Intercostal Drain

Bronchopleural fistula
Intra-op bronchospasm
Laryngospasm
Pulmonary Function Tests & Flow Volume Loops
Temperature regulation and monitoring
Anaesthesia for pneumonectomy
Anaestehsia for pts with COPD posted for lap cholecystectomy
Endotracheal tubes
IV inducing agents and benzodiazepines
Oxygen Therapy
Intercostal Chest Drain.

Anjan Trikha
Why do you need an intercostal chest
drain?

What are the components of a chest

drainage system?
Chest Drains

To evacuate air / fluid into a closed collection

system to restore
Negative intra-thoracic pressure
Promote lung expansion
Prevent lethal levels of pressure from
developing in thorax
What are the indications of inserting a
chest drain?
Indications

• Significant pneumothorax. > 30 %

• Lessor pneumothorax - Requiring ventilation, air
shifting
• Hemothorax, Empyema
• Chylothorax, Pleural Effusion
• Hydropneumothorax
 What are the sites of insertion
What are the sites of insertion?
of a chest drain?
Chest Drains: Sites

• 4th-5th I/C space in Anterior axillary line.

• 2nd I/C space in Mid clavicular line.
• Superior border of the underlying rib.
Chest drain Insertion
Triangle of safety

Posterior border of
Pectoralis Major Anterior border of Latismus
Dorsi

Anterior axillary
line

6th Rib
Chest Tubes

• Red rubber / Silastic PVC

• Right angled / straight
• Sizes 6 - 40 F / Infants: 6 -24 F
• Adults: 24 - 28 for air, 32 - 34 for pleural
effusion, 36 - 40 for blood / pus
Pneumothorax size - Measurement

• Volume of the lung & thorax is a to their

diameter cube.
• Length spine to lateral chest wall - 8cm
• Pneumothorax 2 cm from chest wall
• Volume of lung - (6cm)3 = 216 cm
• Volume of hemithorax - (8cm)3 = 512 cm
• Lung size = 216/516 = 42 %
Pneumothorax size = 58 % size
Chest Drains: Drainage Bottles

• Simple system: single bottle

• Large bottle (8in. / 20cm)
• Disadvantage: increasing resistance as bottle
fills
• 1 / 2/ 3 bottle systems
Physics & physiological aspects
• Under water seal –
A one way valve
Produces a siphon effect, enhances
drainage
• Drainage tube; 1.8m, 9.5 – 12mm ID
• Distal end of drainage tube 2 cm below water
(The depth determines the hydrostatic pressure
needed to overcome during expiration).
Physics & physiological aspects
• Collection chamber always 100cm below the
chest. (To prevent the chamber fluid getting sucked up the
tube during obstructed inspiration).
• Large diameter collection chamber (20cm
diameter) (Minimal resistance to drainage of air, to
prevent loss of underwater seal as water moves up the
drainage tube during deep inspiration).
Complications

• Incorrect positioning
• Intra thoracic / abdominal injury
• I/C neurovascular bundle injury
• Re-expansion pulmonary oedema
• Accidental disconnection
• Infection /Obstruction
 Management of Chest drain

• Bubbling chest tube - never to be clamped.

• Controlled drainage for large pleural effusions
• Avoid clamping in pneumothorax
 Avoiding Re Expansion PE

• Suggestions: Clamp for 1 hour after 1 litre.

• No standard recommendations.
• Not more than 1- 1.5 liters at one time.
• 500 ml per hour.
Contraindications

• Lack of Air fluid

• Coagulopathy
• Complications
• Malposition
• Hemorrhage
Chest drain care

• Avoid clamping, examine daily

• Keep below the level of patient
• Tight fittings connections / no kinking
• Milking with caution
• Pain
• Serial X-rays - Proximal holes
Removal of chest drains
• 24 hours after drainage stopped
• At removal ask patient to inhale deeply and
perform Valsalva
• Chest drain removed swiftly
• Purse string suture closed
• Check CXR
Bronchopleural Fistulas
 Bronchopleural Fistulas
Communication, bronchial tree & pleural space.
Clinically: Persistent air leak 24 hrs after PTX
Identification:
Failure to re inflate lung despite ICD
Continued air leak after evacuation of PTX
Aetiology
Postoperative 2/3, Non-postoperative 1/3
Complication of: Diagnostic or therapeutic
procedure, MV for ARDS•
 Post-operative BPF
• Most commonly follows pneumonectomy
(0-9% v 0.5% in lobectomy)
• Predisposing factors:
Rt pneumonectomy (shorter Rt main bronchus & single Rt
bronchial artery)
Uncontrolled preoperative pleural /pulmonary infection
Preoperative irradiation
Trauma
Postoperative positive pressure ventilation
Faulty closure of bronchial stump
 Non-postoperative BPF

• Causes:
Necrotizing pneumonia, TB, lung abscess & empyema
ARDS
Persistent spontaneous pneumothorax
Thoracic trauma
Iatrogenic (line placement, pleural biopsy, FOB)
Irradiation & chemotherapy
 Clinical Presentation
• Acute
Sudden SOB, hypotension, coughing up of fluid &
blood
• Subacute
Insidious onset with fever, wasting, minimally
productive cough
• Chronic
Fibrosis of pleural space prevents mediastinal shift
 Diagnosis
• Clinical
Instillation methylene blue thru stump,
chest tube

• C T scan to delineate the aetiology

• Bronchoscopy: Diagnostic & therapeutic

 Bronchopleural Fistulas
Problems with a large BPF
Failure of lung re-expansion
Loss of delivered tidal volume
Inability to apply PEEP
Inappropriate cycling of ventilator
Inability to maintain ventilation - hypoxia
Problems of weaning
Attributable mortality
Clinical Scenario

• 40 year old patient with ARDS cannot be

ventilated because of a large BPF in the left
lung.
• Surgery is not possible.
• What are goals of ventilation ?
• What are ventilatory options?
Mechanical Ventilation: issues

• Adequate sized chest drainage system

• Ventilation: Pressure controlled
• Independent lung/ High frequency
• Synchronized closure / positive pressure
to chest tube.
• Consider permissive hypercapnia
• FOB Instillation of sealant
 Anesthesia implications
• Optimization
• Chest drain / Hydration
• Antibiotics
• Sitting upright
• Diseased hemithorax dependent
Clinical Scenario
*A patient with BPF following an empyema
drainage is posted for corrective surgery,
what are the anesthesia implications?

*What are your induction options?

B P Fistula – Surgery options

• Mobilization of IC / Pectoralis muscles

• Thoracoplasty
• Bronchial stump stapling
• Pleural abrasion & decortication
Anesthesia implications

• Prevention of spill into healthy lungs

• Obtaining control of distribution of
ventilation
• Potential of enlargement of fistula with
DLT / BB
 Induction - Options available

• Bronchoscope and intubation under local anesthesia.

• Bronchoscopy and intubation under G A
maintaining spontaneous respiration
• Bronchoscopy and intubation under GA and muscle
relaxation.
• Patient upright and affected side dependent
 Perioperative Care
• Balanced general anesthesia
• Avoid Nitrous oxide
• Multimodal analgesia technique
• Good pain relief
• Thoracic / lumbar epidurals
• Physiotherapy
Thank You
 Intra-operative
bronchospasm

Dr. Neha Gupta

Associate Professor, Dept. of Anaesthesiology
ABVIMS & Dr. RML Hospital
Introduction

• Definition: spasmodic contraction of bronchial smooth muscle,

producing narrowing of the bronchi
• Clinical feature of exacerbated underlying airway hyperactivity
• Rare but potentially lethal intraoperative complication
• Incidence: 1.7 per 1000 pts.
• Higher incidence in presence of irritable airway pathology
• Can occur in isolation or as a part of IgE-mediated anaphylaxis
Anatomy
Tracheobronchial tree
Anatomy

• Down the tracheobronchial tree:

cartilaginous rings recede to finally disappear
muscle layer becomes thinner
relative thickness of muscle layer wrt the wall increases
• Terminal bronchiole – relatively thickest muscle layer
• Actually “bronchiolar spasm” (due to the area mainly involved)
Anatomy
Innervation of bronchi

• Parasympathetic nervous system

• Sympathetic nervous system
• Non-adrenergic non-cholinergic system
Anatomy
Innervation of bronchi
Anatomy
Innervation of bronchi

Sympathetic
T2-T4 ganglia of sympathetic trunk

Adrenergic receptors
• Alpha receptors: clinically insignificant
• Beta-2 receptors
Anatomy
Innervation of bronchi
Sympathetic
Bronchomotor tone
Substances influencing bronchial smooth muscle
tone
Bronchodilatation Bronchoconstriction
• Beta-2 sympathomimetics • Muscarinic cholinomimetics
(salbutamol, isoprenaline, adrenaline, ephedrine)
(neostigmine)
• Xanthine derivatives
(aminophylline) • Beta-2 adrenergic blockers
• Volatile anaesthetics (propranolol)
(halothane, diethyl ether) • Autacoids
• Prostaglandins-E1, E2
 Histamine releasing drugs
• Nitrites
(thiopentone, morphine)
(glyceryl trinitrite)
 Allergic response/Anaphylaxis
• Muscarinic cholinergic R. blockers
(atropine, hyoscine)  Carcinoid tumours
Risk factors

• Recent viral URTI

• Exposure to tobacco smoke
• H/O atopy
• Recent hospital admission for exacerbations of bronchial asthma
• Airway instrumentation (ETT > LMA)
• Surgical stimulation under light anaesthesia
• Airway soiling (secretions, aspiration)
Triggers
• Airway manipulation under light plane of anaesthesia
• Misplacement of ETT
• Surgical stimulation under light anaesthesia
(anal/cervical dilatation, stripping long saphenous vein, traction
on peritoneum)
• Acute exacerbation of asthma
• Inadvertent extubation
• Allergy/Anaphylaxis
• Aspiration of gastric contents
• Pulmonary edema
Triggers

Pharmacological agents which can trigger bronchospasm in high risk

patients:
• Beta-blockers – avoid non-specific agents
• AchE inhibitors – combine with anticholinergic agents
• NSAIDS
• Volatile agents (isoflurane, desflurane) – if introduced/conc.
changed rapidly
• Histamine-releasing drugs (thiopentone, morphine, atracurium,
mivacurium, protamine)
Diagnosis

• Expiratory ronchi
• Decreased breath sounds / silent chest
• Reduced pulmonary compliance
• Falling oxygen saturation
• Spont. breathing pt. – prolonged exhalation
• Positive pressure ventilation – increased peak airway pressure,
decreased tidal volume
Diagnosis

• Capnography – “shark-fin appearance”

• Development of auto/intrinsic PEEP (positive pressure delivered
before expiratory phase over) – increased intrathoracic pressure
reduced venous return
decreased cardiac output
• If associated with anaphylaxis/allergy – in addition – rash,
hypotension, tachycardia
Diagnosis
Capnography change: ‘shark fin’ appearance
Narrowed airways and
prolonged expiration result in
a delayed rise in end-tidal
carbon dioxide, producing
characteristic
‘shark fin’ appearance
Diagnosis
Rule out mechanical causes of increased PAP

• Kinked ETT
• Smaller sized ETT
• Obstruction in breathing circuit, air filters
• Overinflated ETT cuff
• Endobronchial intubation
• Pt’s active respiratory efforts – fighting with the ventilator
• Excessive TV / Inspiratory flow rate settings
Rule out mechanical causes of increased PAP

• Opioid-induced muscle rigidity

• Steep head-down position
• Excessive pneumoperitoneum
• Morbidly obese pts.
• Tension pneumothorax

THESE POSSIBILITIES SHOULD BE RULED OUT AND CORRECTED

FIRST
Ruling out differential diagnosis
Laryngospasm
In non-intubated patients acute laryngospasm can produce upper airway noise (usually
inspiratory), reduced breath sounds and difficulty in ventilation
Bronchospasm Laryngospasm

Expiratory and accompanied by a Inspiratory usually accompanied

wheeze or croup by a stridor

Accessory muscles of respiration Indrawing of the intercostals

suprasternal notch present

Expiration is prolonged Not prolonged

Cyanosis is slow to develop Develops rapidly

Prevention
Preoperative preparation

• Indicators of poor control:

wheeze / ronchi
productive cough
recent RTI
shortness of breath
recent exacerbations / hospital admissions
Prevention
Preoperative preparation

• In COPD pts. – cessation of smoking

control of infection
use of bronchodilators & steroids
incentive spirometry, chest physiotherapy
• In Br. asthma pts. – improve lung function to predicted values
before surgery (consider short course of oral steroids)
• URTI in children - increased risk of intraop. Bronchospasm –
postpone surgery till complete resolution of symptoms (approx. 2
weeks)
Prevention
Anaesthetic management

• Whenever possible – RA should be preferred

• If GA – LMA better than ETT
• Emergency surgery – risk of aspiration vs risk of triggering bronchospasm
• Pre-treatment with inhaled/nebulized beta-2 agonists – 30min prior to
surgery
• Induction – propofol is ideal agent
• Ensure adequate depth of anaesthesia prior to airway instrumentation
Prevention
Anaesthetic management

• i.v lignocaine – 1-1.5mg/kg, 60-90s before intubation (membrane

stabilizing effect)
• Maintainence of anaesthesia – sevoflurane preferred
• Adequate hydration, analgesia
• Humidification of inspired gases
• Airway suctioning under deep plane of anaesthesia
• Ventilatory settings to be altered to limit peak inspiratory pressure
and tidal volume, lengthening of I:E ratio (to prevent auto PEEP)
• Extubation – under deep plane of anaesthesia
Management

A.On suspecting bronchospasm

•Switch to 100% oxygen
•Call for help early
•Manual bag ventilation
•Stop stimulation / surgery
•Consider allergy / anaphylaxis; stop administration of
suspected drugs/ colloids/ blood products
•Thorough ETT suction after deepening of anaesthesia
•In non-intubated patients: exclude larygospasm and
aspiration
Management

B. Immediate management
• Aim: to prevent hypoxia and reverse bronchoconstriction
• Rule out mechanical causes of airway obstruction and inadequate
plane of anaesthesia before initiating treatment:
Check tube position and exclude blocked/misplaced tube
Eliminate breathing circuit occlusion
Management

• Deepen anaesthesia – propofol / volatile agents

• If bronchospasm still persists – beta-2 agonist therapy
• If inspite of deepening anaesthesia and beta-2 agonist therapy
bronchospasm still persists – corticosteroids (effect in 4-6hrs)
• Other drugs: ipratropium bromide
magnesium sulphate
epinephrine
Management
Drug therapy

1st line of therapy

• Salbutamol
Metered dose inhaler: 6-8 puffs repeated as necessary (using in-line
adaptor/barrel of 60ml syringe with tubing or down ETT directly)

Nebulized: 5mg (1ml 0.5%) repeated as necessary

Intravenous: 250mcg slow iv then 5mcg/min upto 20mcg/min

Management
Drug therapy

2 line of therapy
nd

• Ipratropium bromide: 0.5mg nebulized 6 hrly (in combination with beta-2 agonists)
• Magnesium sulphate: 50mg/kg iv over 20min (max 2g)
• Hydrocortisone: 200mg iv 6 hrly
• Ketamine: bolus 10-20mg. Infusion 1-3mg/kg/h
• In intractable cases (esp with hypotension): epinephrine (adrenaline)
Nebulized: 5ml 1:1000
Intravenous: 10mcg (0.1 ml 1:10,000) to 100mcg (1ml 1:10,000) titrated to
response
Management
How to administer drugs via MDI?

• Short-acting beta-2 agonists (salbutamol) via MDI – cornerstone of

management of intra-operative bronchospasm
• Only small fraction absorbed systemically
• MDI delivery should synchronize with onset of inspiratory flow
• HME should be removed during drug delivery
• MDI should be delivered to the inspiratory limb of the circuit
• Majority drug lost in the ETT – large dose like 8-10 puffs to be given
Management
How to administer drugs via MDI?
Management
How to administer drugs via MDI therapy?
Management

C. Secondary management
• Optimize mechanical ventilation
• Reconsider allergy/ anaphylaxis
• Review medications
• If no improvement – consider pulmonary edema / embolus / pneumothorax/
foreign body
• Consider aborting / abandoning surgery
• Request and review chest x-ray
• Consider transfer to critical care area for on-going investigations and therapy
Case scenarios

Case 1
•A 70-year old male patient with suspected intestinal obstruction
scheduled for emergency exploratory laparotomy
•H/O active smoking present
•No H/O atopy / drug allergy
•Preoperative chest auscultation – B/L reduced air entry, conducted
sounds +nt
•Pt. preoxygenated with 100% O2 – RSI using fentanyl and
thiopentone – tracheal intubation using Sch
•Immediately following intubation, chest auscultation revealed B/L
ronchi, peak airway pressure-35 cm H2O, SpO2-88%, capnogram
showed a steep expiratory upstroke
Case scenarios

Case 1
Interpretation and diagnosis
• H/O active smoking with B/L reduced air entry and conducted sounds –
COPD with hyper-reactive airways
• Use of thiopentone – histamine release
• ? Inadequate depth of anaesthesia before intubation – due to RSI

All these factors could have resulted in exacerbation of underlying airway

hyperactivity – leading to bronchospasm
Case scenarios

Case 2
•A 30-year old female pt. with diagnosis of right-sided renal stone,
was scheduled for PCNL
•No H/O any atopy / drug allergy
•Preoperative investigations revealed deranged KFTs
•Chest auscultation – normal
•Anaesthesia induced with fentanyl and propofol – tracheal
intubation facilitated with atracurium
•Around 5min post intubation - BP-60/30 mmHg, HR-130/min,
SpO2-70%, PAP-40cmH2O, capnography-shark fin appearance,
auscultation-silent chest, erythematous rash over chest and arms
Case scenarios

Case 2
Interpretation and diagnosis
• Sudden occurence bronchospasm after anaesthetic induction, with
cardiovascular and cutaneous signs – possible drug-induced
anaphylactic reaction
• Atracurium-induced anaphylaxis – most likely etiology
Stepwise approach to
treatment of perioperative
bronchospasm according
to case scenario
Take-home points

• “Prevention is better than cure” – identify high-risk cases and

situations
• Management begins with switching to 100% oxygen and calling for
help early
• Stop all potential precipitants and deepen anaesthesia
• Exclude mechanical obstruction or occlusion of the breathing circuit
• Aim to prevent / correct hypoxemia and reverse bronchconstriction
• Consider a wide range of differential diagnosis including anaphylaxis ,
aspiration or acute pulmonary edema
References

1. Woods BD, Sladen RN. Peri-operative considerations for the patient

with asthma and bronchospasm. Br J Anaesthesiol 2009;103:57-65
2. Liccardi G, Salzillo A, De Blasio F, D'Amato G. Control of asthma for
reducing the risk of bronchospasm in asthmatics undergoing general
anesthesia and/or intravascular administration of radiographic
contrast media. Curr Med Res Opin 2009;25:1621-30.
3. Dewachter P, Faivre CM, Emala CW, Beloucif S, Riou B. Case
Scenario: Bronchospasm during anesthetic induction. Anesthesiology
2011;114:1200-10.
4. Applegate R, Lauer R, Lenart J, Gatling J et al. The perioperative
management of asthma. J Aller Ther 2013;S11:007.
5. Rajesh MC. Bronchospasm under general anaesthesia. BMH Med J
2018;5(4):98-103.  
Thank you
An Anesthetist’s Nightmare

Laryngospasm
Dr Michell Gulabani
Assistant Professor- Anesthesiology
UCMS, Delhi

Proprietary and confidential — do not distribute

Contents

• Case Scenario

• Definition and Types

• Epidemiology

• Pathophysiology and Diagnosis

• Triggering Factors

• Management

Proprietary and confidential — do not distribute 1/30/2021 2

Case Scenario

Before
tracheal
extubation,
achievement After tracheal
of extubation,
hemostasis, the bag did
8 year old throat free of not show any
boy was secretions or movement Oxygen
scheduled for any gauze was and chest was saturation
tonsillectomy confirmed silent started falling

During the Good oral T he patient CPAP with

surgical suctioning could not be 100% oxygen
procedure was done and ventilated was initiated
bleeding from extubation
the tonsillar performed
bed was
significant

Prompt Recognition is the KEY to Management

Proprietary and confidential — do not distribute 3

Definition and Types

Partial- Both the vocal

Complete- The
Glottic closure due to cords are firmly pressed
ventricular cords are against each other
reflex constriction of the tightly occluded, thus
laryngeal muscles. ,leaving a small lumen
effectively sealing the for minimal ventilation
larynx.
by an anesthetist.

Proprietary and confidential — do not distribute 4

Incidence

Overall incidence:
• 0.87% in adults
• 1.7% in pediatrics
• 2.82% in infants
Incidence of laryngospasm in older children was twice as that of
adults while in younger children thrice that as adults. 1,2

Incidence of laryngospasm in literature has been reported as high

as 25% in patients undergoing tonsillectomy and adenoidectomy. 3

1. A .E. Black, ”Laryngospasm in pediatric practise,”Pediatric Anesthesia, v ol 18, no.4, pp.279-280, 2008.
2. J.Hol zki and M. Laschat, ”Laryngospasm”, Padiatric Anesthesia, vol .18, no.11, pp.1144-1146, 2008.
3. N . Gu lhas,N.Durmus, S.Demirbileks et al, ”The use of magnesium to prevent laryngospasm after tonsillectomy and adenoidectomy: a preliminary study,” Paediatric Anesthesia, vol .13, no.1, pp.43-47, 2003.

Proprietary and confidential — do not distribute 5

Triggering Factors 4-5

Inappropriate depth of anesthesia

Inhalational induced irritation

Secretions

Stimulation of airway

Suction catheter

Induction agents like thiopentone sodium

Tracheal intubation

Airway anomalies

Upper respiratory tract infections

Surgical factors like tonsillectomy, adenoidectomy, appendicectomy, dilation of anus and thyroidectomy.

4. B.C.Wu bie, Y.M.Debas, ”Incidence and Associated Factors of Laryngospasm among Pediatric Patients who underwent surgery under general anesthesia,in University of Gon dar Compressive specialized hospital ,Northwest
Eth opi a,2019: A Cross- Sectional Study”, Anesthesiology Research and Practice, vol 2020, Article ID 3706106, 6 pages, 2020.
5. HE Darryl, M Patrick, F Mark, ” Pediatric l aryngospasm”, Pediatric Anesthesia 2008, vol18, pp.303 -307.
Proprietary and confidential — do not distribute 6
Recognition

Varying
degrees of
airway
obstruction
Paradoxical
Bradycardia chest
movement

Intercostal
Desaturation recession

Tracheal tug

Proprietary and confidential — do not distribute 7

Think of…

Airway irritation Blood/secretions

and/or in the airway
obstruction

Regurgitation Excessive
and aspiration stimulation /
light anesthesia

Proprietary and confidential — do not distribute 8

Treatment Algorithm

• Prompt recognition is the key

• Laryngospasm is a life threatening emergency

Proprietary and confidential — do not distribute 9

Other treatment modalities for laryngospasm

Small sub – hypnotic doses of propofol

• Propofol has been extensively used in the treatment of post extubation laryngospasm and has shown
rapid benefit with no side effects like bradycardia or hypotension6,7

Topical lignocaine

Aerosolized lignocaine

Nitroglycerine

Magnesium

6. A fshan G, Ch ohan U,Qamar UI, Kamal RS. Is there a rol e for a small dose of propofol i n the treatment of laryngospasm? Paediatr Anaesth 2002; 12:625-628.
7. N awfal M, Baraka A. Propofol for relief of extubation laryngospasm. Anaesthesia 2002; 57:1028.
Proprietary and confidential — do not distribute 10
Further care

Careful post operative review of the patient to :

• Ensure a clear airway
• Exclude pulmonary aspiration
• Exclude post obstructive pulmonary edema
• Explain what happened to the patient

Proprietary and confidential — do not distribute 11

Thank You!!!!

Proprietary and confidential — do not distribute 12

References

1. A.E. Black, ”Laryngospasm in pediatric practise,”Pediatric Anesthesia, vol 18, no.4, pp.279-280, 2008.

2. J.Holzki and M. Laschat, ”Laryngospasm”, Pediatric Anesthesia, vol.18, no.11, pp.1144-1146, 2008.

3. N. Gulhas,N.Durmus, S.Demirbileks et al, ”The use of magnesium to prevent laryngospasm after tonsillectomy and adenoidectomy: a
preliminary study,” Paediatric Anesthesia, vol.13, no.1, pp.43-47, 2003.

4. B.C.Wubie, Y.M.Debas, ”Incidence and Associated Factors of Laryngospasm among Pediatric Patients who underwent surgery under general
anesthesia, in University of Gondar Compressive specialized hospital ,Northwest Ethopia,2019: A Cross- Sectional Study”, Anesthesiology
Research and Practice, vol 2020, Article ID 3706106, 6 pages, 2020.

5. HE Darryl, M Patrick, F Mark, ” Pediatric laryngospasm”, Pediatric Anesthesia 2008, vol18, pp.303-307.

6. Afshan G, Chohan U,Qamar UI, Kamal RS. Is there a role for a small dose of propofol in the treatment of laryngospasm? Paediatr Anaesth 2002;
12:625-628.

7. Nawfal M, Baraka A. Propofol for relief of extubation laryngospasm. Anaesthesia 2002; 57:1028.

Proprietary and confidential — do not distribute 13

Pulmonary Function
Tests & Flow Volume
Loops
 Case Scenario

● 56 year old, male ;

● Obese, chronic smoker and alcoholic,
● Diagnosed PIVD at L4-L5 level ;
● Posted for laminectomy.
● H/o breathlessness on exertion,
● Takes inhaler off and on,
● H/o whitish sputum,
● PR-98/min.,BP-150/90 mmHg, SPO2-96%
● Pedal edema, JVP raised
● Chest- B/L occasional Rhonchii
Report
Objectives of the talk

● Indications of PFT

● Information from PFT

● Understanding lung volumes & capacities

● Bedside PFT

● Respiratory lab tests

● Algorithmic approach to PFT interpretation

● PFT application in case scenarios

What are PFTs?

Pulmonary function tests(PFT) are

objective and quantitative measurements of lung function

to provide standardized values

so as to detect presence, type and severity of pulmonary disease

Broad classification of pulmonary diseases

● Obstructive- Patients have difficulty in ‘breathing out’ due to airway obstruction

(COPD;Asthma;Bronchiectasis; Cystic fibrosis)

● Restrictive - Patients have difficulty in ‘breathing in’ due to restriction in increasing lung volume
-Intrinsic causes( ILD like pulm.fibrosis, sarcoidosis; lung resection)
-Extrinsic causes(kyphoscoliosis; obesity; muscular dystrophies)

● Pulmonary Vascular Disease- Primary PAH, Chronic thromboembolic disease

Indications of pre-operative PFT
Indications of pre-operative PFT

● Known pulmonary dysfunction

● Prolonged history of smoking
● Morbid obesity
● Thoracic cage deformity
● Upper abdominal surgery and smoking history or dyspnea
● Lower abdominal surgery and pulmonary disease, particularly if the surgical procedure will be
prolonged or extensive
● Lung resection
● Cardiac Surgery
Information from PFT

● Detect any significant lung dysfunction

● Type of disease (obstructive/ restrictive)
● Severity, progression and reversibility of disease pre-operatively
● Identify patients at risk of peri and post-operative pulmonary complications
● Need: optimization of lung function to minimize the peri-operative pulmonary complications
Pitfalls

● Poor patient compliance give fallacious results

● Clinician unable to interpret the spreadsheet of numerical results
● Incorrect interpretation of PFT can harm the patient
Understanding the lung volumes and capacities

Volume

Time

4 Volumes:TV;IRV;ERV;RV
4 Capacities(Sum of 2 or more volumes):VC=TV+ERV+IRV
IC=TV+IRV
FRC=RV+ERV
TLC=RV+TV+ERV+IRV
 Normal values

4 Volumes:

● TV: 500ml or 6-8ml/Kg

● IRV: 3.1-3.6L
● ERV: 1.2L
● RV : 1200 ml or 1.2L

4 Capacities(Sum of volumes):

● VC=TV+ERV+IRV:60 to 70 mL/kg
● IC=TV+IRV:3500ml
● FRC=TV+ERV:1.8-3.4 liters
● TLC=RV+TV+ERV+IRV:5800 ml
Types of PFT

Bedside tests Respiratory lab tests

Spirometry Lung volume studies Diffusion

capacity of CO
 1. Sabrasez breath holding test
2. Single breath count test
3. Watch and stethoscope test(Forced Expiratory Time)
4. Snider’s match blowing test
5. Debono’s whistleblowing test
6. Wright’s peak flow meter test
7. Greene & Berowitz Cough test
8. Other tests including ABG

Bhavna G and Lalit G. Pulmonary Function Tests-Relevance to

Anesthesiologists. Anaesth Critic Care Med J 2018, 3(1): 000131.
 Sabrasez breath holding test

Ask the patient to take a deep breath and hold it as long as possible

● >25 sec : Normal cardiopulmonary reserve

● 20-25 sec: Mild limitation of cardiopulmonary reserve
● 15-20 sec :Moderate reduction of cardiopulmonary reserve
● <15 sec :Severe reduction in cardiopulmonary reserve
 Single breath count

Ask the patient to take a deep breath and count out loud from 1 onwards in a single breath

● 40~50 : normal cardiopulmonary reserve

● <15 : severe impairment

 Watch and stethoscope test

(Forced Expiratory Time)after a deep breath, patient exhales maximally and

forcefully. Keep stethoscope over trachea and time the exhalation
● 3-5 sec :Normal
● >6 sec : Obstructive lung dis
● <3 sec : Restrictive lung dis
 Modified Snider’s match blowing test

● Ask to blow a match stick from 3”, 6” and 9” distance

● Mouth wide open
● Chin supported
● No head movement
● Match stick at same level as mouth
● It tests Maximum Breathing Capacity (MBC) :a measure of respiratory muscle
endurance
● At 9”- MBC > 150L/min.
6”- MBC > 60L/min; FEV1> 1.6L
3” MBC > 40 L/min. FEV1< 1.6L
 Debono’s whistle

● Measures Peak Expiratory Flow Rate

(PEFR)
● For a given size of leak hole, a minimum
rate of air flow is required to sound the
whistle
● Patient blows in, with the hole
progressively being increased after each
attempt
● The largest hole at which the whistle
blows gives the reading of PEFR
● PEFR primarily reflects large airway flow
● Low PEFR is indicative of large airway
obstruction
 Wright’s peak flow meter test

● Measures PEFR
● Normal: Males- 450-700L/min

Females- 350-500L/min

● PEFR primarily reflects large airway flow

● It is indicative of airway obstruction
 Greene & Berowitz Cough test

● Patient is asked to take a deep inspiration and cough

● Assess ability to cough, strength and effectiveness
● Inadequate cough indicates: FVC<20ml/Kg;

FEV1<15ml/Kg

PEFR<200ml/Kg

● VC at least TV X 3 for effective cough

● Test is positive if there is self propagated productive
cough
● It is suggestive of possible postoperative
complications
 Other tests

Blowing a balloon Exercise capacity tests- Wright’s Respirometer: TV, MV

Stair climbing test
Exercise oximetry
6 min & 12 min walking test
Respiratory lab tests report
1. Name, Age, Gender , Weight, Height, Ethnicity
2. Three types of tests:
● Spirometry
(Numerical and graphical data)

● Lung Volumes
(Whole bodyplethysmography/
N2washout/He dilution)

● Diffusion capacity
(Diffusion capacity of Lung for CO)

3. Predicted/ Reference, Lower Limit of

Normal(LLN),actual & % of Predicted, Pre and
post bronchodilator
● Invented by John Hutchinson
● Cornerstone of all PFTs
● Only measures lung volume compartments that exchange gas with the
atmosphere(FVC,FEV1, IRV, ERV, FEF, PEF)
● Cannot measure RV and hence cannot measure FRC and TLC
● RV, FRC and TLC can be measured by N2 washout , He dilution or Whole
body plethysmography
 Types of Spirometry machines

Portable Digital Spirometer

Computerized spirometer

Benedicts Roth Spirometer

Spirometry
Understanding the lung volumes & capacities
FVC Maneuver - Volume- Time graph

FEV1= 80%; FEV2=94%; FEV3= 97%

FEV1/FVC= >70%;
FEF > 80%
 Numerical data of spirometry

Normal Values:

● FVC > 80% of predicted

● FEV1> 80% of predicted
● FEV1/FVC > 70%(GOLD criteria)
● FEF25-75% > 80% of predicted
● PEFR - Varies with age and height
>450‐700l/min(7.5-11.5l/s) in males

>300‐500l/min(5 - 8.3l/s) in females

FVC Maneuver-Flow volume loop
FVC Maneuver- Normal Flow volume loop
 Interpretation of FEV1, FVC & FEV1/FVC

Disease type FEV1 FVC FEV1/FVC

(Tiffeneau Index)

Obstructive lung Normal Normal

disease ( V.Mild obstr.) (Mild - mod obstr.)

Or Or Decreased
(<70%)
Decreased Decreased
(Mod - Sev obstr.) (Sev. obstr.)

Restrictive lung Normal Normal

disease or Decreased or
Decreased Increased
(> 70%)
 Mild obstructive lung disease

● FEV1
● FVC normal
● FEV1/FVC
● PEFR normal
 Severe obstructive lung disease

● FEV1
● FVC
● FEV1/FVC
● PEFR
 Restrictive lung disease

● FEV1-
● FVC-
● FEV1/FVC-Normal
 Interpretation of graphs & loops

Volume-Time Graph
Upper airway obstruction

Tracheal stenosis Vocal cord paralysis Tracheomalacia

 Staging of COPD on basis of FEV1

Global initiative for Chronic Obstructive Pulmonary Disease

STAGE Post bronchodilator FEV1

GOLD STAGE I FEV1 > 80%

GOLD STAGE II 50% < FEV1 < 80%

GOLD STAGE III 30% < FEV1 < 50%

GOLD STAGE IV FEV1 < 30%

● FEV1/FVC for all categories should be <70%

● >12-15% increase in FEV1 after bronchodilator therapy is significant
 Measuring Lung Volumes

Lung volumes not measured by spirometry

● RV
● FRC
● TLC
 Measuring Lung Volumes

Methods:

● Helium Dilution(Closed circuit method)

● Nitrogen washout(Open circuit method)
● Body plethysmography
● Radiographic measurements(Chest X-Ray and CT)
 Normal lung volume values

Pred CI Pred %Pred

TLC 6.47 0.65 7.30 112.8

RV 1.55 0.67 1.76 113.6

RV/TLC 24.9 3.7 24.1 96.7

● 80% < Normal TLC <120%

● 80% < Normal RV < 120%
● RV/ TLC is useful in the setting of airflow obstruction
● Greater increase in RV compared to TLC is pointing towards air trapping
● High values of TLC & RV are significant only when there is ventilatory limitation
 Diffusion Capacity of Carbon Monoxide (DLCO)

● Patient takes a deep breath of a mixture of air+Helium + 0.3%CO

● CO is used as it is highly soluble in blood, high affinity for Hb and not normally present
in blood
● DLCO is a measure of volume of CO that diffuses /min /unit of pressure across the
alveolar capillary membrane(ml of CO/min./mmHg)
● It is then compared with a predicted value
 Diffusion Capacity of Carbon Monoxide (DLCO)

● DLCO is indicative of functional surface area(alveolar-capillary membrane) available for

diffusion of gases
● Normal is 80% to 120%
● Lung disease that decreases the total area available for diffusion or increases the
thickness of alveolar-capillary membrane, decreases DLCO
 Diffusion Capacity of Carbon Monoxide (DLCO)

● DLCO > 120% with obstructive pattern is indicative of air trapping

● DLCO<40% indicated severe impairment
● Falsely low with active cigarette smoking
● Low DLCO with normal lung volumes and spirometry is indicative of pulm vasc
dis.(PAH)
 Diffusion Capacity of Carbon Monoxide (DLCO)

Pred CI Pre %Pred

DLCO 31.77 8.27 34.23 107.8

VA 6.01

DL/VA 4.71 1.50 5.69 121.0

● DL/VA is diffusion corrected for alveolar volume

● Low DLCO with normal DL/VA indicates the whole V/Q gas exchange units have been
lost(Lung resection)
● Low DLCO with low DL/VA implies capillary bed has been selectively
destroyed(Emphysema)
 Cardiopulmonary Exercise Testing(CPET)

● CPET quantifies the functional capacity of a subject to respond to the increased

metabolic demands of major surgery
● Using three measures: peak V_ O2, anaerobic threshold (AT) and ventilatory equivalent
for carbon dioxide (V_ E/V_ CO2)
● Patients with peak V_ O2 <10 ml kg-1 min-1 or <35% of predicted are at a high risk for
perioperative death and cardiopulmonary complications
Algorithm for interpretation of PFT
Case scenario
Case scenario
Key points

● Important:
○ detailed history
○ thorough clinical examination
○ routine investigations
● Habit : perform bedside PFT in PAC clinic

● Be confident in reading & interpreting a PFT report

Reduce the burden on a

respiratory physician!!
TEMPERATURE REGULATION AND
MONITORING
Dr RACHNA WADHWA
Associate Professor,GIPMER,
G B Pant Hospital, New Delhi
Case Scenario
• A two year old male child was posted for intestinal obstruction
• After rapid sequence GA induction and maintenance of anaesthesia was
continued with low flow anesthesia, N2O, O2 and Sevo (2%)and Inj. Atracurium.
• Surgery was uneventful
• Inj. Paracetamol given at the end for post-op analgesia
• Total duration of procedure was nearly 4.5hrs
• Reversal attempt- patient not taking spontaneous breaths despite 1 hour of the
last dose of relaxant
• Core temperature was 35.2 C
What are all possible causes for delayed reversal?
• Neuromuscular monitoring, ABG required to clinch the diagnosis.
• Hypothermia - definitely present
High risk category
• Extremes of ages
• Extensive burns, major trauma
• Prolonged duration of surgery
• Open chest and abdomen
• Hypothyroid patients
• Major fluid shifts(intestinal obstruction, aortic replacement,
meningiomas, complex cardiac anomalies and major vascular
surgeries, massive intra-op bleeding etc.)
• Eg. Aortic arch surgeries require temp ranging from 170 -350 C -
essential controlled hypothermia for organ protection
Introduction

• Homoeothermic – Ability to maintain body temperatures within

narrow limits despite wide variations in environmental temp(warm
blooded)
• Poikilothermic- (Cold blooded) eg.-fish, reptiles(neonates/ premature
babies- underdeveloped temp control centers)
• Thermoneutral zone - Temp when there is no active heat loss and
heat gain cycle initiated. Most comfortable and well accepted
• So it is the lowest ambient, atmospheric/OT -temp at which we can
maintain our body temp at the basal metabolic rate. Normally it is 27
± 2º C
Body Temperature Classification
• 40-44°C Heat stroke with multiple organ failure and brain lesions
• 38-40°C-- Hyperthermia (as a result of fever or exercise)
• 36-38°C -- Normal range
• 32-35°C -- Mild hypothermia
• 28-32°C– Moderate hypothermia
• 24-28°C -- Cardiac fibrillation
Temperature
Temperature
• Body temperature is a vital sign
• Temperature monitoring- part of minimal mandatory monitoring in GA
• Mean core temp. in healthy humans is 36.5°C–37.3°C and is tightly
regulated for normal physiological functioning
• Incidence of inadvertent hypothermia (90%) -- higher than hyperthermia
• Temperature fluctuations have various harmful physiological effects and
may adversely affect patient outcome
• Therefore, temperature should be monitored and managed strictly
intraoperatively especially in patients having GA exceeding 30 minutes in
duration & in patients having major surgeries under neuraxial anesthesia
Why regulation of body temperature is
required ?
• The enzymes of the body work in optimal temperature
• Speed of chemical reaction varies with temperature
• Very low temperature(260 C) leads to cardiac fibrillation and failure
• Very high temperature(43.50C) leads to heat stroke, tremendous
increase in metabolic requirements
• Keep in mind adverse effects of hypothermia, particularly in relation
to oxygen delivery, coagulopathy, blood transfusion, patient
discomfort, prolonged hospital stay, cardiac dysfunction etc.
Homeostasis
GA
COLD

WARM

Our human body is unique with the ability to maintain a constant internal
environment for perfect functioning of every organ and cell.
Thermoregulation is the mechanism by which hypothalamus regulates body
temperature at a stable level. Infants regulate their temperature remarkably well,
but it is less robust in neonates and elderly.
• Core body temp is tightly regulated. Periphery - 2°C–4°C cooler than the core
• GA produces profound dose-dependent reduction in core temp triggering cold
defenses including arterio-venous shunt vasoconstriction & shivering
• Anesthetic-induced impairment of normal thermoregulatory control, and
resulting core-to-peripheral redistribution of body heat, is primary cause of
hypothermia in most patients
• Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser
extent than general anesthesia
WHY Temperature Monitoring Is Required
• Core temperature monitoring -quantifies hyperthermia and hypothermia and facilitates
detection of malignant hyperthermia.
• Malignant hyperthermia (MH) is a life-threatening clinical syndrome of hypermetabolism
involving the skeletal muscle. It is triggered in susceptible individuals primarily by the
volatile inhalational anesthetic agents and muscle relaxant succinylcholine etc.
• Less observed in this part of world so missed, but mortality is high
• Therefore anaesthesiologist must be vigilant for perioperative hyperthermia
• Hyperthermia may be marked, with an increase in core temp at a rate of 1–2 °C every
five minutes. Severe hyperthermia (core temperature greater than 44 °C) may occur
• This hypermetabolism causes increased carbon dioxide production, metabolic and
respiratory acidosis, accelerated oxygen consumption, heat production, activation of the
sympathetic nervous system, hyperkalemia, disseminated intravascular coagulation (DIC),
myoglobinuria and multiple organ dysfunction and failure
WHY Temperature Monitoring Is Required
• Controlled hypothermia is also pertinent in few situations
Thermoregulation
• Hypothalamus-primary central structure regulating temp
• It integrates thermal input & activates effector, mechanisms which
normalize temperature by altering metabolic
heat production and environmental heat loss
• Afferent signals for cold and hot sensations are transmitted via A-
delta and C nerve fibers, respectively
• Sensory nerve fibers -sense environmental temp changes through skin projections
• These cutaneous “sensors” are characterized as transient receptor potential receptors
located in both skin and spinal cord. Temp signals from the skin, spinal cord, deep
abdominal/thoracic tissue, and other parts of the brain coalesce mainly within anterior
spinal cord & travel to primary area of temp regulation- hypothalamus
• Hypothalamus then activates both behavioral & autonomic responses to temp changes
• Hypothalamus controls core temp through variety of mechanisms
including behavioral modification, ANS stimulation, surface skin
sweating, & increased heat production via shivering & non-shivering
thermogenesis
• Behavioral regulation is most powerful mechanism & requires
conscious perception of body temp; eg. warm clothes, it is 50%
mediated by skin temp
• Autonomic responses include various mechanisms like peripheral
vasoconstriction or dilatation.
• Sweating is only mechanism by which body dissipates heat in hot
surroundings; each gram of sweat evaporated dissipates 0.58 kcal of
heat
• Bindu B, Bindra A, Rath G. Temperature management under general anesthesia: Compulsion or option. J Anaesthesiol Clin Pharmacol.
2017;33(3):306-316
• As strict temp control is imp. for normal organ, enzymatic, cellular
function, temp control is tightly regulated by body to within 0.2 ℃
• This is referred to as interthreshold range. Within this range, active
methods of heating or cooling are not triggered.
• Threshold temp is temp at which a response is triggered. Thresholds
for vasoconstriction & shivering are 36.5°C - 36.0°C
• GA lowers this threshold by 2°C–3°C.
• The thresholds vary daily in both genders (circadian rhythm)
• Exercise, food intake, infection, and hypothyroid and hyperthyroid
states also alter threshold temp
Thermoregulation –Under anaesthesia

Inter
threshold
range
• Under GA, behavioral regulation plays no role as patients are
unconscious and may be paralyzed. They rely on autonomic defenses
and external temperature management for thermoregulation.
Marked attenuation of autonomic responses exists as most drugs
increase warm response and reduce cold response thresholds.
• The interthreshold range increases up to 10-fold, from 0.3°C to about
2°C–4°C. Temperatures within this range do not trigger
thermoregulatory defense and patients become poikilothermic.
• Midazolam slightly impairs thermoregulatory control
• Painful stimulation can slightly increase vasoconstriction threshold;
therefore, regional or local anesthesia decreases vasoconstriction
threshold.
• Isoflurane and halothane impair thermoregulatory vasoconstriction in
infants and children. Propofol and volatile anesthetics inhibit non-
shivering thermogenesis. Infants are at further higher risk of
hypothermia due to large surface area to body mass ratio.
• Therefore, sweating is the best preserved thermoregulatory defense
during GA. Its threshold is only slightly increased, and gain and
maximum intensity remain normal.
• In contrast, vasoconstriction and shivering thresholds are markedly
reduced, and efficacy of these responses is diminished even after
being activated.
Metabolic problems-hypothermic infants

• Hypoglycaemia. Common cause of mortality in hypothermic infants and the most

important complication of hypothermia. Cold infants use a lot of energy in an attempt
to warm themselves. As a result they use up all their energy stores, resulting in
hypoglycaemia.
• Hypoxia. When haemoglobin becomes cold it takes up, but will not release, oxygen.
Oxygen dissociation curve shifted to left. The oxygen is trapped in the haemoglobin and
not released to the body cells. The cold infant, therefore, appears centrally pink even
while dying of hypoxia. Hypothermia also increases the oxygen needs of the body and
this make the hypoxia worse.
• Metabolic acidosis. Due to poor peripheral perfusion, blood does not carry enough
oxygen to the cells. The resulting hypoxia causes a metabolic acidosis.
Measurement of Intraoperative Body
Temperature
• Combination of core and mean skin temp- required to accurately estimate
body heat content
• Mercury in-glass thermometer–slow-cumbersome-not recommended
• Electronic thermometers use thermistors and thermocouples. They are
sufficiently accurate (±0.5°C), inexpensive, and most dependable modality
• Infrared monitors detect heat given off by radiation & can measure temp
from tympanic membrane and forehead skin but are less reliable
• Though, temp can be monitored at various sites, none of the existing
guidelines specify the best device or best site to monitor temp. The site
and device selection depend on physician, type of surgery, and accessibility
of monitoring sites.
Temp monitoring sites
• The least invasive modality that gives reliable
assessment of core temperature is preferred

• Tympanic membrane monitoring-one such option

• National Institute for Clinical Excellence (NICE) guidelines recommend

temperature measurement at 1 h before induction, every 30 min
intraoperatively, every 15 min in the postanesthesia care unit, and every 4
h in the ward or every 30 min, if active warming is required in the ward
• Nasopharyngeal temperature under general anesthesia and tympanic
temperature during regional anesthesia are most frequently measured
Inadvertent Intraoperative Hypothermia

• Most common perioperative thermal disturbance (core temp. <36°C)

• Incidence -6% to 90% depending on the surgical population and
demographic characteristics of patients
• Risk increases with prolonged surgery, extremes of age, extensive
burns, lower preoperative temperature, severe trauma, and major
intraoperative fluid shifts
Hypothermia during General Anesthesia

Hypothermia during GA occurs from a combination of-

• Anesthetic-induced impaired thermoregulation
• Vasodilatation
• Inhibition of vasoconstriction
• Reduced metabolic rate by 20%–30%
• Exposure to cold environment – OT temp, cold cleaning and irrigating fluids
• Cold intravenous fluids
• Heat transfer from the human body occurs in four ways: conduction,
convection, radiation, and evaporation. Radiation and convection
contribute most to perioperative heat losses
Mechanism of Heat Loss
Hypothermia under GA
• Hypothermia under GA has three phases: initial rapid decrease, slow
linear reduction, and plateau phase
• Like GA, neuraxial anesthesia also impairs behavioral and autonomic
thermoregulation
• Core temperature may decrease by 0.5°C–1.0°C
• It blocks all thermal input from anesthetized regions & reduces
vasoconstriction and shivering thresholds by 0.6°C above the level of block.
Reduction in these thresholds is proportional to the number of spinal
segments blocked
• Hypothermia during neuraxial blocks may be as severe as GA
• Supplementation – analgesics & sedatives also impairs thermoregulation
• Decrease may not plateau since nerve block inhibits peripheral
vasoconstriction. Hence, under regional, patients often do not recognize
being hypothermic
Hypothermia- Consequences

• Prolonged anesthesia drugs duration, especially neuromuscular blockade

• Impaired coagulation and platelet function
• Increased blood loss and transfusion requirements
• Increased wound infections
• Prolong hospital stay
• Increased heart rate, blood pressure, and plasma catecholamine levels
• Mild hypothermia is associated with threefold increase in morbid
myocardial outcomes
• Besides, extreme vasoconstriction & volume depletion may obliterate pulse
oximetry signals
The Outcomes Research Consortium guidelines state as follows:
Body temperature should be monitored in most patients under GA
exceeding 30 min in duration
Body temperature ideally monitored continuously- mandatory on CPB
and rewarming times however, 15 min intervals in all patients
Core temperature should be measured during spinal or epidural
anesthesia in patients whom clinicians believe are likely to become
hypothermic
Intraoperative core temperatures should usually be maintained >36°C
unless hypothermia is specifically indicated.
NICE- GUIDELINES
Clinical Practice Guidelines for Management of Inadvertent Perioperative
Hypothermia in Adults
• Hypothermia - core temperature < 36.0°C.
Perioperative pathway divided into three phases:
• Preoperative phase (1 h before induction of anesthesia),
• Intraoperative phase (total anesthesia time),
• Postoperative phase (24 h after entry into recovery area in the theater suite).
They recommend assessing patients for risk of developing perioperative
hypothermia before transfer to the operation theater (OT). Anesthesia should be
induced only after core temperature is more than 36°C. IV fluids and blood
products must be warmed to 37°C using fluid warming device. Use of FAWs is
recommended to prevent and treat perioperative hypothermia.
• NICE. Inadvertent Perioperative Hypothermia: The Management of Inadvertent Perioperative Hypothermia in Adults. NICE Clinical
Guideline No. 65.: NICE; 2008. Available from http://www.nice. org.uk/guidance/cg65 [Last accessed on 03-06-2017
ACC/AHA 2007 and 2014 Guidelines
Perioperative Cardiovascular Evaluation and Care for Noncardiac
Surgery Class I (Level of Evidence: B) recommendation in 2007
To maintain body temperature in normothermic range for most
procedures other than during periods, in which hypothermia is
intended to provide organ protection.
However, 2014 ACC/AHA Guidelines on Perioperative Cardiovascular
Evaluation and Management of Patients Undergoing Noncardiac
Surgery makes Class IIb recommendation (Level of Evidence: B) that
maintenance of normothermia may be reasonable to reduce
perioperative cardiac events in patients undergoing noncardiac surgery.
Postanesthetic shivering
• Occurs in up to 40% of patients
• Higher incidence in younger patients, low core temperature
• Increased oxygen consumption, raised intraocular and intracranial
pressures and cardiac dysfunction.
• Management-normal ambient temperature, skin surface warming,
pharmacological options -meperidine (25 mgIV), clonidine (75μg/IV),
dexmedetomidine, magnesium sulfate (30 mg/kg IV), tramadol,
physostigmine (0.04 mg/kg IV)and nefopam (0.15 mg/kg)
• Meperidine – time tested drug
• Dexmedetomidine- reduces vasoconstriction and shivering thresholds and
is effective in reducing shivering
 Intra-operative Temperature Management
• Intraoperative warming, especially when patients are vasodilated due to anesthetic agents
• Postoperatively- Preventing Redistribution Hypothermia
• Initial redistribution hypothermia -difficult to treat as heat flow from core to periphery is
massive, but transfer of peripheral heat to the core needs hour, even in vasodilated patients
• Cutaneous warming prior to induction -may not increase core temp but increase peripheral
tissue temp & total body heat content, thus decreasing the temp gradient.
• NICE guidelines recommend preop temp>36°C and keep patient warm at 36.5°C–37.5°C.
• Skin surface warming 30 min before induction- prevents redistribution hypothermia.
• Warm patients for an hour before induction using FAW undergoing spinal surgery under
GA—Less fall in core temperature & decreased intraop hypothermia
• The efficacy of prewarming children by increasing ambient temperature in the induction
room and OT to 26°C for 30–40 min has been found to be safe and effective
Temperature management
• Airway heating and humidification with use of low flow rates & semi-closed
circuits –so- heat loss by evaporation from respiratory system is minimal.
• As less than 10% of metabolic heat produced is lost through the respiratory tract,
heating and humidification of anesthetic gases is not very effective in preventing
fall in core temp
• Warming intravenous fluids – as--- large quantity of cold fluids causes significant
heat loss
• One unit of refrigerated blood or one-liter crystalloid at room temperature can
reduce mean body temperature by 0.25°C
• At flow rate <35 ml/min, warming of fluids is not required in adults.
• Fluid warming is the only method that produces direct core warming and is
recommended for all intraoperative infusions ≥500 ml in adults
Sessler DI. Mild perioperative hypothermia. N Engl J Med. 1997;336:1730–7
• Fluids cannot be heated to temperatures much higher than normal
body temperature; most fluid warmers deliver fluid around body
temperature.
• Red blood cells are stored at 4°C. Rapid transfusion (>100 ml/min)
may cause sudden decrease in temp with serious consequences.
• According to the WHO guidelines, keeping the patient warm is more
important than warming blood; warming of blood is required in
settings of large volume transfusions (adult: >50 ml/kg/h; children:
>15 ml/kg/h), exchange transfusions in infants and in patients with
clinically significant cold agglutinins.
Fluid Warming Devices

• Dry warming systems

• Countercurrent heat exchanger
• Water bath
• Convective air systems
• Insulators.
• Delivery of warm fluids depends on the warming method used, flow
rate, and length of tubing between warmer and patient.
Cutaneous warming
• The amount of heat lost through skin is roughly proportional to the exposed body
surface area
• So, OT temp plays critical role in cutaneous losses- radiation, convection, and
evaporation
• OT temp more than 23°C for adults and 26°C for infants is comfortable
• In OT, passive insulation or active warming can achieve cutaneous warming
• Passive insulation- Cotton blankets, surgical drapes, plastic sheets, space blankets
• Insulation- layer of air trapped. Single layer reduces heat loss by 30%
• Active warming devices include circulating-water mattresses/garments, Forced
Air Warmers, resistive heating devices, and radiant heaters.
• Warming devices/mattresses are used for surgeries where blankets cannot be
used, cardiac surgeries . However, contrary to belief, these are not superior to
over the body warming devices due to reduced perfusion of dependent areas.
• Revised National Accreditation Board for Hospitals and Health Care
Providers guidelines for air conditioning in OTs require temp and
relative humidity in OTs to be 21°C ± 3°C and 40%–60%, respectively,
with a relative humidity of 55%. Appropriate display and minimum of
25 air changes/h is required and airflow must be unidirectional and
downward on the OT table
• Intraop warming also depends on age of patient, type of surgery,
disease state, and drugs used
Postoperative warming therapy

• Forced air blankets and radiant heaters are most commonly used to
warm patients in postanesthesia recovery room.
• Due to continued peripheral vasoconstriction, they have low
efficiency and take long time to warm patient. Intraoperative warming
is therefore ideal. Active warming is better compared to passive
warming alone in the postoperative phase also.
• Active warming helps regain temperature an hour faster.
• Evidence suggests that active warming with convection is slightly
superior to conductive
Bair hugger blanket
Bair
Warming mattress
Fluid warming devices
• Warming cabinets- Cheap, simple, convenient, safe, large volumes can
be kept pre-heated and ready to use for massive transfusions. E.g.
trauma, burns etc
• Water baths
• Countercurrent heat exchange
• Microwave technology
• Forced-air warming
Warming cabinets
Hotline
Hyperthermia and Fever

• Hyperthermia is more dangerous than a similar degree of hypothermia.

• It causes discomfort and increases metabolic demand and cardiovascular stress.
• “Hyperthermia” indicates core temperature exceeding normal values; “fever” indicates
regulated increase in core temperature targeted by the thermoregulatory system.
• Passive hyperthermia- from excessive patient heating without core temperature
monitoring. It may occur in infants and children as sweating under GA is less effective in
them
• Treated – discontinue active warming and removing excessive insulation.
• Fever develops when endogenous pyrogens increase the “set point” of thermoregulatory
system. Fever is relatively rare under GA as volatile anesthetics and opioids inhibit
expression of fever.
• Perioperative fever Causes- infection, mismatched blood transfusions, blood in fourth
ventricle, allergic reactions, release of inflammatory mediators
Cardiopulmonary bypass
• Hypothermia -- potential benefits in myocardial infarction, organ
transplantation, cardiopulmonary bypass (CPB), spinal cord injury (SCI),
intestinal ischemia, and neonatal hypoxic ischemia
• However, there is a need for systematic approach in patients on CPB
• Generally, divided into three groups according to the nasopharyneal
temperature: mild hypothermia group (32-35°C), moderate hypothermia
group (26-31°C) and deep hypothermia group (25°C).
• Usually, patients are cooled to 31-32°C after the beginning of CPB.
Rewarming begins 10-15 min before release of aortic cross-clamp. The
gradient between heat-exchanger and nasopharynx during rewarming will
be maintained at 2-3°C.
Saad H, Aladawy M. Temperature management in cardiac surgery. Glob Cardiol Sci Pract. 2013;2013(1):44-62.
Deep Hypothermic Circulatory Arrest
• To facilitate meticulous and complex cardiac procedures including aortic
arch surgeries
• Total aortic arch replacement is generally performed with DHCA at 15-
22°C
• Despite low temperatures, chances of neurological ischemia co-exist
• Therefore, adjuvants for neuroprotection- pharmacotherapy and ice
cooling of head is done.
Rewarming-
• Basically we are trying to protect the brain, "The rest of the body can deal
fairly well with heat and cold, but the brain is the most adversely affected
by temperature, especially overheating
Engelman et al 2015
Special caution
• Hypothyroid
• Myasthenia gravis
• Neonates
• Preterm kids
• Elderly undergoing major surgeries
• All high risk category for hypothermia
APPLIED PHYSICS
Three techniques are commonly used for measuring temperature:

(1) those based on expansion of a material as its temperature increases

(2) those based on changes in electrical properties with temperature
(3) those based on optical properties of a material.
• As heat is added to most substances (e.g., gases, liquids, solids),
motion of molecules increases, and volume of material increases
• Depending on material, this expansion can be directly calibrated to
changes in temp. Liquids are most commonly used, for example,
mercury, because its effective range extends from its freezing point of
−39° C to approximately 250° C.
Mercury thermometers have two disadvantages. They require 2 to 3
minutes for complete thermal equilibration (mercury is a liquid metal
with a high specific heat). In addition, they are enclosed in a glass tube,
which may break and cause injuries
Bimetallic thermometers
• Thermometers based on bimetallic strip are frequently used in
thermostats because they also slowly respond to transient changes in
temperature.
• A thermometer which uses two different metal strips for
converting the displacement of temperature into mechanical
change. The metals used in the thermometer are steel, copper
& brass. These strips are connected and they will enlarge at
different rates once they heated. This change will compare with
the real temperature & moves a needle beside the scale.
These thermometers are low-cost, simple, and strong
Electrical techniques
• Electrical techniques for measuring temperature can be subdivided
into three categories: resistance thermometers, thermistors, and
thermocouples.
• Resistance thermometers operate on the principle that the electrical
resistance of metals increases with temperature. These devices most
frequently use a platinum wire as the temperature-sensitive resistor,
a battery, and a galvanometer to measure current, which can be
calibrated to temperature. The platinum wire is incorporated into a
Wheatstone bridge circuit, which accurately measures very small
changes in resistance
• Thermistor - a semiconductor and displays opposite behavior with regard to
electrical resistance
• when thermistor is heated, its resistance decreases
• Thermistors, being solid-state devices, can be manufactured in extremely small
sizes and therefore have a fast response to changes in temperature (i.e., little
heat is needed to increase their temperature)
• Most of the temperature probes used in anesthesia, from the ones at the end of
pulmonary artery catheters to esophageal probes, are thermistors.
• Physical problems with thermistors are few: cracked or broken wires lead to high
resistance and incorrect temperature readings.
• More common are poor probe placement and a misinterpretation of the resulting
value, for example, placing an esophageal probe in the oropharynx and
measuring airway temperature rather than core temperature.
• Thermocouples are conductors that generate a voltage in response to a
temperature gradient.
Optical properties
The optical properties of materials can be used to measure
temperature in two ways:
(1) a device known as a thermopile can measure the infrared black-
body emissions of an object, and the emission is then converted to
temperature
(2) a liquid crystal matrix can be placed in direct contact with the
desired zone, and an optical change in color can be observed.
• The Infrared Temperature Measurement System-- Each body with a
temp above the absolute zero (–273,15 °C = 0 Kelvin) emits an
electromagnetic radiation from its surface, which is proportional to its
intrinsic temp
• A part of this so-called intrinsic radiation is infrared radiation, which
can be used to measure a body’s temperature
• This radiation penetrates the atmosphere.
• With the help of a lens (input optics) the beams are focused on a
detector element, which generates an electrical signal proportional to
the radiation- thermopile
• The signal is amplified and, using successive digital signal processing,
is transformed into an output signal proportional to the object
temperature.
• The measuring value signal, which supports an easy connection to
control systems of the process- displays temp
The advantages of non-contact temperature measurement are
• temperature measurements of moving objects and of objects in
hazardous situations
• very fast response and exposure times
• measurement without inter-reaction, no influence on measuring
object
• non-destructive measurement
• long lasting measurement, no mechanical wear
• The most commonly encountered example of infrared temperature
measurement involves the tympanic membrane temperature monitor
used in recovery rooms, pediatrics, and hospital wards.
• The infrared detector produces an electrical signal that is proportional
to the fourth power of the difference in absolute temperatures of the
objects.
• The following formula describes this phenomenon: Q1 , 2 =K (T 4 1 −T
4 2 ) (7) where Q1,2 is net heat transfer (W/cm2), K is the Stefan-
Boltzmann constant, and T1 and T2 are the absolute temperatures of
the two objects (degrees K).
• Theoretically, this method is accurate, but practically, improper
placement and lack of calibration contribute to errors.
Forehead thermometer Gun
• Just as the molecules in a liquid crystal watch display change their
optical properties with a small electric current and become polarized
and dark, the molecules in a liquid crystal temperature device change
their optical properties with temperature, resulting in a rainbow of
colors.
• The crystal matrix is sensitive to pressure and temperature. The
reported clinical accuracy of liquid crystal devices varies.
TAKE HOME MESSAGE

• Intraoperative temperature monitoring, though essential, but still not

done in all requisite scenarios
• Temperature fluctuations are quite common intraoperatively, and
careful monitoring, prevention, and treatment is mandatory for
favorable patient outcomes after anaesthesia
• Depending on the surgery, a strategic plan should be devised for
perioperative warming using warm fluids and warming
• The site and device of temperature monitoring depends on the
surgery and accessibility of monitoring
 APPEC 2021

ANESTHESIA FOR PNEUMONECTOMY

PRESENTER: DR. FANTIN

MODERATOR: DR. PRIYANKA SINGH
EXAMINER: DR. PAVAN GURHA

This is to certify that most of the facts presented in this slide show has been collected from text books and world wide web
service and compiled for academic purpose only.
2/20/2021 1
 INTRODUCTION

• Pneumonectomy- pulm resection surgery with highest morbidity and

mortality rates 5-14%. Right sided lung resections have a far worse
postoperative outcome compared to left sided due to the difference in
volumes of the two lungs with the right being 10% larger than the left and
therefore its higher overall contribution to pulmonary perfusion
Extrapleural pneumonectomy is a rare but extensive thoracic resection,
which would include a dissection of the lymph nodes, the pericardium, the
diaphragm, the parietal pleura and the chest wall.
Sleeve pneumonectomies are performed for lesions involving proximal
main stem bronchus and carina. They are an option for patients with
limited pulmonary reserve that are unfit for a pneumonectomy

• Lobectomy, Segmentectomy, Wedge resections

• Video-assisted thoracoscopic surgery (VATs)- VATs is minimally invasive

alternative to certain lung resection procedures with a 15% decrease in
morbidity and mortality. Patients that have undergone VATs have less
intraoperative blood loss, a better perioperative course, with less
postoperative pain. faster recovery with a shortened overall postoperative
hospital stay.
2/20/2021 2
ANESTHESIA FOR PNEUMONECTOMY
• Pre operative assessment
• Pre operative preparation
• Intra operative management
Induction & maintenance
Monitoring
positioning
lung isolation techniques
one lung ventilation
• Post operative management
• Post op.analgesia
• Post op complications

2/20/2021 3
 PRE ANESTHESTIC EVALUATION
• Preoperative period for evaluation for fitness prior lung resection surgery
• Coexisting disease
• Functional capacity
• h/o smoking, IHD, chemotherapy
• Investigations:
• CBC
• LFT
• KFT
• Clotting profile
• Chest x ray
• ECG-signs of lt or rt heart dysfuntion
• ABG
• PFT- evaluate obstructive or restrictive pattern, to assess responsiveness to
bronchodilators and suitability of resection, static spirometry, before and after
bronchodilator therapy, FEV1>2l for pneomonectomy (BTS). High risk:- FVC,50%,
FEV1< 2l, FEV1/FVC <50%, RV/TLC> 50%, PaCO2>45mmhg
• V/Q scanning -should be considered for any pneumonectomy patient who has a
2/20/2021 preoperative FEV1 and/or DLCO less than80% 4
2/20/2021 5
 ACCP GUIDELINES

2/20/2021 6
2/20/2021 7
PREOP RESPIRATORY CARE REGIMEN

1. Stop smoking
2. Dilate airways- b2agonists, theophylline, C/S, cromolyn Na
3. Loosen secretions- airway/ systemic hydration, mucolytics, antibiotics
4. Remove secretions- postural drainange, cough, chest PT
5. Education, facilitation of post op care- psychological preperration, Incentive
Spirometry, teaching secretion removal manouvers, stabilise medical issues

2/20/2021 8
 SUMMARY OF INITIAL PREOPERATIVE
ASSESSMENT • COPD patients: ABG analysis
• All patients: Physiotherapy
Assess exercise tolerance bronchodilators
estimate predicted postoperative • Increased renal risk:
FEV1%
Measure creatinine and
ABG
blood urea nitrogen
discuss postoperative analgesia
discontinue smoking
FINAL ASSESSMENT
• Patients with predicted postoperative
FEV1< 40%:
Dlco • Review initial assessment
Ventilation perfusion Scan and test results
Vo2 max • Assess difficulty of lung isolation:
• Cancer patients: consider the “4 Ms”: examine chest radiograph and
mass effects computed tomography scan.
metabolic effects • Assess risk of hypoxemia during
Metastases one-lung ventilation.
2/20/2021 medications 9
Factors That Correlate With an
Increased Risk of Desaturation During One-
Lung Ventilation

1. High percentage of ventilation or perfusion to the operative lung on preoperative

V/Q scan
2. Poor PaO2 during two-lung ventilation, particularly in the lateral position
intraoperatively
3. Right-sided thoracotomy
4. Normal preoperative spirometry (FEV1 or FVC) or restrictive lung disease
5. Supine position during one-lung ventilation

2/20/2021 10
 ANESTHETIC PLAN
• GA with controlled ventilation is the safest method
• Combined with thoracic epidural(T7-8)
• Preoxygenation is mandatory
• Maintain two lung ventilation as long as possible
• PREMEDICATION- Continue medications for co morbidities
Antisialagogue (facilitate bronchoscopy)
Anxiolytic (iv midazolam)
Avoid over sedation
Antibiotic prophylaxis
• Iv induction
• Iv fentanyl 3-5µg/kg
• NDMR
• Choice of anesthetic : less than or equal to 1 MAC of iso, sevo, desflurane ( 20% inhibition of HPV ~ 4% of shunt )
• Nitrous oxide - usually avoided because :
- higher incidence of post thoracotomy atelectasis
- inc PA pressures in pulm HTN pt(redirects blood to NDL)
- inhibits HPV minimally
- contraindicated in pts with blebs or bullae.
• M/o during OLV- propofol & o2/air mixture
• Lung isolation , selective ventilation of the left lung to allow collapse of right lung and access to the bronchovascular structures.
• Maintain normothermia and adequate hydration
• Prevention of bronchospasm
2/20/2021 11
INTRAOP MONITORING

• ECG
• pulse ox-(Oxygenation ), direct PaO2
• Capnometry (ETCO2)
• Invasive hemodynamic (ABP- transient severe hypotension, ABGs CVP- as fluid gt is
critical, PACs PAP&PCWP- i/op PAP msr less accurately lt heart preload in LDP)
• Ventilation (Fiberoptic bronchoscopy- placing & reconfirming DLTs, continuous
spirometry- continuously measure I&E volumes, pressures & flow interactions)
• TEE- continuous real time monitor of myocardial function & cardiac preload

2/20/2021 12
INDICATIONS OF OLV
Absolute
• Isolation of one lung from
another to prevent spillage or
contamination (infection,
massive hemorrhage)
• Control of distribution of
ventilation
• Bronchopleural fistula
• Surgical opening of major
conducting airway
• Giant unilateral cyst
• Unilateral bronchopulmonary
lavage (pulmonary alveolar
proteinosis)
2/20/2021
Relative
• Surgical exposure- high
priority
– Thoracic aortic aneurysm
– Pneumonectomy
– Upper lobectomy
– Mediastinal exposure
• Surgical exposure- lower
priority
– Middle/lower lobectomies
– Esophageal resection
– Thoracoscopy
– Thoracic spine procedures
13
FACTORS AFFECTING RESPIRATORY PHYSIOLOGY IN LATERAL
DECUBITUS POSITION

The changes further accentuated by several factors:

1) Induction of anesthesia
2) Initiation of mechanical ventilation
3) Use of neuromuscular blockade
4) Opening the chest/pleural space
5) Surgical Retraction/ Compression
6) Pressure by mediastinum/ Abdominal content

• Perfusion continue to favor dependent lung (Due to gravitational

effect)
• Ventilation favor the less perfused lung.
• End result is V/Q mismatch(shunt) giving rise to hypoxemia.
SUMMARY OF V/Q RELATIONSHIP IN AWAKE & ANAESTHETISED PT

Awake/Closed Anaesthetised
Closed Open
V/Q V Q V Q V Q
NDL
DL
HYPOXIC PULMONARY VASOCONSTRICTION

• local response of pulmonary vascular smooth muscle (PVSM),

decreases blood flow to the area of lung where a low alveolar
oxygen pressure(NVL), hence improves arterial oxygen saturation.
• Increases pulmonary arterial pressure and increases risk of
arrhythmias
• Rapid onset over 30 min then peaks at 2 hrs
• Surgery may oppose HPV by release of vasoactive metabolites
• Decreased by NTG, nitroprusside, inhalational agents
• Aim- try to maintain HPV, avoid factors decreasing HPV

2/20/2021 16
LUNG ISOLATION METHODS

• Double lumen tubes

• Left sided DLT
• Right sided DLT
( Carlen's tube (with hook) ,Robertshaw tube)
• Bronchial blockers
(Arndt/cohen/Fuji/ EZ- blocker)
• Single-lumen ET with a built-in bronchial blocker( Univent Tube )
• Single lumen Endobronchial tubes
• Endotracheal tube advanced into bronchus

2/20/2021 17
 DLT TYPES
• Type:
• Carlens, a left-sided + a carinal hook
• White, a right-sided Carlens tube
• Bryce-Smith, no hook but a slotted cuff
• Robertshaw,

• All have two lumen and cuffs, one terminating in

the trachea and the other in the mainstem
bronchus.

• Right-sided or left-sided available

• Available size: 41,39, 37, 35, 32,28,26

French (ID=6.5, 6.0, 5.5, 5.0 and 4.5 mm

respectively)
Basic pattern of a Right-Sided DLT
2/20/2021 20
Rt Lt
2/20/2021 22
2/20/2021 23
 Selection of DLT

Left sided DLT is most commonly used

irrespective of the surgical procedure because
right sided DLT’s bronchial cuff usually obstructs
right upper bronchus d/t its proximity(1-2.5cm)
to the carina hampering ventilation/ suctioning
of that segment.

• Indications for Right sided DLT:

1. Distorted anatomy of entrance of Lt main bronchus(LMB)
1. Ext. / intraluminal tumor compression
2. Descending thoracic aortic aneurysm
2. Site of Sx involving LMB
1. L lung transplantation
2. L pneumonectomy
3. L sleeve resection
4. Left-sided tracheobronchial disruption 24
 Size of DLT

➢Best→largest size as per calculation

➢Depth of insertion = 12 +(height(cms)/10)
➢Less reliable for <155cms
➢Tracheal cuff (high vol,low pressure cuff), filled up to 20ml
➢Bronchial cuff (low vol, high pressure cuff) inflation <3ml 25
 INSERTION
• Laryngoscopy
• DLT is passed with direct laryngoscopy with the distal concave
curvature facing anteriorly and then turned 90 degrees counter
clockwise (for a left-sided DLT placement) after the Endobronchial
cuff has passed beyond the vocal cords

• Fibreoptic bronchoscopy
• Tip of the endobronchial lumen is guided into the correct
bronchus after the DLT passes the vocal cords using direct vision
with a flexible fiberoptic bronchoscope.
POSITION
• Auscultation and bronchoscopy should both be used each time a DLT
is placed and again when the patient is repositioned
• Through tracheal lumen to confirm position of endobronchial tube
and rule out cuff herniation
2/20/2021 • Through endobronchial lumen to check tube patency 26
2/20/2021 27
2/20/2021 28
 Double lumen tube
Advantages
• Easy to place successfully
• Repositioning rarely required
• Bronchoscopy to isolated lung
• Suction to isolated lung
• CPAP easily added
• Alternate OLV to either lung
• Can be inserted even if
fibreoptic not available
Disadvantages
• Size selection more difficult
• Difficult to place in difficult
airways or abnormal trachea
• Need to change to SLT for
postop ventilation
• Resistance
• Potential laryngeal and
bronchial trauma
29
COMPLICATIONS OF DLT

• Failure of intubation
• Failure of lung isolation
• Tracheal injury
• Bronchial injury
• Airway edema
• Obstruction of tube(teeth/phlegm)
• Dislodgement above glottis
• Cuff rupture/pressure leak
• Intubation trauma/perforation
• Mucosal ulceration-prolonged intubation

2/20/2021 30
BRONCHIAL BLOCKERS

• Advanced distally into mainstem bronchus to allow distal lung collapse

• Can be advanced even further to achieve lobar collapse
• Can be used with a normal single lumen endotracheal tube or modified one
ADVANTAGES
• Can be used in difficult airway
• Lobar isolation possible
• No need for reintubation if post op ventilation to both lungs required
• Can be used easily with tracheostomy tubes
• Can be used in paediatric patients.

2/20/2021 31
2/20/2021 32
33
 SINGLE LUMEN TUBES

• Used as the last resort, emergency, some cases of difficult airway

• ETT pushed beyond carina into the bronchus of the non-operated lung
• dedicated endobronchial tubes (Gordon-Green tubes )

34
 POSITION OF PATIENT
• Lateral decubitus position with the operative lung/area being non dependent
• Proper positioning is crucial to avoid injury and facilitate surgical exposure
▪ Lower arm is flexed
▪ Upper arm extended in front of the head pulling the scapula way from the operative field
▪ Recheck for tube displacement after appropriate positioning
• Neuro vascular injuries-Dependent eye
• Dependent ear pinna
• Dependent arm: (i) brachial plexus, (ii) circulation
• Nondependent arm*: (i) brachial plexus, (ii) circulation
• Dependent and nondependent suprascapular nerves
• Nondependent leg sciatic nerve
• Dependent leg: (i) peroneal nerve, (ii) circulation

35
VENTILATION STRATEGIES

• Maintain two lung ventilation as long as possible

• Tidal volume 5-6 ml/Kg of ibw
• RR 12/min (maintain pCO2 within normal limits)
• PEEP of 5- 10 cmH2O to ventilated lung
(not in patients of COPD)
• Pressure control for patients at risk of lung injury
• Saturation more than 90% acceptable

2/20/2021 36
 FLUID MANAGEMENT

1) Total positive fluid balance in first 24-hour perioperative period should

not exceed 20 mL/kg.

2) Average adult patient, crystalloids: < 3 L in first 24 hrs

3) No fluid for third-space fluid losses

4) Urine output greater than 0.5 mL/kg/h is unnecessary.

5) To increase tissue perfusion postoperatively-use invasive monitoring and

inotropes
INTRAOP COMPLICATIONS

1) Hypoxemia- intrapulmonary shunt during OLV

2) Sudden severe hypotension- surgical compression of heart / great vessels
3) Sudden changes in ventilating pressure or volume
4) Arrhythmias- irritation of heart
5) Bronchospasm – airway stimulation, reactive airway
6) Massive haemorrhage – great vessels or inflamed pleura
7) Hypothermia- loss from open hemi thorax
8) Neurovascular injuries

2/20/2021 38
MANAGING HYPOXIA

• Ensure that delivered FIO2 is 1.0.

• Resume two lung ventilation-Intermittent reinflation of the nonventilated lung
• Check position of double-lumen tube or blocker with fiberoptic bronchoscopy.
• Ensure that cardiac output is optimal; decrease volatile anaesthetics to < 1 MAC.
• Apply a recruitment manoeuvre to the ventilated lung (this will transiently make the
hypoxemia worse). PEEP 5cmH2O to ventilated lung except in emphysema

2/20/2021 39
MANAGING HYPOXIA

• CPAP 1-2 cm H2O nonventilated lung

• Partial ventilation techniques of the nonventilated lung ( Oxygen insufflations- 3L/min to
non ventilated lung , High-frequency ventilation, Lobar collapse using a bronchial
blocker)
• Pharmacologic manipulations-Eliminating the known Vasodilators : NTG, Halothane, decreasing
MAC to < 1, inhaled Nitric Oxide(NO) to ventilated lung
• Mechanical restriction of the blood flow to the nonventilated lung
• Persistent refractory hypoxia- suspected PFO.(25-30yrs- 25% pts have PFO)- RA>LA prs-
R→L shunt: Rx- ↓PAP, improve RV function, Pulmonary VDs, ionotropes
• Venovenous ECMO
• Last resort- bypass

2/20/2021 40
EXTUBATION

2/20/2021 41
 POSTOPERATIVE PERIOD

• Before resuming both lung ventilation do suction and fully inflate lungs.
• Postoperative x-ray is advised to rules out pneumo, hemothorax, collapse,
misplaced drains.
• Adequate pain relief, ability to cough, moisturised air/ oxygen therapy,
breathing exercises , physiotherapy are essentially appropriate to prevent
complications.
• Judicious fluid therapy - Positive fluid balance is kept below 20 ml/kg.
 POSTOPERATIVE ANALGESIA

• SYSTEMIC ANALGESIA:
1. Opioids
2. NSAIDS
3. Ketamine: 1mg/kg i.m.
4. Dexmedetomidine: 0.3-0.4 ug/kg/hr

• LOCAL ANESTHETICS/ NERVE BLOCKS:

1. Intercostal nerve blocks
2. Intrapleural analgesia
3. Epidural analgesia
4. Paravertebral blocks
5. Cryoanalgesia- -60˚temp of probe to exposed
intercostal nerves
POSTOPERATIVE COMPLICATIONS

PNEUMONECTOMY

• Incidence 2-4%
I. Respiratory failure
II. ARDS
III. Empyema
IV. RVF
V. Arryhtmias
VI. Cardiac herniation
2/20/2021 45
 THANK YOU

2/20/2021 46
Presented by : Dr. Saagari Gupta
DEFINITION

 COPD is a disease of progressive loss of alveolar

tissue and progressive airflow obstruction that is
not reversible.
COPD
Chronic Bronchitis
➢ Chronic productive cough for atleast 3 months in each of 2
successive years in a patient in whom other causes of productive
chronic cough have been excluded.
Emphysema
➢ The presence of permanent enlargement of the airspaces distal to
the terminal bronchioles, accompanied by destruction of their walls
and without obvious fibrosis
Symptoms

➢ The most common respiratory symptoms include dyspnea,

cough and/or sputum production.
Risk Factors
➢ cigarette smoking,
➢ occupational exposure to dust and chemicals,
especially in coal mining, gold mining ,and the
textile industry,
➢ indoor and outdoor pollution,
➢ recurrent childhood respiratory infections,
➢ low birthweight.
➢ α1-Antitrypsin deficiency
 Diagnosis Of COPD

Symptoms:
•Dyspnoea: persistent & progressive, worse with exercise

•Chronic cough: maybe intermittent or unproductive

•Sputum production

Exposure: Smoking,in pack year

Spirometry
Pulmonary Function Tests

➢ An FEV1:FVC less than 70% of predicted that is not

reversible with bronchodilators confirms the diagnosis.
GOLD Classification
Global initiative for Chronic Obstructive Lung disease

Stage Characteristics
I: Mild FEV1/FVC < 70%
FEV1 > 80% predicted, with/without chronic symptoms
II: Moderate FEV1/FVC < 70%
50% ≤ FEV1 ≤ 80% predicted, with/without chronic
symptoms

III: Severe FEV1/FVC < 70%

30% ≤ FEV1 ≤ 50% predicted, with/without chronic
symptoms
IV: Very FEV1/FVC < 70%
severe FEV1 < 30% predicted or < 50% predicted plus chronic
respiratory failure (PaO2 < 60mm Hg &/or PaCO2 >
50mm Hg)
Treatment
➢ Smoking cessation
➢ Inhaled long-acting bronchodilators
➢ Inhaled corticosteroids
➢ mucolytic
➢ Inhaled long-acting anticholinergic drugs
➢ Antibiotics against chest infections
➢ Annual vaccination against influenza
➢ Vaccination against pneumococcus
➢ Home oxygen therapy if Pao2 < 55 mm Hg, hematocrit > 55%, or
there is evidence of cor pulmonale
➢ Diuretics if evidence of right heart failure with
peripheral edema
➢ Lung volume reduction surgery
➢ Lung transplantation
Laparoscopic Cholecystectomy

Advantages

➢ Reduced stress response

➢ Reduced pain and analgesic requirements
➢ Decreased postoperative respiratory
dysfunction
➢ Reduced hospital stay
Pneumoperitoneum
➢ Abdominal insufflation w/ CO2, helium, nitrous oxide, or
oxygen to ~ 15 mmHg

➢ Normal Intra-abdominal pressure (IAP) < 5 mmH

➢ CO2 most commonly used gas.

➢ Noncombustible = safe to use with electrosurgical

devices

➢ Solubility in blood and reactivity with soluble buffering

system minimizes the risk of air embolism
Pathophysiological effects of
laparoscopy

Due to
- creation of a pneumoperitoneum
- positioning
Effects of Pneumoperitoneum...

➢ Respiratory
➢ CVS
➢ regional blood flow
➢ GIT
Respiratory Changes

Changes in ventilation
➢ Increase in PaCO2
➢ Endobronchial intubation
➢ CO2 subcutaneous emphysema
➢ Pneumothorax
➢ Gas embolism
Cardiovascular Effects

➢ Biphasic effect on Cardiac Output

➢ Initial transient increase due to splanchnic

compression (IAP<15) .Then decrease in CO (10-
30%) due to decrease in venous return

➢ Increase in SVR
Due to direct compression of abdominal aorta and
abdominal organs and reflex sympatethic response
to decrease Cardiac output
➢ Increase in PVR
➢ HR unchanged
➢ Inrease in arterial BP despite decrease in
CO
➢ Cardiac arrhythmias
Positions in laparoscopic surgeries

➢ Trendelenburg / head down;

➢ Reverse Trendelenburg / head up;
➢ Lateral
➢ Lithotomy
HEAD DOWN
CVS effects;
➢ Increase in CVP

➢ Increase in CO
Respiratory effects;
➢ Atelactasis
➢ Decrease in FRC, TLC
➢ Decrease in pulmonary compliance
HEAD UP

CVS effects;
➢ venous return
➢ CVP
➢ CO
➢ MAP
➢ Respiratory changes are less significant
Pre-Operative Evaulation
 Anaesthetic Considerations in patients
with COPD undergoing Laparascopic
cholecystectomy
Patient Related:
 Advanced age
 smoker
 Co morbid conditions
➢ HTN
➢ Diabetes
➢ Heart Disease
➢ Obesity
➢ Sleep Apnea
 Disease Related

➢ Exacerbation of Bronchial inflammation

➢ Preoperative airway infection
➢ Hyperreactive airway,secretions
➢ Cor pulmonale
 Problems due to Anaesthesia:
➢ V/Q mismatch
➢ FRC reduced during anaesthesia,
➢ Anaesthetic drugs blunt ventilatory responses to
hypoxia & hypercapnia
➢ Postoperative atelectasis & hypoxemia

➢ Problems due to Surgery:

 Investigations
➢ Complete Blood count
➢ BUN,Serum Electrolytes
➢ Blood Sugar
➢ ECG
➢ Arterial Blood Gases
➢ Diagnostic Radiology
➢ Chest X Ray
➢ Spiral CT
➢ Preoperative Pulmonary Function Tests
Pre-operative preparation

➢ Cessation of smoking
➢ Continuation of all the medications as Prescribed
➢ Loosening & Removal of secretions
➢ Treatment of infection by antibiotics
➢ Recognition of Cor Pulmonale and treatment
➢ Improve strength of skeletal muscles – nutrition,
exercise
➢ Correct electrolyte imbalance
➢ Incentive spirometry, chest physiotherapy
Anaesthetic Technique
Premedication
➢ ↑ Sensitivity to the effect of respiratory
depressants
➢ Opioids & Benzodiazepines - ↓ response to
hypoxia, hypercarbia but short acting drugs like
➢ Alprazolam can be prescribed on night before
surgery
➢ Educate the patient to continue all medications as
prescribed
 Choice of Anaesthesia

➢ General Anaesthesia
➢ Allows control of ventilation, excellent muscle
➢ relaxation
➢ Ensures oxygenation and CO2 elimination
➢ IPPV overcomes decrease in lung compliance, increased
resistance and decreased FRC
➢ Comfort to patient, prolonged procedures
➢ Monitoring
➢ ECG, NIBP
➢ Pulse Oximetry
➢ Capnography
➢ temperature
General Anaesthesia: Induction
 Opioids:
 Fentanyl(DoC)
 Avoid morphine-histamine release, sensitive to its ventilatory depressant
effects

 Propofol (DoC)
 Better suppression of laryngeal reflexes
 Agent of choice in stable patient
 Hemodynamic compromise
Intubation

➢ Attenuation of Intubation Response:

➢ IV lignocaine (1- 1.5 mg/kg) 90s prior to laryngoscopy
➢ Gentle laryngoscopy with minimal time
➢ Adequate plane of anaesthesia prior to intubation
Maintenance
➢ Muscle relaxant
➢ Prefer Vecuronium, Rocuronium, Cisatracurium

➢ Avoid Atracurium, ( histamine release)

➢ Volatile anaesthetic
➢ NO → Caution in pulmonary bullae
➢ Inhalational agents attenuate HPV
➢ Iso/des: airway irritants
➢ Sevoflurane: non pungent, bronchodilator
➢ Halothane: Non pungent, bronchodilator.
➢ Slower onset & elimination, Sensitises to
catecholamines
Maintenance
Ventilatory Strategy:
 Aim: Maximise alveolar gas emptying
Minimise dynamic hyperinflation, iPEEP
 Settings:
➢ Large tidal volumes(8-10ml/kg) if bullae absent,low tidal
volumes(6-8ml/kg) if bullae present
➢ Low respiratory rate(6-10/min)
➢ Slow inspiratory flow rate
➢ Longer expiratory phase
 Warm humidified gases
Intraoperative Complications

➢ Bronchospasm
➢ Endobronchial intubation
➢ Pneumothorax
➢ Pulmonary embolism
Definition of Bronchospasm

 Reversible constriction of bronchial smooth muscles

in response to noxious stimulus.
Causes
➢ Airway Irritation
➢ Anaphylaxis
➢ Misplacement of endotracheal tube
➢ Aspiration of gastric contents
➢ Exacerbation of bronchial asthma and copd
Management of intraoperative bronchospasm

➢ Increase FiO2

➢ Deepen anaesthesia
➢ Commonest cause is surgical stimulation under
light anaesthesia
➢ Incremental dose of Propofol

➢ Relieve mechanical stimulation

➢ Stop surgery
➢ β2 agonists – Nebulisation or MDI

➢ s/c Terbutaline,

➢ Intravenous corticosteroid indicated

➢ intravenous Aminophyline

➢ Intraveneous magnesium sulphate

Reversal/ Recovery:
 Neostigmine - may provoke bronchospasm
 Glycopyrrolate before Neostigmine
 Extubation :
 Deep extubation may reduce chance of
bronchospasm

Deep
NO YES
Good airway - accessible
Difficult airway
Easy intubation
Difficult
intubation No Residual NMB
Residual NMB Normothermic
Post operative care

➢ Monitor vitals,spO2,etCO2
➢ Oxygen therapy
➢ Continue bronchodilator,mucolytic,antibiotics
➢ Chest physiotherapy & postural drainage
➢ Voluntary Deep Breathing

➢ Incentive Spirometry

➢ Early Ambulation
Postoperative analgesia –

➢ Parenteral NSAIDS

➢ Subcostal TAP block

Endotracheal Tubes

Dr Rajesh Kumar Meena

Associate Professor
Department of Anaesthesiology
IMS, BHU
 History
• 1869- first inflatable cuff by Trendelenberg.
• 1893- first use of cuffed ETT with Pilot ballon by Eisenmenger.
• 1968- Disposable polyvinyl chloride (PVC) tube with a high-
pressure low-volume cuff was introduced.
• 1970- High volume low pressure cuffed tube.
 Standard Endotracheal Tube
• Patient end
• Curvature
• Markings
• Material
• Cuff
• Machine end
 Patient End

• Bevelled tip
• Murphy’s eye
a. Murphy type
b. Magill’s type
 Curvature
• Anatomic curvature of oral cavity
• Arc – 140 mm
 Markings
• Written on bevel side
• Common markings:
➢ Oral/nasal
➢ Size
➢ Radio opaque line
➢ Distance
➢ Manufacture
➢ Disposable
➢ MRI Compatibility
 Materials
1.Red Rubber/natural latex
➢ Reusable
➢ Less traumatic
➢ Rigid
 Materials
2. PVC
➢ Inexpensive
➢ Disposable
➢ Compatible with tissue
➢ Pre sterilized
➢ Transparent
➢ Difficult to insert
➢ Traumatic
 Materials
3. Silicon Rubber
➢ PVC+ SILICON OIL
➢ Less surface adhesion
➢ Inexpensive
➢ Can be reused
 Cuff
On the basis of pilot ballon
➢ With pilot ballon
➢ Without pilot ballon
 Cuff
On the basis of Cuff Pressure
A.LVHP
➢ Red rubber
➢ Circular
➢ Advantage : Better sealing
Better visibility
Less sore throat
Less expensive
➢ Disadvantage : Ischemia
Scarring
Stenosis
 Cuff
B. HVLP
➢ Thin enalstic material
➢ Large resting volume and diameter
➢ Adaptive to trachea
➢ No pressure related injury
➢ Possible to regulate and measure
pressure
➢ Disadvantage: Difficult to insert
Sore throat
Not effective seal
Micro folds
N2O Diffuse
Can be overfilled
 Cuff
Foam cuff
➢ Polyurathane foam
➢ Bigger diameter
➢ Deflate first with suction then
reinflate
➢ Good seal
 Cuff
Lanz cuff
➢ Latex pilot ballon inside
transparent plastic bag
➢ Pressure regulating valve
➢ Automatically maintain 20-25
torr pressure at end Tv
 Machine end
• Male type of connector
• Plastic /metal
• Universally designed to fit 15 mm
female plug
 Specialty Tubes

• Designed to met the requirement for specific conditions

 Cole’s Tube
• Emergency neonatal
resuscitation
• Narrow patient end
• Shoulder
• Blocked easily
• Resistance
 Microcuff Tube
• Pediatric cuffed tubes
• Effectively seal at an average cuff
pressure of 11 cm H20
• High volume, low pressure
(HVLP)
• Short, cylindrical PU cuff near
tracheal tube tip allow adequate
placement with a cuff-free
subglottic zone, without the risk
of endobronchial intubation.
 RAE Tube

• The RAE ETT was introduced in

the 1970s,named after the 3
inventors Ring, Adair, and
Elwyn.
• Preshaped oral or nasal
tracheal tube
• Types- 1.South facing
2. North facing
• Uses- For facial-oral surgery
and dental procedures
 Microlaryngeal Tube
• Microlaryngeal surgeries with
narrow airway
• Small cuff size, ID and OD
• Available ID 4,5 or 6 mm
• Can be inserted through LMA
• Forceps is required
 Laryngectomy Tube
• Designed to be inserted through
tracheostomy
• J shaped
• To be made straight before
intubation
• No bevel end
 Jet tube
• Uncuffed tube with additional
lumen
• Jet ventilation
• Monitoring airway pressure
• Gas sampling
• LA Administration
 Hunsaker Mon-Jet Tube
• Narrow laser compatible tube
• Providing a channel for
subglottic high frequency jet
ventilation
• Outer diameter of 4.3 mm
• Additional channel for
measuring airway pressure or
carbon dioxide levels.
• Open cuff less design-
contamination of the
environment and requires the
use of total intravenous
anesthesia.
 Laser Resistant Tubes
A. The Norton tube
• Reusable
• Stainless steel
• Flexible tube
• No cuff
 Laser Resistant Tubes
B. The Laser Flex tube
(Mallinckrodt laser tube)
• Airtight stainless steel tube
• Flexible
• Uncuffed or with two cuffs
 Laser Resistant Tubes
C. The Laser-Shield II (Xomed-laser
shield II tube)
• Silicone tube
• Inner aluminum wrap
• Outer Teflon coating
 Laser Resistant Tubes
D. The Bivona Foam-Cuff Laser
tube
• Designed to solve the perforated-
cuff-deflation- problem.
• Aluminum wrapped silicone tube
with unique self inflating foam
sponge filled cuff which prevent
deflation after puncture.
 Wrapped standard tubes
• Standard tracheal tubes (rubber, silicon, and PVC), Wrapped
with laser resistant material (except the cuff).
• The wrapped material may be :
➢ Aluminum or copper foil tape with adhesive back.
➢ Merocel laser guard (merocel wrap).
 Disadvantage of wrapping
• No cuff protection
• Add thickness to the tube.
• Not an FDA approved device.
• May reflect laser beam to non target tissue. Protection varies with
the type of the metal foil used.
• Airway obstruction
• Rough edges
 Protection of the cuff
• Filling the cuff with saline colored with Methylene blue.
• Place the cuff distally in the trachea and covered visible cuff
with moistened cotton pledgets
 Nerve integrity monitor ETT
• Silicone-based tube with a special
silicone elastomeric cuff
• The anatomic proximity of the
recurrent laryngeal nerve to the
vocal cords allows sensors to be
adhered to or embedded on an ETT
• Monitor vocal cord electromyogram
activity during surgery
• Use – Thyroid surgery
 Reinforced Tube
• Also known as Wire-reinforced or
Armored or Flexomettalic
• Concentric steel wire rings
embedded in the wall of the tube
along its entire length
• flexible and resist kinking with
positioning
• Use- Head and neck surgeries
• Disadvantage- if crimped or
kinked, it cannot return to its
normal shape and must be
changed.
 Intubating LMA tube
• Used with LMA
• Wire reinforced silicon tube
• Size: 6 to 7.5 mm
• Reusable
• MRI compatible
• Used for submental intubation
 Parker Flex-Tip Tube
• Soft, flexible, hemispherical,
curved tip pointing toward
the center of the distal
lumen of the tube
• Greater incidence of initial
success and faster tube
passage
 LITA Endotracheal Tube
• Separate channel for injection
of topical anesthetic via 8 holes
above and 2 holes below the
cuff
• To decrease Airway irritability,
coughing and incidence of
laryngospasm during
emergence
 Endotrol Tubes
• Ring loop
• Directional tip control
• Facilitate blind nasal
intubation
• Better with McGrath VL
 Oxford Tube
• L shaped
• Angle lies in Pharynx
• Reduces risk of bronchial
intubation
• Less risk of kinking
 Tehran tube
• Specially designed for nasal
intubation
• Silicon
• Typical upper airway curve
• Reusable
• Can be inserted blindly
 Subglottic Suction Tube
• Dedicated lumen in the dorsal
wall of the tube exiting above the
cuff
• used to evacuate secretions
 Silver-coated Tube
• Prevent bacterial
colonization and bio film
formation
• VAP incidence
 PneuX Tube
• Soft silicon material
• Tracheal seal monitor which
continuously measures the
pressure in between the cuff
and the trachea
• Optimal tracheal seal and
significantly helps reduce the
risk of aspiration.
• Non-stick coating inside
• Adjustable flange
• Atraumatic tip
THANK YOU
INRAVENOUS INDUCING AGENTS & BENZODIAZAPENES

Dr Himanshu Sikri
MD Anaesthesiology, FICM (Apollo), PGDHM
Senior Medical Officer(SMO) (CHS)
Department of Anaesthesia
ABVIMS & DR RML Hospital
 Scope
• Covering the Basics
• From point of view of drug table viva
What are IV inducing agents?
• Drugs given intravenously, appropriate dose, rapid loss of
consciousness, one arm brain circulation time (depends on CO & EF,
approx. 11-15 secs).
• Also may be used to maintain anaesthesia via an infusion and also
provide sedation.
Drugs which will be covered here:
(Commonly used ones in daily practice)
1. Thiopentone
2. Propofol
3. Etomidate
4. Ketamine
5. Benzodizapenes – Diazepam
Midazolam
Lorazepam
Mechanism of Action of Most IV Inducing
Agents
• The most commonly used intravenous anesthetic agents—the Barbiturates,
Propofol, Benzodiazepines and Etomidate act at GABA receptor (a ligand-
activated ion channel, composed of five subunits).

• Bind to “a” subunit and increase the transport of chloride (Cl−) ions across
the membrane and into the postsynaptic neuron. The postsynaptic neuron
becomes hyperpolarized, which functionally inhibits further propagation of
nerve signals.
• These drugs do not bind at the same location as GABA itself (the
orthosteric binding site), instead they bind at other locations (allosteric
sites) and are positive allosteric modulators of the GABA receptor.
Mechanism of Action of Most IV Inducing
Agents
 About Every Drug

1. What is this?
2. How to recognise it?
3. Mechanism of action?
4. Clinical uses with doses?
5. Pharmacokinetics?
6. Pharmacodynamics?
7. Special points to mention if any?
 What is this?

THIOPENTONE
Thiobarbiturate (Barbituric Acid) carbonate
 How to recognise it?

• Yellow coloured powder formulation.

• 1gm or 500 mg.
• Reconstituted in normal saline to make a 2.5% solution, has a alkaline
pH of approx. 10.1. Hence, when added to lactated ringers or other
acidic drug preparations, crystalline precipitation occurs, may
irreversibly occlude intravenous tubing and catheters.
 Mechanism of action?

• Same as described previously.

(potentiation of the chloride current mediated through the γ-
aminobutyric acid type A (GABAA) receptor complex).
Clinical uses with doses?
Induction doses are reduced in the
geriatric population by 30% to 40%, in
obstetric patients in early term (7 to 13
weeks’ gestation), in patients with
advanced ASA 3 or 4 and when used in
conjunction with other medications.
 Pharmacokinetics?

• Undergoes hepatic metabolism mainly by oxidation, also by N-

dealkylation, desulfuration, and destruction of the barbituric acid ring
structure.
• Resulting metabolites are inactive and excreted through urine and,
after conjugation, through bile.
• Redistribution to inactive tissue sites.
• Long context-sensitive half-time.
 Pharmacodynamics?

• CNS: dose-dependent CNS depression, anti-analgesic, potent cerebral

vasoconstrictor and decreases CBF, CBV and ICP. Hence decreases
CMRO2. Decreases electrical activity on the EEG.
• CVS : modestly decreases systemic arterial blood pressure.
Exaggerated decreases in blood pressure are likely to follow the
administration to patients with hypovolemia, cardiac tamponade,
cardiomyopathy, coronary artery disease, or cardiac valvular disease.
• Respiratory System: respiratory depressant, Suppression of laryngeal
cough reflexes is not as profound as after Propofol administration.
 Special points to mention if any?

• Accidental intra-arterial injection:

crystal accumulation, excruciating pain, intense vasoconstriction, often
leading to severe tissue injury (gangrene).
maintain perfusion, reduce the drug concentration by dilution,
blockade of the sympathetic nervous system in the involved extremity.
• Induced histamine release: not preferred in asthma, COPD
• Through stimulation of aminolevulinic acid synthetase, the
production of porphyrins is increased. Therefore, barbiturates should
not be administered to patients with acute intermittent porphyria.
 Special points to mention if any?

• Methohexital, an Oxybarbiturate
activates epileptic foci, thus facilitating their identification during
surgery targeted to ablate these sites. For the same reason, a popular
choice for anaesthesia to facilitate electroconvulsive therapy.
• Phenobarbital is mainly eliminated unchanged via renal excretion.
 What is this?

PROPOFOL

(2,6 di-isopropylphenol),
an alkyl phenol
 How to recognise it?

• A milky white liquid emulsion.

• Constituents: 10% soybean oil, 2.25% glycerol, and 1.2% lecithin,
ethylenediaminetetraacetic acid (0.05 mg/mL) or metabisulfite (0.25
mg/mL) or benzyl alcohol (1 mg/mL) are added to the emulsions by
the different manufacturers as retardants of bacterial growth,
solutions should be used as soon as possible or at least within 12
hours after opening the Propofol vial.
• pH is approximately 7.
• concentration is 1% (10 mg/mL). In some countries, a 2% formulation
is available.
 Mechanism of action?

• Same as described previously

(potentiation of the chloride current mediated through the γ-
aminobutyric acid type A (GABAA) receptor complex)
 Pharmacokinetics?

• Rapidly metabolized in the liver, resulting water-soluble compounds

inactive and excreted through the kidneys.
• Extrahepatic metabolism : lungs probably play a major role in this and
likely account for the elimination of up to 30% of a bolus dose.
• Onset of action approx. 30 secs.
• Redistribution seen.
• Context-sensitive half-time is brief, used as infusion.
• Awakening usually seen within 8 to 10 minutes after an induction
dose.
 Pharmacodynamics?

• CNS: dose-dependent CNS depression, no analgesic properties,

decreases CBF, CBV and ICP. Hence decreases CMRO2. Decreases
electrical activity on the EEG. Reduced mean arterial pressure caused
by peripheral vasodilation can critically compromise cerebral
perfusion. Twitching or spontaneous movement can be observed
during induction (similar to seizures but not seizures), anticonvulsant ,
safely administered to patients with seizure disorders.

• CVS: larger decreases in SAP, profound vasodilation, direct myocardial

depressant, markedly inhibits the normal baroreflex response.
 Pharmacodynamics?

• Respiratory System: respiratory depressant, Suppression of laryngeal

cough reflexes is more profound as after thiopentone administration.

• Other effects : antiemetic activity, propofol infusion syndrome

(metabolic acidosis, rhabdomyolysis, or hyperkalemia), Pain from
injection (selecting an antecubital vein -larger, faster venous flow
rate,injecting a small dose of lidocaine (20 to 40 mg intravenously and
applying proximal venous occlusion for 15 to 60 seconds), small dose
of opioid).
 Clinical uses with doses?

1. Induction and Maintenance of General Anesthesia : 1 to 2.5 mg/kg

IV adults, 2.5 to 3.5 mg/kg IV children, 100 - 200 μg/kg/min.
2. Sedation : 25 - 75 μg/kg/min IV.
3. Antiemetic : 10 to 20 mg IV, or 10 to 20 μg/kg/min as an infusion.
 Special points to mention if any?

• Lipid emulsion formulation of Propofol has several disadvantages

including pain on injection, risk of bacterial contamination, and
hypertriglyceridemia, Propofol Infusion Syndrome, with prolonged
infusion.
• Hence, Fospropofol - water-soluble phosphate ester prodrug of
Propofol, 2,6-diisopropylphenoxymethyl phosphate disodium salt,
single dose vial at a concentration of 35 mg/mL. Bolus (6.5 mg/kg IV),
onset of sedation is slower (4 to 8 min) and duration of action is
longer (5 to 18 min) than an equivalent dose of Propofol.
 What is it?

ETOMIDATE

(Carboxylated imidazole derivative)

 How to recognise it?

• White solution, poorly soluble in water.

• 2 mg/mL solution in 35% propylene glycol.
• Solution has a pH of approx. 6.9.
 Mechanism of action?

• Same as described previously

(potentiation of the chloride current mediated through the γ-
aminobutyric acid type A (GABAA) receptor complex)
 Pharmacokinetics?

• Metabolism - primarily hepatic , ester hydrolysis to inactive

metabolites, which are then excreted in urine (78%) and bile (22%).
• Primarily bound to albumin.
• 0.1 mg/kg provides about 100 seconds of unconsciousness.
• Redistribution to inactive tissue sites (comparable to thiopental and
propofol).
• Onset approx. 11- 15 secs, Duration of action 3 to 8 mins.
• Short context sensitive and elimination half lives.
 Pharmacodynamics ?
• CNS: dose-dependent CNS depression, anti-analgesic, potent cerebral
vasoconstrictor and decreases CBF, CBV and ICP. Hence decreases
CMRO2, but no neuroprotection, may activate seizure foci,
manifested as fast activity on the EEG, spontaneous movements
characterized as myoclonus occur in more than 50% of patients.

• CVS: modestly decreases Arterial BP, SVR, HR & CO, minimal

depression on myocardial contractility. Hypotensive effects
exaggerated in the presence of hypovolemia. Overall cardio stable.
 Pharmacodynamics ?
• Respiratory System: respiratory depressant, but less than other
inducing agents.
• Other significant effects: Adrenocortical suppression by producing a
dose-dependent inhibition of 11β-hydroxylase, lasts at least 4 to 8
hours, hence use controversial in critically ill.
 Clinical uses with doses?
1. Induction : Rapid intravenous induction of anesthesia, especially in
patients with compromised myocardial contractility, coronary artery
disease, or severe aortic stenosis, standard induction dose 0.2 to
0.3 mg/kg IV.
2. ECT: Etomidate remains a useful hypnotic for electroconvulsive
therapy as it provides a longer seizure duration than propofol or
methohexital.
 Special points to mention if any?

• PONV may be more common than after the administration of

Thiopental or Propofol.
• ABP-700: Development of novel short-acting Etomidate derivative is
under way with the goal of finding an analog with limited adrenal side
effects.
 What is this?

KETAMINE
(Phencyclidine derivative)
 How to recognise it?

• Clear liquid formulation.

• Partially water-soluble and highly lipid soluble.
• Two stereoisomers: S(+) form is more potent than the R(−) isomer.
• Available as a Racemic mixture (10/50/ 100 mg/mL).
 Mechanism of action?
• Inhibition of the N-methyl-d-aspartate (NMDA) receptor complex.
• Causes incomplete amnesia, potent analgesia, airway reflexes
preserved, increased lacrimation and salivation, hence co -
administered with an anticholinergic.
• “Dissociative anesthesia,” wherein the patient’s eyes remain open
with a slow nystagmic gaze (cataleptic state).
 Pharmacokinetics?
• Metabolism occurs primarily in the liver and involves N demethylation
by the cytochrome P-450 system to form mainly Norketamine, active
metabolite but less potent, subsequently hydroxylated and
conjugated into water-soluble inactive metabolites that are excreted
in urine.
• Redistribution to inactive tissue sites.
• Low protein binding.
• Onset of action in 30 to 60 secs after IV and in 2 to 4 minutes after IM
injection, duration of action 10 to 20 mins.
 Pharmacodynamics?
• CNS: cerebral vasodilator, increases CBF , CMRO2. Thus, ketamine is
usually avoided in patients with intracranial disease, especially
increased ICP. Potential to produce myoclonic activity, but still an
anticonvulsant and may be considered for treatment of status
epilepticus.
Emergence Reactions: vivid colourful dreams, hallucinations, out-of-
body experiences and increased and distorted visual, tactile, and
auditory sensitivity. Euphoric state, abuse potential. Limited by co
administration of a BZP.
 Pharmacodynamics?
• CVS: Centrally mediated sympathetic stimulation transiently increases
in SBP, HR, CO. Direct myocardial depressant which becomes
prominent in critically ill or hypovolemic patients.

• Respiratory System: minimal depression, airway reflexes preserved, in

children laryngospasm chances increased due to increased induction
of secretions, relaxes bronchial smooth muscles, hence used in
reactive airway disease.
 Clinical Uses with doses?
• Can be administered by multiple routes (intravenous, intramuscular,
oral, rectal, epidural), useful option for premedication in mentally
challenged/uncooperative paediatric patients.
• Induction and Maintenance of Anesthesia : 1 to 2 mg/kg IV or 4 to 6
mg/kg IM, 30 to 90 μg/kg/min, Short context sensitive half life.
• Analgesia : 0.2 to 0.8 mg/kg IV bolus, 3 to 5 μg/kg/min infusion. Burn
dressings, caesarean section under neuraxial anesthesia with an
insufficient regional block, post operative period.
• Treatment of Major Depression : single intravenous infusion of
ketamine 0.5 mg/kg over 40 minutes.
What are these ?
Commonly used Benzodiazepines:
1. Diazepam
2. Midazolam
3. Lorazepam
Benzene ring fused to a seven-member
diazepine ring.
 How to recognise them?
MIDAZOLAM DIAZEPAM LORAZEPAM
Clear colourless liquid formulation Clear to slightly yellow liquid Clear colourless liquid formulation
formulation

1mg/ml or 5mg/ml 5mg/ml 2mg/ml or 4mg/ml

 Mechanism of Action?
• Same as described previously
(potentiation of the chloride current mediated through the γ-
aminobutyric acid type A (GABAA) receptor complex)

MIDAZOLAM DIAZEPAM LORAZEPAM

Amnesia> Sedation Sedation> Amnesia Sedation= Amnesia, most
potent amongst the three
 Pharmacokinetics?
• Metabolism of benzodiazepines occurs in the liver predominantly through
microsomal oxidation and glucuronide conjugation.
• Lorazepam is does not undergo oxidative metabolism and is excreted after
a single-step conjugation to glucuronic acid.
• Diazepam undergoes hepatic metabolism to active metabolites
desmethyldiazepam and oxazepam.
• Midazolam is selectively metabolized by hepatic cytochrome P450 3A4 to a
single dominant metabolite, 1-hydroxymidazolam which is half as active as
Midazolam.
• Slower effect-site equilibration time.
• Midazolam has the shortest context-sensitive halftime.
 Pharmacodynamics?
• CNS: decrease CBF, CMRO2 and ICP, but less pronounced as compared to
other agents, no neuroprotection, potent anticonvulsants.
• CVS: decrease MAP, virtually no change in CO.
• Respiratory system : no significant depression when administered alone, be
cautious with opioids.
• Diazepam and Lorazepam- propylene glycol formulation, hence pain on
injection site.
• Exposure of the acidic midazolam preparation to the physiologic pH of
blood causes a change in the ring structure that renders the drug more
lipid soluble.
• All three drugs are highly protein bound.
 Clinical Uses?
• Preoperative Medication : Midazolam IV 0.5- 1 mg bolus. Oral syrup (2
mg/mL) at a dose of 0.25-0.5 mg/kg 30 minutes before induction of
anaesthesia.
• Intravenous Sedation: Midazolam in doses of 1.0 to 2.5 mg IV (onset within
30 to 60 seconds, time to peak effect 3 to 5 minutes, duration of sedation
15 to 80 minutes).
• Induction of Anaesthesia: Midazolam, 0.1 to 0.15 mg/kg.
• Maintenance of Anaesthesia.
• Postoperative Sedation.
• Paradoxical vocal cord motion post operatively, a cause of nonorganic
upper airway obstruction, midazolam 0.5 to 1 mg IV may be an effective
treatment.
 Special points to mention if any?

• Remimazolam (CNS-7056) : ultrashort-acting benzodiazepine,

carboxylic ester group that is rapidly hydrolyzed by tissue esterases,
analogous to Remifentanil, less prolonged sedation compared with
midazolam, particularly in patients with liver disease or those taking
cytochrome P450–inhibiting drugs.

• Flumazenil : specific and exclusive benzodiazepine antagonist,

recommended initial dose is 0.2 mg IV (8 to 15 mcg/kg IV), which
typically reverses the CNS effects of benzodiazepine agonists within
about 2 minutes. If required, further doses of 0.1 mg IV (to a total of
1mg IV) at 60s interval.
“Life is a chain reaction taking you day by day,
nothing is permanent is this crazy world”

This time shall too pass!!!

ALL THE BEST.

THANK YOU
Oxygen Therapy
Prof (Dr) Neerja Banerjee
Consultant Anaesthesia
ABVIMS, Dr. RML Hospital
Objectives
• Physiology

• Oxygen Transport

• Oxygen Therapy Devices

• High Flow Nasal Oxygen Therapy

• Hyperbaric Oxygen Therapy

• Oxygen Toxicity
Journey Of Oxygen
AIR

MITOCHONDRIA
Journey…
• Breathing - Inspired gas transported to alveoli

• Gas Exchange - Between Oxygen in alveoli and blood

• Transport - Oxygenated blood transported to tissues

• Diffusion - Between tissue capillaries and mitochondria

 Oxygen Cascade
Atmosphere air (dry) (159 mm Hg)

Humidification
Lower resp tract (moist) (150 mm Hg)

O2 consumption and
alveolar ventilation Alveoli PAO2 (104 mm Hg)

Venous
admixture Arterial blood PaO2 (100 mm Hg)

Tissue
extraction Venous blood PV O2 (40 mm Hg)

Mitochondria PO2 (7 – 37 mmHg)

Oxygen Cascade
159mm Hg
Atm. Air (Dry)
(21 % of 760)

Humidification
47mm Hg

Lower Resp. Tract 149mm Hg

(Moist 37oc) 21% of 713 (760-47)
Oxygen Cascade
Lower Resp. Tract 149mm Hg
(Moist 37oc) 21% of 713 (760-47)

101mm Hg
Alveolar Air
Oxygen Cascade
101mm Hg
Alveolar Air

Venous admixture

97mm Hg
Arterial Blood

PaO2 = 100 – 0.3 x age (years) mm Hg

A – a = 4 – 25 mmHg
Oxygen Cascade
Pa O2 = 97mm Hg
Alveolar Air (Sat. > 95 %)

Utilization by tissue

Mitochondria Mixed Venous PV O2 = 40mm Hg

Sat. 75%
PO2 7-37mmHg blood

Pasteur point – The critical level for aerobic metab. to continue

(1 – 1-2 mmHg PO2 in mitochondria)
Oxygen Cascade
Venous admixture
(physiological shunt)

Low VA/Q Normal True shunt

(normal anatomical shunt)

Pulmonary
Extra Pulm.
(Bronchial veins)
(Thebesian veins)

Normal = upto 5 % of cardiac output

Oxygen Transport

• Oxygen Content

• Oxygen Flux

• Oxygen Uptake

• Oxygen Extraction Ratio

How is oxygen transported in blood

• Combined with Haemoglobin - 97%

• Dissolved in plasma - 3%
Oxyhaemoglobin Dissociation Curve

• Percentage of haemoglobin saturation with Oxygen

(SpO2) at different partial pressures of oxygen in
blood

• Sigmoid curve

• P 50 - PaO2 at which haemoglobin is 50% saturated

• 27mmHg
Oxyhaemoglobin Dissociation Curve (ODC)
Dissolved in plasma

• 0.003ml/100ml/mmHg PaO2

• Breathing air- PaO2 - 100mmHg

• Oxygen dissolved in plasma - 0.3 ml/100ml of blood

Oxygen Content

• Amount of oxygen carried by 100ml of blood

• Dissolved Oxygen + Oxygen bound to haemoglobin

• PO2 x 0.03 + SO2 x Hb X 1.34

• Oxygen content
• Arterial blood - CaO2
• Venous blood- CvO2
Oxygen content of Arterial blood -
CaO2
• PaO2 x 0.03 + SaO2 x Hb X 1.34

• 100 x 0.03 + 100 x 14 x 1.34 = 20ml/100ml

• 20ml/100ml
Oxygen Content of venous blood -
CvO2
• PvO2 x 0.03 + SvO2 x Hb X 1.34

• 40 x 0.03 + 75 x 14 x 1.34 = 15ml/100ml

• 15ml/100ml

• Arterio venous difference C(a -v )O2

• 20 - 15 = 5ml/100ml
Oxygen Flux/ Oxygen Delivery -DO2

• Amount of oxygen leaving left ventricle per minute

and delivered to tissues each minute

• Arterial oxygen content (CaO2) x Cardiac Output

• 20ml/100ml x 5000ml/min = 1000ml /min

• 1000ml /min
Oxygen returning to lungs

• Venous oxygen content CvO2 x cardiac output

• 15ml/100ml x 5000ml = 750ml/min

• 750ml/min
Oxygen uptake VO2

• Amount of oxygen taken up by tissues per minute

• VO2 = CO x C (a-v )O2

= 5000ml x ( 20 - 15 )ml /100ml

= 250ml/min

• 250ml/min
Oxygen Extraction Ratio

• An index of efficiency of oxygen transport

• Oxygen Uptake / Oxygen Delivery

• VO2 / DO2

• 250 / 100 = 25 %

• 25%
Indices to evaluate transfer of oxygen
in lungs
• Shunt Equation

• P(A -a) O2 - 5-25 mmHg

• PaO2/FiO2 - 400-500

• PaO2 /PAO2 - 0.75

Hypoxia

• Hypoxia - Deficiency in either the delivery or the

utilisation of oxygen at tissue level

• Hypoxemia - Reduction of oxygen in blood ie

decreased partial pressure of oxygen in blood

• PaO2 <60mmHg
Types of hypoxia

• Hypoxic hypoxia

• Anaemic hypoxia

• Stagnant hypoxia

• Histotoxic hypoxia
Hypoxic hypoxia

• Reduced inspired oxygen tension - High altitude, hypoxic

gas mixture

• Hypoventilation

• Shunts- septal defects, cardiovascular malformations

• V/ Q mismatch- pneumonia, lobar collapse

• Increased oxygen demand - shivering, fever, convulsions,

thyrotoxicosis

• Diffusion defects
Anemic hypoxia

• Anemia

• Carbon monoxide poisoning

• Methaemoglobinemia

• Sickle cell disease

Stagnant hypoxia

INSUFFICIENT BLOOD FLOW

• Decreased circulating blood volume
• Cardiac failure
• Venous pooling
• Vasodilatation
• Localised hypoperfusion
Histotoxic hypoxia

IMPAIRED UTILISATION OF OXYGEN BY

TISSUES
• Cyanide Poisoning
Causes of peri-operative hypoxia
• Airway
• Laryngospasm, Airway Obstruction
• Misplaced endotracheal tube- inadvertent extubation, endobronchial
intubation, Endotracheal tube obstruction
• Occlusion/ kinking/ Detachment of anesthesia circuit

• Breathing
• Hypoventilation, secretions
• Pneumothorax
• Bronchospasm
• Positioning , V/Q mismatch
Causes cont….
• Circulation
• Low cardiac output
• Embolism
• Drugs
• Respiratory depressants
• Inadequate reversal of neuromuscular blocking agent
• Anaphylaxis
• Equipment failure
• Breathing circuit failure
• Delivery of hypoxic mixture
• Monitoring failure
 Signs and symptoms of hypoxia
Mild to moderate Severe
Airway Air hunger

Dyspnoea
Tachypnea
Shallow & laboured breathing Increasing dyspnoea
Breathing
Tachypnoea, possible bradypnoea
Somnolence, confusion
Disorientation

Tachycardia Bradycardia
Cardiac Mild hypertension Arrhythmia
Peripheral vasoconst Hypotension

Anxiety
Restlessness
Neurological Loss of coordination
Impaired judgement
Disability Obtunded mental status
Lassitude
Headache

Exposure Pale, cold, clammy Cyanosis

Case scenario
• Diagnosed case of Covid
• Pulse rate-110/min
• BP-110/80mmHg
• SpO2- 90%

Oxygen Therapy
Case scenario
• Polytrauma
• Chest trauma
• B/L Femur fracture
• Pulse- 120/min
• BP- 90/60mmHg
• RR- 35/min
• GCS -14

Oxygen Therapy
Case scenario
• Morbid obesity posted for bariatric surgery
• Difficult intubation
• Preoxygenation

Oxygen Therapy
Case scenario
• Postoperative case of peritonitis
• Extubated
• Conscious, complaining of severe pain
• Pulse 110/min
• BP- 100/70mmHg
• RR- 34/min
• SpO2- 92%

Oxygen Therapy
Oxygen Therapy
• Oxygen therapy is the administration of oxygen at
concentration greater than ambient air to treat or
prevent hypoxia

• Orthobaric - Administration of oxygen more than 21% at

ambient atm pressure

• Hyperbaric - Administration of oxygen more than 21% at

more than ambient atm press i.e. >1ATA
Indications of Oxygen Therapy

• Acute hypoxaemia - Trauma, acute MI, hypoventilation

• Chronic hypoxemia
• Anemia, Carbon monoxide poisoning
• Increase oxygen demand - hyperthermia, shivering, thyrotoxicosis
• Palliative care
• Preoxygenation
• Apneic Oxygenation
• Intraoperative and postoperative hypoxemia
Preoxygenation

• Administration of oxygen prior to intubation to increase

safe apnea time
• Safe apnea time - Time duration until oxygen desaturation
occurs ie 88%-90% after stopping ventilation/breathing
• Denitrogenation of lungs
• ETO2 gold standard for monitoring denitrogenation - 90%
Principle of Preoxygenation

• Oxygen stores- 1500ml

• Haemoglobin 80%,Lungs 30%,myoglobin 20%
• High affinity of oxygen to Hb, myoglobin
• Lungs - main source of oxygen in apnea ie FRC
• FRC - 2300ml
@21% - Oxygen content 480ml - safe apnea - 90secs
@100% - Oxygen content 2300ml - safe apnea - 4-5 mins
• Resting oxygen consumption 200-300ml/min
Technique of Preoxygenation

• Flush breathing circuit with 100% oxygen

• Head up position
• Ensure proper seal of mask
• 10-15 l/min of 100% Oxygen
• 3 mins of normal Tidal volume breaths
• 8 vital capacity breaths in 1 min
• PEEP 4-6 cm H2O
• Patients with poor respiratory efforts - NRB mask,
BVM@15l/min, HFNO
Apneic Oxygenation

• Used to extend Apnea Time beyond which can be achieved

by preoxygenation
• An adjunct to pre oxygenation
• Airway should be patent
Principle of Apneic Oxygenation

• Alveolar Oxygen removal - 200-300ml/min

• CO2 excretion in alveoli - 10-20ml/min

• This difference generates negative pressure ~ 20cm H2O

• Mass flow of gases from pharynx to alveoli through
unobstructed airway
NO DESAT (Nasal Oxygenation During Efforts Securing A
Tube)

• Use of supplemental oxygen via nasal cannula ,during

intubation to increase apnea time
• Apneic Oxygenation
• Preoxygenation
• Mask ventilation after muscle relaxant
• Continue Nasal oxygenation - 15 l/min throughout
• No ventilation
• No CO clearance
THRIVE - Transnasal Humidified Rapid Insufflation
Ventilatory Exchange

• Oxygenation and ventilation without ventilatory movements

• Apneic Oxygenation
• Prolongs apnea time
• High Flow Nasal Oxygen therapy
• Oxygen flow- 70l/min
• Warm and humidified gases
• CPAP- 5-7cm H2O
• Use jaw thrust to maintain airway patency
Oxygen Delivery Systems
Oxygen Delivery Systems
ORTHOBARIC OXYGEN THERAPY

• Ambient Pressure
• Variable Performance Devices
• Fixed Performance Devices

• Positive Pressure Ventilation

• Non Invasive - CPAP, BIPAP
• Invasive
Oxygen Delivery Systems
HYPERBARIC OXYGEN THERAPY
• Monoplace Hyperbaric Oxygen Therapy Chamber
• Multiplace Hyperbaric Oxygen Therapy Chamber
Classification of Oxygen Delivery Systems
According to design According to performance
• Low Flow • Variable performance Device
• High flow • Fixed Performance Device
• Reservoir
• Enclosures
Oxygen Delivery Systems- According to
Design
LOW FLOW RESERVOIR
• Nasal Cannula • Reservoir cannula
• Nasal catheter • Simple Mask
• Partial Rebreathing Mask
HIGH FLOW • Non Rebreathing Mask
• Venturi mask
• Air Entrainment Nebulisers ENCLOSURE

• Blending Systems • Oxyhood

• High Flow Nasal Cannula • Oxygen Tent

Oxygen devices
Low Flow system High Flow System

• Gas flow insufficient to • Gas flow is sufficient tp

meet patient’s PIFR and meet patients PIFR and
minute ventilation minute ventilation
requirement requirement

• FiO2 dependent on • FiO2 independent of

patients ventilatory patients ventilatory
pattern pattern
Oxygen Devices- According to Performance
Fixed Performance Variable Performance
Patient Independent Patient Independent

• High Airflow Oxygen • No Capacity - Nasal cannula,

Enrichment Systems - HAFOE Nasal catheter

• Anaesthesia circuits • Small Capacity - Simple Mask

• Ventilators • Large Capacity - Partial

Rebreathing Mask, Non
• High Flow Oxygen Therapy Rebreathing Mask
Cannula - HFNC
Variable performance Device
PATIENT FACTORS DEVICE FACTORS

• Inspiratory Flow Rate • Oxygen Flow Rate

• Minute Ventilation • Capacity of Device

• Duration of Inspiration • Resistance

LOW FLOW SYSTEMS
Nasal Cannula
• Plastic Disposable device with two prongs (1cm) , inserted in
vestibule of nose

• 1 l/min - 24%

• 2 l/min - 28%

• 3 l/min - 32%

• 4 l/min - 36%

• 5 l/min - 40%

• 6 l/min - 44%
 Estimation of Fio2 from a low-flow system for
patient with normal ventilatory pattern
Cannula 6 L/min VT, 500 mL
Mechanical reservoir None Rate, 20 breaths per min
Anatomic reservoir 50 mL I/E ratio, 1:2
100% O2 provided/sec 100 mL Inspiratory time, 1 sec
Volume inspired O2 expiratory time, 2 sec
Anatomic reservoir 50 mL
Flow/sec 100 mL
Inspired room air 0.2 × 350 mL = 70 mL
O2 inspired 220 mL
220 O2 = 0.44
FiO2
500 TV

A patient with ideal ventilatory pattern who receives 6L/min O2 by nasal cannula
is receiving FiO2 of 0.44.
Nasal Catheter
• Catheter with several holes at tip

• Depth - Nose to Tragus

• Should visualise tip behind uvula

• Flow rate 1-6 l /min

• 24- 44% oxygen

• Contraindications
• Faciomaxillary injury, Nasal blockade, deformity
• Base skull fracture
• Epistaxis, coagulation abnormality
Transtracheal catheter
• Teflon catheter

• Inserted over guidewire

between 2nd - 3rd tracheal
rings

• 1-4 l/ min

• 24% - 36% Oxygen achieved

Reservoir Systems
Nasal Reservoir and Pendant Reservoir
Nasal Reservoir Pendant Reservoir
Reservoir Masks
• Simple Face Mask

• Partial Rebreathing Face Mask

• Non Rebreathing Face Mask

Simple Face Mask
• Variable Performance Device

• 100- 200ml Reservoir

• Open ports for exhalation

• Air dilution occurs during

inhalation

• Minimum 5l/min flow

• 5- 8 l/min

• 40% -60% Oxygen achieved

Tracheostomy Mask
Partial Rebreathing Mask
• Reservoir 600ml- 1000ml

• No valves

• Reservoir bag filled with oxygen and

exhaled gases (first one third of gases)

• Flow > 6l/min

• 50%-70% Oxygen achieved

• The bag should remain inflated to

prevent rebreathing
Non Rebreathing Masks
• Reservoir bag - 600ml-1000ml
• Unidirectional valves
• Inspiratory valve - prevents
exhaled gases from entering
reservoir bag
• Expiratory valve- prevents air
entrainement
• Flow - 10-15l/min
• 80%-90% oxygen achieved
• Reservoir bag should be
completely inflated
Reservoir Bag
Enclosures
Incubator

• Heating with supplemental oxygen

• Provides temperature control

• Flow - 10-15 l/min

• 40%-50% Oxygen
Oxygen Hood
• It covers only head

• Useful for paediatric

patients, facial injuries,
burns

• Heated and humidified

gases

• Flow rate >6l/min

• 24% - 90% oxygen

Oxygen Tent
• Canopy covers head and
shoulder or over entire body
• Flow - 12-15l/min
• 50%-60% oxygen achieved
• Disadvantage
• Cumbersome
• Difficult to clean
• Leakage of gases
• Limits patient mobility
High Flow Devices
High Flow Devices
• Air Entrainment Devices
• Venturi Mask
• Nebulisers

• Blending Systems
Air Entrainment Devices
• Based on Bernoulli’s Principle

• A rapid velocity of gas exiting from a restricted

orifice Creates SUBATMOSPHERIC LATERAL
PRESSURE

• Results in atmospheric air being entrained into

main stream
Characteristics of Air Entrainment devices
• Amount of air entrained varies with the size of
oxygen port and O2 jet velocity

• The entrained air dilutes the oxygen in a particular

ratio to deliver the set FiO2

• The higher entrainement results in lesser FiO2 and

higher delivered flow rate

• The FiO2 can be varied by altering the oxygen port

size and the entrainment port
Venturi masks
• HAFOE - High Air Flow Oxygen Enrichment

• Colour coded with varying oxygen port size

• 24%- 60%

• Different Flow rates with different port

size

• Single Adapter with one oxygen port size

and varying entrainment port is also
available
Approximate Air Entrainment Ratio and
Gas Flows for different FiO2
Recommended O2 Total Gas Flow (to Port)
FiO2 (%) Ratio
Flow (L/min) (L/min)
24 25.3:1 3 79

26 14.8:1 3 47

28 10.3:1 6 68

30 7.8:1 6 53

35 4.6:1 9 50

40 3.2:1 12 50

50 1.7:1 15 41
Air Entrainment Nebuliser
• Fixed Orifice

• Variable Entrainment port size

• Flow rate - 15 l/min

Aerosol Face tent
• 28 -100% mask

• Used in Intubated and

Tracheostomised patients

• Provides humidity and

temperature control
Tracheostomy T tube
collar
Blending Systems
• Separate pressurised Air
and Oxygen input

• Mixture of gases manually

or with blender

• Flow rate - 60l/min

• 24%-100%

• Fixed performance device

HFNC Oxygen Therapy
HIGH FLOW NASAL OXYGEN THERAPY
• Air Oxygen blender delivers 21%-100% oxygen

• Flow rates -60 l/min

• Gas HEATED and HUMIDIFIED through active heated humidifier

• CPAP 4-8 cm H2O

Physiological effects
• Nasopharyngeal dead space wash
out, CO2 washout
• Decreased nasopharyngeal
resistance
• Decreased work of breathing
• CPAP
• Alveolar recruitment
• Heated and humidified gases, better
tolerated , great comfort
• Better control of FiO2
• Better Mucociliary clearance
HFNO

• Wide bore prongs and

tubings- less resistance
• Flowmeter- 60l/min
• Oxygen Air blender
• Warm Humidifier
• Single tubing with
heated wire
• Distilled water for
humidification
• 30 days
Physiological basis
• Peak Inspiratory Flow Rate (PIFR) - 15l/min -20 l/min
• In distress increased 100-120l/min
• Normal breathing heating and humidification-- 36deg C, 80-90%
• Cold and High flow gases-
Increased fluid and heat losses, increased metabolic oxygen requirement,
patient discomfort
Drying of secretions
Poor mucociliary clearance
Poor compliance
Mechanism of action And Effects
WASHOUT OF PHARYNGEAL DEAD SPACE

• Generates Oxygen reservoir

• Rebeathing of CO2 minimised

• Decreases dead space

• Increases alveolar ventilation beyond MV ratio

Cont…...
DECREASED WORK OF BREATHING

• Warm and humidified gases- Reduced energy

required for gas conditioning

• Reduced upper airway resistance bcoz of high flow -

Decreased respiratory effort
Cont...
• Alveolar Recruitment/CPAP

• CPAP- 2.7 - 7.4mmHg

• Improvement in Mucociliary clearance

• Provides accurate & constant FiO2

Indications- Anaesthesia
• Preoxygenation
• Apneic Oxygenation -
• THRIVE( Transnasal humidified Rapid Insufflation
Ventilatory Exchange)- apnea time 5-60 mins, SPO2
>90%, etCO2 rise 1.13mmHg/min
• Rapid Sequence Induction
• Awake Fibreoptic Intubation
• Extubation and post-operative oxygenation
Indications cont...
• Surgery of Airway
• Surgery involving shared airway
• Laryngotracheal surgery
• Fibre optic bronchoscopy
• Fibre optic guided Airway management
• Obstetric Anesthesia
• Paediatric Anesthesia
Indications - Critical Care
• Acute Hypoxemic Respiratory Failure

• Pulmonary edema

• Post extubation respiratory failure

• Weaning off Mechanical ventilation

• Palliative care

• Chest trauma

• Asthma
Advantages
• Reduces respiratory rate, work of breathing
• Increased comfort & Unobtrusive
• Tracheostomy option
• Precision with FiO2
• One interface for all FiO2
Contraindications
• Decreased level of consciousness
• Uncooperative patient
• Faciomaxillary injury
• Epistaxis
• Airway obstruction
• DO NOT DELAY TRACHEAL INTUBATION
Hyperbaric Oxygen Therapy

Administration of 100% Oxygen

at greater than
atmospheric pressure (1 ATA)
Henry’s Law

Amount of oxygen dissolved in solution

is proportional to its partial pressure

The effect of pressure on oxygen solubility
in blood
Physiological Basis
•Air 19 ml O2 combined with Hb
0.3 ml dissolved in
plasma
•100% O2 20 ml O2 combined with Hb
1.5 ml.O2 dissolved in
plasma
•Hyperbaric O2 20 ml O2 combined with Hb
5-6 ml O2 carried in
solution
 Physiological Basis
Total pressure Content of oxygen dissolved in plasma(vol %)
ATA MmHg Breathing Air 100% Oxygen

1 760 0.32 2.09

1.5 1140 0.61 3.26
2 1520 0.81 4.44
2.5 1900 1.06 5.62
3 2280 1.31 6.80
4 3040 1.80 O2 is not
administered at
5 3800 2.30 pressures above 3

6 4560 2.80 ATA

 Mechanism of Action

• Mechanical
• Reduces bubble size in air embolism and DCS
• Hyper oxygenation
• Immune stimulation
• Neovascularization
• Bactericidal
• Edema reduction
Indications of HBOT
Undersea & Hyperbaric Medical Society USA

• Decompression sickness
• Carbon monoxide poisoning / smoke inhalation
• Clostridia myonecrosis (gas gangrene)
• Crush injury, compartment syndrome, and other acute traumatic
ischemias
• Air or gas embolism
• Enhancement of healing in selected problem wounds
Indications of HBOT
Undersea & Hyperbaric Medical Society USA
• Exceptional blood loss (anemia)
• Necrotizing soft tissue infections (subcutaneous tissue, muscle, fascia)
• Osteomyelitis (refractory)
• Radiation tissue damage
• Skin grafts and flaps (compromised)
• Thermal burns
• Intracranial Abscess
• Idiopathic Sensorineural Deafness
Oxygen Toxicity

100% - not more than 12hrs

80% - not more than 24hrs
60% - not more than 36hrs

Use lowest possible FiO2 compatible with

adequate tissue oxygenation
Oxygen Toxicity cont...

• CNS - Paul Bert Effect

• Pulmonary- Lorraine Smith Effect
• Retinopathy Of Prematurity( ROP)
• Absorption Atelectasis
• Fire Hazard
• Mechanism
Free Radical generation
Alteration of cellular metabolism
Enzyme Inhibition
Paul Bert Effect

• >3ATA HBOT therapy

• In high risk patients - at lower pressures
• Perioral twitching
• Tremors
• Vertigo
• Altered behaviour
• convulsions
Lorraine Smith Effect

• Tracheobronchitis
• ARDS
• Pulmonary Interstitial Fibrosis
Retrolental Fibroplasia

• In premature/ Low birth weight infants

• Retinal Vasoconstriction causes necrosis and Haemorrhage
• Retinal detachment
• Blindness
• Target paO2 < 80mmHg
 THANK YOU
BEST OF LUCK!