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Session Summary

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Session Summary

1. Move to a new topic - just type the topic name (e.g., Ischaemic Heart Disease, Thyroid Disease, Renal Failure, Obesity, Obstructive Sleep Apnoea, etc.)
2. Deeper dive into a specific subtopic within Hypertension - for example:
   • Hypertensive emergencies in detail
   • Phaeochromocytoma anaesthetic management
   • Pharmacology of specific antihypertensives
   • Neuraxial anaesthesia in hypertension
   • Postoperative hypertension
3. A clinical case scenario based on hypertension - e.g., uncontrolled hypertensive patient for emergency laparotomy
4. A focused viva drill on hypertension - rapid-fire questions and model answers

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Session Summary

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PULMONARY OEDEMA

Comprehensive MD Anaesthesiology Teaching Session

Sources: Miller's Anesthesia 10e | Barash's Clinical Anesthesia 9e | Morgan & Mikhail's Clinical Anesthesiology 7e | Harrison's Principles of Internal Medicine 22e

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1. DEFINITION

Standard Textbook Definition

Clinical Importance

• Pulmonary oedema is a life-threatening emergency requiring immediate recognition and treatment
• It is the final common pathway of many cardiac, renal, oncological, and inflammatory disorders
• Perioperative significance: Postoperative pulmonary oedema occurs in ~0.1-2% of all surgical patients; the most common forms are cardiogenic (volume overload/LV failure) and negative pressure (post-obstructive/NPPE from laryngospasm)
• ICU: Flash pulmonary oedema, ARDS-associated, and TRALI account for significant ventilator dependence

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2. INTRODUCTION

Background

Epidemiology

Relevance in Anaesthesia

1. Preoperative: Heart failure with pulmonary oedema = high-risk surgical patient; must be optimised before elective surgery
2. Intraoperative: Fluid overload → cardiogenic pulmonary oedema; acute MI → flash pulmonary oedema; transfusion → TRALI
3. Post-extubation (PACU): Laryngospasm → negative pressure pulmonary oedema (NPPE) - a classic anaesthetic complication
4. ICU: Mechanical ventilation management (PEEP, tidal volume) critically affects pulmonary oedema resolution

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3. BASIC SCIENCES

A. Physiology of Fluid Movement in the Lung - The Starling Equation

• Q = Net fluid flow across capillary (normally ~10-20 mL/hr in adults)
• K = Filtration coefficient (related to capillary surface area and permeability)
• σ (sigma) = Reflection coefficient for albumin (0 = freely permeable; 1 = completely impermeable; pulmonary endothelium ≈ 0.7)
• Pc' = Capillary hydrostatic pressure (normally 7 mmHg average; ranges 0-15 mmHg due to gravity)
• Pi = Interstitial hydrostatic pressure (normally -4 to -8 mmHg - slightly negative)
• πc' = Capillary oncotic pressure (plasma oncotic pressure ≈ 25-28 mmHg)
• πi = Interstitial oncotic pressure (≈ 14 mmHg; albumin concentration ~50% of plasma)

• Forces favouring fluid OUT (filtration): Pc' (~7) + Pi (negative = facilitates filtration) + πi (~14) ≈ favours mild filtration
• Forces favouring fluid IN (reabsorption): πc' (~26) ≈ dominates
• Net: Small amount of fluid (~10-20 mL/hr) filtered out, entirely removed by lymphatics

Key concept: The lung's lymphatic reserve is the crucial protective factor. Lymphatics can increase flow 20-fold over baseline. Pulmonary oedema develops only when this lymphatic reserve is overwhelmed.

B. Stages of Pulmonary Oedema (Pathological Progression)

Stage 1 - Interstitial Oedema (Compensated)

• Fluid enters the interstitium; lymphatics cope initially
• Lung water increases but alveoli remain dry
• CXR: Haziness of vascular markings; Kerley B lines (horizontal lines at lung periphery from distended interlobular septa); peribronchovascular cuffing
• Clinical: Mild dyspnoea; cough; orthopnoea; paroxysmal nocturnal dyspnoea (PND)

Stage 2 - Interstitial Oedema (Decompensated)

• Lymphatic capacity exceeded; Pi becomes less negative
• Interstitial pressure rises toward zero
• CXR: Upper lobe venous diversion; hilar prominence; Kerley A lines (longer, non-septal lines)
• Clinical: Progressive dyspnoea; tachycardia; hypoxaemia begins (V/Q mismatch)

Stage 3 - Alveolar Flooding

• Pi becomes positive; fluid breaches alveolar epithelium (tight junction disruption)
• Alveoli fill with fluid → complete atelectasis of flooded alveoli
• CXR: Bilateral alveolar opacities ("bat wings" or "butterfly pattern"); air bronchograms
• Clinical: Severe dyspnoea at rest; tachypnoea; pink frothy sputum; coarse crackles; cyanosis; severe hypoxaemia (intrapulmonary shunt)

C. Pathophysiology by Mechanism

1. Cardiogenic / Hydrostatic / High-Pressure Pulmonary Oedema

2. Non-Cardiogenic / Increased Permeability Pulmonary Oedema

3. Special Types of Pulmonary Oedema (Perioperatively Relevant)

a. Negative Pressure Pulmonary Oedema (NPPE) / Post-Obstructive Pulmonary Oedema

1. Laryngospasm/upper airway obstruction → patient makes forceful inspiratory effort against a closed glottis (Müller manoeuvre)
2. Markedly negative intrathoracic pressure (can reach -50 to -100 cmH2O; normal = -5 cmH2O)
3. Negative intrathoracic pressure → increases venous return to right heart → dilates right heart → increases pulmonary blood flow → increases Pc'
4. Simultaneously increases left ventricular afterload (transmural pressure increases) → decreases EF → increases LVEDP → increases left atrial pressure → increases pulmonary venous pressure
5. Combined effect: Massive acute increase in pulmonary capillary hydrostatic pressure → acute pulmonary oedema

HIGH-YIELD EXAM POINT (Miller's 10e): NPPE is caused by laryngospasm post-extubation. It is a combination of hydrostatic AND mixed mechanisms. Muscularly healthy patients are at HIGHEST risk because they can generate the most powerful negative intrathoracic pressures.

b. Neurogenic Pulmonary Oedema

c. High-Altitude Pulmonary Oedema (HAPE)

d. Re-expansion Pulmonary Oedema (RPO)

e. TRALI (Transfusion-Related Acute Lung Injury)

• New acute lung injury (ALI) within 6 hours of transfusion
• Bilateral CXR infiltrates
• PaO2/FiO2 <300 mmHg (or SpO2 <90% on room air)
• No pre-existing ALI before transfusion
• No alternative explanation (hydrostatic oedema)

VIVA GOLD: TACO = give diuretics. TRALI = do NOT give diuretics. Getting this wrong in viva is a critical error.

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4. CLASSIFICATION

A. By Mechanism

B. By Cause (Comprehensive Classification)

Cardiogenic

1. Left Ventricular Systolic Failure - ischaemic cardiomyopathy, DCM, myocarditis
2. Left Ventricular Diastolic Failure (HFpEF) - HTN, hypertrophic cardiomyopathy
3. Flash Pulmonary Oedema - acute severe hypertension, acute MI, acute MR
4. Valvular Disease - mitral stenosis, acute aortic regurgitation, acute mitral regurgitation
5. Fluid Overload - excessive IV fluid administration (common in perioperative period)
6. Arrhythmias - AF with rapid ventricular response, acute LV dysfunction

Non-Cardiogenic

1. ARDS (see separate section) - most common cause
2. Sepsis/Septic shock
3. Aspiration pneumonitis
4. TRALI (transfusion-related)
5. Inhalation injury (toxic gases, smoke)
6. Near-drowning
7. Pancreatitis
8. Drug overdose (heroin, aspirin, tricyclics)
9. Neurogenic (SAH, TBI)
10. Reperfusion injury (post-cardiopulmonary bypass)

Special Perioperative Types

1. Negative Pressure Pulmonary Oedema (NPPE) - laryngospasm, post-extubation
2. TRALI - intraoperative or PACU blood transfusion
3. Re-expansion Pulmonary Oedema - post-thoracentesis
4. Volume overload - excessive crystalloids/colloids

C. By Severity (Modified Killip Classification for Cardiogenic Pulmonary Oedema)

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5. ETIOLOGY AND RISK FACTORS

Perioperative Risk Factors for Pulmonary Oedema

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6. CLINICAL FEATURES

Symptoms

Signs

Clinical Pearl: The presence of bilateral basal fine crackles + elevated JVP + S3 gallop = classic cardiogenic pulmonary oedema triad. Wheeze alone does NOT distinguish cardiogenic from bronchospasm - always consider "cardiac asthma."

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7. DIAGNOSIS

Investigations

1. Arterial Blood Gas (ABG) - Essential

• PaO2: Reduced (hypoxaemia); severity reflects extent of alveolar flooding and shunt
• PaCO2: Initially REDUCED (hyperventilation drives CO2 down); if fatigue supervenes → PaCO2 RISES → type II respiratory failure → imminent respiratory arrest
• pH: Respiratory alkalosis early; metabolic acidosis (tissue hypoperfusion) in severe cardiogenic shock
• A-a Gradient: Markedly elevated (shunt physiology)

2. Chest X-Ray

• Cardiogenic: Cardiomegaly; bilateral symmetrical; perihilar; Kerley B lines; pleural effusions; normal/enlarged vessels
• Non-cardiogenic (ARDS): Normal heart size; peripheral/patchy distribution; no Kerley B; no pleural effusions

3. Echocardiography - Gold Standard for Differentiation

• Cardiogenic: Reduced LVEF (<40%); dilated LV; diastolic dysfunction (E/e' ratio >13); wall motion abnormalities; valvular disease
• Non-cardiogenic: Normal or hyperdynamic LV; normal filling pressures; no structural abnormality
• Point-of-care ultrasound (POCUS): B-lines on lung US (vertical hyperechoic artefacts arising from pleural line, reaching edge of screen = "lung rockets") indicate pulmonary oedema. ≥3 B-lines per intercostal space in ≥2 bilateral zones = significant pulmonary oedema

4. BNP / NT-proBNP

• BNP >100 pg/mL (or NT-proBNP >300 pg/mL): Supports cardiac cause
• BNP >400 pg/mL (NT-proBNP >900 pg/mL): High probability cardiogenic oedema
• BNP <100 pg/mL: Makes cardiac cause unlikely (useful to exclude cardiogenic in non-cardiogenic oedema)
• BNP in TRALI: Normal or minimally elevated (not volume overloaded)
• Limitations: Elevated in renal failure, PE, sepsis (non-specific elevation)

5. Pulmonary Artery Catheter (PAC/Swan-Ganz)

• PCWP >18 mmHg = Cardiogenic pulmonary oedema
• PCWP <18 mmHg + clinical pulmonary oedema = Non-cardiogenic (ARDS or other)
• Caveat (Morgan & Mikhail): In "flash" pulmonary oedema, PCWP may be normal at time of measurement even though elevated at time of oedema onset (PCWP normalises rapidly after haemodynamic event)
• PAC does NOT improve mortality (PACMAN trial); use selectively when:
  • Aetiology uncertain after non-invasive testing
  • Refractory to standard therapy
  • Accompanied by haemodynamic instability

6. ECG

• ST elevation/evolving Q waves → acute MI → flash pulmonary oedema → trigger STEMI protocol immediately (Harrison's 22e)
• AF with rapid ventricular rate → tachycardia-mediated cardiomyopathy
• LVH (voltage criteria) → diastolic dysfunction
• Atrial enlargement (P mitrale, P pulmonale) → valvular disease

7. Additional Blood Tests

• Troponin I/T: Elevated → acute MI as trigger
• LFTs, albumin: Hypoalbuminaemia contributes to oedema (reduces πc')
• U&E/creatinine: CKD, electrolyte disturbance
• FBC: Anaemia (reduces O2 delivery, exacerbates LV stress)
• Thyroid function: Hypothyroidism causes pericardial effusion + HF; hyperthyroidism causes high-output HF

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8. MANAGEMENT

Immediate Management of Acute Pulmonary Oedema (APO)

Mnemonic: "LMNOP" (classic teaching, still valid)

• L - Lasix (Furosemide) - IV diuresis
• M - Morphine - reduces anxiety + venodilation (falling out of favour - see below)
• N - Nitrates - potent venodilators; reduce preload
• O - Oxygen (+ positive pressure ventilation)
• P - Position (sit patient upright - legs dependent)

Step-by-Step Acute Management

• Sit upright (reduces venous return → reduces preload → improves respiratory mechanics)
• High-flow O2 via non-rebreather mask; target SpO2 92-96% (avoid >98% which may be harmful)
• Secure IV access (large-bore)
• Continuous monitoring: ECG, SpO2, NIBP every 5 min

• Furosemide IV: Initial dose 20-40 mg (0.5 mg/kg) IV bolus; higher doses (1 mg/kg) if CKD, chronic diuretic use, or hypervolaemia
• Furosemide has an immediate venodilatory effect before diuresis begins (within 5-10 minutes) → rapid preload reduction
• Diuresis begins within 30-60 minutes; maximum at 2-4 hours
• If inadequate response: Double dose; add thiazide (metolazone) for synergy; consider bumetanide
• Monitor urine output (Foley catheter); target 1-2 mL/kg/hr initially
• Target: Euvolaemia; avoid excessive diuresis (→ hypotension, AKI)

• IV Glyceryl Trinitrate (GTN/NTG): Start 5-10 mcg/min; titrate up to 200 mcg/min
  • Primarily venodilator (preload reduction) at low doses
  • Arterial dilation (afterload reduction) at higher doses
  • Has coronary vasodilating effects (important if ischaemic cause)
  • Contraindication: SBP <90 mmHg; recent PDE-5 inhibitor use (sildenafil within 24h, tadalafil within 48h)
• Oral nitrates: Isosorbide dinitrate sublingual 5-10 mg (fast onset, useful in prehospital)
• IV Sodium Nitroprusside: For severe hypertensive APO; combined arteriovenous dilation; titratable; cyanide toxicity risk with prolonged use

1. Decreases preload and afterload → improves cardiac function
2. Redistributes lung water from intraalveolar to extraalveolar space (where it interferes less with gas exchange)
3. Increases lung volume → prevents atelectasis → recruits alveoli
4. Reduces work of breathing → reduces myocardial O2 demand

• CPAP (Continuous Positive Airway Pressure): 5-10 cmH2O; first-line for cardiogenic APO
  • Provides constant expiratory pressure → keeps alveoli open → reduces shunt
  • Reduces intubation rate
  • Cochrane review: Equivocal overall mortality benefit but reduces intubation need
• BiPAP (Bilevel Positive Airway Pressure): IPAP 10-15 cmH2O; EPAP 4-5 cmH2O
  • Better for hypercapnic respiratory failure (COPD + APO)
  • HFNC (High-Flow Nasal Cannula): For non-CS patients with normal PaCO2 - Harrison's 22e: Better outcomes than BiPAP in this specific group
• Indications for intubation:
  • PaO2 <60 mmHg despite NIV
  • GCS <8, inability to protect airway
  • Haemodynamic deterioration (cardiogenic shock)
  • Respiratory rate >35/min with fatigue
  • Rising PaCO2 (>45 mmHg) with acidosis (pH <7.25) on NIV

• FiO2 1.0 initially; titrate to SpO2 92-96%
• PEEP 8-12 cmH2O (higher PEEP recruits flooded alveoli)
• Low tidal volume 6 mL/kg IBW (lung-protective)
• Accept mild permissive hypercapnia if PEEP and FiO2 requirements are high

• Dobutamine: Beta-1 agonist + mild beta-2; increases CO + mild vasodilation; drug of choice for low-output cardiac failure with pulmonary oedema
  • Dose: 2.5-20 mcg/kg/min IV infusion
  • Increases HR (proarrhythmic) - use with caution in tachycardia
• Milrinone: Phosphodiesterase-3 inhibitor → increased cAMP → inotropy + vasodilation ("inodilator")
  • Dose: 0.375-0.75 mcg/kg/min IV
  • Particularly useful in right heart failure + pulmonary hypertension
  • Does not increase myocardial O2 demand as much as dobutamine
• Dopamine: At higher doses (>5 mcg/kg/min): alpha-adrenergic vasoconstriction + beta-1 inotropy; useful if hypotensive; not preferred in pure pulmonary oedema (increases afterload)
• Levosimendan: Calcium sensitiser; positive inotrope + vasodilator; available in some countries; evidence in acute HF but not universally adopted

• IV GTN (as above)
• IV Sodium Nitroprusside (0.25-10 mcg/kg/min) - for severe hypertension
• IV Enalaprilat (ACE inhibitor) - 1.25-5 mg IV q6h; reduces afterload; useful in hypertensive APO
• Hydralazine 10-20 mg IV (slower onset; less predictable)

• Acute MI → Emergency percutaneous coronary intervention (PCI) (not thrombolysis if PCI available within 90 min)
• Acute AF with APO → Rate control (beta-blocker, digoxin) or cardioversion
• Severe aortic/mitral stenosis with APO → Emergency valve surgery or balloon valvuloplasty
• Hypertensive APO → Aggressive BP reduction with IV agents

• Historical use: Morphine 2-4 mg IV; reduces anxiety; mild venodilation; reduces sympathetic drive
• Current evidence (ALARM-HF Registry 2024): Morphine use in APO associated with increased mortality, more intubations, more ICU admissions
• Current position (ESC 2021): Morphine is NOT routinely recommended in APO; use only if associated with extreme anxiety/distress that cannot be managed otherwise
• Anaesthetic relevance: Do not reflexively give morphine; opioids suppress hypercarbic drive; in a patient already struggling with ventilation, opioid respiratory depression can be catastrophic

HIGH-YIELD EXAM POINT: Morphine is no longer routinely recommended in acute pulmonary oedema based on contemporary registry data showing increased adverse outcomes.

• Intra-Aortic Balloon Pump (IABP): Counterpulsation; reduces afterload (deflates systole) + augments diastolic perfusion pressure (inflates diastole); first-line in refractory cardiogenic shock post-MI + APO
• VA-ECMO (Veno-Arterial ECMO): For refractory cardiogenic shock; provides complete cardiopulmonary bypass support; bridge to recovery/transplant
• Impella: Catheter-based LV assist device; reduces LV filling pressure; unloads LV; improves forward flow

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9. ANAESTHETIC CONSIDERATIONS

A. Preoperative Assessment

Key Assessment Points

1. NYHA functional class - dyspnoea at rest or minimal exertion (NYHA III/IV) = very high risk
2. Echocardiography - LVEF, diastolic function, valvular disease, wall motion abnormalities
3. Current medications - ACEi/ARBs, beta-blockers (never stop preoperatively), diuretics, digoxin, inotropes
4. Biomarkers - NT-proBNP: if elevated, delay elective surgery and optimise heart failure
5. Fluid status - Is patient euvolaemic? Signs of congestion (JVP elevation, pitting oedema, crackles)?
6. Renal function - CKD affects diuretic response and fluid management
7. Precipitating factor - Has the cause of pulmonary oedema been identified and treated?

Preoperative Optimisation

• Target: Absence of signs of congestion + euvolaemia + LVEF as optimised as possible before elective surgery
• Optimise with diuretics + ACEi/ARBs + beta-blockers (guideline-directed medical therapy)
• NT-proBNP >300 pg/mL preoperatively → high risk; delay elective surgery if possible
• Echo is mandatory if new or unknown pulmonary oedema in a preoperative patient

B. Intraoperative Anaesthetic Management

Positioning

• Keep head-up (semi-recumbent, 15-30°) throughout to reduce venous return and improve respiratory mechanics
• Avoid prolonged Trendelenburg position (worsens pulmonary congestion)

Induction

• Propofol: Vasodilation + cardiac depression → may precipitate severe hypotension in a patient with already elevated filling pressures; use with caution; etomidate preferred if LVEF <30%
• Ketamine: Increases HR and BP (sympathomimetic) → may worsen tachycardia-induced pulmonary oedema; use with caution; may be beneficial if low output state (sympathomimetic support)
• Careful fluid management at induction: Avoid boluses; have vasopressors ready (phenylephrine, norepinephrine)
• RSI if any concern about aspiration (pulmonary oedema causes frothy secretions, impaired airway reflexes)

Airway Management

• Presence of frothy secretions requires thorough suctioning before and during intubation
• Have a large-bore suction device ready at the head of the bed
• Post-intubation: Immediate PEEP (8-10 cmH2O) to recruit atelectatic alveoli
• Confirm position and start mechanical ventilation with lung-protective settings

Intraoperative Monitoring

• Standard: ECG (ST analysis), SpO2, NIBP, capnography, temperature
• Invasive arterial line: Essential in moderate-severe pulmonary oedema for continuous BP and ABG monitoring
• Central venous pressure (CVP): Guides fluid management; limited value alone (CVP does not accurately reflect LV filling pressures)
• Pulmonary artery catheter (PAC): For refractory cases, cardiac surgery; guides PCWP, CO, SVR
• Transoesophageal Echocardiography (TOE/TEE): Gold standard for intraoperative cardiac function assessment; guides fluid and vasopressor decisions; identifies new wall motion abnormalities
• Urinary catheter: Essential; hourly urine output monitoring

Intraoperative Fluid Management

• Goal-directed fluid therapy (GDT): Use dynamic indices (pulse pressure variation, stroke volume variation) to guide fluid administration; avoid fixed-volume protocols
• Avoid crystalloid overload: Each litre of normal saline contains 154 mmol Na → sodium-mediated fluid retention → worsens pulmonary oedema in susceptible patients
• Balanced crystalloids (Hartmann's, PlasmaLyte): Preferred over normal saline
• Furosemide intraoperatively: If significant fluid positive balance or rising plateau pressures: furosemide 20-40 mg IV; target zero fluid balance or slight negative balance in HF patients

Ventilation Strategy

• FiO2: Start 1.0 at induction; titrate to SpO2 94-98%
• PEEP: 8-12 cmH2O (recruits alveoli, redistributes lung water, reduces shunt)
• Tidal volume: 6-8 mL/kg IBW (lung-protective)
• Inspiratory flow pattern: Decelerating (best for distribution of ventilation in oedematous lung)
• Peak airway pressure: Monitor; keep Pplat <28-30 cmH2O

Drug Considerations in Pulmonary Oedema

C. Postoperative Care

PACU Management

• SpO2 monitoring: Continuous; target >94%
• Position: Semi-recumbent (head-up 30-45°)
• Fluid balance: Strict hourly; aim neutral to negative in HF patients
• Suspect NPPE: Any patient developing frothy secretions, hypoxia, bilateral infiltrates within 90 minutes of airway obstruction/laryngospasm → diagnose clinically → treat with O2 + furosemide ± CPAP
• Suspect TRALI: Any patient developing acute hypoxic respiratory failure within 6 hours of blood transfusion → stop transfusion → supportive treatment
• Early resumption of cardiac medications: ACEi/ARBs (if haemodynamically stable), beta-blockers, diuretics

ICU Management (If Intubated)

• Lung-protective ventilation (tidal volume 6 mL/kg IBW; PEEP as above)
• Daily spontaneous breathing trials when: FiO2 ≤0.4; PEEP ≤5 cmH2O; neurologically intact; haemodynamically stable
• Fluid balance: Target neutral to negative daily balance
• Treat underlying cause aggressively (revascularisation for ischaemic APO, rate control for AF-induced APO)

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10. DRUGS

A. FUROSEMIDE (First-line for Cardiogenic APO)

B. GTN/NITROGLYCERIN

C. DOBUTAMINE

D. MORPHINE (Use with Caution/Avoid)

E. MILRINONE

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11. SCORES, FORMULAE, AND NUMERICAL VALUES

Key Numerical Values

Formulae

1. Starling Equation (Pulmonary Fluid Balance)

• Normal Q ≈ 10-20 mL/hr (entirely removed by lymphatics)
• In cardiogenic oedema: Pc' rises to >18-25 mmHg → Q exceeds lymphatic capacity

2. Lung Water Estimation (Transpulmonary Thermodilution - PiCCO/VolumeView)

• Normal: 3-7 mL/kg
• Pulmonary oedema: >10 mL/kg
• Severe: >15 mL/kg

3. Oxygen Delivery (DO2)

• In pulmonary oedema: SaO2 and PaO2 fall → reduced DO2 → tissue hypoxia

4. PaO2/FiO2 Ratio (P:F Ratio)

• Normal: ~400-500 mmHg (on room air, FiO2 0.21: PaO2 ~85/0.21 = ~400)
• Mild pulmonary oedema: 200-300 mmHg
• ARDS (non-cardiogenic): <200 mmHg (moderate); <100 mmHg (severe)

5. NYHA Functional Classification

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12. GUIDELINES

1. ESC Guidelines on Acute Heart Failure (2021)

• CPAP or BiPAP recommended (Class IIa) to reduce respiratory distress
• IV diuretics (furosemide) first-line for volume overload
• IV nitrates for afterload reduction in hypertensive APO
• Morphine NOT recommended (Class III: harm in ESC 2021)
• Dobutamine for low-output APO
• Routine PAC not recommended; selective use only
• Target SpO2 92-96% (not >98%)

2. ESC/ESICM Definition of TRALI (Updated 2019)

• Acute non-cardiogenic pulmonary oedema within 6 hours of transfusion
• PaO2/FiO2 <300 mmHg
• Bilateral chest infiltrates
• No alternative explanation

3. NICE Guidance on Acute Heart Failure (NG196, 2023)

• CPAP/NIV in acute APO not responding to standard therapy
• High-flow nasal oxygen for non-hypercapnic patients
• IV furosemide first-line
• Consider IV nitrates if BP adequate

4. High-Altitude Pulmonary Oedema (Wilderness Medical Society Guidelines 2019)

• Descent is definitive treatment
• Nifedipine 30 mg extended-release for treatment and prevention
• Dexamethasone for high-altitude cerebral oedema co-existence
• Portable hyperbaric chamber if descent not possible

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13. IMPORTANT TABLES

Table 1: Cardiogenic vs Non-Cardiogenic Pulmonary Oedema - Comprehensive Comparison

Table 2: TRALI vs TACO - Differential Diagnosis

Table 3: Types of Pulmonary Oedema - Anaesthetic Perioperative Relevance

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14. FLOWCHARTS AND ALGORITHMS

Algorithm 1: Acute Pulmonary Oedema - Emergency Management

ACUTE PULMONARY OEDEMA SUSPECTED
               ↓
    IMMEDIATE: ABC + O2 + MONITORING
    • Sit upright • SpO2/ECG/NIBP
    • IV access × 2 • ABG • CXR (portable)
    • Echocardiography (POCUS if available)
    • BNP/NT-proBNP; Troponin; ECG
               ↓
        IS BP ADEQUATE (SBP >90 mmHg)?
         /                          \
       YES                           NO
        ↓                             ↓
  STANDARD TREATMENT             CARDIOGENIC SHOCK
  • Furosemide 40 mg IV           + PULMONARY OEDEMA:
  • GTN 5-10 mcg/min IV           • Dobutamine
    (if SBP >100 mmHg)            • ± Noradrenaline
  • CPAP 5-10 cmH2O              • Urgent IABP/ECMO
  • Target SpO2 92-96%           • PCI if STEMI
               ↓
       Response adequate?
       /              \
     YES               NO
      ↓                 ↓
  Continue;         ESCALATE:
  Address cause     • Increase furosemide
                    • Add nitroprusside
                    • Consider intubation
                    • PAC/TOE guidance
                    • ICU admission
               ↓
    IDENTIFY AND TREAT CAUSE:
    • STEMI → emergency PCI
    • AF → rate control/cardioversion
    • Fluid overload → strict restriction
    • Valvular crisis → surgical consultation

Algorithm 2: Postoperative Respiratory Deterioration - Differentiating Pulmonary Oedema Types

PATIENT IN PACU: ACUTE HYPOXIA + BILATERAL INFILTRATES
               ↓
    RECENT TRANSFUSION (<6h)?
         /              \
       YES               NO
        ↓                 ↓
   TRALI vs TACO        RECENT LARYNGOSPASM
   Check BNP, echo      OR AIRWAY OBSTRUCTION?
   • High BNP → TACO         /         \
   • Normal BNP → TRALI     YES          NO
   TACO: Furosemide           ↓            ↓
   TRALI: Supportive        NPPE         CARDIOGENIC or
   BOTH: Stop transfusion   Furosemide   VOLUME OVERLOAD
                            + O2 + CPAP  Check fluid balance,
                            Monitor 24h  BNP, echo; treat
                                         accordingly

Algorithm 3: NPPE Prevention and Management

EXTUBATION CRITERIA MET?
               ↓
  PRE-EXTUBATION CHECKLIST:
  • Reverse all NMB (confirm TOF ratio >0.9)
  • Suction pharynx thoroughly
  • Semi-recumbent position
  • Have IV lignocaine 1.5 mg/kg ready (reduces
    laryngospasm risk in at-risk patients)
  • Prepare for re-intubation
               ↓
    POST-EXTUBATION MONITORING:
    Monitor for laryngospasm:
    Stridor + SpO2 ↓ + respiratory distress
         /                        \
   NO SPASM                    LARYNGOSPASM
       ↓                            ↓
  Monitor 30 min           IMMEDIATE INTERVENTION:
  in PACU (standard)       1. 100% O2 by facemask
                           2. Jaw thrust + mask hold
                           3. IV succinylcholine
                              0.1-0.2 mg/kg (larson's point)
                           4. Re-intubate if necessary
                                    ↓
                        MONITOR FOR NPPE:
                        SpO2 + breathing pattern
                        every 15 min × 90 min
                                    ↓
                        If NPPE develops (hypoxia,
                        frothy secretions, bilateral
                        infiltrates):
                        • O2 + SpO2 target 94-98%
                        • Furosemide 40 mg IV
                        • CPAP 5-10 cmH2O if SpO2 <92%
                        • Intubate if deteriorates
                        • Expect resolution 12-48h

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15. FREQUENTLY ASKED MD VIVA QUESTIONS

1. Preload and afterload reduction: Positive intrathoracic pressure reduces venous return (reduces RV preload) and increases LV transmural pressure (reduces LV afterload) → improves forward CO and reduces pulmonary venous congestion
2. Redistribution of lung water: PEEP moves fluid from intraalveolar to extraalveolar compartments (peribronchial spaces), where it interferes less with gas exchange
3. Alveolar recruitment: Opens collapsed, fluid-filled alveoli → reduces intrapulmonary shunt → improves oxygenation Target PEEP in cardiogenic APO: 8-12 cmH2O. Excessive PEEP: Reduces venous return → hypotension; overdistends healthier alveoli → barotrauma; may impair RV function.

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16. MD THEORY EXAMINATION POINTS

High-Yield Facts

• PCWP >18 mmHg = cardiogenic pulmonary oedema; PCWP <18 mmHg = non-cardiogenic
• NPPE = laryngospasm → forced inspiration against closed glottis → negative Pit → hydrostatic + afterload mechanism → onset within 90 min; risk: muscular young patients; treat: furosemide + CPAP
• TRALI = within 6h of transfusion; non-cardiogenic; antibody-mediated neutrophil activation; DO NOT give diuretics; stop transfusion
• TACO = within 6h of transfusion; cardiogenic; volume overload; GIVE furosemide; high BNP
• Morphine NOT recommended in APO (ESC 2021 Class III)
• CXR Kerley B lines = PCWP ~18-20 mmHg; horizontal peripheral lines from oedematous interlobular septa
• "Bat wings" or "butterfly" pattern on CXR = bilateral alveolar oedema with central predominance
• BNP >400 pg/mL = likely cardiogenic
• PEEP three mechanisms: preload/afterload reduction; redistribution of lung water; alveolar recruitment
• Maximum safe CPAP for cardiogenic APO: 5-10 cmH2O (higher risks CO reduction by reducing venous return)

Mnemonics

Types of Pulmonary Oedema: "CATCH-RN"

• Cardiogenic (LV failure, fluid overload)
• Altitude (HAPE)
• TRALI / TACO (transfusion)
• Capillary permeability (ARDS, sepsis)
• High pressure non-cardiac (NPPE, neurogenic)
• Re-expansion (after thoracentesis)
• Neurogenic (SAH, TBI)

Cardiogenic APO Treatment: "LMNOP" (modified)

• Lasix (furosemide)
• Morphine (use with caution/avoid - ESC 2021)
• Nitrates (IV GTN)
• Oxygen + positive pressure ventilation
• Positioning (sit up) + Pressure monitoring

Kerley Lines Memory: "B is for Bottom, A is for Arise from hilum"

• Kerley B lines = short horizontal lines at the base (periphery)
• Kerley A lines = longer lines arising from the hilum

Common Mistakes

1. Giving diuretics in TRALI - it is non-cardiogenic; diuretics worsen hypotension
2. Continuing transfusion in TRALI/TACO - stop immediately
3. Targeting SpO2 >98% in APO - current guidance recommends 92-96%
4. Not applying PEEP immediately after intubating APO patient - leaving PEEP at zero in flooded lungs causes catastrophic shunting
5. Missing NPPE because onset is delayed up to 90 minutes - any frothy secretions/hypoxia after extubation in a patient who had laryngospasm = suspect NPPE until proven otherwise
6. Confusing Kerley B lines with ARDS infiltrates - Kerley B lines are fine, short, horizontal, peripheral; ARDS = bilateral, patchy, peripheral, non-gravity-dependent opacification
7. Giving morphine routinely - not recommended per ESC 2021

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17. CLINICAL PEARLS

1. "The classic cardiogenic APO triad" in the PACU: Bilateral fine crackles + elevated JVP + S3 gallop. If you hear these after major surgery with large fluid infusion, act immediately.
2. Pink frothy sputum through the ETT = alveolar flooding. This is not a sputum plug; it is protein-rich alveolar fluid. Do NOT just suction and move on. Apply PEEP, start furosemide, get ABG, inform surgeon.
3. The NPPE "young muscular man" profile: Young fit male, difficult intubation requiring multiple attempts, bites the ETT at emergence, develops laryngospasm after extubation, then deteriorates within 1 hour with hypoxia and bilateral white-out on CXR. This is textbook NPPE. Furosemide + CPAP; resolve without intubation in most cases.
4. PEEP is your friend in pulmonary oedema - but respect its haemodynamic effects. In a patient with cardiogenic APO who is also hypotensive, high PEEP (>12 cmH2O) can reduce venous return and worsen cardiac output. Start at 5-8 cmH2O and titrate.
5. BNP in the perioperative period: A preoperative NT-proBNP >300 pg/mL predicts perioperative cardiac events. A postoperative rise in NT-proBNP (especially >3-fold the preoperative value) indicates perioperative myocardial injury/stress and mandates cardiology review.
6. Flash pulmonary oedema in a hypertensive patient: This patient does NOT need inotropes. They need aggressive afterload reduction. IV GTN or nitroprusside rapidly reduces afterload, LV fills less in diastole, LVEDP drops, pulmonary venous pressure drops, and oedema resolves. Giving dobutamine to a hyperdynamic LV in hypertensive APO worsens matters.
7. In ICU patients with ARDS-type non-cardiogenic oedema: Aggressive diuresis will NOT improve the CXR opacity (it is permeability oedema, not volume-dependent primarily). Lung-protective ventilation + treat the underlying cause is the key.
8. TACO is underdiagnosed. Any elderly patient, any patient with cardiac disease, receiving >2 units of blood products in the perioperative period is at high TACO risk. The onset during transfusion + hypertension + bilateral infiltrates + elevated BNP = TACO until proven otherwise.

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18. KEY TAKE-HOME MESSAGES

1. Pulmonary oedema = fluid in the interstitium and alveoli from overwhelmed lymphatic capacity. Normal lymphatic reserve is 20× baseline; oedema develops only when this reserve fails.
2. Two fundamental mechanisms: Cardiogenic (high PCWP >18 mmHg, low-protein oedema) and Non-cardiogenic (permeability increased, PCWP <18 mmHg, high-protein oedema).
3. Three immediate actions in APO: Sit the patient upright; give O2 (target SpO2 92-96%); start IV furosemide + IV GTN (if SBP adequate).
4. PEEP is the most powerful acute treatment for alveolar flooding - it recruits alveoli, redistributes lung water, and reduces LV afterload simultaneously.
5. Morphine is NO LONGER recommended in cardiogenic APO (ESC 2021 Class III). It increases intubation rates and mortality.
6. NPPE = laryngospasm post-extubation → negative intrathoracic pressure → hydrostatic and afterload-mediated pulmonary oedema. Onset within 90 minutes. Risk: Young muscular patients. Treatment: Furosemide + CPAP; resolves 12-48h; mortality 40% if delayed.
7. TRALI = stop transfusion + supportive care + NO diuretics. TACO = stop transfusion + furosemide. BNP is the key differentiator.
8. The CXR progression of cardiogenic oedema: Upper lobe diversion → Kerley B lines → hilar haziness → "bat wings" bilateral alveolar oedema → pleural effusions.
9. BNP >400 pg/mL = likely cardiogenic oedema. BNP <100 pg/mL makes cardiac cause unlikely.
10. Dobutamine is the inotrope of choice in low-output APO. Milrinone is preferred when pulmonary hypertension or right heart failure coexists (avoids further beta-receptor stimulation, provides pulmonary vasodilation).
11. In the perioperative period, always consider NPPE, TRALI, and TACO when any patient develops bilateral infiltrates and hypoxia. The temporal relationship to extubation and transfusion is the diagnostic key.
12. Mechanical ventilation target in APO: FiO2 titrated to SpO2 92-96%; PEEP 8-12 cmH2O; TV 6 mL/kg IBW; Pplat <30 cmH2O.
13. Flash pulmonary oedema in hypertension: Pathophysiology is LV diastolic dysfunction with afterload mismatch; treatment is aggressive afterload reduction (GTN, nitroprusside), NOT inotropes.
14. In ARDS-type (non-cardiogenic) oedema: Diuretics are adjuncts, not primary treatment. Lung-protective ventilation, prone positioning, and treating the cause are the priorities.
15. "The lung's water balance is extraordinarily well-buffered." By the time pulmonary oedema is visible on CXR, EVLW has already increased by >30-50% above normal. Interstitial oedema (Stage 1) is invisible on standard CXR but detectable on POCUS (B-lines) and CT.

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References

• Morgan & Mikhail's Clinical Anesthesiology 7e - Chapter 54 (ICU Pulmonary Care), pp. 2461-2470: Pathophysiology, Starling equation, classification, treatment
• Miller's Anesthesia 10e - Chapter 40 (PACU), p. 11583-11584: NPPE mechanism and TRALI in PACU
• Barash's Clinical Anesthesia 9e - PACU Complications: Negative Pressure Pulmonary Oedema
• Harrison's Principles of Internal Medicine 22e - Chapter 39 (Pulmonary Oedema): Diagnosis, BNP, PPV, diuretics, nitrates; Chapter 264 (Heart Failure management)
• ESC Heart Failure Guidelines 2021 - Morphine: Class III (harm); CPAP/NIV: Class IIa
• ESC/ESICM TRALI Definition 2019

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Session Progress Summary

Note on Topic 6 (Pneumothorax): The research was completed but the document was interrupted before delivery. When you request it, I can deliver the full 18-section Pneumothorax document immediately from gathered sources plus the 2024 ERS/EACTS/ESTS Joint Guidelines on Spontaneous Pneumothorax (PMID 38806203) and the 2025 meta-analysis on needle decompression for tension pneumothorax (PMID 40383767).

What Was Covered

Three Most Common Exam Traps

1. CPAP vs BiPAP confusion - CPAP has no pressure support above the set level; BiPAP's PS = IPAP minus EPAP. Very frequently asked.
2. COPD SpO2 target 88-92% - examiners routinely test this and expect the explanation (Haldane effect + hypoxic drive + V/Q worsening).
3. THRIVE does NOT eliminate CO2 - it slows the rise to 1.1 mmHg/min, not zero. Candidates who claim "THRIVE removes CO2 completely" are incorrect.