Pulmonary edema

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Pulmonary edema is the accumulation of fluid in the lung interstitium and alveoli. Causes can be broadly classified as cardiogenic, most commonly acute decompensated heart failure (e.g., due to acute myocardial infarction), and noncardiogenic, most commonly ARDS (e.g., due to pneumonia). Clinical features include progressive dyspnea, signs of hypoxemia (e.g., cyanosis, tachycardia), and features of the underlying cause, such as S3 gallop on cardiac auscultation in cardiogenic pulmonary edema. Laboratory studies (e.g., BNP, cardiac biomarkers) and imaging studies (e.g., chest x-ray, POCUS) are performed to help determine the underlying cause and confirm the diagnosis. Management often involves hemodynamic and respiratory support to prevent and treat respiratory failure. The decision of whether to use pharmacotherapy and which agent to use depends on the cause.

The etiology of pulmonary edema is multifactorial in ∼ 10% of patients. ^[2]

Pulmonary and nonpulmonary causes of noncardiogenic pulmonary edema can occur simultaneously.

• General symptoms ^[2]
  • Progressive dyspnea and/or tachypnea
  • Cough, possibly with pink frothy sputum or expectoration
  • Fever (e.g., secondary to pneumonia or sepsis)
• Physical examination findings ^[2][4]
  • Signs of hypoxia (e.g., cyanosis, tachycardia)
  • Agitation, diaphoresis and/or confusion
  • Dullness upon chest wall percussion
  • Increased tactile fremitus
  • Inspirational crackles on lung auscultation
  • In cardiogenic pulmonary edema:
    • S3 gallop or murmurs on cardiac auscultation
    • Jugular vein distention
    • Peripheral edema

General principles

• The diagnosis of pulmonary edema is usually confirmed by chest x-ray.
• Additional studies (e.g., BNP, ECG) can help identify the underlying cause.
• There is no single test to distinguish cardiogenic vs. noncardiogenic pulmonary edema.

Imaging studies

Chest x-ray ^[2][3][5]

• Indication: all patients with suspected pulmonary edema
• Views: PA, lateral, or AP
• Typical findings in cardiogenic pulmonary edema
  • Opacities in the perihilar areas (bat wing pattern)
  • Kerley B lines: horizontal, linear opacities that represent thickened interlobular septa; 1–2 cm in length and perpendicular to the pleural surface
  • Pleural effusions
  • Enlarged cardiac silhouette
  • Peribronchial cuffing
• Findings suggestive of noncardiogenic pulmonary edema
  • Peripheral, patchy ground-glass opacities
  • Peripheral air bronchograms and pulmonary consolidations

Other studies

• Indications: as an alternative to chest x-ray or to further assess radiographic abnormalities
• Modalities
  • POCUS lung: B lines and pleural effusions ^[5]
  • CT chest: similar findings to plain film, with higher resolution

Additional assessment

Routine studies ^[6][7]

Results from the following studies can help to rule out common causes of pulmonary edema:

• ECG: ECG findings in STEMI, ECG findings in AHF ^[5]
• Cardiac biomarkers
  • BNP ; ^[6][7]
    • < 100 pg/mL: suggestive of noncardiogenic pulmonary edema
    • > 400 pg/mL: suggestive of cardiogenic pulmonary edema
  • ↑ Troponin T/I, CK-MB, and/or myoglobin: suggestive of cardiogenic pulmonary edema ^[2]
• Blood gas analysis: Respiratory failure and/or acid-base disorders may be present.
• CBC: Leukocytosis may be present in many causes of pulmonary edema, e.g., sepsis, acute pancreatitis, and ACS.
• BMP
  • ↑ Creatinine in kidney disease
  • Serum osmolality and/or electrolyte abnormalities in IV fluid overload

Additional studies ^[2]

Consider the following based on clinical suspicion:

• Lipase, amylase: to rule out acute pancreatitis
• Blood cultures and gram stain: to assess for bacteremia and sepsis
• Echocardiography: to assess for left ventricular systolic dysfunction and/or valvular dysfunction
• CT brain: if neurogenic pulmonary edema is suspected
• Pulmonary artery catheterization (gold standard) if findings from other studies are inconclusive and results of catheterization would affect management ^[2][5]

Approach

• Provide respiratory support as needed.
  • Supplemental oxygen
  • Ventilatory support (invasive or noninvasive)
  • See “Respiratory support in AHF” and “Lung-protective ventilation strategies” for more information.
• Treat the underlying cause (e.g., AHF, ARDS, HAPE).
• Maintain adequate perfusion (e.g., with IV fluids) to prevent end-organ damage in patients with noncardiogenic pulmonary edema.
• Tailor pharmacotherapy based on the complete clinical picture.

For patients with respiratory and/or hemodynamic instability, involve a critical care specialist early (e.g., rapid response team).

Pharmacotherapy

Indications for pharmacotherapy vary based on the underlying disease process. See disease-specific articles for dosing.

• Loop diuretics (e.g., furosemide)
  • First line for cardiogenic pulmonary edema
  • May be considered for other causes of pulmonary edema (e.g., ARDS) if there are signs of fluid overload
  • See also “Pharmacotherapy for HF.”
• Vasodilators (e.g. IV nitroglycerin)
  • First-line for cardiogenic pulmonary edema caused by a hypertensive emergency
  • Decreases preload and pulmonary congestion
  • See also “Vasodilator therapy in acute heart failure.”
• Inotropes (e.g., dobutamine or dopamine) for patients with low systolic blood pressure
• Nifedipine OR phosphodiesterase inhibitors (e.g., sildenafil) for HAPE if immediate descent and oxygen therapy are not feasible
• Opioids (e.g., morphine) may be used for palliative treatment of dyspnea ^[7][8]

Diuretics and vasoactive drugs can cause hemodynamic instability and are not appropriate for all causes of pulmonary edema (e.g., HAPE, reexpansion pulmonary edema).

Opioids have historically been used to treat acute pulmonary edema.

• ARDS with progressive hypoxemia
• Respiratory failure, requiring mechanical ventilation
• Further complications depend on the underlying condition.

We list the most important complications. The selection is not exhaustive.

• Description
  • Sudden-onset, potentially life-threatening cardiogenic pulmonary edema that can cause acute hypoxemic respiratory failure
  • Can occur in de novo heart failure and acute decompensated heart failure (ADHF)
• Risk factors ^[11]
  • Long-standing poorly controlled hypertension ^[10]
  • LVH and diastolic dysfunction
  • Bilateral renal artery stenosis ^[12]
  • Coronary artery disease
  • Obstructive sleep apnea
• Triggers: similar to those of ADHF ^[11]
  • Sympathetic activation: exertion, sympathomimetics (e.g., cocaine), medication nonadherence, psychosocial stress or anxiety ^[10]
  • Abrupt hemodynamic changes
    • Hypertensive emergency
    • Volume overload
    • Myocardial ischemia
    • Acute mitral regurgitation
    • Tachyarrhythmias
• Pathophysiology: Multiple processes lead to a vicious cycle of sympathetically-driven ↑ LVEDP and pulmonary edema. ^[10][11]
  • Long-term hypertension → ↑ atherosclerosis and cardiac remodeling → ↑ afterload and ↑ MVO₂, LVH, and ↑ diastolic dysfunction
  • Sympathetic activation → peripheral and splanchnic vasoconstriction→ ↑ venous return and ↑ afterload → ↑ pulmonary edema and ↓ cardiac output
  • ↑ Pulmonary edema and ↓ cardiac output → end-organ dysfunction and hypoxemia → ↑ sympathetic activation
• Clinical features ^[8]
  • Hypertension, hypoxia
  • Features of pulmonary congestion: e.g., crackles, signs of increased work of breathing, respiratory distress signs
  • Minimal peripheral edema
  • See also “Wet and warm” in “Classification of acute heart failure.”
• Diagnostics: similar to other types of pulmonary edema
  • CXR: x-ray findings in pulmonary congestion
  • Ultrasound
    • B lines often present on lung ultrasound (See “POCUS in acute heart failure” for details)
    • Echocardiography: See “Echocardiographic findings in AHF.”
• Management: See “Management of acute heart failure.”
  • Stabilization with NIPPV and vasodilators for ADHF ^[8][11]
  • Treatment of the underlying condition and trigger management.