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Pulmonary Edema — Comprehensive MD Exam Notes (15 Marks)

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1. Definition

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2. Classification & Etiology

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3. Pathophysiology

Starling Forces (Normal)

Qf = Kf [(Pc − Pi) − σ(πc − πi)]

• Pc = capillary hydrostatic pressure (~7 mmHg normally)
• πc = plasma oncotic pressure (~25 mmHg)
• Net force: small amount of fluid leaks into interstitium → drained by lymphatics (~500 mL/day)

Sequence of Fluid Accumulation

Stage 1 (Interstitial edema)
↑ Pulmonary venous/capillary pressure → fluid in peribronchovascular spaces
→ Kerley B lines, vascular redistribution (cephalization)

Stage 2 (Alveolar flooding)
Interstitial capacity overwhelmed → fluid floods alveolar spaces
→ Bat-wing opacities, frothy sputum, severe hypoxia

Stage 3 (Respiratory failure)
V/Q mismatch → intrapulmonary shunt → refractory hypoxemia

Cardiogenic Mechanism

• ↑ Left atrial pressure (e.g., from LV dysfunction or mitral stenosis)
• ↑ Pulmonary venous pressure → ↑ capillary hydrostatic pressure (PCWP >18–20 mmHg)
• Fluid transudation exceeds lymphatic clearance → interstitial then alveolar edema

Non-Cardiogenic Mechanism (ARDS)

• Endothelial and epithelial injury (e.g., from sepsis mediators, aspiration)
• ↑ Capillary permeability → protein-rich exudate floods alveoli
• Surfactant destruction → alveolar collapse
• PCWP remains normal (<18 mmHg)

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4. Clinical Features

Symptoms

• Acute breathlessness — sudden onset, often worse at night (PND)
• Orthopnea — inability to lie flat; patient sits upright
• Paroxysmal nocturnal dyspnea (PND)
• Cough — productive of frothy, pink-tinged (blood-stained) sputum
• Anxiety, sense of impending doom
• Wheeze ("cardiac asthma")
• Diaphoresis, pallor, cold extremities (in cardiogenic shock)

Signs

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5. Investigations

Bedside / Emergency

Chest X-Ray (CXR)

1. Vascular redistribution / cephalization — upper lobe vessels >lower (earliest sign)
2. Kerley B lines — horizontal lines at lung bases (interstitial edema)
3. Kerley A lines — radiating lines from hilum
4. Perihilar "bat-wing" / "butterfly" opacity — bilateral perihilar haziness
5. Alveolar consolidation — diffuse bilateral opacities
6. Cardiomegaly (CTR >0.5)
7. Pleural effusions — blunting of costophrenic angles
8. Prominent upper lobe veins

Blood Tests

Echocardiography

• Assesses LV systolic/diastolic function, EF, wall motion, valvular lesions
• Differentiates cardiogenic from non-cardiogenic etiology (Harrison's, p. 8301)

Pulmonary Artery Catheterization (Swan-Ganz)

• PCWP >18 mmHg → Cardiogenic
• PCWP ≤18 mmHg → Non-cardiogenic (ARDS)
• Indicated when etiology is uncertain, edema is refractory to treatment, or accompanied by refractory hypotension (Harrison's, p. 8301)

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6. Diagnosis

Diagnostic Criteria Summary

ARDS Berlin Definition (2012)

• Onset within 1 week of precipitating event
• Bilateral opacities on CXR/CT not explained by effusion/collapse
• Respiratory failure not fully explained by cardiac failure
• PaO₂/FiO₂ ratio: Mild 201–300, Moderate 101–200, Severe ≤100 (on PEEP ≥5 cmH₂O)

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7. Management

Immediate / Emergency Measures (ABC approach)

A — Airway: maintain, prepare for intubation if needed
B — Breathing: high-flow O₂ (15 L/min via non-rebreather mask)
C — Circulation: IV access, monitoring, treat underlying cause
Position: Sit patient upright (reduces venous return, improves FRC)

Pharmacological Treatment

Non-Invasive Ventilation (NIV)

• CPAP (Continuous Positive Airway Pressure): First-line for cardiogenic pulmonary edema
  • Recruits alveoli, ↓ work of breathing, improves oxygenation, ↓ preload & afterload
• BiPAP (Bilevel Positive Airway Pressure): For hypercapnic respiratory failure
• Indications: SpO₂ <90% despite high-flow O₂, RR >25/min, accessory muscle use

Invasive Mechanical Ventilation

• Indications: Failure of NIV, GCS ≤8, apnea, refractory hypoxemia
• Settings: Low tidal volume (6 mL/kg IBW) — "lung-protective" strategy (especially in ARDS)
• PEEP titrated to optimize oxygenation

Treatment of Non-Cardiogenic PE / ARDS

• Treat underlying cause (antibiotics for sepsis/pneumonia, etc.)
• Lung-protective ventilation (low VT, permissive hypercapnia)
• Prone positioning (for severe ARDS, PaO₂/FiO₂ <150)
• Conservative fluid strategy after initial resuscitation
• Corticosteroids: Methylprednisolone in early moderate-severe ARDS (evidence-based)
• No role for diuretics/nitrates in non-cardiogenic PE

Treatment of Specific Causes

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8. Complications

• Respiratory failure — hypoxic and/or hypercapnic
• Cardiac arrhythmias
• Cardiogenic shock
• Multi-organ dysfunction (renal failure, hepatic congestion)
• Pulmonary fibrosis (post-ARDS)
• Death — in-hospital mortality: cardiogenic PE ~10–20%; ARDS ~30–40%

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9. Differential Diagnosis

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10. Prognosis

• Cardiogenic pulmonary edema: In-hospital mortality ~10–20%; depends on underlying cause (STEMI has higher early mortality)
• ARDS: Mortality 30–40% for severe ARDS; survivors may have long-term pulmonary fibrosis and cognitive impairment
• HAPE: Excellent if promptly treated (descent + O₂)
• Patients with repeated episodes of cardiogenic pulmonary edema have poor long-term prognosis (5-year survival ~50%)

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11. Key Points for Exam (Quick Recall)

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Sources: Harrison's Principles of Internal Medicine, 21st Edition (p. 8301); AHA Heart Failure Guidelines 2022; ARDS Berlin Definition 2012; Davidson's Principles of Medicine.