ca2+, lactate
Metabolic/respiratory acidosis on ABG
MH confirmation?
Biopsy of a fresh section of living skeletal muscle is exposed to a caffeine, halothane,
or combination caffeine-halothane bath
How does MH differ from Neuroleptic Malignant Syndrome?
NMS is characterized by hyperthermia, muscle rigidity with extrapyramidal signs
(dyskinesia), altered consciousness and autonomic lability in patients receiving antidopaminergic agents or withdrawal from dopaminergic agonists
Not inherited, takes 24-72 hours to develop after the use of neuroleptic drugs
(phenothiazines, haloperidol, metoclopramide, butyrophenones, abrupt withdrawal of
Succinylcholine and volatile anesthetics are NOT triggers for NMS
NMB agents reverse the rigidity of NMS, but not that associated with NM
Treatment dopamine agonists (bromocriptine, amantadine), dantrolene
What is a safe anesthetic in susceptible MH patients?
SAFE: Thiopental & pancuronium appear to be protective by raising the triggering
N20, local anesthetics, opiates, BZD, barbiturates, nondepolarizing agents
NOT SAFE: succinylcholine, decamethonium, curare(?), all volatile anesthetics
Summary NMB to Nerve Stimulation


Single twitch
Tetanic stimulation
Train of four

Phase I
Decreased height, no

Phase II




All twitches same,

Marked fade
decrease in height
Train of four ratio
Enhances effect
*Post-tetanic facilitation occurs when a single twitch is induced, short
tetanic stimulation is larger than the amplitude of the tetanus

tidal volume
twitch height
Sustained tetanus at 50
Sustained tetanus at 100
Head lift and hand grip


Marked fade
period of time after,

% receptors
occupied when
response returns
to normal

Prolonged Block with Sux

Pseudocholinesterase = plasma cholinesterase
Metabolizing esters: ACh, SCh, mivacurium, trimethaphan, ester-type L.A.,
remifentanil, esmolol, quinidine
Distinct from acetylcholinesterase found in nerve endings and in RBCs
Synthesized by the liver, t = 12 days
Qualitative tests, dibucaine number and fluoride number reflect reduced PChE
activity resulting from addition of dibucaine or sodium fluoride to the assay
Pseudocholinesterase Abnormalities
Heterozygous atypical plasma cholinesterase o
Homozygous atypical =
prolonged blockade for 2-3 hours after Sux o
Dibucaine number is a lab assay
to characterize quality, not quantity of plasma cholinesterase.
Dibucaine is an AMIDE local anesthetic which is an inhibitor of
plasma cholinesterase
Normal plasma cholinesterase is 80% inhibited in vitro by dibucaine
Heterozygous atypical are only 60% inhibited = D60
Homozygous patients are only 20% inhibited = D20


Physiologic Variances in Activity:

o Birth to 6 months 50% of activity, 70% by age 6, 100% at puberty o
Pregnancy by 30% from week 10 to post-partum week 6
Acquired PChE Defects:
o Disease states PChE activity: hepatitis, cirrhosis, malnutrition, cancer,
myxedema, acute infection, MI, hypothyroidism, shock, burns, uremia
Drugs that inhibit PChE activity: acetylcholinesterase inhibitors,
pancuronium, procaine, hexafluorenium, organophosphate insecticides,
MAO-I, cyclosphosphamide
o Decreased synthesis PChE: steroids, chemotherapy agents

Cardiac Arrhythmias & Sux

Directly stimulates post-junctional cardiac muscarinic receptors at SA node
sinus bradycardia, junctional rhythms, asystole o Non-depolarizing agent 3 mins
before 1st dose of sux reduces bradycardia
Stimulates nicotinic autonomic ganglia transmission at sympathetic &
parasympathetic NS
Muscle Relaxants & Renal Failure
Anti-vagal at cardiac mAChR (MAP, HR and C.O.) & indirect sympathomimetic by
blocking reuptake of NE
Vagolysis is prominent with gallamine predisposition to arrhythmias because
o Vagal block with shift toward adrenergic tone o
Indirect sympathomimetic
activation o AV nodal block > SA nodal block
Renal failure slows elimination! 80% eliminated unchanged in the urine
Requires hepatic metabolism
Decreases MAC by 25%

10% eliminated unchanged in the bile up to 40% during renal failure

DOES NOT undergo significant hepatic metabolism better choice than
pancuronium in setting of liver failure
Neonates & infants are more sensitive to d-TC, but Vd is much larger so dose is same
Histamine hypotension & tachycardia
Can block autonomic ganglia contribute to hypotension

Hepatic metabolism & biliary excretion
T is prolonged in patients with renal failure decreased clearance of the drug
The only NMB without CV effects
Atracurium (intubate: 0.5 mg/kg, intra-op: 0.1 mg/kg)
Hoffman elimination & ester hydrolysis inactive metabolite LAUDANOSINE
excitation CNS, caution in seizure pts
Side effect: transient SVR, HR with 3 x ED95
Avoid in asthmatics 2nd bronchospasm from histamine release at high doses


3 x more potent than atracurium

No metabolites or histamine release
Given by infusion non-cummulative

Mivacurium chloride (Mivacron)

First rapid acting non-depolarizer 2.5 mins, re-dosing q 15 mins
Side effect: transient flushing, high doses histamine release, hypotension,
Metabolism: hydrolyzed by plasma cholinesterase not prolonged in renal failure
Removed from the market due to severe bronchospasm death
Active, 2 x potent metabolite, 3-desacetylrapacurium liver metabolism
Reversal Agents & Renal Failure
Renal excretion is the principal route of elimination for edrophonium,
neostigmine, and pyridostigmine. Prolonged t in renal patients.
Reduce dose by 50%, if Cr Cl < 10 ml/min reduce dose by 75%
Potentiation NM Blockade
Antibiotics (decrease release of ACh)
- Aminoglycosides (gentamicin, tobramycin, netilmicin, amikacin, kanamycin)
- Streptomycins
- Tetracycline
- Polymyxin
- Lincomycin
- Clindamycin
- Bacitracin
- **Erythromycin, penicillin, cephalosporins do not potentiate NMB**
Antidysrhythmics: quinidine, lidocaine, Ca channel blockers
Nitroglycerin only prolongs affects on pancuronium
Anticholinesterase echothiophate
Volatile agents Isoflurane >> halothane
Local anesthetics procaine can augment NMB
Magnesium sulfate, Furosemide due to K+
Ca2+ channel blockers
Electrolytes Na+ or Ca+, K+
Physiologic states (1) hepatic dysfunction, (2) hypothermia, (3) acidosis, (4)
Burn victims have upregulation of receptors resistant to standard dose
Botulism toxin prevents calcium dependent release of ACh state of paralysis
Porphyria & Heme Synthesis
Autosomal dominant
Rate limiting step in heme synthesis: succinyl CoA + glycine -amino
levulinic acid (ALA) catalyzed by ALA synthetase
Heme (the end product) exerts negative feedback regulation on ALA synthetase


The specific enzyme deficit in each type of porphyria results in a partial block in
heme biosynthesis and lower intramitochondrial heme levels negative feedback
from low levels of heme elevated baseline ALA synthetase activity
Si/sx are due to (1) high ALA synthetase activity, (2) increased porphyrin
accumulation in tissues, or (3) decreased heme production
Elevated heme precursors that are colorless and non-fluorescent porphyrinogens
Porphyrins are highly reactive oxidants
Accumulation of porphyrins in the epidermal skin layers cutaneous
photosensitivity Acute porphyria causes severe neuropathy
Unsafe drugs:
o Barbiturates thiopental, etc
o Etomidate
Enflurane o
Alpha-methyl dopa o
Hydralazine o
o Oral contraceptive pills
Only the inducible forms (acute intermittent porphyria, variegate porphyria,
hereditary coproporphyria) show acute symptoms (e.g. neurologic) from drug
Porphyria cutanea tarda is non-inducible form (not affect by drugs) and most
often appears as photosensitivity in males older than 35 yrs avoid excessive
pressure or irritation of the skin (.e.g during mask ventilation, taping OETT, etc)
Acute intermittent porphyria is the most serious form! Affects central &
peripheral nervous system pain, change mental status, paralysis (respiratory
distress) o
Triggers: starvation, dehydration, stress, sepsis, drugs (ketorolac,
pentazocine, BZDs, barbiturates, etomidate)

Pure opioid antagonist pt. will have opioid requirments if taking at time of
T = 24 hrs, stop the day before surgery
N-cyclopropylmethyl derivative of oxymorphone
Blocks the euphoric effects of injected heroin in addicts who have been detoxified
Mixed agonist-antagonist strong affinity for -receptor (50 x MSO4)
Prolonged duration )8 hrs) due to affinity for -receptor & resistant to naloxone
Delirium tremens
Occurs 2-4 days after abstinence from EtOH
Treat with fluid replacement, electrolyte replacement, Thiamine
Beta-blockers to suppress overactivity of SNS
Lidocaine for cardiac dysrhythmias
Aggressive use of BZDs to prevent seizures
Smoking Cessation
Restoration of P50 to normal value of 26 mmHg within days


Incidence of pulmonary complications begins to decrease only when abstinence

from cigarette smoking is > 8 weeks

Post-Op Shivering Treatment meperideine (via K), butorphanol (via K), clonidine,
serotonin antagonists, propofol, physostigmine

CV parasympathetic effect = hypotension due to arrhythmias, bradycardia,

asystole; followed by sympathetic activation = tachycardia, HTN, mydriasis
(pupillary dilation), gooseflesh
Cerebrovascular brief cerebral vasoconstriction, followed by vasodilation concern
if patient has hx elevated ICP
Tourniquet is used to block the circulation of succinylcholine in one extremity to see
tonic-clonic activity
Effects of IV anesthetic drugs on Duration of ECT-induced seizure activity
(Miller Ch. 68)
Increase duration

No change


Internal Jugular Bulb PaO2

CMRO2 decreases 7% per 1 C drop in temperature Jugular Bulb PaO2
Isoflurane causes burst suppression at 2 MAC lower CMRO2 Jugular Bulb PaO2
SNP poisons cytochrome system and tissue cant use oxygen Jugular Bulb PaO2
Hyperventilation cerebral vasoconstriction, no effect on CMRO2 lower jugular
Bulb PaO2

Associated with cerebral aneursyms, HTN, coarctation of aorta, polycystic kidney

disease, fibromuscular dysplasia, cigarette smoking
Risk of rebleeding, vasospasm (70% incidence), intracranial HTN, seizures
N2O increases CBF and CBV AVOID with hx intracranial HTN, high ICP
EKG findings canon T waves, QT prolongation, ST depression and U waves
Clinically significant vasospasm noted in 30% patients, peak incidence 7 days
after SAH o Calcium channel blockers (e.g. nimodipine) decrease morbidity
and mortality, no significant change in incidence or severity of vasospasm.
Beneficial effect may be due to inhibition of primary and secondary
ischemic cascades, rather than direct vasodilation
o triple H and cerebral angioplasty
o Hypervolemia & HTN aid ischemic regions of the brain that have impaired
autoregulation, thus CBF is perfusion pressure dependent.
o Hemodilution increases flow through microcirculation

4 Important Influences on CBF


1. Respiratory gas tensions

CBF directly proportional to CO2 b/t 20-80 mmHg
Only marked changes in PaO2 alter CBF, O2 < 50 mmHg
2. Temperature
Directly changes CBF 7% per 1 C drop temperature, pyrexia increases CBF
3. Blood viscosity
Blood viscosity b/t 30-50% do not alter
< 30% CBF increases, > 50% CBF decreases
4. Autonomic influences
Sympathetic stimulation CBF


Cerebral Metabolism & Flow

Brain weighs 1350 g
CMRO2 = O2 consumption = 3 - 5 ml/100g/min o
x 1350 g = 50 ml/min = 20% of
VO2 (total body O2 consumption) o Greatest in gray matter (unmyelinated)
CBF = 50 ml/100 g/min o
x 1350 g = 675 ml/min = 15% C.O. o
mL/100g/min = 1 sign of cerebral ishemia o
15-20 ml/100 g/min = isoelectric
EEG o < 10 ml/100 g/min = irreversible ischemia
CBF 1 ml/100 g/min for every 1 mmHg PaCO2 = 2% o Due to CO2-mediated pH of
the extracellular fluid cerebral vasodilation
Critical CBF with isoflurane, desflurane, sevoflurane = 10 ml/100 g/min
Critical CBF with enflurane = 15 ml/100g/min
Critical CBF with halothane = 20 ml/100 g/min
Cerebral Autoregulation
CBF remains nearly constant b/t MAP 50-150 mmHg, beyond these limits, CBF becomes
pressure-dependent. Pressures > 150 mmHg can disrupt BBB cerebral edema &
Final common pathway of dysfunction, in its most extreme form = vasomotor paralysis
Distrubed in acute cerebral ischemia, mass lesions, trauma, inflammation, prematurity,
neonatal asphyxia, diabetes mellitus, volatile agents (> 2 MAC abolished!)
Unaffected/persevered during: hyperoxia, modrate hypothermia, cardiopulmonary
Right shift curve - HTN
Hyperventilation recommended to PaCO2 25-30 mmHg to allow maximal ICp & minimal
cerebral ischemia.
Cerebral ischemia if PaCO2 < 20 mmHg
Left shift Hgb curve with hyperventilation decrease O2 off-loading

Produced by choroid plexus, by oxidation of glucose and ultrafiltartion by cerebral capillaries

CSF [Na+] = Serum [Na+]

Compared to plasma:
o CSF has higher levels Cl-, Mg2+
o CSF has lower levels glucose, K+, HCO3, Ca2+, PO4-

Glascow Coma Scale






Open to pain
le sounds
Extension to

Open to
e words
flexion to

w to pain

to pain


Venous Air Embolism

Occurs when the pressure within an open vein is subatmospheric. Exists in any position
where the wound is above the level of the heart

1. TEE most sensitive!
2. Precordial Doppler U/S - able to detect 0.25 ml



PA catheter see reflex vasoconstriction due to pulmonary hypoxemia

Mass spectrometry for end-tidal nitrogen - exhaled N2 < 2%
End-tidal CO2 not specific for air embolism
Drop in BP

1. Pulmonary microvascular occlusion results in increased dead space
2. PA pressure rises C.O. due to high RV afterload
3. M & M is directly related to the volume & rate of air entry
4. Presence of patient foramen ovale (10-25% incidence) paradoxical air embolism

Clinical signs:
1. Drop in ETCO2 or arterial PaO2
2. ABG may show slight PaCO2 from pulmonary dead space
3. Reappearance (or increase) of nitrogen in expired gases
4. Mean PA pressure increases in direct proportion to the amount of air entrained
5. Hemodynamics: sudden hypotension, circulatory arrest by obstructing RV outflow,
changes in BP and heart sounds (mill wheel murmur) are late manifestations

1. Notify surgeon flood field with saline or packs and bone wax applied
2. D/C nitrous oxide, 100% oxygen
3. Head down (Trendelburg) so operative site is below the heart
4. Aspirate multi-orifice central line located at SVC-RA junction
5. Give volume to increase CVP
6. d/c PEEP as it may increase risk of paradoxical embolism or decrease venous effluent
from calvarium increased CBV, ICP
7. Bilateral jugular vein compression slow entrainment, back bleeding to see source
8. If able, place in L lateral decubitus position

Carbon Dioxide Response Curve

Left shift
Right shift
( sensitivity to ( sensitivity to

Metabolic acidosis
- Central
causes: high ICP,
anxiety, fear,
Drugs: doxapram

Down ( response)

- Opioids
- volatile anesthetics:
enflurane >>
halothane >
Metabolic alkalosis isoflurane Denervation of
chemoreceptors Normal sleep

Down and to
Right (
sensitivity &
response to
- High dose
opioids neuromuscular


- Ketamine
- droperidol
- N 2O

Ventilatory Control - Central Response

Chemosensitive areas located in the medulla
CO2 (not H+ b/c poor permeability) diffuses from arterial blood into the CSF combines with
H2O --> H+ + HCO3-. H+ acts directly on the central chemoreceptors in medulla
Ventilatory response to CO2 = minute ventilation = RR & Tv, peaks within 1 min


During apnea, CO2 rises 6 mmHg 1st minute, 3 mmHg every minute thereafter
Apneic threshold is 5 mmHg below the resting PaCO 2 Hyperventilation to PaCO2 > 20
mmHg x 2 hrs causes transport of HCO3 out of CNS threshold to spontaneously breath seen
at a lower PaCO2 (more likely to breath)

Ventilatory Control - Peripheral Response

Carotid (bifurcation) & aortic bodies (aortic arch) response primarily to hypoxemia o
Afferent limb = CN IX (glosspharyngeal), efferent limb = CN X (vagus)
o Interact with central centers via glossopharyngeal nerves, producing reflex
increases in alveolar ventilation
Most sensitive to PaO2 < 60 mmHg, followed by arterial pH
Decreases in arterial PO2 hyperventilation
Increases in arterial PCO2 hyperventilation
Increases in arterial [H+] stimulate carotid body peripheral chemoreceptors directly,
independent of changes in PCO2. E.g. RR is increased during metabolic acidosis
Criteria for Determination of Brian Death
Absent cerebral and brainstem function
Well-defined irreversible etiology
Persistent absence of all brain function after observation or treatment
Hypothermia, drug intoxication, metabolic encephalopathy, and shock excluded
Clinical Tests of Brain Death
Cerebral unresponsiveness
No spontaneous motor activity
Absent brainstem reflexes - pupillary, corneal, oculocephalic/oculovestibular
Absent cough reflex with deep tracheal suctioning
No increase in HR after IV atropine (2 mg)
No respiratory efforts on apnea testing with PaCO2 > 60 mmHg
Electrocerebral silence documented by electroencephalography
Absence of cerebral perfusion by angiographic study
Absent brainstem auditory evoked potentials
Somatosensory Evoked Potentials (SSEPs)
Provides ability to assess the integrity of the peripheral nerve (1st order sensory neuron) with
cell body in dorsal root ganglia ipsilateral dorsal column (synapse with 2nd order cells)
axon decussate (cross over) at medulla oblongata project on to 3rd order sensory cells in
thalamus contralateral somatosensory cortex
Ischemia, volatile agents, barbiturates, propofol = amplitude and/or latency
Fentanyl = amplitude and/or latency
Nitrous oxide = amplitude, no effect on latency
Ketamine = amplitude, no effect on latency
Etomidate = amplitude and latency
Non-depolarizing muscle relaxants have no effect on sensory pathways
1 MAC of isoflurane, enflurane or halothane is compatible with SSEP monitoring

Beta = 12-30 = active concentration, barbiturates, BZDs

Alpha = 8-12 = dominant frequency in the awake state, closing the eyes and by
Theta = 4-8 Hz = sleep, hyperventilation, anesthesia
Delta = 0-4 Hz = deep sleep, deep anesthesia, hypoxia, slow wave sleep


N20 30-70%
Volatile < 1 MAC

Volatile > 1 MAC

frequency &
Severe hypoxia
Severe hypercarbia
Large dose

Electrical silence
Brain death
Severe hypoxia
Coma dose
Isoflurane 2 MAC

Propofol produces a decrease in frequency, increase in activity

Seizures with enflurane 3% with hypocapnia


Autoimmune disease loss of AChR at the post-synaptic NMJ due to destruction by
circulating antibodies
Antibodies reduce # AChR in 3 ways:
o Competitive blockade of receptors by blocking access to
receptor o
Complement-mediated lysis of receptor &
muscular end plate o
Increasing degradation of the
Hallmark: voluntary muscle weakness with exercise & improvement with rest, respiratory
insufficiency, aspiration, cardiomyopathy and cardiac failure
Clinical features:
o Muscles innervated by CN most frequently involved o
Pharyngeal or ocular weakness ptosis, diplopia,
dysphagia o
Severe MG progresses to proximal
weakness, respiratory failure o Cardiac muscle is impaired
2/2 to cardiomyopathy
Work up:
o Tensilon test = 10 mg of edrophonium
Distinguishes a myasthenic vs. cholinergic crisis
If weakness is from MG then strength will improve
If due to cholinergic crisis, added ACh will worsen symptoms bradycardia,
bronchoconstriction, ciliary constriction, salivation, lacrimation, urination. Must
then treat with atropine.
o Pyridostigmine to increase ACh available. Excessive
anticholinesterase drug effects precipitates cholinergic crisis
increased weakness, excess mACh effects (salivation, diarrhea, miosis,
bradycardia). Must treat with atropine!
o Anticholinesterase therapy should not be discontinued before surgery o
Steroids o
Immunosuppressive drugs - azathioprine,
cyclophosphamide o
Plasmapheresis o
Thymectomy for
drug resistant disease

Anesthetic Implications:
o More sensitive to the respiratory depressant effects of narcotics and anxiolytics
b/c have reduced respiratory reserve
o Resistant to depolarizing agents, requires 2-3 x SCh dose o Sensitive to
non-depolarizing agents, avoid if possible o
Profound muscle relaxation


with volatile agents o

Avoid ester-type L.A. b/c anticholinesterase therapy
affects pseudocholinesterase o
MG crisis can be precipitated by:
inadequate pyridostigmine, nondepolarizing NMB, excessive neostigmine, or
intubating dose of SCh.
Group of diseases characterized by delayed muscle relaxation after stimulation
Autosomal dominant with variable penetrance
Contractures are not relieved by nondepolarizing relaxants or regional anesthesia
Infiltration of L.A. may produce relaxation
3 major groups:
1. Myotonic dystrophica most common & serious
Presents in 2nd, 3rd decade of life
Muscle weakness (restrictive lung disease) and cardiomyopathy, dysrhythmias (RBBB,
heart block)
2. Myotonia congenita
Presents at birth, widespread muscle weakness
3. Paramyotonia
Rarest, mild and develop only in response to cold
Anesthetic Considerations in Muscular Dystrophy
AVOID SCh sustained contractions to point of impaired ventilation, hyperkalemia
Sensitivity to non-depolarizers
Anticholinesterases to revere NMB often precipitates myotonia
IV regional (Bier block) or local infiltration will ensure muscle relaxation.
Increased sensitivity to IV induction agents; Etomidate can cause contractures, myoclonus
Very sensitive to depressant effects of barbiturates, BZDs, narcotics
Full stomach precautions RSI due to delayed gastric emptying
Duchenne muscular dystrophy
X-linked recessive, lack formation of dystrophin
Dx: elevated serum CK levels (10-100 x normal) o
Cardiac contractility & papillary
muscle dysfunction mitral regurgitation, systolic dysfunction, ventricular thinning
o Pulmonary weak cough, poor reserve, aspiration risk, restrictive
pattern o GI risk of regurgitation and aspiration (GI hypomotility with
delayed emptying)
SCh can cause massive rhabdomyolysis, hyperkalemia and death
Halothane, can exaggerate myocardial depressant effects, risk of arrhythmias
Higher rate of malignant hyperthermia
Beckers Muscular Dystrophy
X-linked recessive, also due to mutation in the dystrophin gene
Similar presentation to Duchennes, however present later in life and progresses more slowly
Huntingtons Chorea

Low levels of pseudocholinesterase sensitive to succinylcholine May also be

sensitive to non-depolarizing agents as well

Autonomic Hyperreflexia
Appears after spinal shock in association with the return of spinal cord reflexes
Most common 6 months to 2 years from time of injury


Occurs after cord injury at or above T6

M & M occur from retinal, subarachnoid, cerebral hemorrhages; strokes; basilar artery
insufficiency, HTN encephalopathy
Cutaneous or visceral stimulation below the level of injury o
Below the
transection = HTN, vasoconstriction (blanching), piloerection, sweating o Above the
transection = baroreceptor-mediated reflex bradycardia, vasodilation, flushing,
severe HA, blurry vision, shivering, nausea, inability to protect body temperature
and poikilothermia (equilibrate with surrounding temperatures)
o Deep level of anesthesia o Regional (spinal is best)
anesthesia or deep GA to prevent o
Ganglionic blockers:
trimethaphan o - receptor antagonists: phentolamine o
Vasodilators: sodium nitroprusside or nitroglycerin
o Risk succinylcholine-induced hyperkalemia is decreased 6
months after injury, but best to use non-depolarizing agents
AVOID -blockers (i.e. propranolol) due to (1) bradycardia potentiated by beta-1, and (2)
beta-2 blockade in skeletal muscle will leave the alpha-properties unopposed, causing a
paradoxical HTN response, even CHF

Anesthetic Considerations for Acute Transection

High-dose corticosteroids first 24 hrs (methylprednisolone 30 mg/kg, then 5.4 mg/kg/hr)
Patients with high transections often have impaired airway reflexes and are further
predisposed to hypoxemia by a FRC
Safe to use succinylcholine in 1st 24 hrs
Anesthetic Considerations for Chronic Transection
Monitor body temperature closely b/c transections above T1 result in chronic vasodilation
and loss of normal reflex cutaneous vasoconstriction hypothermia
Progressive renal insufficiency due to recurrent calculi & amyloid deposition avoid
primarily renally excreted drugs
Carotid Endarterectomy
Carotid bodies are near the carotid bifurcation bilaterally, aortic bodies near the aortic
arch all respond to hypoxemia (low PaO2) and to a lesser degree hypercarbia (high PaCO2)
Blood flow to these receptors is so high that O2 demands are met largely by dissolved O2
alone not stimulated in conditions such as anemia or CO poisoning in which the dissolved
amount is generally normal.
In those without carotid bodies, little change in ventilation is seen at rest, but the ventilatory
response to hypoxia is lost and there is a 30% reduction in ventilatory response to CO2
chronic CO2 elevation
As PaO2 drops below 60 mmHg the carotid bodies activate the medullary respiratory center
via CN IX (glossopharyngeal) MV. Medullary chemoreceptors are denervated, thus
the hyperventilation response to PaCO2 is altered.
Denervation of the carotid sinus nerves & baroreceptor reflexes may result in post-op
HTN Preoperative Considerations
Origin of the internal carotid artery is the most common site of atherosclerosis
Ophthalmic branch emboli can cause transient monocular blindness (amaurosis fugax)
Larger emboli enter the middle cerebral artery contralateral motor & sensory deficits
affecting the arm & face. Aphasia also develops if the dominant hemisphere is affect.
Indications for CEA:
o TIAs associated with ipsilateral severe carotid stenosis > 70% or
ulcerated plaque o
Severe ipsilateral stenosis (>70%) in patients with a


minor stroke (incomplete stroke) o

Asymptomatic, but stenotic lesions
>60% o Fluctuating neurologic deficits
Increased operative risks = age > 75 yrs, symptomatic lesions, uncontrolled HTN, angina,
carotid thrombus & occlusions near the carotid siphon

Anesthesia & Surgical Concerns

Isoflurane is the volatile agent of choice b/c it has the greatest protection against cerebral
Surgical retraction of the recurrent laryngeal n. hoarseness; hypoglossal n.(CN XII)
ipsilateral tongue deviation
Monitoring of Cerebral Function
Shunt need is determined by stump pressure distal to cross-clamp, EEG, and SSEPs
**Distal stump pressure < 50 mmHg or EEG signs of ischemia = need for shunt**
No difference in outcome seen in GA + EEG vs. awake with regional block
Regional Anesthesia
Superficial & deep cervical plexus blocks to cover C2-C4
Cervical plexus block may result in ipsilateral phrenic nerve paralysis, usually transient
If Horners syndrome develops injection is superficial to the deep cervical plexus
Perinatal Cardiorespiratory Physiology
Fetal circulation is in parallel vs. adult in series R.V. 2/3 of C.O.
PVR due to (1) lung expansion, (2) breathing, (3) alkalosis, (4) PAO2 tension. C/S
neonates have PVR compared to vaginal delivery
Ductus arteriosus closes when PAP < SBP (10-14 days = 2-3 weeks)
Apgar Score
A measure of fetal asphyxia --- severe, mild, or nonexistent


Appearance (Color)

Blue or pale

Grimace (reflex
irritability in response
to catheter in nose)
Activity (muscle tone)


Body pink,
extremities blue
< 100

All pink

Some flexion
Slow, irregular

Active motion
Good, crying

> 100

1-min score => acidosis, survival

5-min score => neurological outcome
Bulb suction as head emerges; neonate held at level of introitus o
If below introitus
blood volume polycythemia o If above introitus blood volume
o If cut cord too early blood volume (30 ml/kg)

Meconium-Stained Neonates


Thick or particulate meconium obstructs small airways and causes severe respiratory distress

Can see persistent fetal circulation

Amnioinfusion prior to delivery can reduce the severity of meconium aspiration syndrome
Thin watery meconium does not require suctioning beyond careful suctioning of the
Thick meconium may require intubation and suction of the trachea immediately after
delivery, but before the first breath is taken. If meconium is aspirated, the procedure should
be repeated until no meconium is obtained --- but no more than 3 times after which little
benefit is seen
Newborns with meconium aspiration have an increased incidence of pneumothorax (10%
vs. 1% for all vaginal births)

Care of the Depressed Neonate

Grouping by the 1-min Apgar score facilitates resuscitation:

o Apgar 5-7 = mild asphyxiation, require stimulation with 100% oxygen blown across
face o Apgar 3-4 = moderate asphyxiation, temporary assisted PPV with bag &
mask o
Apgar 0-2 = severely depressed neonate, immediate intubation
and possible CPR Indications for PPV:
o Apnea
o Gasping respirations
o Persistent central cyanosis with 100% oxygen
o HR < 100 beats/min
Assisted ventilation by bag & mask at rate of 40-60 beats/min with 100% oxygen Correct
depth of ETT = 6 cm + weight in kg or Morgans formula = infant length/10 + 5

Indications for CPR: o

HR < 60
o HR 60-80 beats/min and not rising after 30 secs of adequate PPV with 100% oxygen
Chest compressions should be at 120/min
Should be interposed with ventilation in a 3:1 ratio --> 90 compressions, 30 ventilations/min
Vascular Access

If neonatal condition does not improve with ventilation & tactile stimulation cannulation of
umbilical artery with 3.5F (<1500g) or 5F (>1500g) umbilical catheter. If catheter does not
advance, leave in place and attempt at 2nd artery as this often relaxes 1 or 2 vessels.
If place catheter in umbilical vein can result in infusion of hypertonic solutions directly into

Volume Resuscitation

10 ml/kg of LR, NS, or type O-negative blood (5 ml/kg) crossmatched with maternal blood
Causes of neonatal hypotension:
o Hypocalcemia o
Hypoglycemia o
o Polycythemia (Hct >65%) PVR, LV filling pressure R L shunt via ductus
arteriosus & foramen ovale. Can see with delayed cord clamping or stripping blood
from cord.

Correction of Acidosis & Problems with NaHCO3 administration

NaHCO3 is hypertonic, if rapidly given intra-vascular volume intracranial

Generation of CO2 cardiac arrest or dilated cerebral vessels cause higher CBF risk
intracranial hemorrhage


May induce hypotension. Correcting acidosis PVR & hypovolemia is unmasked

Who Requires Alkali Therapy?
o Apgars < 2 at 2 or < 5 at 5 give 2 meq/kg with ventilation. Do not give if catheter
tip in the liver hepatic necrosis
o Metabolic acidosis with pH < 7.0. Resuscitate with volume, r/o CDH, hypoglycemia

Drug Therapy

Epinephrine, 0.1 ml/kg of 1:10,000 soln for asystole or spontaneous HR < 60

Naloxone, 0.1 mg/kg IV or 0.2 mg/kg IM if opioids given to mother within last 4 hours of labor
Sodium bicarbonate, 2 mEq/kg, only for severe metabolic acidosis
Calcium gluconate 60 mg/kg only with documented neonatal hypocalcemia or Calcium
chloride 20 mg/kg
Atropine 0.02 mg/kg
Glucose only for hypoglycemia
Dopamine at 5 mcg/kg/min to support BP
Surfactant via ETT to premature neonates with respiratory depression syndrome

Spinal Cord
Epidural space: extends from foramen magnum to sacral hiatus covered by the
sacrococcygeal ligament
Spinal cord ends L2 in adults, L3 in children
Dural sac extends to S2 in adults, S3 in children
Extension of pia mater, the filum terminale, penetrates the dura and attaches conus
medullaris (terminal spinal cord) to coccyx

Total volume = 150 mL; of which 25-35 mL is in the spinal subarachnoid space
Pressure = 60-80 cm H20
Acid-Base status o
pH 7.32 (slightly lower than serum)
o PCO2 48 mmHg,
o HCO3- 23 mEq/L
Specific gravity = 1.006

Blood Supply
Vertebral artery single anterior spinal artery anterior 2/3 of the cord, found in the
midline of the cord. Gives off numerous circumferential vessels o
Injury = motor lesion,
including anterior horn cells
Posterior inferior cerebellar arteries (PICA) 2 posterior spinal arteries posterior
1/3 of the cord; fed by 25-40 radicular arteries.
Artery of Adamkiewicz (radicularis magna) unilateral, arising from the aorta anterior,
lower 2/3 of the cord, supplies the anterior spinal artery o
T9-T12 (60%), T4 region is
the most tenuously supplied

Injury = Anterior Spinal Artery Syndrome Disruption of the anterior spinal

cord leads to bilateral disruption of the corticospinal tract = motor deficits,
AND disruption of the spinothalamic tract = sensory deficits pain &
temperature deficits

Cardiovascular Manifestations of Neuraxial Technique

Vasodilation of venous capacitance vessels pooling of blood preload,
Arterial vasodilation may also SVR


Cardiac output o Total sympathectomy denervation has no effect on C.O. provided

patient is normovolemic and legs elevated above the level of the heart.

Heart rate o
Bradycardia due to blocked pre-ganglinonic T1-T4 & significant RA
pressure (BezoldHarisch reflex )place patient in head down position

Myocardial Oxygenation demand decreases with spinal anesthesia for 3 reasons:

o Afterload decreases, thus LV work decreases o
Preload decreases, workload of
RV & LV then decrease o
HR decreases

Pulmonary Manifestations of Neuraxial Technique

Resting TV & IRV are unaffected by intercostal paralysis b/c diaphragmatic activity is intact
TLC & ERV, including forced exhalation & cough
Transient respiratory arrest during high spinal is ischemia of medullary respiratory neurons
Phrenic nerves are unaffected by midcervical levels of sensory anesthesia b/c the level of
motor blockade is below the level of sensory anesthesia.
Clonidine causes bradycardia and sedation when given SAB or epidural
-agonists produce analgesia
Addition to lidocaine or bupivacaine has not clinically significant, prolongation of spinal if
added to tetracaine
Cardiovascular effects of epidural to T5 with epinephrine:
o SV and C. O. o MAP and SVR
o Without epinephrine MAP, SV, CO, SVR
Distribution of L.A. in CSF: Factors with Proven Effects
Site of injection
Anatomic configuration of spinal column
Patient height (only in extremes)
Direction of needle during injection (cephalad vs. caudad)
Volume & density of CSF (e.g. CSF volume with intra-abdominal pressure such as
obesity) Baricity the MOST important factor controlling spread of L.A.**
Dose of L.A. hastens onset & duration
Volume L.A. solution
Position during & after injection
Uptake of L.A. From CSF
Surface area of nerve tissue exposed to CSF
Concentration of local anesthetic in CSF
Lipid content of nerve tissue
Blood flow to nerve tissue
General order of uptake by fiber size
1) Sympathetic
2 segments above pinprick, measured by temperature (C fiber)
fibers are the most sensitive to L.A.

Pre-ganglionic nerve


2) Pain: (A-delta fibers) 1 segment above level of anesthesia to

light touch 3) Touch/Proprioception
4) Motor: (A-) 2 segments below pinprick
Elimination of L.A. From CSF
Vascular absorption via subarachnoid and epidural blood vessels. i.e. spinal anesthesia at T12
lasts longer than T3 b/c the absorptive surface to which L.A. exposed is greater with T3 than
No significant metabolism of L.A. in CSF
Lipid solubility = Duration of action
Physiochemical Properties of Local Anesthetics
Lipid solubility = potency
Protein binding = duration of effect & toxicity, metabolism
pKa = speed of onset
Weak bases, pKa closer to physiologic pH = higher concentration non-ionized base, faster

Anesthetic Toxicity
CNS manifestations are FIRST!
CNS tinnitus, perioral paresthesias, dizziness, lightheadedness grand mal seizure
Cardiac o < 5 mcg/ml - no symptoms are seen
o 5-10 mcg/ml - prolonged PR interval and wide QRS, low C.O. and peripheral
o > 10 mcg/ml - asystole
o Treatment 100% O2, hyperventilation:
o Prevents ypoxia
o Induced hypoK+ hyperpolarizes neurve membrane to seizure threshold o
pH lidocaine non-ionized increases & get cerebral vasoconstriction causing
less drug delievery to brain

Max Doses with 1:200 K Epi

Lidocaine 500 mg

Prilocaine 600 mg

Mepivicaine 500

Bupivacaine 225

Tetracaine 200

Systemic toxicity is much greater with epidural blockade than spinal b/c higher doses given
Onset of spread is faster cephalad (head) than caudad
Areas first blocked are the last to return to normal
Tetracaine is not used b/c it spreads poorly. Chloroprocaine is not used often b/c of the risk of
adhesive arachnoiditis, likely related to a preservative, sodium bisulfite
Addition of Epi
increases duration of sensory block, NOT motor block
*Factors Affecting Epidural Spread
Major: Age & Site
Minor: weight, height, position
Epidural Opioids

Lipid solubility predicts clinical behavior.

Advantages of epidural opioids vs. spinal opioids:



Better post-op analgesia o Higher post-op PaO2

Lower incidence of pulmonary complications

Sacral hiatus, covered by the sacrococcygeal ligament.
Dural sac extends S2 in adults, S3 in infants (spinal cord ends at L3 in infants)
Most common complications - intravascular or subarachnoid injection
Dose: 0.5-1.0 mL/kg of 0.125% to 0.25% bupivacaine with or without Epi.


Headache - Post-dural puncture headache (PDPH)
Bilateral, frontal or retro-orbital, occipital and extending into the neck, +/- photophobia
Hallmark = body position, aggravated by sitting or standing, relieved or lessened by lying
flat Onset, 12-72 hours post-procedure
Results from ICP as CSF leaks from the dural defect faster than it is produced

Risk Factors for PDPH

Not Risk Factors o Age: younger more
Continuous spinals
o General: F > M
Timing of ambulation
o Needle bevel, transverse cut more common o Needle size o Pregnancy o # of
Rx: recumbent position, hydration, NSAIDS, caffeine (500 mg tid) to stimulate CSF production
Blood patch: 15-20 mL of autologous blood injection into the epidural space at or one
interspace below. 90% respond to a single patch.

Transient Neurologic Symptoms

Risks: lithotomy position, demography, NOT drug concentration
Characterized: back pain radiating to the legs without sensory or motor deficits, occurring
after the resolution of spinal block and resolving spontaneous within several days.
Associated with hyperbaric lidocaine (11.9%), tetracaine (1.6%), bupivacaine (1.3%).
Highest incidence among outpatients (early ambulation) after surgery in the lithotomy
High Spinal

Diminish coughing, but no change in ABGs!

ERV by 20% with total thoracic block
Inspiratory capacity (IRV + TV) is minimally affect b/c it is a diaphragmatic function (C3-5)
Spinal block causes the greatest motor blockade, affecting cough more than epidural
Severe sustained hypotension with lower sensory blocks can lead to apnea via medullary
hypoperfusion. **Must treat with epinephrine**
Can see pupillary dilatation

Cauda Equina Syndrome

A mild acute myelopathy affecting smaller nerve fibers, or autonomic fibers urinary and
fecal incontinence, lower extremity paresis (loss of movt), perineal hypesthesias (absent or
reduced sensitivity to cutaneous stimulation
Onset of symptoms is rapid unless it is caused by adhesive arachnoiditis
Has been associated with subarachnoid catheters (small or large)
Common causative factors = pooling/maldistribution of L.A. in dependent areas of the


Adhesive Arachnoiditis
Proliferative overgrowth of the pia-arachnoid that can obliterate the subarachnoid space
Typically chronic progressive, chronic, sensory loss and paresis of the lower extremities
Subarachnoid steroid injection is not recommended!
Probably due to the preservative ethylene glycol
Epidural Abscess (EA)
4 classic stages of EA
1. Back or vertebral pain, intensified by percussion over the spine
2. Radicular pain develops
3. Motor and/or sensory deficits or sphincter dysfunction
4. Paraplegia or paralysis
Staphylococcus aureus and Staphylococcus epidermidis
Rx: ABX, decompression (laminectomy)
Prevention: (1) minimize catheter manipulations, (2) micropore bacterial filter, (3) remove
epidural catheter after 96 hours ( 4 days)
Spinal or Epidural Hematoma
Sx/Si are more sudden than epidural abscess
Rx: surgical decompression within 8-12 hours
Anticoagulants & Antiplatelet Agents
Subcutaneous heparin (BID) is not a contraindication
Those requiring intraoperative heparin gtt, blocks may be performed 1 hour or more before
heparin administration. Removal should occur 1 hour prior to, or 4 hours after subsequent
heparin dosing.
LMWH Neuraxial guidelines
Produce a more predictable anticoagulant response than unfractionated heparin, have a
better bioavailability, longer t , and dose independent clearance
Low dose LWMH
o Placement: 12 hrs after last dose, avoid placement if given within 2 hrs o
Postop: resume dosing 8 hrs after block placement, then q 24 hr
o Removal: remove catheter 12 hours after the last dose, resume dosing 2 hours
after catheter removal
High treatment dose LWMH (enoxaparin 1 mg/kg q12, enoxaparin 1.5 mg/kg daily,
dalteparin 120 U/kg every 12 hours, dalteparin 200 U/kg daily, or tinzaparin 175 U/kg daily) o
Placement: 24 hrs after last dose o
Post-op: 24 hrs after placement o
Removal: 12 hours after the last dose, subsequent dosing 2 hours after catheter
o Do not maintain continuous catheters while on twice daily dosing


CNS Effects
MAC 40%, normal by 3rd day post-partum o Due to surge in -endorphin and high
levels of progesterone (sedating effects)
pain tolerance due to activation of endorphin system


sensitivity to local anesthetics; dose requirements reduced by 30%; progesterone

mediated o No increased risk of local anesthetic toxicity
Obstruction of IVC distends the epidural venous plexus and epidural blood volume o
CSF volume enhances cephalad spread
o potential volume of epidural space enhances cephalad spread o
epidural (space) pressure higher risk of dural puncture

Respiratory Effects
MV (50%): progesterone VT, little change in RR
O2 consumption (20-40%): FRC 20% + O2 consumption hastens hypoxemia
airway resistance: progesterone effect
FRC 20% due to RV; closing capacity > FRC
NO CHANGE Vital capacity = ERV + IRV
PaO2 PaCO2: PaO2 103 mmHg, PaCO2 32 mmHg respiratory alkalosis
HCO3- 22 mmHg
o 2,3-DPG offsets the effect of hyperventilation (R-shift Hgb curve) o P50
30 mmHg (vs. 27 mmHg)
Elevation of the diaphragm is compensated by anteroposterior diameter of the chest
Flow-volume loops are unaffected
dead space (pulmonary vasodilation)
Fast rate of induction due to FRC and MV
Cardiovascular Effects
Increase in plasma volume in excess of an increase in red cell mass (blood volume increased
by 1000-1500ml) dilutional anemia and lower viscosity
Hemoglobin remains > 11 g/dL, Hct > 33%
C.O. by 40% ( HR & SV ) & R- shift of Hgb curve (P50 = 30 mmHg) SVR, diastolic >
Greatest increase in C.O. is seen during labor and immediately after delivery.
Returning to normal within 2 weeks post-delivery
Cardiac chambers enlarge and myocardial hypertrophy is often noted on Echo o
PA wedge pressures remain unchanged
Renal Effects
Renal vasodilation RBF & GFR 50% in 1st trimester, decline to normal during 3rd
trimester serum Cr & BUN a normal Cr during pregnancy is highly abnormal!
renin & aldosterone levels Na+ retention
renal tubular threshold for glucose and amino acids mild glyucosuria or proteinuria
**Gastrointestinal Effects**
Lower LES sphincter tone from elevated progesterone levels & upward/anterior
displacement of the stomach
Hypersecretion of gastric acid (pH < 2.5) from production of gastrin by placenta
Higher gastric volumes b/c of hormonal & mechanical obstruction high intragastric
Narcotics and anticholinergics reduce LES sphincter pressure
Hepatic Effects
Hepatic function and blood flow are unchanged
30% decrease in serum pseudocholinesterase activity rarely significant prolongation of
succinylcholine. Takes up to 6 weeks post-partum to return levels to normal
Elevated tests: SGOT, LDH, cholesterol, alkaline phosphatase (due to placental secretion)
Breakdown of mivacurium and ester-type anesthetics is not noticeably altered


Progesterone inhibits release of cholecystokinin incomplete emptying of the gallbladder

Hematologic Effects
Hypercoagulable state
Fibrinogen and factors VII, VIII, IX, X, and XII all increase
Only factor XI levels may decrease
Leukocytosis (up to 21,000) and platelets can be seen
Cell-mediated immunity is markedly depressed increase risk of viral infections
Metabolic Effects
Diabetogenic state insulin levels rise; secretion of human placental lactogen by the
placenta is likely responsible for relative insulin resistance o
Maternal glucose crosses
placenta, insulin does not severe neonatal hypoglycemia following delivery
o Fetal hyperglycemia & hyperinsulinemia may delay fetal lung
maturation and surfactant synthesis
Pancreatic cell hyperplasia occurs in response to increased demand for insulin secretion
Hypertrophy of the thyroid gland and thyroid-binding globulin
T4 & T3 levels, but free T4 & T3 and TSH remain normal
Uterine Blood Flow = 500-700 ml/min
50% decrease is required before see fetal distress (scalp pH normal = 7.25)
Autoregulation is absent, but remains sensitive to -adrenergic agents
uterine blood flow IF severe hypocapnia (PaCO2 < 20 mmHg) fetal hypoxemia, acidosis
Decrease flow after phenylephrine, dopamine & dobutamine
Increase in blood flow after ephedrine
Placental Physiology & Anatomy
Placenta is composed of projections of fetal tissue (villi) that lie in maternal vascular spaces
(intervillous space)
Fetal blood within villi is derived from 2 umbilical arteries (deoxygenated) and returns to
the fetus via 1 umbilical vein (oxygenated)
Respiratory Gas Exchange/Cord Blood Gases
Oxygenated umbilical vein: PaO2 = 30 mmHg, PaCO2 40 mmHg, pH 7.35, SpO2 70%
Deoxygenated 2 umbilical arteries, PaO2 = 20 mmHg, PaCO2 50 mmHg, pH 7.28,
SpO2 40%
Transfer of oxygen across the placenta is dependent on ratio of maternal uterine blood flow to
fetal umbilical blood flow
To aid oxygen transfer, fetal hemoglobin curve is L-shifted (high affinity)
Fetal hemoglobin = 15 g/dL = Hct 45% (maternal = 12 mg/dL)
Maternal hyperventilation (PaCO2 32 mmHg) increases gradient for the transfer of CO2
from fetus into the maternal circulation
Fetal hemoglobin has less affinity for CO2 than maternal hemoglobin
Vein (Birth)












1st stage of labor: pain from uterine contraction and

cervical dilation o
Latent phase: T11-T12
dermatomes o Active phase: T10-L1
Pain carried in visceral afferent C fibers accompanying sympathetic nerve fibers first to
uterine & cervical plexuses hypogastric & aortic plexuses spinal cord with T10-L1 nerve
Paracervical block carries 10-40% risk of fetal bradycardia & acidosis likely direct cardiac
2nd stage of labor: onset of perineal pain signals the beginning of fetal descent
Sensory of the perineum is provided by pudendal nerve (S2-S4)
Requires T10-S4 dermatomes
Lumbar sympathetic block does not provide reliable relief for 2nd stage labor

Frank Breech (remember Frank Butt) feet against the face and butt presenting
Complete breech butt and feet present together
Incomplete breech one or both feet together
Dx by manual exam
Associated increase risk of maternal mortality with hemorrhage, infection, retained placenta
Fetal risk of cord compression and intracranial hemorrhage (trama)
If uterine relaxation is needed for extraction, a volatile anesthetic with OETT is

Pudendal Nerve Block

Perineal anesthesia for the 2nd stage of labor (S2-S4)
Needle placed transvaginally under ischial spine, advance 1.5 cm through the
sacrospinous ligament, deposit 10ml 1% lidocaine
Complications: intravascular, retroperitoneal hematoma, retropsoas or subgluteal abscess
Paracervical Plexus Block

40% incidence of fetal bradycardia & acidosis because high fetal blood levels cause
direct cardiotoxicity
Effective during 1st stage of labor
Injection submucosally at 3 oclock & 9 oclock positions on either side of the cervix
Visceral sensory fibers of the Frankenhuser ganglion from the uterus, cervix, and upper
vagina are blocked as they pass through the paracervical plexus Does not cause
uterine atony, may increase uterine activity
Does NOT cause motor blockade!
Performed prior to 8 cm cervical dilation to prevent fetal injury

Lumbar Sympathetic Nerve Block

1st stage of labor, not reliable for 2nd stage
Sensory fibers from the lower uterus and the cervix join the sympathetic chain between L2 &
Bilateral paravertebral sympathetic block beneath the spinous process of L2
2 Side Effects Terbutaline
Pulmonary edema


*Bradycardia has been reported with low dose terbutaline

Hemabate (15-Methyl prostaglandin F2a)

2nd line uterotonic drug (1st line is Oxytocin 40U/L)
Dose: 0.25 mg IM or intra-myometrial
Side effects: Asthma, AVOID in severe cardiac disease b/c increases PVR & C.O.
Ergonovine or Methergine (ergot alkaloids)
3rd line uterotonic drug, used when Hemabate is contraindicated
Dose: 0.2 mg IM or IMM
Side effects: receptor activation HTN, coronary artery spasm, stroke
AVOID in PIH or those with CAD
Fetal Heart Rate/Patterns of Decelerations
Normal HR 120-160
Early decelerations:
o Begins at the onset and ends at the conclusion of uterine contraction o Fetal
head compression 2nd vagal stimulation

Late decelerations:
o Begin after onset of uterine contraction and persist after its conclusion
o Uteroplacental insufficiency 2nd maternal hypotension, HTN, or uterine
hyperactivity o Immediate delivery is NOT mandatory check fetal scalp pH

Variable decelerations (MOST COMMON) o NOT related to contractions o Umbilical cord

o Last longer than 1 min = > severe fetal distress

Placental Exchange
Placental exchange from other to fetus primarily occurs by diffusion, which depends on:
o Concentration gradient
o Protein binding of drug in maternal circulation
50% lidocaine bound compared to 95% of bupivacaine o
Molecular weight, lipid
solubility, and degree of ionization of the drug
Non-depolarizing NMB are TOO large (MW to big) to cross placental barrier
Sux is too ionized and has low lipid solubility to cross placenta o
Fetal pH fetal
acidosis can cause ion trapping of local anesthetics and narcotics (weak bases)

Almost all drugs cross the placenta, except He Is Going Nowhere Soon
Non-depolarizing NMB

Fetal Lung Maturity

Surfactant secreted by type II pneumocytes
During 3rd trimester, rate of growth slows and isolated values for the biparietal diameter are
much less accurate in predicting gestational age
Lecithin-sphingomyelin ratio > 2.0 = fetal maturity. Can still see fetal respiratory
distress syndrome in infants of mothers with diabetes and L:S ratio > 2.0



(1) Chronic HTN HTN persistent before, during and after pregnancy (e.g. 6 wks post-partum)
(2) Gestational HTN increase in BP without generalized edema or proteinuria, resolves by 2-6
(3) Preclmapsia-eclampsia
(4) Chronic HTN with preeclampsia-eclampsia
Preeclampsia refers to the triad of (1) HTN, (2) proteinuria (>500 mg/day), and (3)
edema (hand and face) occurring after 20 weeks and resolves within 48 hrs after delivery
2 of the 3 manifestations must be present for diagnosis
Defined as SBP > 140 mmHg or DBP > 90 mmHg or as a consistent increase in SBP of 30
mmHg or DBP of 15 mmHg > baseline
Maternal deaths are usually due to stroke, pulmonary edema, and hepatic necrosis or rupture
Pathophysiology & Manifestations of Preeclampsia

Incidence of about 7%, affects chiefly primigravidas

Appears to be related to abnormal prostaglandin metabolism and endothelial dysfunction that
leads to vascular hyperreactivity
thromboxane A2 - a potent vasoconstrictor & promoter of platelet aggregation
prostacyclin - potent vasodilator and inhibitor of platelet aggregation
Endothelial dysfunction may reduce nitric oxide production and endothelin-1 (a potent
vasoconstrictor and platelet activator)
Abnormal regulation of oxygen-derived free radical and lipid peroxidation may play a role
Increased sensitivity to catecholamines

Mild Pre-eclampsia:
o BP 140/90 or SBP > 30 mmHg and DBP > 15 mmHg over pre-pregnant levels o
Proteinuria > 300 mg/day o
Generalized edema

Severe Pre-eclampsia: o BP > 160/110 mmHg o Proteinuria > 5 g/day o Edema

pulmonary edema CHF, general edema airway swelling o Hypovolemia, oliguria
o Thrombocytopenia-DIC prolonged PT/PTT, thrombocytopenia, fibrinogen
o CNS irritability seizures, coma, hypoxic cerebral encephalopathy, vertigo,
blindness, hyperreflexia
o HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count)

Most patients have low-normal cardiac filling pressures with high SVR, but C.O. may be low,
normal, or high

Magnesium Sulfate Effects

Skeletal muscle relaxant: (1) release of Ach at the NMJ, (2) sensitivity of motor end
plate to Ach, (3) excitability of muscle membrane
Sensitivity to depolarizing & non-depolarizing NMB
Tocolytic, uterine activity uterine blood flow
Vasodilator due to smooth muscle relaxation
Magnesium Sulfate Side Effects


Therapeutic level = 4-6 meq/l

5-10 meq/L = EKG changes
10 meq/L = loss of deep tendon reflexes (hyporeflexia) and muscle weakness
15 meq/L = Respiratory insufficiency /paralysis treat with supportive measures if possible
20 meq/L = Cardiac failure/arrest treat with CaCl2
Neonates have muscle tone at birth respiratory depression & apnea. Treat with IV
No fasciculations are seen with succinylcholine. dose of succinylcholine should be used
*B/c calcium antagonizes the anti-convulsant effects of magnesiumexcept in cases of gross
magnesium overdose & cardiac depression, it is probably better to support the mothers
depressed respirations and AVOID calcium.

*Other Side effects of Magnesium

Vasodilation hypotension
CNS depression
Pulmonary edema
Placental Anomalies
Placenta accreta placenta is adherent to the surface of the myometrium
Placenta increta placenta invades the myometrium
Placenta percreta placenta penetrates the myometrium, serosa, possible surrounding
Myasthenic in Labor
Anticholinesterase therapy should be continued
Epidural anesthesia is an excellent choice
Neonatal myasthenia is present in 20-30% of neonates whose mothers are afflicted;
neonatal anti-cholinesterase therapy is needed for 3 weeks post delivery.
Non-obstetric Surgery During Pregnancy > 20 weeks
Aspiration prophylaxis
After 24 weeks, use left uterine displacement
Fetal monitoring when possible
Fiber Type

Modality served
Motor efferents &


Touch, Pressure


Motor efferents to muscle




Pain somatic

Dorsal root


-Pain visceral via




Differential Blockade
Sympathetic B & C fibers (temp) > pain & touch (A) > proprioception (A) > motor (A)
Pain Terminology
Nociceptive pain is due to activation or sensitization of peripheral nociceptors
Neuropathic pain is the result of injury or acquired abnormalities of peripheral or central
neural structures
Allodynia - perception of an ordinarily non-noxious stimulus as pain
Analgesia - absence of pain perception
Anesthesia dolorosa - pain in an area that lacks sensation
Dysesthesia - unpleasant or abnormal sensation with or without a stimulus
Hypoalgesia - diminished response to noxious stimulation
Hyperalgesia - increased response to noxious stimulation
Hyperesthesia - increased response to mild stimulation
Hypoesthesia - reduced cutaneous sensation (eg, light touch, pressure, temp)
Hyperpathia - presence of hyperesthesia, allodynia and hyperalgesia usually associated
w/overreaction, persistence of the sensation after the stimulus
Paresthesia - abnormal sensation perceived without an apparent stimulus
Radiculopathy - functional abnormality of one or more nerve roots

Excitatory Pain Neurotransmitters

substance P
somatostatin, cholecystokinin
vasoactive intestinal polypeptide
enkephalin (kappa receptor)
endorphins (mu receptor)

Inhibitory Pain Neurotransmitters

- NorEpi & serotonin at dorsal horn



A, C

Marginal layer
Substantia gelatinosa
* major role in processing & modulating nociceptive
input from cutaneous nociceptors and major site


of opioids


A, A
A, A, C

Nucleus proprius
Visceral & somatic pain
WDR neurons
Nucleus proprius
Intermediolateral column; pre-ganglionic
sympathetic neurons
Ventral (motor) horn
Central canal

- mu

- kappa

- delta


Physiologic Effect
Supraspinal analgesia
Prolactin secretion (1)
Respiratory depression
Spinal analgesia (2)
Tolerance & dependence
Muscle rigidity
Spinal analgesia
Supra- & Spinal Analgesia
Epileptogenic (myoclonus)
Depersonalization reactions

Endogenous agonist



- epsilon
*all side effects diminish with time, EXCEPT constipation & myoclonus
L-isomer is agonist at receptor, D-isomer is antagonist at NMDA blocks hypersensitivity
& central sensitization in neuropathic pain & tolerance to opioids

Non-opioid analgesic, weak -receptor agonist

Analgesic effect by inhibition of reuptake NorEpi & Serotonin, can enhance serotonin
Dose 50-100 mg q6-8 hrs
Side effects respiratory depression (reversed with naloxone), constipation
Can develop physical & psychological dependence
AVOID in patients taking SSRI or TCAs, MAO-I risk seizures
Reduce does in those taking cimetidine



Synthetic opioid, NOT ideal for chronic pain due to short duration and high abuse potential
Normeperidine, secreted via kidneys myoclonus, tremulous, hallucinations, seizures
Anti-cholinergic (looks like atropine) mydriasis (dilation), orthostatic hypotension,
Rarely causes puritis when given neuraxially, has local anesthetic effects!
AVOID with MAO-I (Selegiline) hyperthermia, rigidity, seizures
Myocardial depression with large doses, related to local anesthetic effect

WHO Stepladder
Step 1: manage pain by non-opioid medications with or without adjuvants
Step 2: if pain is persisting or increasing, add weak opioids (codeine, hydrocodone,
tramadol, oxycodone) to existing non-opioid analgesics and adjuvants
Step 3: strong opioids (morphine, hydromorphone, fentanyl) are used with non-opioids
and adjuvants until patient achieves complete analgesia
Step 4: if pain persists, neurolytic and/or interventional procedures should by employed
*adjuvants = steroids, amitriptyline, gabapentin, NMDA antagonists, clonidine, antihistamines
Neuraxial Opioid Infusions
Advantage of producing profound analgesia WITHOUT motor, sensory or ANS blockade!
Oral MSO4: epidural MSO4 = 1:30
Oral MSO4: SAB MSO4 = 1:300
Central Pain
If patient fails to obtain pain relief despite complete sympathetic, sensory, and motor
blockade, a
central mechanism for pain is likely or the lesion is higher in the CNS that level of blockade
Central pain states may include encephalization, psychogenic pain, or malingering
Persistence of pain in the LE after successful spinal blockade suggests a central source or
psychological source
Phantom Limb Pain
Type of Central Pain
Of those who get it, 85% develop it within the first 4 days
Higher incidence w/ more proximal amputation
NO difference of incidence b/t tramatic & non-tramatic
Can reactivate limb pain with
w/ spinal or epdiural technique
o Sympathetic chain activation. Although bilateral sympathetic blocks fail to
relieve pain o Central mechanisms. Somatosensory cells begin to fire at will
Treatment Phantom Limb Pain:
o TENS and Tegretol o
Epidural morphine o
o IV opioids dont work very effectively
o Nerve blocks trigger pt injections, peripheral & central, sympathetic bocks
Classified by the presence of chronic widespread pain and tactile allodynia
Research has demonstrated that FM is associated with polymorphisms of genes in the
serotoninergic, dopaminergic and catecholaminergic systems
Studies have shown that stress is a significant precipitating factor in the development of
fibromyalgia, and that PTSD is linked with fibromyalgia.
Electroencephalography show a lack of slow-wave sleep and circumstances that interfere with
stage 4 sleep (pain, depression, serotonin deficiency, certain medications or anxiety) may
cause or worsen the condition
Women (10:1), ages 20-60 yrs


75% experience fatigue, restless sleep, widespread stiffness

25% irritable bowel syndrome, subjective swelling, paresthesias, anxiety or depression
Dx: (1) history of widespread pain lasting more than 3 monthsaffecting all 4 quadrants
of the body, AND (2) pain is present 11 of 18 tender points
o 1st line amitriptyline
o 2nd - analgesics NSAIDs, tramadol, pregabalin (marketed as Lyrica)

Reflex Sympathetic Dystrophy (CRPS Type I)

RSD is NOT a definitive diagnosis
Hallmark is pain, trans dermatomal, and autonomic changes
Major nerve damage does not occur
May follow carpal tunnel release, palmar fasciotomy, or arthroplasties
Cure rate of > 90% if treatment is initiated within 1 month of symptoms






3 Phases

Localized, severe,

More diffuse,


Dry and red


Cold, discolored,
edematous Muscle

1-3 months

3-6 months

Less severe; often
involves other
Severe muscle
Glossy and atrophic
ankylosis of joint

Causalgia (CRPS Type II)

Most severe form of RSD. Causalgia means burning pain, and typically follows high velocity
(eg, gunshot) incomplete injuries to large nerve(s)
Onset within 1 month of injury
In contrast to RSD, sustained, constant, burning pain, NOT paroxysmal!! General
o Constant burning pain beginning distally and spreads centrally o
Hyperesthesia: light touch can produce unbearable pain
o Vasomotor and sudomotor changes: extremity can be cold and cyanotic or
warm, dry, and erythematous
o Wasting of skin, muscles, and bone (decalcification). Skin can be thin and
glossy with hair loss and nail changes
Increased sympathetic tone (fear, anxiety, light, noise or touch) exacerbates the
Major Forms of Treatment for CRPS
Sympathetic nerve blocks: stellate ganglion, lumbar sympathetic, brachial plexus,
epidural, spinal blocks
IV Regional Blocks with bretylium acts to cause release of norepinephrine and inhibit
further release of norepinephrine.
Aggressive physical therapy plays a central role
Some benefit from TENS or dorsal column stimulation


Systemic medications: amitriptyline, steroids, propranolol. Oral alpha- blockers

(phenoxybenzamine or prazosin), clonidine, anti-convulsants, anti-depressants .
Surgical sympathectomy for chronic causes is often disappointing due to only transient relief

Myofascial Pain Syndrome

Onset 3rd-4th decade
Characterized by widespread aching which is deep, discrete trigger points and poorly
Associated with erythema, stiffness, fluctuation in pain intensity
Can see autonomic dysfunction = vasoconstriction, piloerection
Aggravating factors fatigue, mental stress, cold damp weather, under- or over activity
Treatment rest, heat, massage, L.A. injection into trigger points
Mixed - opioid antagonist at 1-receptor and agonist at K
Antagonistic properties can attenuate efficacy of co-administered opioid agonists
withdrawal symptoms
Advantages: low potential for respiratory depression and physical dependence
Disadvantage: dysphoric reaction is very common, analgesic ceiling effect (increasing the
dose does not give more analgesia)
Transdermal fentanyl
More effective pain relief & higher quality of life scores
Lower constipation rates
Disadvantages: more nausea & higher rates of rescue drugs
Conversion 45 mg oral morphine = 12.5 mcg/hr fentanyl patch
1 oxycodone = 1.5 oral morphine
Tolerance = the point at which a person adapts to a specific substance, so larger amounts
of the prescribed medication or a new medication is needed to achieve the same results.
Physical dependence = a physical condition in which rapid discontinuation of a substance,
such as alcohol, tobacco or a drug, causes a withdrawal reaction.
Addiction = the continued compulsive use of drugs in spite of adverse health or social
Post-Herpetic Neuralgia o
Defined as pain persisting beyond the healing of
herpes zoster o
Incidence with age, > 50% at age 80 o Rx TCA,
anticonvulsants, topical lidocaine patch, topical capsaicin, +/- L.A. injection


Respiratory Parameters for Boards
O2 consumption
TV (ml/kg)
MV (liters)
Vd/Vt (dead space)
FRC (ml/kg)
VC (ml/kg)
PaO2 (mmHg)





NPO Guidelines = 2-4-6-8 Rule

2 hours clear liquids
4 hours breast milk
6 hours formula or light meal
8 hours fatty or solid meal

Weight Gain
Average newborn = 3.5 kg
1 year-old = 10 kg
2 - 6 year-old gain 2 kg/yr = 12 kg 20 kg
6 - 10 year-old gain 3 kg/yr

Cardiovascular Parameters for Boards


0-30 days
1-12 months

Blood Volume
85 ml/kg
80 ml/kg


1-12 yrs

75 ml/kg



Retinopathy of prematurity (ROP) = Retrolental fibroplasia

Newborns < 35 weeks gestational age, risk is negligible after 44 weeks
Risk inversely related to age & birth weight highest risk < 1500g
Hyperoxia constriction of retinal arterioles swelling, degeneration endothelium
vascularization resumes in an abnormal fashion when normoxic conditions return retinal
detachment and blindness are possible
GOAL: keep PaO2 < 80 mmHg, SpO2 93-95% during anesthesia. Do not compromise O2
delivery to brain just to protect the eyes. ROP does develop in cyanotic CHD patients not
exposed to supplemental O2.
Pyloric Stenosis
1/500 births, male >> females, occurs equally in preterm & term neonates, 2-6 weeks, but
as early as 36 hrs
Most common GI obstruction in pediatrics
Hypokalemia, hypochloremic, hyponatremic metabolic alkalosis, +/- metabolic
acidosis from severe dehydration
Vomiting HCl gastric fluid, kidneys correct alkalosis by holding onto H+ and excreting
alkaline urine with K+ & Na+.


In severe cases, will conserve Na+ at the expense of wasting H+ ions in the
urine paradoxic aciduria = vomit and pee H+
Fluid resuscitation with Normal Saline (LR contains NaHCO3 & worsens alkalosis), once UOP
returns, add KCl to infusion
Risk of post-op ventilatory depression from central apena depression due to metabolic
alkalosis that is worsened by intra-op hyperventilation
Na deficit = (140 current Na) x 0.6 x wt in kg 1 liter NS has 154 mEq

Pierre Robin & Treacher Collins Syndromes

Pierre Robin: micrognathia, congenital heart defects, cleft palate, *glossoptosis can
cause asphyxiation requiring tongue suture to pull it forward
Treacher Collins: micrognathia, congenital heart defects, choanal atresia, aplastic
zygomatic arches, microsomia
Infectious croup, FB aspiration, Acute epiglottitis
Infectious croup = follows a viral URTI, ages 3 mos 3 yrs.
o A subglottic problem (below cords) o
Present with inspiratory &
expiratory stridor, steeple sign on CXR, hoarse o
Managed with
racemic epi, cool mist, O2, IV dexamethasone

Foreign body aspiration = ages 6 mos 5 years o Present with stridor if supraglottic
or glottic o Present with wheezing if subglottic o
Inhalational induction with extraction
of supraglottic object by endoscopy o
RSI with OETT if subglottic

Acute epiglottitis = commonly due to Haemophilus influenzae type B o

Ages 2- 6 yrs o
Located supraglottic, thumbprint sign on CXR, inspiratory stridor, high fever, drooling
To OR for definitive diagnosis by laryngoscopy followed by intubation o Inhalational
induction in sitting up position o
Rx: ampicillin & chloramphenicol

Post-extubation Stridor/Croup
Oxygen, cool mist, racemic epi 2.25% 0.5 ml into 3 ml NS, dexamethasone 1.5 mg/kg
if all fails, intubate
Downs Syndrome
Short neck, irregular dentition, mental retardation, hypotonia, large tongue, strabismus,
cataracts Cardiac anomalies (40%): AV canal, PDA, endocardial cushion defects with
VSD (50%) , TOF
GI anomalies: congenital duodenal atresia
Associated with subglottic stenosis, TE fistula, chronic pulmonary infections, seizures
Endocrine: congenital hypothyroidism
Anesthetic concerns:
o Neck flexion may result in atlanto-occipital dislocation due to laxity of
ligaments o Risk of post-op stridor and apnea o Narrow nasopharynx, large
tongue, large T & A chronic obstruction o
Impaired alveolar
development hypoxemia, pulmonary HTN
o Smaller trachea use 2 size smaller OETT o
High risk malignant
hyperthermia Omphalocele and Gastroschisis
Omphaloceles = occur at the base of umbilicus, have a hernia sac lower risk
dehydration, due to failure of gut to return within abdominal wall o
Associated with
Trisomy 21, diaphragmatic hernia, cardiac & bladder malformations o BeckwithWiedemann Syndrome refractory hypoglycemia, hyperviscosity syndrome, associated
with visceromegaly, hemi-hypertrophy


Gastroschisis = lateral to umbilicus (defect to omphalomesenteric artery), does not have

hernia sac, often isolated finding

Tracheoesophageal Fistula Anomaly

Most common type C (86%) , upper esophagus ends in a blind pouch, lower esophagus to
Dx: regurgitation 1st feeding, intra-uterine polyhydramnios
Type C (86%)

Type A (8%)

Type E (4%)

Type D (1%)

Type B (1%)

Part of VACTERL syndrome o Vertebral, VSD or other Vascular problems (ASD, PDA,
coarctation) o Anal stenosis (imperforate anus) o Cardiac defects
o TE Tracheoesophageal fistula o
Renal or radial abnormalities
o Limb anomalies

o Pre-op, strict NPO and catheter placed in esophagus to drain saliva
o Awake OETT R main stem bronchus placement then pulled slowly back
until BS heard on the L. Ideally tip of OETT lies b/t the fistula & carina. Not
possible if fistula connects to the carina or a main-stem bronchus, requiring
venting via gastrostomy tube.
o L-lateral position, precordial stethoscopy is placed L side in axilla, since
obstruction of the main-stem bronchus during retraction is not uncommon.
o A-line as retraction can compress the great vessels, trachea, heart and vagus
nerve o
Surgeon 1st performs gastrostomy tube placement; chest
opened and fistula ligated

Congenital Diaphragmatic Hernia

3 defects: L or R posterolateral foramen of Bochdalek or the anterior foramen of Morgagni.
Left-posterior foramen of Bochdalek is the most common (90%)
Incidence is 1:5000
Hallmarks: hypoxia, scaphoid abdomen, evidence of bowel in thorax
Associated anomalies: polyhydramnios (30%), cardiac defects (25%), pulmonary
hypoplasia with
HTN, incomplete cecal rotation, umbilical defects and duodenal
defects Ability to control PaCO2 reflects severity of lung pathology,
ECMO can help
Anesthetic concerns:
o DO NOT BMV intubate immediately!!
o Hypoxemia due to primary pulmonary HTN, pulmonary hypoplasia
o Systemic hypotension by kinking major vessels, esp. liver


Overdistention of stomach herniation across midline hypotension,

hypoxia; must place NGT and avoid high PPV
o Tachypnea o Cyanosis o
Metabolic acidosis o Severe dehydration
o Awake OETT without BMV to prevent overdistention o Insert A-line in R
side to monitor preductal levels o Maintain PaO2 between 50-80, increase
MV by increasing RR and decreasing Tv o Avoid hypothermia to O2
consumption o
Avoid agents that cause myocardial depression until
chest is decompressed o
Monitor for barotraumas-induced pneumothorax
of opposite lung. Aggressive attempts to expand ipsilateral lung after
decompression are detrimental!!

Meningomyelocele = hernial protrusion of a part of the meninges AND spinal cord

Underestimation of fluid & blood loss from the defect is common
High association with hydrocephalus
Possible cranial nerve palsy inspiratory stridor
Latex allergy precautions taken for their 1st & all subsequent anesthetics
Arnold-Chiari malformation-hydrocephalus: caudal displacement of brainstem blocks CSF from
4th ventricle ICP apnea, HTN
Surgical emergency due to risks of CSF leakage and infection
Prune-Belly Syndrome
Agenesis of the abdominal musculature protuberant abdomen, associated with club feet,
cryptorchidism, GU abnormalities
Anesthetic concerns:
o Multiple pulmonary complications due to ineffective cough o
Risk for
o Awake OETT
Cleft Lip & Palate
Rule of 10s: Hgb of 10, weight 10 kg, age of 10 weeks
Cerebral Palsy
No reports of succinylcholine-induced hyperkalemia! secure airway by RSI & Sux
Neurofibromatosis (Von Recklinghausens Disease)
Autosome dominant
Neurofibromas involve skin, peripheral & central NS
1% pheochromocytoma
Intracranial HTN due to expanding intracranial tumor
Airway can have laryngeal neurofibroma
Klippel-Feil Syndrome
Spinal canal stenosis, cervical fusion, short neck
Congential heart disease
Renal abnormalities
Hemolytic Disease of the Newborn (Erythroblastosis fetalis)


Alloimmune condition that develops in a fetus, when IgG antibodies that have been produced
by the mother pass through the placenta and attack fetal RBCs reticulocytosis and
Fetal disease ranges from mild to very severe, death from heart failure (hydrops fetalis)
Usually does not occur in 1st pregnancy. Contamination of maternal blood with fetal RBCs
occurs at delivery or abortion
Bilirubin crosses the placenta and is cleared by the mother newborn at birth may not be
clinically jaundiced

Ductus arteriosus
Closes primarily due to [PaO2] & requires arterial muscular tissue by 2-3 weeks
Maintenance of patent ductus include: hypoxia, hypercarbia, acidemia all due to smooth
muscle vasodilation and pulmonary HTN
Prostaglandin E1 = Alprostadil maintains patency o
o Inhibition of platelet aggregation o Stimulation of intestinal & uterine smooth
muscle o
Patient with low initial PO2 values and < 4 days old respond
best! o
Helpful in liver transplantation by increasing blood flow and
making liver cells more resistant to ischemic injury
o Serious effects = apnea, bradycardia, hypotension, fever o Used to
treat R L shunt lesions cyanotic lesions
Pulmonary atresia/stenosis
Tetralogy of fallot
Coarctation of aorta
Transposition great vessels requires patent foramen ovale for
Fetal Hemoglobin
P50 = 19 mmHg (vs. 27 in adults)
[Hgb] neonate = 17 g/dL, then at 3 - 6 mos. 11 g/dL resulting in O2 carrying capacity
Anemia at 1.5 3 mos as HgbF (gamma, subunit) converted to HgbA (beta,
Minimal Hbg = 10 g/dL
Fetal hemoglobin has higher oxygen affinity than that of the maternal carrier due fetal hgb
subunit (gamma), instead of the b (beta) subunit.
The subunit has less positive 2,3-DPG is less electrostaticly bound to fetal hemoglobin as
compared to adult hemoglobin less effective in lowering the oxygen affinity of the fetal
hemoglobin allowing adult Hgb to readily transfer its oxygen to the fetus

anesthesia in Children
Spinal cord extends to L3
Loss of sympathetic tone rarely presents as hypotension in children
Respiratory depression = apnea & hypoxia are the first signs of a high-spinal in infants
Endotracheal Tubes
Cuffed OETT used for children < 10 yrs old
Size = age /4 + 4
Depth of insertion = age / 2 + 12

Differences b/t Adult Airway

Head, tongue, arytenoids are larger
Larynx and glottic opening are more anterior & cephalad, C4
Larger & stiffer epiglottis
Narrowest part cricoid ring, C4



Vocal cords are in a diagonal position in larynx more likely to lodge OETT in anterior
Larynx is funnel shaped
Inhalational Induction b/c:
Greater % of CO distributed to VRG vs. adults
Greater % of extracellular TBW
Higher alveolar ventilation
Incrased blood solubility of volatile anesthetics
Diminished FRC

Other Important Facts

TBW 85% in pre-term, 75% term newborns, 60% @ 6 months
Lower PVR at birth due to (1) improved PaO2, (2) lung expansion during inspiration, (3)
alkalosis. PVR approaches adult levels at 1 year-old
Neonates have decreased GFR, ability to concentrate urine, urea clearance, and reabsortpion
of HCO3 - => pH (compared to adults)
Metabolism inhibited by erythromycin, cimetidine, Ca2+ channel blockers
H2O soluble, converted to a lipid-soluble drug when exposed to blood
Highly protein bound BZD, used IV/IM/PO
Rapid onset of action and elimination
Lack of active metabolites
Significant respiratory depression at high doses due to 6x higher potency than diazepam
Suitable for oral and IV, not IM due to pain at site of injection and unreliability of action
H2O soluble, must mix w/propylene glycol to be soluble => painful with injection
Active metabolites contribute more significantly to the sedative effect
Peak 5-8 mins
Reverses all BZD CNS effects sedation, amnestic, muscle relaxant, anti-convulsant
Has some weak anti-convulsant effects
Side effects N/V
Methylxanthines = Theophylline & Aminophylline
Inhibit phosphodiesterase inhibit cAMP breakdown amount cAMP bronchodilation
Aminophylline o
Narrow therapeutic range
o Side effects Ventricular arrhythmias & seizures, decreases the threshold of
epinephrine to induce arrhythmias.
Theophylline o
Metabolized faster in smokers
o Liver metabolism toxicity risk in CHF, liver disease
o Improves pulmonary function and resolves obstruction in asthmatic patients in a
dosedependent manner
o Decreases PVR and increases C.O. (even in presence of beta-blockade)
o Side effects > 20 mcg/ml N/V, seizures, decrease sensitivity to non-depolarizing
NMB agents (increase dose)


An anti-cholinergic most effective in preventing & treating beta-blocker bronchospasm

Best for COPD patients
Can increase viscosity of secretions

Prednisone 50 mg = Dexamethasone 7.5 mg = Hydrocortisone 200 mg

Mineralocorticoid = fluticasone
Mixed mineral & glucocorticoid = methylprednisolone, prednisone, hydrocortisone
Glucocorticoid = dexamethasone
May block chronotropy (heart rate)
Decreases sympathetic system outflow
Disrupts subsequent defibrillation and cardioversion by increasing current & energy
requirements, worsened by acidosis
Asystole has been associated with prophylactic use of lidocaine
Toxicity increases with decreased protein binding, cirrhosis
Decreased blood volume higher concentrations b/c of lower Vd
Low cardiac output
potentiates toxicity by decreasing hepatic flow
Hypokalemia potentiates cardiac toxicity, NOT CNS toxicity!
An ester, metabolized by plasma cholinesterases in the liver patient with enzyme
deficiency are at risk of sudden death
Mech: blocks uptake of catecholamines at the nerve terminal sympathetic NS activation
i.e. mydriasis
Can facilitate the development of epinephrine induced cardiac dysrhythmias during halothane
Max dose = 200 mg
Contraindicated in HTN patients or those receiving guanethidine, reserpine, TCAs, or MAO-I
Drug of choice to treat HTN crisis = labetalol
Chronic abusers of amphetamines or cocaine lower MAC
Metoclopramide dopamine antagonist
Speeds gastric emptying
Increases LES pressure
Decreases pyloric pressure
DOES NOT change gastric pH
Side effects o Dystonic, Extrapyramidal symptoms o Abdominal cramps, cardiac dysrhythmia
Competitive blocker at H2 receptors blocks histamine induced secretion of H+ from gastric
parietal cells
More potent and longer lasting (8 hrs) than cimetidine
hepatic blood flow (histamine vasodilates hepatic vessels)
Side effects o HA, fatigue, dizziness
Competitive blocker at H2 receptors blocks histamine induced secretion of H+ from gastric
parietal cells
Inhibits oxidative metabolism prolongs midazolam, diazepam, NOT lorazepam or oxazepam
that undergo conjugation rxn.
Side effects o
CV bradycardia, heart block, asystole


Resp - airway resistance by leaving unopposed H1 receptors o

confusion, agitation, hallucinations, seizures, delayed awakening o
retards metabolism of digitalis, diazepam, propranolol, meperidine,
aminophylline, verapamil, lidocaine; LFTs


Penicillin Allergy
Okay to give cefazolin as long as the allergic reaction is only a mild rash, otherwise need to
give vancomycin for more severe reactions
Mechanism: inhibits synaptic transmission in CNS by inhibiting adenylate cyclase cAMP
100% renally cleared!
Potentiates duration succinylcholine & non-depolarizers (pancuronium). NOT
associated with sux & hyperkalemia
Li is exchanged for Na+ in proximal convoluted tubules if low Na+ => high Li+, risk
toxicity, especially in patient taking diurectics
Treatment Li induced polyuria: thiazide diuretics (metolazone, chlorthalidone,
Lasix reduces renal clearance of lithium retain Lithium
o Nephrogenic DI o
Hypothyroidism due to Li blocking release of thyroid
hormones o Sedative effects = MAC
Thomboxane: (1)
vasoconstriction, (2)
platelet aggregation by inhibiting
adenylate cyclase cAMP
Prostacyclin: (1) vasodilation, (2)
platelet adhesiveness by
stimulating production of cAMP
PGF2: vasoconstriction
COX 1 constitutive enzymes
(present in
all cells)
COX 2 induced by inflammatory



Arachidonic acid prostaglandin production via cyclooxygenase or lipoxygenase

Lipoxygenase facilitates conversion of arachidonic acid to 5-hydroyperoxy-arachidonic acid
leukotrienes = potent bronchoconstrictor

Inhibits cyclooxygenase and prevents for the formation of thromboxane (a potent platelet

COX 2 inhibitors (Celocoxib, Refocoxib)

Causes very few cases of stomach ulceration
No effect on platelets or bleeding time do not need to d/c before surgery Used for OA, RA
Specific COX-1 inhibitor


Provides analgesia by inhibiting prostaglandin synthesis via inhibition of

cyclooxygenase (does not cross BBB) o
Inhibition of platelet aggregation, prolongs bleeding
10 mg Ketorolac = 50 mg Meperidine = 6 mg MSO 4
T = 6 hours
Contraindications: (1) bronchospasm/asthma, (2) angioedema, (3) nasal polyps, (4)
concurrent use of other NSAIDs, (5) allergy to ASA, (6) h/o GI bleeding or ulcer, (7) daily ASA
Side effects: renal toxicity papillary necrosis, GI ulceration, hypersensitivity
Peripheral & CNS stimulant
Selective activation of carotid chemoreceptors stimulates hypoxic drive TV &
Clinical use: mimics low PaO2, used in pts with COPD
Side effects: AVOID h/o epilepsy, CVD, acute head injury, CAD, HTN, bronchial asthma o
CNS stimulation: confusion, dizzy, seizures, tachycardia, HTN, dysrhythmias,

Effects of Cholinesterase Inhibitors CHOLINERGIC CRISIS

*volatile agents slow onset
Bronchial constriction
Pupillary constriction (miosis)
Edrophonium = Quaternary ammonium
Binds acetylcholinesterase by electrostatic attachment and strengthened by Hbonding. No appreciable inhibition of plasma cholinesterase (unlike neostigmine)
Rapid onset of action due to a pre-synaptic (i.e. ACh release) rather than a post-synaptic
(i.e., acetylcholinesterase inhibition) action
Onset is well matched to atropine little change in HR
Least muscarinic side effects
Dx of Myasthenia Gravis* since t is very short o
Used to differentiate myasthenic
vs. cholinergic crisis (over medication) improves myasthenic, but worsens
cholinergic crisis
Neostigmine = Quaternary ammonium
Is stronger than edrophonium as an inhibitor of pseudocholoinesterase, yet its inhibition of
acetylcholinesterase still predominates dose of succinylcholine will last longer after a
neostigmine reversal
Binds covalently to acetylcholinesterase
Large doses potentiate blockade!!
Can cross placenta fetal bradycardia
Relies on renal excretion in renal failure neostigmine lasts longer; reduce the
dose by 50%75%
Effectiveness decreases in ACIDOSIS
Onset: 7-11 mins
Pyridostigmine = Quaternary ammonium


Lipid insoluble cannot pass BBB

Longest t , if administer atropine with it (short t ) will see bradycardia from continue
pyridostigmine effects
Onset: 15 mins (longest)

Physostigmine = Tertiary amine

Lipid soluble, crosses BBB, GI, mucous
Rx: atropine intoxication
Almost all metabolized by plasma esterases, so renal excretion is not important
Echothiophate = Tertiary amine
An organophosphate, can cross BBB
Irreversibly binds to pseudocholinesterase & acetylcholinesterase
Prolongs Succinylcholine & Mivacurium stop medication x 3 weeks for elective
Organophosphates = CHOLINERGIC CRISIS
Most common clinical scenario is insecticide poisoning or chemical warfare (nerve gases
tabun, sarin)
Echothiophate is used to treat glaucoma
o 1st line = termination of exposure relocating patient and removing soiled clothes
Atropine to off-set muscarinic effects
o Pralidoxime to reverse nicotinic muscle weakness , acts by reactivating
cholinesterase activity
Prophylaxis in anticipation of nerve gas exposure is by Atropine to off-set cholinergic
effects will occupy a % of receptors, preventing them from binding with irreversible
Anti-Cholinergic Poisoning
Central anticholinergic effects are biphasic CNS excitation, followed by depression
Summary of Anticholinergic effects (Opposite to SLUDE) o
Hot as a hare fever,
no sweating
Blind as a bat loss of accommodation & blurred vision, photophobia
Dry as a bone no saliva, sweat or tears
Red as a beet flushed
Mad as a hatter CNS excitation, hallucinations,
ataxia o Tachycardia o Bronchial dilation o
Pupillary dilation
o *Atropine causes relaxation of Sphincter of Oddi*
Common causes of poisoning are eating seeds or flowers of:
o Dautra stramonium (jimson weed) o
Mandragora officinarum (mandrake) o
Hyoscyamus niger (henbane) o
Atropa belladonna (deadly nightshade)
Treatment induced vomiting or gastric lavage with activated charcoal. Physostigmine b/c
crosses BBB and able to treat both central & peripheral effects o
Physostigmine can
cause asystole, bronchospasm, hypotension
Anti-Cholinergic Drugs
Atropine & Scopolamine are tertiary amines penetrate BBB; can both cause central
anticholinergic syndrome, treated with physostigmine
Glycopyrrolate is poorly lipid soluble quaternary compound does not cross BBB
Scopolamine is the best anti-salagogue
Glycopyrrolate has the least effect upon pupil size (pupillary dilation), scopolamine the most


Atropine causes relaxation of Sphincter of Oddi, most increase in HR

Thiopental 2.5 % Sodium salt solution

Highly protein bound to plasma proteins (albumin), but this DOES NOT impact awakening.
Patients with uremia or cirrhosis have decreased protein binding increased effect, need to
decrease the dose
Rapid brain penetration due to high lipid solubility and low degree of ionization
Termination of action due to redistribution, metabolism and renal excretion
Awakening is due to redistribution alone!
Elimination is highly dependent upon liver metabolism, cirrhosis DOES NOT prolong a single
dose b/c metabolism is slow enough.
Weak acid (pKa 7.6, pH 10.5), thus during acidosis a greater non-ionized fraction is present
more rapidly crosses BBB decrease the dose
HD effects (1) peripheral vasodilation-venous pooling causing decline BP hypovolemia
potentiates effects, (2) sympathetic stimulation (BP would be lower if not true)
Cerebral protection is limited to focal ischemic events
Rx intra-arterial injection stellate block, heparin, intra-arterial injection lidocaine, papavarine
Water soluble imidazole
Myoclonic movements, NOT associated with EEG changes
CNS: ICP, CMRO2 & CBF due to direct vasoconstriction & coupling; NO effect on CO2
Eye: IOP
Resp: Tv, RR, MV
Side effects: laryngospasm, cough, hiccough, adrenal suppression from inhibiting the
conversion of cholesterol to cortisol
Unsafe in porphyria
Ketamine = phencyclidine
Acts through neurotransmitter L-glutamate at NMDA receptor, monoaminergic,
muscarinic, opioid, voltage-sensitive Ca2+ ion channels
Direct sympathetic stimulation indirect HR & vasoconstriction
muscle tone (hypertonous), purposeful skeletal movts
Retention pharyngeal/laryngeal reflexes, profuse secretions
airway resistance excellent for asthmatics
Direct myocardial depression with cardiac out due to sympathetic stimulation. When
systemic catecholamines have been depleted or when patient is under deep
anesthesia, myocardial depressant properties dominate.
CBF, CMRO2, ICP by cerebral vasodilation
No change in IOP!
Metabolized to norketamine, 1/5 as potent
Analgesia somatic >> visceral

Esters Local Anesthetics = Chloroprocaine, Cocaine, Procaine, Tetracaine

Metabolized by pseudocholinesterase & partially by RBC esterases via ester hydrolysis
alcohol + para -aminobenzoic acid (associated with allergic reactions)
Cocaine, tetracaine have active metabolites!
Amide Local Anesthetics = Bupivacaine, Dibucaine, Etidocaine, Lidocaine, Mepivacaine,
Prilocaine, Ropivacaine


Metabolized by microsomal liver enzymes decrease metabolism in hepatic function

(cirrhosis) or diminished liver blood flow (CHF) will reduce metabolic rate
Lidocaine has an active metabolite (MEGA) high risk toxicity in cirrhosis b/c has high 1st
pass metabolism
Prilocaine metabolites convert hemoglobin to methemoglobin. Avoid in epidural!!
Benzocaine (common in anesthetic sprays) can cause methemoglobinemia o
methemoglobinemia with IV methylene blue (1-2 mg/kg 1% solution). It reduces
methemoglobin (Fe3+) to hemoglobin (Fe2+)
Ropivacaine is the only single enantiomer (pure-S), less cardiac & CNS toxicity vs.
Bupivacaine toxicity due to blocked Na+ channels, alters mitochondrial fx hypotension,
AV block V. fib o Risk increased with pregnancy, acidosis, hypoxemia
o Treatment bretylium, amiodarone for VF, Epi for PEA, intralipid

Freely filtered at the glomerulus and not reabsorbed increased osmolality in the renal
tubules free water follows free water excreted in excess of Na+
Free radical scavenger
Vasodilation effect, dependent on dose and rate of administration
Given IV over 20 mins, takes 15 mins to work, lasting about 2 hours
Loop Diuretics = Furosemide (Lasix), bumetanide (Bumex), ethacrynic acid (Edecrin)
Inhibit Na+ and Cl- reabsorption in the medullary portion of the ASCENDING limb
Increases urinary Ca+ and Mg+ excretion
Uses: Na+ overload states, acute pulmonary edema, cardiac failure, HTN, hypercalcemia,
rapid correction of hyponatremia, alterations in BBB do not influence ability of Lasix to
decrease ICP
Side effects:
o Increased delivery of Na+ to the distal and collecting tubules increases K+ and
H+ secretion hypokalemia and metabolic alkalosis
o Marked Na+ losses will lead to hypovolemia and prerenal azotemia o
Hypercalciuria can result in stone formation o
o Deafness in high doses
Thiazide-Type Diuretics = Metolazone, Chlorthalidone, Indapamide
Reduce reabsorption of Na+ & Cl- in DISTAL convoluted tubule and part of cortical
ASCENDING loop of Henule
Competes for Cl- site at Na+-Cl- carrier protein Na+ excretion
Use: HTN, Na+ overload, hypercalciuria ( Ca+ excretion), nephrogenic DI
K+-Sparing Diuretics
(1) Spironolactone (Aldactone)

Direct aldosterone receptor antagonist in collecting tubule & distal of convoluted

tubule inhibits Na+ reabsorption and K+ secretion
Side effects: hyperkalemia, especially in patients taking beta-blockers or ACE-I; diarrhea,
lethargy, ataxia, gynecomastia, sexual dysfunction

(2) Triamterene, Amiloride


Inhibit Na+ reabsorption and K+ secretion by decreasing the number of open Na+
channels likely in the proximal tubule

Carbonic Anhydrase Inhibitors = Acetazolamide (Diamox)

Interfere with Na+, HCO3- reabsorption and prevents H+ secretion in PROXIMAL tubules
dumps HCO3- hyperCl-, hypoK+ acidosis
Uses: reduction of intraocular pressure (reduces formation of aqueous humor),
alkalinization of urine
Loop diuretics = Furosemide, Bumetanide, Ethycrynic Acid, Torsemide

Inhibit Na- & Cl- reabsorption in medullary portion ASCENDING loop of Henule
Treatment of acute pulmonary edema best choice for CHF b/c reduces pulmonary
wedge pressure before diuresis occurs. Decreases ICP, able to give with disrupted BBB

Freely filtered at the glomerulus, NOT reabsorbed increases osmolality in the renal tubules
reduced efficiency of Na+ reabsorption
Do not use if BBB is disrupted mannitol enters brain causing edema
Maximum effect in rx of ICP occurs within 1-2 hours, lasting 6 hours

60% filtered and reabsorbed

Crosses BBB rebound intracranial HTN
High incidence of venous thrombosis should extravasation occur

Aldosterone antagonist, in the absence of aldosterone, it has NO effect
Amiloride, Triamterene

Directly blocking the epithelial sodium channel thereby inhibiting Na+ reabsorption in the
distal convoluted tubules and collecting ducts in the kidneys. This promotes the loss of
sodium and water from the body, but without depleting potassium.

Acetazolamide: Carbonic Anhydrase Inhibitor

Inhibits reabsorption of HCO3 and prevents the secretion of H+ (dump HCO3) hypokalemic
metabolic acidosis

Haldoperidol = butyrophenone

Side effects:
o Anti-cholinergic effects rarely with Haldol
o Highly sedating
o -blockers orthostatic hypotension o
Lowered seizure threshold
o Cardiac toxicity in overdose prolong QT, torsades de pointe

Droperidol = butyrophenone

o Inhibits histamine-N-methyl-transferase ,which metabolizes
histamine o
Inhibits dopamine in chemoreceptor trigger zone
of medulla

Metabolized in the liver


duration of fentanyl (Innovar 50:1, droperidol: fentanyl) orthostatic hypotension

Side effects:
o Extrapyramidal reactions treat with diphenydramine
or benzoprine (anti-cholinergics that cross BBB)
o Dysphoria - unmask tremendous fear of surgery o
Cerebral vasoconstrictor = CBF, no effect
on CMRO2 o SSEPs latency and amplitude o
Peripheral -blocker = BP
o Anti-dysrhythmic, especially arrhythmias
epinephrine-induced o
Useful in WPW o
cause tachycardia o Resting CO2 response curve is NOT
altered o
Some local anesthetic effects

Parkinsonism Treated with Levodopa

Drugs that inhibit or prevent the action of dopamine in the basal ganglia o
= chlorpromazine, promazine o
Butyrophenones = droperidol
o Metoclopramide
o Viral
encephalitis o

Levodopa to the precursor of dopamine, t 1 hr.

o Metabolized in stomach & intestines 95% decarboxylated to dopamine
peripherally and will NOT cross BBB. Only 5% reaches brain for effect
o Risk of cardiac dysrhythmias from dopamine palpatations, sinus tachycardia, V.


Chlorpromazine a phenothiazine
Effective anti-psychotic drug, blocks D2 receptors
Anti-emtic, sedative
Lowers seizure threshold
Blocks anti-HTN effects of guanethidine & guanadrel
Potentiates depressant effects of narcotics
-Methyl Dopa
Pre-synaptic central
2 receptor agonist
RARE rebound HTN (more common with clonidine or propranolol)
Nicotinic AChR antagonist at autonomic ganglia blocks sympathetic &
parasympathetic outflow
Side effects mydriasis, orthostatic hypotension, tachycardia, constipation
Causes LEAST CBV & ICP compared to other anti-hypertensive drugs

Selective post-synaptic dopapmine-1 receptor agonist with significant vasodilating

Indiction short term control (<48 hrs) of HTN emergencies and malignant HTN in
patient with deteriorating end-organ function: reduced renal fx, encephalopathy, ICH,
pulmonary edema, dissecting aneurysm, acute MI

Contains sodium bisulfite AVOID in patients allergic to sulfites


Advatnages of SNP ntriuresis, diuresis, incrase Cr clearance, preserves renal function

Sodium Nitroprusside

Side effects:
o CN- & thiocyanate toxicity o
Rebound HTN o
Intracranial HTN o
Blood coagulation abnormalities o
Inhibits hypoxic pulmonary vasoconstriction shunt
hypoxemia o

Cyanide Toxicity

Toxic blood levels (= 100 mcg/dL) occur when 1 mg/kg sodium nitroprusside given over 2
hours; max rate 10 mcg/kg/min. Can see toxicity at really any level.

Definitive test = blood cyanide levels

Renal failure patients are NOT at increased risk of cyanide toxicity thiocyanate formed in
the liver by thiosulfate + CN via rhodanase accumulates. They are risk for thiocyanate
toxicity b/c diminished excretion.

Toxicity risk greatest if nutritionally deficient in cobalamines (Vitmaine B12) or dietary

substances with sulfur
1) CN- + methemoglobin cyanomethemoblogin
2) CN- + thiosulfate, vitamin B12 thiocyanate
* *rate limiting, facilitated by
in liver & kidney.
thiosulfate as sulfur donors
3) CN- + cytochrome oxidase tissue cyanide toxicity

Si/Sx: metabolic acidosis, SvO2, acute tachyphylaxis, also see dysrhythmias, N/V,
confusion, muscle weakness

Drug treatment includes:

o 1st - Sodium thiosulfate 150 mg, provides sulfur to convert cyanide into
thiocyanate. o 2nd - Sodium nitrate 5 mg/kg to oxidize Hgb to methemoglobin
cyanmethemoglobin o 3rd - Hydroxocobalamine, used especially in renal
failure patients

Thiocyanate Toxicity

Potential hazard in renal failure patients

Si/Sx: nausea, mental confusion, skeletal-muscle weakness, hyperreflexia, seizures

Mechanism: metabolized to nitric oxide (NO) in vascular SM wall cGMP SM relaxation
dilate veins > arteries myocardial O2 demand by preload & wall tension. See
subendocardial O2 delivery. Does not increase total coronary blood flow in angina
Indications: pulmonary HTN, MI, HTN
Side effects:
o Nitrate, a metabolite, can cause methemoglobinemia; Rx: IV methylene blue (1-2
mg/kg) o
Hypotension, reflex tachycardia
o Arrhythiamis
o MI
Relative contraindications: angina due to AS or IHSS, tachyarrhythmias


Peripheral post-ganglionic adrenergic blocker

Enters sympathetic neurons, replaces NorEpi in storage vesicles depleting catecholamines.
Indirect acting vasopressors (mephenteramine, ephedrine) are ineffective
Used to Rx severe HTN or IV sympathetic blocks for CRPS

Indirect sympathomimetics ephedrine, mephentermine, metaraminol

Direct sympathomimetics methoxamine (-agonist), phenylephrine, norepinephrine
1 & 2 agonist HR, SVR and bronchodilation
Chemotherapy Agents
Bleomycin pulmonary fibrosis & hypoxemia. Risk factors: elderly, 200-400 U, pre-existing
lung disease, prior radiotherapy and high concentration of O2 during surgery
Doxorubin cardiomyopathy
Cyclophosphamide cardiomyopathy, inhibition plasma cholinesterases
Vincristine peripheral neuropathy, impaired sensorium, encephalopathy & renal toxicity
ALL cause bone marrow suppression (e.g. anemia, thrombocytopenia)
Selectively inhibits helpter T-cells, NOT B-cells
Side effects nephrotoxicity, HTN, limb paresthesias (50%), HA, confusion, seizure, high
LFts, gum hyperplasia, hirsutism, hyperglycemia


Celiac Plexus Block


EtOH is most effective

tumors present in pancreas, liver, gallbladder,
stomach, adrenal glands, kidney, spleen,
transverse colon
Formed from the greater and lesser splanchnic nerves
at L1 vertebral body
Posterior to vena cava on the right
Lateral to aorta on the Left (aortic drifts to the right)
Posterior to pancreas

Side effects
Orthostatic hypotension (most common) correct
with fluid bolus LR
Intravascular injection into the vena cava is more
likely to produce a severe systemic rxn than intraaortic
SAB is the most serious complication
Retroperitoneal hematoma (rare)
Diarrhea unopposed parasympathetics

Lumbar Sympathetic Block

Indication pelvic or LE pain (i.e. peripheral vascular disease)
o L2 vertebral level o
Anterior to the psoas
muscle o Right - Posterior
to vena cava o Left Lateral to aorta
Side effects
o Puncture of a major vessel, renal pelvis, or disk o Neuralgia L1 o
nerve damage genitofemoral N.
o Ejaculatory failure o Chronic back pain
Completeness of block is ascertained by skin temperature ( 2C) measurements and
increases in blood flow.
o Blood flow determined by laser Doppler flowmeter, occlusion skin plethysmography,
transcutaneous oxygen electrodes, mass spectrometry

Hypogastric Plexus Block

Indication pain in the pelvis that is unresponsive to lumbar or caudal epidural blocks;
cancer of cervix, uterus, bladder, prostate, or rectum, chronic nonmalignant pelvic pain
o Contains post-ganglionic fibers from lumbar sympathetic chain & visceral sensory
fibers from cervix, etc
o Superior hypogastric plexus lies at L5
Ganglion Impar Block
Indication visceral or sympathetically maintained pain in the perineal area


Anatomy the ganglion impar is the most cadual part of the sympathetic trunk located
midline, anterior to the coccyx

IV Regional Sympathetic Blockade

A Bier block using guanethidine, reserpine, bretylium can selectively interrupt
sympathetic innervation
Guanethidine causes depletion of NorEpi and inhibits its reuptake at the post-ganglionic
Blockade lasts 3-7 days
Premature TQ release hypotension, bradycardia, edema, diarrhea, nausea
Safe alternative to standard sympathetic blocks in those with hemostatic issues
Bier Block
Duration determined soley by tourniquet time, once released the block is rapidly lost,
regardless of type or amount of agent used
0.5% lidocaine, 40 ml; Prilocaine is most rapidly metabolized = least toxic
TQ inflated 100 mg above systolic pressure, minimum time 30 mins, max time 2 hrs
Stellate Ganglion Block
Indications: patients with head, neck, arm
and upper chest pain; vasospastic disorders
of the upper extremity
Anatomy: fusion of the lower cervical and
1st thoracic ganglia. Lies between the base
of the TP of C7 and the neck of the 1st rib.
Sends post-ganglionic fibers to cardiac
plexus o
Anterior to ganglia:
carotid sheath, sternocleidomastoid
o Anterior and inferior: dome of the lung
lies anterior and inferior
o Medial to ganglia: prevertebral fascia,
vertebral body of C7, esophagus, and
thoracic duct
o Posterior to ganglia: longus colli muscle,
anterior scalene muscle, vertebral artery,
brachial plexus sheath, and neck of the first

Technique: needle inserted at medial edge of SCM just below the level of the cricoid cartilage
at the level of the TP of C6 or C7.
Success interruption of sympathetic supply = Horners syndrome ipsilateral ptosis,
myosis, enophthalmos (sunken eye ball), unilateral nasal congestion, anhydrosis, flushing of
the conjunctiva & skin.
Complications: intravascular, SAB, hematoma, pneumothorax, epidural anesthesia, brachial
plexus block, hoarseness from recurrent laryngeal nerve (avoid bilateral blocks), osteitis or
mediastinitis following esophageal puncture
If block fails, using guanethidine or reserpine can be used with Bier block technique.

Trigeminal Nerve Block (Gasserian Ganglion Block)

Indications: trigeminal neuralgia & intractable cancer pain in the face


Anesthesia of the ipsilateral face, cornea, sclera, anterior tongue (posterior tongue by
CN IX) o
Trigeminal neuralgia: sharp facial pain in the maxillary br of V2 o
Definitive Rx: neurolytic block with glycerol or pulse radiofrequency ablation o
Pharmacologic Rx: carbamazepine
Anatomy: CN V roots join one another to form the gasserian ganglion in Meckels cave
(middle cranial fossa) which contains CSF risk total SAB

Brachial Plexus
Anterior primary divisions (ventral rami) of C5-T1
Roots, Trunks, Divsions, Cords, Branches (Robert Trunk Drinks Cold Beer)
Brachial plexus begins with 5 nerves and terminates with 5 nerves (ARM MU): Axillary,
Radial, Median, Musculocutaneous, Ulnar
In the axilla, 3 cords are formed, named by relationship to the axillary artery:
o Lateral cord (flexor surface): superior and
middle trunks
lateral head of the median nerve (C6-T1)
terminates as musculocutaneous nerve (C4-6) o
Medial cord (flexor surface):
inferior trunk
medial head of the median nerve (C5-T1)
terminates as ulnar nerve (C8, T1)
medial antebrachial nerve
medial brachial cutaneous nerve o
Posterior cord (extensor surface): posterior
division of all 3 trunks
axillary nerve (C5-6)
terminates as radial nerve (C6-T1)
Interscalene block
Progresses proximal to distal, interosseous muscles (abduct & adduct fingers) are most
distal & last blocked, innervated by ulnar nerve
If need to cover skin over the shoulder, must block superficial cervical plexus (C1-C4) at
posterior border SCM
Onset of block is faster than either supraclavicular or axillary
Supraclavicular block
Blocks trunks (superior, middle, inferior)
**Miss suprascapularis nerve which supplies supraspinatus, infraspinatus, shoulder
capsule** Axillary Nerve Block
Best for procedures distal to the elbow
Proximal spread of L.A. in axillary perivascular space is promoted by (1) increased volume of
agent, (2) digital pressure distal to injection site, (3) cephalad direction of needle, (4)
adduction of shoulder after injection
(1) Musculocutaneous nerve (C6 dermatome) - sensory to lateral forearm, motor to
coracobrachialis & biceps, must block with injection into the coracobrachialis.
(2) Intercostobrachial nerve (T2 dermatome) apex of axilla
(3) Median cutaneous nerve medial upper arm (part of T2 dermatome)
Radial Nerve


Radial nerve is motor to arm, forearm, wrist extension; innervates triceps; sensory to mid
forearm, wrist, extending onto (medial) dorsum hand and small bit of thenar (palmar surface)
At the wrist lateral to medial: N A / N / A N radial n. - radial a. - flexor carpi radialis
median n. - palmaris longus - ulnar a. - ulnar n.
At the elbow 4 fingers above the lateral epicondyle, b/t brachioradialis & biceps
Injury wrist drop

Ulnar Nerve
Motor to all hand muscles (interosseus), except 1st & 2nd lumbricals & thenar muscles (median
n.); sensory little finger & medial of ring finger (palmar & dorsal sides)
At the wrist
N A / N / A N medial to ulnar a.
At the elbow b/t olecranon & medical epicondyle
Injury interosseus atrophy = clawed hand
Median Nerve
Motor to thenar eminence & 1st & 2nd lumbricals, wrist & finger flexion, allows you to oppose
thumb and little finger
Sensation palmar aspect of thumb, palmar aspect lateral 2 fingers + finger tips dorsal
At the wrist N A / N / A N radial n. - radial a. - flexor carpi radialis median n. palmaris longus - ulnar a. - ulnar n.
At the elbow medial to the brachial artery b/t 2 heads of pronator teres
Injury thenar atrophy
Absorption rates of local anesthetics
IV > intra-tracheal > intercostal = intrapleural > caudal > epidural > brachial plexus >
sciatic Neurolytic Nerve Blocks
Not used directly on peripheral nerves b/c risk development of denervation dysesthesia
Used in epidural block bilateral block
Used in subarchnoid unilateral block
Ethanol 100% (hypobaric) cause more intense neural destruction and is more painful
Phenol 5-10% in glcerine (hyperbaric) gives a more predictable block, painless b/c dual
action as a local anesthetic & neurolytic. Initial block wears off in 24 hrs then neurolysis



Lumbar plexus = ventral rami of (T12) L1-L4 o
Femoral: posterior divisions of L2-L4 o
Obturator: L2-L4 o Lateral femoral cutaneous: L2-L3
o Genitofemoral o
Ilioinguinal o Iliohypogastric
Sciatic nerve: L4-5 and S1-S3
Femoral Nerve and Three-in One Block
Sensory: anterior thigh from inguinal ligament to the knee; medial side of leg below the knee
to big toe via saphenous n.
Motor: anterior compartment = quadriceps, sartorius, pectineus muscles knee
extension & hip flexion
Obturator Nerve Block
Exits the pelvis and enters the medial thigh via obturator foramen, just beneath the superior
pubic ramus
Sensory: hip, lower medial thigh
Motor: hip/thigh adductor muscles
Technique: needle inserted 2 cm lateral and 2 cm inferior to pubic tubercle. Needle is
walked off the superior ramus and advance 3-4 cm until it enters the obturator foramen, 1520 ml
Lateral Femoral Cutaneous Nerve Block
Sensory: anterolateral thigh to the knee & lateral thigh from hip to mid-thigh
Technique: needle inserted 2cm medial and 2 cm caudal to ASIS
Sciatic Nerve Block
Used for all procedures on the lower extremity that do not require a tourniquet. Can only use
as sole technique for surgery on the sole of the foot, otherwise needs to be supplemented.
Leaves the greater sciatic notch beneath the piriformis, courses b/t the greater trochanter
and ischial tuberosity popliteal fossa to divide into tibial & common peroneal nerves
Sensory: posterior thigh, everything below the knee except a medial strip supplied by the
saphenous n.
Motor: hamstrings, all muscles of the leg and foot
Classic Technique of Labat:
Lateral position: ipsilateral hip & knee are flexed and line drawn connecting the
greater trochanter and PSIS at midpoint, 4 cm perpendicular line is drawn caudally
(Labatts lines) now a 3rd line is drawn b/t greater trochanter and the sacral hiatus,
which will cross the perpendicular at a point 35 cm along the line



Compartment Block = Block of lumbar plexus at L4

Lumbar plexus lies b/t psoas and quadratus lumborum muscles at level of L4-5
Provides anesthesia of the hip flexors and LE
More effective at blocking the lateral femoral cutaneous and obturator nerves than anterior
approaches I.e. Winnies 3-in-1 block
Technique: patient in lateral position, knees tucked on chest, L4 spinous process marked.
Mark a point 3 cm caudal and 5 cm lateral from the L4 spinous process. Insert needle until
transverse process of L5 is hit walk off medial and cephalad until quadriceps or adductor
twitch is obtained or lateral femoral cutaneous nerve paresthesia
Complications: Epidural spread of L.A. can occur causing block of the contralateral leg or

Ankle Block

5 nerves supply sensation to the foot:

1. Saphenous (terminal br of femoral n.)
Anterior to medial malleolus
Sensory: anteromedial leg & medial foot
2. Deep peroneal
b/t anterior tibial and extensor hallucis longus tendons
Lateral to anterior tibial artery & extensor hallucis longus
Motor: toe extensors
Sensory: medial half of the dorsal (top) foot & web space b/t great & 2nd toes
3. Superficial peroneal
Lateral to extensor digitorum longus at the level of the lateral malleolus


Sensory: dorsum (top) of the foot and all 5 toes, except b/t great & 2nd toes

4. Posterior tibial
Posterior to medial malleolus with posterior tibial artery, branching into lateral and
medial plantar nerves & medial calcaneal branches
Sensory: heel (medial calcaneal br), plantar surface of the foot (plantar n)
Motor: plantar flexion & inversion
5. Sural
Continuation of the tibial nerve & 1 br of common peroneal nerve
Between the Achilles tendon and posterior to lateral malleolus
Sensory: lateral foot, lower posterolateral leg, 5th toe

Deep peroneal, superficial peroneal, and saphenous nerves can all be blocked using a
single injection site
At ankle only sensory only nerves = sural, saphenous, superficial peroneal


Superficial Cervical Plexus Block
Useful for carotid endarterectomy
Adjunct to interscalene block for shoulder
surgery to get tip of shoulder
Cervical plexus is formed from anterior
(ventral) rami of C1-C4, emerging from
platysma muscle lateral (posterior) to SCM
Sensory: jaw, neck, occiput posteriorly
and areas of the chest & shoulder close to
the clavicle
Complication: anesthetize phrenic, RLN,
cervical sympathetic chain, NOT spinal

Intercostal Block
Exits from the spine at the intervertebral foramen and travel along the underside of
the corresponding rib, with artery & vein; nerve is most inferior (VAN)
Technique: mid & posterior axillary line.
Complications: highest blood levels of L.A. per volume injected of any block in
the body
Common Nerve Injuries

Brachial plexus stretching by head of the humerus or compression b/t clavicle & 1 st
Radial n. wrist drop (cant extend metocarpophalangeal jts), weakness thumb
Median n. inability to oppose thumb and little finger, loss sensation palmar
surface lateral 3 fingers
Ulnar n. due to compression of posterior aspect of medial epicondyle of humerus
inability to abduct little finger, loss sensation over both dorsal & palmar surfaces of
medial 1 fingers
Sciatic n. due to stretching in lithotomy position weakness below the knee and
loss sensation of all of the foot EXCEPT inner arch (saphaneous n.)


Common peroneal n. - **most commonly injuryed n. in lower extremity** due to

compression b/t head of fibula and metal brace used in lithotomy position foot drop,
loss of dorsiflexion and inability to evert foot (PED = peroneal/dorsiflex/evert)
Femoral n. injured at pelvic brim by retractor or excessive thigh angulation in
lithotomy loss of hip flexion & knee extension, loss sensation over superior aspect of
Saphenous n. injured if foot is suspended lateral to vertical brace loss sensation
ONLY (no motor component) over anteriomedial aspect of leg & medial aspect
foot/inner arch
Obturator n. injured during difficult forceps delivery or excessive flexion of thigh
inability to adduct leg & loss sensation over medial aspect of thigh



ABGs for certain physiologic states

Hiker at altitude




Criteria for extubation

Stable vital signs, RR < 30-35
Afebrile, no inotropic support
ABG on 40% PaO2 > 70, PaCO2 < 55
MIF < -20 cm H2O
Vital capacity > 15 ml/kg ( 70 kg = > 1 liter)
Criteria for intubation
RR > 35
Vital capacity < 15 ml/kg and 10 ml/kg children
MIF < - 20 cm H20
PaO2 < 70 mmHg on 40%
PaCO2 > 55 (except in those with chronic hypercarbia)
A-a gradient > 350 on 100%
Vd/Vt > 0.6
Measurement of Negative inspiratory force (NIF) or max inspiratory force (MIF)
Patient cooperation
Hope in adapter to OETT is occluded
Fresh gas is NOT flowing during measurement
After the effort, the hole (pop-off valve) is opened
No rebreathing bag is necessary for measurement
ABG concentration gradients
Room air, alveolar PAO2 is 150 mmHg, while arterial PaO2 is 75-100 mmHg
Room air PCO2 is very small, while arterial PaCO2 is 40 mmHg
Air bubble in ABG syringe would result in higher PaO2, lower PaCO2
Effects of PEEP
FRC decreases shunting (ventilation without perfusion)
dead space (ventilated, but not perfused) by opening up West zone 1
Vd/Vt ratio
pulmonary compliance
extravascular lung water
Factors that

increase closing capacity (= closing volume + residual volume)

Chronic bronchitis
LV failure


Supine position

Decreases in FRC (PANGOS) Increases in FRC

- Emphysema
- Elderly
General anesthesia
Supine position
A-a Gradient
Room air, A-a gradient = 5-10 mmHg
100%, A-a gradient = 10-20 mmHg
If A-a gradient > 350 mmHg on 100% INTUBATE
Most common cause of increased A-a gradient is SHUNT
Each 20 mmHg of A-a gradient = 1% shunt

A-a gradient = age


Shunt Equation
Qs/Qt = CcO2 CaO2
CcO2 CvO2

% shunt = A-a gradient


If >30% shunt (normal 5%), administration of O2 is ineffective in increases PaO2

Causes of shunt: thesbesian veins, bronchial veins, R L shunt, PTX, bronchospasm,
General anesthesia increases venous admixture to 5-10% due to atelectasis and airway
collapse in dependent areas of the lungs

Dead Space
Vd/Vt = PaCO2 PETCO2, normal < 0.3 (intubate if > 0.6)
Normal Vd = 150 ml or 2 ml/kg = weight in lbs.
Normal Vt = 450 ml or 6 ml/kg
Factors that increase physiologic (anatomic + alveolar) dead space (thus Vd/Vt)
Upright position
Hypotension, hypothermia, hypovolemia
PE, pulmonary hypoperfusion
Positive pressure ventilation
Neck extension
General anesthesia
ARDS maybe due to hypoxic vasoconstriction
Shock/low cardiac output
Factors that decrease dead space (thus Vd/Vt)


Neck flexion
Artificial airway
Increased cardiac output increases perfusion to apical zones (West zone 1) of the lung

Causes of Low Mixed SVO2: COAL

Cardiac output low
Oxygen consumption high
Anemia severe
Loading problems caused by right shift Hgb curve with increased unloading at the tissue
level, resulting in decreased O2 as it returns to the right heart)
SvO2 = SaO2%
mL/min x Hgb/dL x 1.34

ml O2/g Hgb

Increase SvO2
permeanently wedged PA catheter
Cyanide toxicity due to (VO2)
Methemoglobinemia (VO2)
Sepsis (VO2)
Hypothermia (VO2)
High C.O. states burns, L R
shunts, AV fistula, excessive
inotropic drugs,
hepatitis, pancreatitis
Side effects of Bicarbonate
L shift Hgb curve due to
Intracerebral hemorrhage 90%
Left shift Hgb Curve = Hgb

Decrease SvO2

Low SaO2
Low C.O. MI, CHF, hypovolemia
High VO2
Right shift Hgb curve

700 mmHg
100 mmHg
60 mmHg
40 mmHg
26 mmHg

rebound alkalosis (pH)

affinity for O2, P50 < 26

Cyanide, nitric acid, ammonia all combine with Hgb at O 2 binding sites displace O2
Methemoglbinemia, carbon monoxide, sulfhemoglobin, fetal hgb
H+ = metabolic & respiratory alkalosis
2,3 DPG (occurs with blood txn)

Right shift Hgb Curve = Hgb affinity for O2, P50 > 26 mmHg
H+ = metabolic & respiratory acidosis
2,3 DPG
Abnormal hemoglobins sickle cell (P50 = 31), thalassemia
Volatile anesthetics at 1 MAC
Bohr Effect
The effects of PaCO2 and pH on the position of the oxyhemoglobin dissociation curve
Attributed primarily to the action of CO2 and pH on erythrocyte 2,3 DPG metabolism


Hgb is oxidized to ferric (3+) unable to bind O2 & left shift Hgb curve, difficult to unload O2

Adequate PaO2, but SpO2= 85%
Chocolate urine & blood
Cyanosis when methemoglobin > 1.5 gm/dl
2 types
(1) congenital
(2) acquired i.e. nitroglycerin, nitroprusside, EMLA cream, benzocaine, phenacetin, Prilocaine
due to metabolism to o-toluidine oxidizes Hgb
Treatment: methylene blue 1-2 mg/kg, if fail then require exchange transfusion

Non-smokers 1-3%, smokers 15%
Si/Sx: HA, dizzy, N/V, confusion, cherry red skin of COHb >40%
CO can result from interaction of desiccated absorbent, soda lime or baryalyme 30% level.
Predisposition to production of CO: o Degree of absorbent dryness o Use of Baralyme
o High concentration of volatile anesthetic (more CO at higher
concentrations) o High temperatures o Type of volatile used:
desflurane >> sevoflurane

Diagnosis: Overestimated SpO2 in presence of normal or low PaO2 o Carotid

bodies are sensitive to PaO2, not dissolved O2 no tachypnea o Must measure
COHb using spectrophotometer (co-oximeter)

Treatment: Oxygen!
o T CO 4-6 hrs while on room air, reduced to 1 hr on 100%
o If hyperbaric therapy fails, consider transfusion fo blood, sedation to alter O 2 demans,
diuretics, steroids

Hyperbaric Oxygen therapy if: o

Carboxyhemoglobin >30% o
Pregnancy with levels > 15% o
Signs of cardiac ischemia or
arrhythmias o
Hx of CAD with
levels > 20%
o No improvement in symptoms after 6 hours on 100% O2
TPN HASComplications

Hypo & Hyperglycemia

Hypophosphatemia Left shift Hgb curve, muscle weakness & respiratory failure
Acid (fatty) deficiency
Acidosis (metabolic) as amino acids are metabolized, HCl is liberated

Gaussian distribution = data sets follow a normal distribution around a center point.
Derived from the assumption that there is a center, true value and that deviations from the
center are random and diminish in likelihood the farther the values get from the center
When data follow a normal distribution or any specific mathematical distribution, the methods
of parametric statistics can be used refers to the ability to describe the distribution when
a specific set of values


Frequently data does not follow a normal distribution non-parametric statistical methods
need to be used

Measures of Central Tendency

Median = middle data point if the data can be ordered from smallest to largest
Mean (average) = average value of the numerical data, with each data point being counted
Mode = most common value in a set of data points
Example: data set of 2, 2, 3, 7, 14
- median = 3
- mean = 5.6
- mode = 2
Measures of Dispersion
Standard deviation (SD) o
68% of observations fall within 1 SD of the mean
(average value) o
95% of observations fall within 2 SD of the mean o
99.7% of
observations fall within 3 SD

The larger the SD, the wider the bell-shaped curve, and the smaller the SD, the
narrower the curve

1ST step is to choose the variables that will be used as independent variables
Univariate analysis only one variable is used for the data fit, and the data are plotted and
the computations performed by using that one variable to describe the data.
o i.e. the weights of a group of subjects may be compared with their heights
Multivariate analysis more than one variable can almost always be used to determine an
outcome o
i.e. the subjects weight might be analyzed by using heights, ages, and gender
Null hypothesis = there is no difference b/t 2 groups of data
Alternative hypothesis = there is a difference b/t 2 groups of data
A level of significance, termed the alpha () value, and declare that if P < alpha, the result
is statistically significant and accepted as true
If P > alpha we reject the hypothesis = accept the null hypothesis that there is no difference
b/t 2 groups of data
P value is the chance that the null hypothesis was true
Typically alpha = 0.5 (5%) and desire P < 0.5 if, in fact, there was no association in the
population b/t the independent and dependent variables, the observed association would be
expected to occur by chance less than 5 times in 100 samples.

Beta error probability of falsely accepting the null hypothesis
Power = 1 = 1 probability of making type II error
Sample size sample size = power
As power increases, the chance of a type II error () decreases
Type I error ()
Rejecting null hypothesis incorrectly (should have been accepted)
Probability of observing difference between 2 groups when there is actually no difference
E.g. positive pregnancy test in a patient that is not pregnant


Type II error ()
Accepting null hypothesis incorrectly (should have been rejected)
Probability of observing no difference between 2 groups when there is actually a difference
E.g. negative pregnancy test, when in fact patient is pregnant
Confidence Intervals
A range of values may be given such that it is determined with some likelihood (often picked
at 95%) that the true values lie within that range
For expressing simple results, the CI is equivalent to providing a mean +/- SD
Observational study: if CI includes 1 findings are NOT statistically significant
Randomized control trial: if CI includes 0 findings are NOT statistically significant


true positives
false negatives

no disease
false positives
true negatives

sensitivity = TP/(TP + FN)

specificity = TN/(TN + FP)

Sensitivity = ability of the test to rule in the

Specificity = ability of the test to rule out the disease o
TP = patient has disease, test
(+) o FP = patient does not have disease, test (+) o
TN = patient does not have disease,
test (-) o
FN = patient has disease, test (-)

Must first determine what kind of data is being collected --- categorical or
Categorical = male/female; blood type; sick/well; receive drug/dont receive drug. One
either has it or not, one receives a drug or not. There is NO average.
o Requires chi-square
Continuous = blood pressure; weight; height; reaction time. These are numbers and taking
an average makes sense. I.e., taking an average blood pressure makes sense, but taking an
average of maleness does not.
o Requires linear regression or student t-test
Students t-test
Most valid for comparing mean values of 2 groups!!
Considered a robust test, especially when small sample size < 30
Used to test the null hypothesis that there is no difference b/t 2 means, 3 circumstances:
o To test if a sample mean differs significantly from a given population mean
o To test if the population means estimated by 2 independent samples differ
= unpaired t-test o
To test if the population means estimated by 2
dependent samples different significantly = paired t-test

Paired t-test used if the means for the 1st category come from the same people as the
means in the 2nd category. Occurs when you can test the same people under 2
conditions or circumstances

Analysis of variance
Must use when 3 or more means are present
Identical to the t-test when more than 2 means are being compared


Chi-Square Test
Most appropriate test to determine statistical significance
When the exposure (independent variable) and the result (observed data) are both
The only method used to evaluate whether categorical data is associated with categorical

OBSERVATIONAL studies = data is gathered without performing any specific intervention

the assignment of groups or effect on group members

Case report = individual case or group of cases is reported

Cross-sectional (prevalence) study = exposure and disease assessment examined at

one point in time (lacks incidence)

Case-control study = groups of subjects are compared, usually in regard to the effects
of some intervention. However, the factor separating the groups is determined AFTER
the intervention
Comparison groups defined by outcome (disease) and look
historically for exposure.
Persons are followed over time to determine the frequency of disease occurrence.
Cases are compared to controls.
Can be done prospectively or retrospectively

Cohort study = groups of subjects are compared, usually in regard to the effects of
some intervention, followed over time
Study group is monitored BEFORE the intervention
Relative risk used to measure of strength of association between exposure and

o Randomized controlled trial (RTC)
reason to randomize: equally distribute confounding factors
between groups
assessment: single blind vs. double
Strengths of RCT design

Limitations of RCT design

- avoids selection bias and confounding

not always ethically justifiable
not suitable to study risk factors (i.e. smoking)
- ideal to study effect of treatment
- provides evidence that intervention preceded
- not always practical:
- patients and providers must relinquish freedom
- allows quantitative measure of benefits
- inefficient for rare or delayed outcomes
- allows quantitative measure of adverse events
- limited number of interventions studied at one
- convinces skeptics time
- time and money are required

Selection bias occurs when we are comparing groups with respect to some
variable, but do not realize that the groups are different in other ways o


More problematic in case-control & retrospective cohort studies because

exposure & outcome have occurred at time individuals were selected into study
o Prospective studies are best to eliminate selection bias because individuals are
selected prior to occurrence of outcome

Confounding bias occurs when multiple variables are intimately intertwined so

that although we may assume that the variable under study is important, the truth
is that the confounding variable is more important o
i.e. b/c DM is very closely
correlated to obesity, a result that purported to be about obesity might easily be
more accurate about DM

Measurement bias occurs if the methods used for making measurements when
comparing different groups have different scales or sensitivities o
consider attempting to get a h/o chest pain in groups of patients with and w/o
known CAD. Patients who know they have heart disease might be imagined to
remember brief pain more thoroughly than healthy patient do
o Minimized in blinded studies

**Odds ratio
odds ratio (OR) =


Blood flow distribution

Upright and supine positions Right lung = 55% total blood flow, Left lung 45%
Gravity causes a vertical gradient in distrubtion of blood flow in lateral decubitus position
dependent lung has significantly greater flow.
Rigid Bronchoscopy
Venturi jet ventilation (ventilation through side port) relies on 50 psi successful
oxygenation and normocarbia. Best used with paralyzed patient, chest wall passively
relaxes to complete exhalation
Disadvatnages of HFV (high frequency ventilation) adequacy of ventilation cannot be
judged from motion of chest or lung, use of anesthetic agents is high, assessment of lung
volume is difficult
Obstructive and Restrictive Lung Disease

VC (> 60 ml/kg)
FRC (= wt in lbs.)
Spirometry, Flow-Volume Loops

Normal or

Normal or


Variable Extrathoracic Obstruction o Inspiration = pressure around the

extrathoracic airway is atmospheric, and the transmural pressure favors narrowing
o In the presence of a nonrigid extrathoracic obstruction, such as bilateral vocal cord
paralysis, there is a decrease in airway pressure distal to the obstruction, which causes
further narrowing and obstruction of the airway
o The flow-volume loop will show a flattening of the inspiratory component AND ratio
expiratory:inspiratory flow at mid-vital capacity > 2.0 L

Variable Intrathoracic Obstruction o Expiration = pleural pressure becomes positive

relative to the airway pressure, which favors narrowing of the intrathoracic airway o
In the flow-volume loop it is seen as a flattening of the expiratory component


Fixed Upper Airway Obstruction o

When the airway obstruction is rigid, as in
tracheal stenosis or intraluminal tumors, the flow will be limited during both
inspiration and expiration, flattening both components of the flow-volume loop


Best test for assessment of small, peripheral airways is FEF25-75 and MMEF
CANNOT measure FRC & RV by spirometry
DLCO determined by:
Area & thickness of alveolar membrane
Glood/gas solubility & MW of gas
Transmembrane partial pressure difference of the gas
Pulmonary blood volume
Hgb concentration
DLCO => anemia, emphysemia, dehydration, pulmonary HTN
DLCO = Asthma (unknown mech.)

Chronic Bronchitis

Dx = productive cough on most days of 3 consecutive months x 2 years

Intrapulmonary shunting is prominent, hypoxemia is common blue bloater
erythrocytosis, pulmonary HTN, right heart failure chronic CO2 retention
Clinically severe hypoxia (PaO2 < 65 mmHg) and hypercarbia (PaCO2 > 45 mmHg),
congestion on CXR


Loss of elastic recoil premature collapse during exhalation patients purse their lips to
delay closure of small airways pink puffers
Clinically DYSPNEA
Destruction of pulmonary capillaries in alveolar septa DLCO pulmonary hypertension
Normal PaCO2 & overinflation on CXR


Perfusion favors the dependent (lower lung), ventilation progressively favors the less
perfused upper lung V/Q mismatch increasing hypoxemia


The Awake State

Ventilation & perfusion (V/Q) are preserved during spontaneous ventilation in the lateral
decubitus position
The lower lung receives more perfusion & more ventilation o
More perfusion due
to gravity
o More ventilation due to more efficient contraction of the dependent (lower)
hemidiaphragm b/c it assumes a higher position and has a more favorable
compliance curve
Induction of Anesthesia
Upper lung to a more favorable compliance, but the lower lung to a less compliant position
upper lung is ventilated more, but lower lung (dependent) continues to have greater
perfusion V/Q mismatch
Positive Pressure Ventilation
PPV favors the upper lung in the lateral position b/c it is more compliant
Muscle paralysis enhances this by allowing abdominal contents to rise further against the
dependent hemidiaphragm and impede ventilation of the lower lung
Collapsed lung continues to be perfused and no longer ventilation large R-to-L shunt (2030%)
Mixing of unoxygenated blood from the collapsed upper lung with oxygenated blood from
the still ventilated lower lung (dependent) wide PA-a O2 gradient hypoxemia
HPV decreases blood flow to non-dependent lung by 50% i.e. non-dependent lung
should be able to reduce its blood flow from 40% to 20%

Factors known to inhibit HPV worsen R-to-L shunt o

Very high or very low PA
pressures o Hypocapnia done by hyperventilating the dependent lung o High or very
low mixed venous O2
o Vasodilators such as nitroglycerin, nitroprusside, agonists (e.g. dobutamine, isoproterenol,
salbutamol), Ca2+ blockers
o Pulmonary infection o
Inhalation anesthetics
especially Halothane

Factors that decrease blood flow to the ventilated (dependent) lung counter act
the effect of
HPV by indirectly increasing blood flow to the collapsed lung o
High mean peak airway pressures in the ventilated lung o
Low FiO2 HPV in the ventilated lung o
Vasoconstrictors that may have greater effect on
normoxic vessels o
Intrinsic PEEP that develops due to
inadequate expiratory times
CO2 elimination is not affected by one-lung ventilation provided minute
ventilation is unchanged arterial CO2 tension is usually not appreciably altered


Indications for Double-Lumen Tube/One-Lung Ventilation


(1) Avoid contamination of blood and/or pus

Pulmonary abscess or infection
Pulmonary hemorrhage
(2) Control the distribution of ventilation
Bronchopleural fistula
Lung cysts or bulla
Tracheobronchial disruption
(3) Perform unilateral bronchopulmonary lavage (BAL)
(4) Surgical exposure
Repair of thoracic aortic aneurysm
Upper lobectomy
Esophageal surgery
Single lung transplant
Management of One-Lung Ventilation
Hypoxemia during one-lung ventilation requires intervention: most important
problem is shunt ( =perfusion, w/o ventilation)
1. Check tube position with fiberoptic scope
2. Ventilate with 100% oxygen
3. Periodic inflation of the collapsed lung with oxygen
4. Treat with CPAP-PEEP:
5-10 cm H2O of CPAP to the collapsed/non-ventilated lung
5-10 cm H2O of PEEP to the ventilated lung
Place a ligature around the PA to the nonventilated lung to shunt

Methods for Ventilating the Dependent Lung o FiO2 of 1.0

protects against hypoxemia & promotes vasodilation resulting in
PaO2 150-

250 mmHg
High FiO2 can cause absorption atelectasis, oxygen toxicity, bleomycin-induced
injury o
Ventilate dependent lung with VT = 10-15 ml/kg; > 15 mg/kg
PVR, shunt blood to the non-ventilated lung
Maintain PaCO2 = 40 mmHg. Hypocarbia vasodilates lung vasculature &
inhibits HPV o
CPAP to the non-dependent lung is the most effective way to
PaCO2 elminiation. CPAP
= 5-10 cm H2O maintains patency of nondependent alveoli allowing gas
exchange o
PEEP to the dependent lung FRC & improves gas exchange.
PEEP may compress small interalveolar vessels increasing shunt to the nondependent lung ultimately PaO2

Factors Affecting Oxygenation During One-lung Ventilation o

Degree of active
hypoxic pulmonary vasoconstriction (greatest benefit when 30%-70% of the lung is made
o Increased pulmonary vascular pressure mitral stenosis, volume overload, mitral
insufficiency, pulmonary embolism (SM cant constrict against high vascular pressure)
o Vasoconstrictor drugs preferentially constrict normoxic lung vessels and defect
HPV mechanism
o Surgical ligation of the pulmonary artery for pneumonectomy improves oxygenation
by removing perfusion to the unventilated lung


Alternatives to One-Lung Ventilation o

Ventilation can be stopped for short periods
if 100% O2 is insufflated at a greater rate than O2 consumption (apneic oxygenation)
o PaCO2 rises 6 mmHg in 1st minute, 3 mmHg during each
subsequent minute o High-frequency PPV and high-frequency jet
ventilation using single-lumen ETT


Small cell = 20% incidence
Central masses with endobronchial lesions
Paraneoplastic syndromes ACTH (Cushings syndrome), arginine vasopressin
(hyponatremia), parathyroid hormone (hypercalcemia)

Lambert-Eaton syndrome o
Seen with bronchial carcinomas
o Antibody-mediated destruction of pre-synaptic voltage gated Ca2+
channels deficient release of ACh at NMJ muscle weakness o
Proximal myopathy, muscle strength increases with repeated
o Autonomic disturbance hypo- or hypertension, sinus tachycardia, diaphoresis
No improvement with administration of anticholinesterases o
sensitivity to both depolarizers & non-depolarizers; risk of sux induced hyperK+
Required A-line for BP monitoring given dysautonomia
o Treatment - plasmapheresis or IV immunoglobulins and supportive care;
Guanidine hydrochloride and 3,4 diaminopyridine (DAP) increase level of
ACh and improve symptoms
o Death may occur if severe pulmonary complications & dysautonomia are

Non-small cell = 80% squamous cell, adenocarcinomas, large cell; peripheral lesions
involving the pleura adenocarcinoma occurs in non-smokers
Clinical Manifestations
Involvement of mediastinal structures:
o Hoarseness from compression of the recurrent laryngeal nerve o Horners syndrome o
Elevated hemidiaphragm from phrenic n. compression
o Dysphagia from compression of the esophagus
o SVC syndrome

Pancoast syndrome = extension of apical tumors to involve C7-T2 nerve roots of the
brachial plexus shoulder or arm pain
Metastases liver, bone, brain, adrenal glands

Surgical resection for non-small cell in the absence of advanced LN involvement Small
cell is infrequently operated on!!
Lobectomy via posterior thoracotomy, 5th or 6th intercostal space is the procedure of choice o
Mortality = 2-3%
Pneumonectomy is necessary for curative treatment of lesions involving the L or R main
bronchus or when tumor extends to the hilum o Mortality = 5-7%, Right sided >> Left sided
b/c of greater loss of lung tissue o Pre-op FEV1 < 1 L = 40% mortality o
Most post-op
deaths are due to cardiac cause


Predictors of poor post-op Respiratory Function s/p Pneumonectomy

Predicted post-op FEV1
Max voluntary ventilation
Maximum VO2
RV/TLC ratio
Vital capacity

High-Risk Patients
PaCO2 > 45 mmHg (on room air)
PaO2 < 50 mmHg
800 ml or < 40% of predicted
< 50% predicted
< 50% predicted
< 10 mL/kg/min
> 50%
< 2 L (normal = 60 ml/kg = 4.2

The most commonly used criteria for operability is predicted post-op FEV 1 > 800 ml
% contribution of each lung to total FEV1 is assumed to be proportionate to % of total
pulmonary blood flow it receives, determined by radioisotopic scanning (133 Ke or 99 Tc)

Post-op FEV1 = % blood flow to remaining lung x total FEV1

Pneumonectomy Preoperative Work-Up
1. PFTs o
FEV1 < 70% and DLCO < 60% must go onto phase
2. Estimation of post-op function using quantitative split
function lung scan o
Poor outcome = FEV1 (< 800 mL =
40%) and DLCO < 40% predicted must go onto more testing
3. Post-op conditions mimicking pneumonectomy by
occluding PA with a balloon on the
resected side
o Poor outcome = PAP > 35 mmHg, PaCO2 > 60 mmHg, PaO2 < 45 mmHg
4. Post-op VO2 max using exercise study o
> 20 mL/kg/min =
minimal morbidity o
<15 mL/kg/min = increased M & M,
okay for lobectomy o
< 10 mL/kg/min = very high risk,
reconsider resection

Vasodilator, acetylcholine stimulates its release from endothelial cells
In the lungs, NO synthetase combines oxygen with L-arginine to produce NO and L-citrulline
NO stimulates c-GMP decrease intracellular Ca2+ relaxation & vasodilation of vascular
SM decrease PA pressures and V/Q mismatching
A selective pulmonary vasodilator with NO systemic hemodynamic effects!
< 2 ppm is acceptable exposure, NO > 100 ppm and high FiO2 results in production of
NO2, a potent oxidant
>150 ppm for short duration is fetal

Tracheal Resection


PFTs are required by all patients undergoing elective tracheal resection b/c severe lung
disease necessitating post-op ventilation is a relative contraindication b/c PPV may cause
wound dehiscence.

Nitrous oxide

MAC (%)




MAC = Minimum Alveolar Concentration

Defined as the concentration of that agent in alveolar gas necessary to prevent movement in
50% of patients when a standard skin incision is made
MAC is most closely associated with Oil/Gas partition coefficient
150 / MAC Oil/Gas partition coefficient
1.3 MAC immobility in 95% of patients
MAC-awake = patient will open his or her eyes to command, generally 0.3-0.4 MAC
MAC-BAR (block adrenergic response) = blunts sympathetic response to noxious stimuli
= 1.5
MAC is not affected by altitude or hyperbaric pressure
No change in MAC
-Duration of anesthesia
-Anesthetic metabolism
-Thyroid function
- Potassium K+ levels

MAC ( potency)
-Hyperthermia (>42C)
-Drugs that CNS
catecholamine levels: MAOI, TCA, ephedrine - Acute
cocaine, amphetamines
- Chronic EtOH abuse
-Infants at age 1 yr

- age (elderly)
-Hypercapnia (PaCO2 > 90)
-Hypoxia (PaO2 < 40)
-Hypotension (MAP < 40
mmHg) -CNS depressant:
sympatholytics, ketamine,
pancuronium -Acute EtOH
-Chronic amphetamines
-Lithium, Reserpine, methyldopa
-Cholinesterase inhibitors
- 2 agonists = Clonidine
-Neonates (0-30 days)
-Anemia (Hct < 10%)
-Cardiopulmonary bypass

Trace Concentrations, Personnel Hazards, OR pollution


Studies have not shown an association b/t trace concentrations of waste gases found in
scavenged location and adverse health effect in health personnel
OSHA recommendations (not requirements!) o
N2O alone < 25 ppm o
N2O +
volatile anesthetics, with N2O < 0.5 ppm o Halogenated anesthetics < 2 ppm

Anesthetic Uptake Factors

Partition coefficients of volatile
agents (least soluble --> most
Uptake = x soluble)
Q x (PA-PV)
Nitrous oxide
1. Solubility

Blood/gas partition coefficient ()

describes the affinity of anesthetic for 2 phases o
E.g. enflurane = 1.9 at
equilibrium the [blood] will be 1.9 times the concentration in the gas (alveolar) phase
Blood solubility is the most important single factor in the speed of induction &
recovery o Insoluble agents (ie. N2O = 0.47) are taken up by the blood less avidly -->
rapid rise in alveolar concentration (FA/FI) --> faster rate of induction
Cold solubility slows induction
2. Cardiac Output (Q): Q = FA/FI ratio
Affects uptake of soluble agents (i.e. halothane, isoflurane)
Q = uptake = slower induction ( FA/FI ratio) remove more agent from alveoli
Q = uptake = faster induction (FA/FI ratio ) remove less agent o Low output
states predispose patients to overdosage with soluble agents b/c rate of rise in
alveolar concentrations markedly increases
o Shock ventilation with Q rapid rise FA/FI faster induction

Children have greater perfusion of VRG, FA/FI rises more rapidly o VRG
receives 75% of cardiac output

Intracardiac Shunts o
Impact of the shunt is greater with the less soluble
agents, most dependent on blood flow o
Right-to-Left Shunt portion of Q
bypasses the lung slows induction o
Left-to-Right Shunt no
significant change in the speed of induction
3. Alveolar to Venous partial pressure difference (PA-PV)
The uptake of anesthetic by blood perfusing the lung will increase (rate of rise of F A/FI will
decrease) as the gradient between the partial pressure of anesthetic between the alveoli &
blood increases. This gradient is large early in the course of anesthetic administration
o The factors that determine the fraction of anesthetic removed from blood traversing
a given tissue include: (1) tissue solubility, (2) tissue blood flow, (3) arterial to tissue
anesthetic partial pressure difference
4. Altitude & Barometric pressure
Altitude lowers barometric pressure uptake = FA/FI = slower induction
Vaporizers are NOT compensated for changes in barometric pressure.


o High altitude = vapor output compared to what is

dialed o Hyperbaric chamber = vapor output
compared to what is dialed Transfer of inhaled anesthetic
from anesthetic machine to alveoli (anesthetic input)
Inspired partial pressure Fresh gas flow o
The higher the fresh gas flow rate -->
smaller the breathing system volume --> lower the circuit absorption --> closer the inspired
gas concentration will be to the fresh gas concentration
Alveolar ventilation o
A change in ventilation produces a greater relative change in
FA/FI with more soluble agents (they are subject to uptake by the pulmonary circulation)
o FA/FI is already high for insoluble anesthetics, so increasing ventilation has
minimal effect
o Hyperventilation more anesthetic is delivered to the lungs FA/FI
faster induction
o Hypoventilation rate of [alveolar] increase is slowed because of decreased
delivery of anesthetic gas to the lungs
Right mainstem intubation slow induction for insoluble agents
(halothane, isoflurane)
o An increase in inspired [anesthetic] does not produce a proportional increase
in [alveolar]
Characteristics of anesthetic breathing system any absorption by machine or circuit
Halothane, isoflurane, methoxyflurane are absorbed by circuit
= faster induction (as in children)

Transfer of inhaled anesthetic from alveoli to arterial blood (anesthetic loss)

Blood:gas partition coefficient
Pulmonary blood flow/Cardiac output
Alveolar-to-venous partial pressure difference
Transfer of inhaled anesthetic from arterial blood to brain (anesthetic loss)
Brain:blood partition coefficient
Cerebral blood flow
Arterial-to-venous partial pressure difference

**Conditions that affect Blood/Gas Coefficient**

Anemia RBCs have fat in them and volatile agents are lipid soluble, fewer red cells less
lipid solubility
Protein binding is very minor, but does occur low albumin levels = lowers B/G
coefficient Gases are less soluble at high temperature = lower B/G coefficient
Amount dissolved in liquid is determined by the partial pressure ONLY, not total
pressure Barometric pressure DOES NOT affect B/G coefficient!
Concentration Effect
Described by .. increasing the inspired concentration increases the [alveolar] &
FA/FI faster induction
Second Gas Effect
The factors that govern the concentration effect also influence the concentration of any gas
given concomitantly with nitrous oxide (i.e., second gas effect). Uptake of large volumes of
a 1st gas accelerates the alveolar (arterial) rate of rise of a 2nd gas.
Increased ventilation plays the greater role in raising the second gas concentration when the
fraction of the second gas removed by uptake into the blood is large (i.e. with more soluble
second gases)


Factors Affecting Elimination

Recovery depends on lowering anesthetic concentration in brain tissue
Elimination occurs: (1) biotransformation (methoxyflurane 40%, halothane 20%,
enflurane 2%, sevoflurane 1.5%, isoflurane <0.2%, desflurane <0.2%), (2) transcutaneous
loss, (3) exhalation
Speed of recovery is influenced by:
o Elimination of rebreathing o High fresh gas flows o
circuit volume o
Low absorption by circuit o
solubility = blood:gas partition coeffecient
o High cerebral blood flow o
Increased alveolar
o Cardiac output
o Metabolism for some agents (Halothane)
Ventilation/Perfusion Mismatch
V/Q mismatch tends to increase the alveolar-anesthetic partial pressure and decrease the
arterial anesthetic partial pressure
With less soluble agents (N2O), arterial partial pressure of the agent decreases markedly
b/c of mixing with blood from areas with inadequate ventilation
With more highly soluble agents, blood from the hyperventilated alveoli contains more
anesthetic compensating for blood emerging from under ventilated alveoli.
Vapor Pressure
Contemporary inhaled volatile agents exist in the liquid state below 20C
The % of an anesthetic delivered increases with increasing vapor pressure o
If halothane (VP=240 mmHg) is used in an enflurane (VP=175 mmHg) vaporizer, the
delivered concentration will be higher. Worst situation would be Ether (VP =450 mmHg) in a
methoxyflurane (VP = 22 mmHg) vaporizer
Molecules escape from the liquid phase to the vapor phase until # molecules in the vapor
phase is constant = saturated vapor pressure
Vapor pressure is temperature dependent; a decrease in temperature of a liquid lower
vapor pressure and fewer molecules in the vapor phase
Vapor pressure is independent of atmospheric pressure o At low barometric
pressure (high altitude) variable-bypass vaporizers will deliver about the same anesthetic
partial pressure, but increased % concentrations. Since VP remains the same and BP ,
the ratio of VP/BP increases delivered % concentration is higher than that indicated
on the dial
o At high barometric pressure (hyperbaric) vaporizers deliver decreased
anesthetic concentration as measured in volume %
Latent heat of vaporization of a liquid = number of calories required at a specific
temperature to convert 1 g of liquid into a vapor.
o The temperature of the liquid decreases during vaporization in the absence of an
outside energy source
o Temperature drop will greatly decrease vaporization
Specific Heat = # calories required to increase the temperature of 1 g of a substance by
o Specific heat value is important for volatile agent b/c it indicates how much heat
must be supplied to the liquid to maintain a constant temperature when heat is lost
during vaporization.
Nitrous Oxide
34 x more soluble than nitrogen


No change in MAP, SV, SVR or baroreceptor reflexes

Slight HR = slight CO/CI
Dose-dependent direct myocardial depression is overcome by sympathetic activation
Encounters less barriers to diffusion in the blood than in crossing other membrane faster
expansion in blood than other locations in the body o
Nitrous enters the pleural
space by diffusion, not by vascular delivery. Explains the rapid increase in the volume of PTX
o However, a still more rapid expansion of volume occurs if air inadvertently
enters the blood stream
o A PAC balloon would fill almost instantaneously whereas the PTX is more remote
from the blood; there is direct contact of the balloon with the blood containing
N 2O
Following equilibration:
o 50% N20 = 2 x size of air
containing cavity o
70% N20 = 3 x
size of air containing cavity o
75% N20 = 4 x size of air
containing cavity
Change in volume (%) = N2O in alveoli (%)
1 - fraction %N2O

80% N2O: 80%/ 1 0.8 = 400% increase in volume

Mild sympathomimetic stimulation = mild pulmonary vascular

vasoconstriction, CO ( SV & HR), circulating catecholamines

All volatile agents sensitize the myocardium to epinephrine,

greatest for Halothane
Drugs that block the reuptake of NE: cocaine, ketamine,
arrhythmogenicity of all agents

Effects on CV system







SVR = Desflurane >>

Isoflurane, Enflurane,
No effect on SVR =
Coronary artery dilation possible coronary steal syndrome
associated with Isoflurane


MAP in a dose dependent manner = Enflurane >>
Desflurane, Isoflurane > Halothane (least)



CO/myocardial contractility/CI
CO = Halothane, Enflurane
Maintain CO = Isoflurane, Sevoflurane,
(profoundly SVR, with compensatory

HR is unaffected by Halothane, due to altering carotid
HR = Desflurane > Isoflurane > Sevoflurane




Fluoride-induce nephrotoxicity (high-output renal failure) was most noticeable with

Impairs ability to concentration urine by direct inhibition of adenylate cyclase which is
necessary for normal ADH function ADH resistant DI (nephrogenic DI) polyuria,
hyperNa+, serum osmolality
The only ALKANE, all others are ether compounds
The only modern agent (methyoxyflurane also contained a preservative) that contains a
preservative, thymol. Added to prevent spontaneous oxidation.
Reductive pathway = fluoride, chlorodifluroethylene, chlortrifluoroethylene o Occurs with
hypoxia, hypoperfusion of liver
Oxidative pathway = trifluoroacetic acid, bromide, chloride
Serum [fluoride] can reach 10 uM/L, far below 50-80 uM/L that causes renal toxicity
Halothane Hepatitis a diagnosis of exclusion
Si/Sx: post-op fever, eosinophilia, hepatic dysfunction +/- jaundice, rash, arthralgia ?
immune mediated mechanism
Physiology: 2nd to centrilobular necrosis, seems to be linked to hepatic hypoxia &


Risks: multiple short intervals (within 4 weeks) , middle age obese women (higher rate
defluorination), familial predisposition

Biotransformation/Metabolism of Volatile
Anesthetics o Methoxyflurane:
o Halothane: 20% (oxidative
metabolism) o Sevoflurane: 3% o
Enflurane: 2% o
0.2% o
Desflurane: < 0.02%
Metabolism dependent on P450 enzymes in the endoplasmic reticulum of hepatocytes o
Cirrhosis & CHF may decrease overall metabolism o
Morbid obesity =>
increased defluorination of VA o
Inducing enzyme systems of the liver ARE NOT
associated with increased metabolism!!
Compound A
Sevloflurane is degraded in temperature-dependent fashion in soda & baralyme
nephrotoxin at proximal renal tubules
Increased concentrations seen with:
o Baralyme (instead of soda lime) o High
absorbent temperatures o
concentrations o
Closed circuit or low-flow
anesthesia o
Desiccated Baralyme (vs.
desiccated soda compound)
Combining MACs
Isoflurane 1% + N20 70% 1%/1.15% + 70%/104% = 0.86 + 0.7 => 1.5 MAC