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Respiratory System

Pulmonary edema

Abnormal accumulation of extravascular fluid in the lung parenchyma.

Abnormal accumulation of extravascular fluid in the lung parenchyma.


Etiology

Cardiogenic pulmonary edema:

Volume-overload pulmonary edema due to elevation in hydrostatic pressure of pulmonary capillaries.
  • Left ventricular systolic and diastolic function (acute myocarditis including other etiologies of non-ischemic cardiomyopathy, acute myocardial infarction)
  • Valvular function (aortic/mitral regurgitation and stenosis in the moderate to the severe range)
  • Rhythm (atrial fibrillation with a rapid ventricular response, ventricular tachycardia, high degree, and third-degree heart block)

Noncardiogenic pulmonary edema:

Caused by lung injury with a resultant increase in pulmonary vascular permeability leading to the movement of fluid, rich in proteins, to the alveolar and interstitial compartments. Acute lung injury with severe hypoxemia is referred to as acute respiratory distress syndrome (ARDS) and is seen in various conditions directly affecting the lungs, such as the following:
  • Direct lung injury: Pneumonia, inhalational injury
  • Indirect lung injury: Sepsis, acute pancreatitis, severe trauma with shock, multiple blood transfusions
Acute Respiratory Distress Syndrome Pathogenesis and clinical findings

Presentation

Common features:

  • Progressive worsening dyspnea + hypoxia
  • Tachypnea, and rales/crackles on examination

Cardiogenic pulmonary edema:

  • Cough with pink frothy sputum (noted due to hypoxemia from alveolar flooding)
  • Auscultation: S3 gallop, murmurs
  • Elevated JVP

Non-cardiogenic pulmonary edema:

  • Symptoms of infections: Fever, cough with expectoration, dyspnea
  • History of recent trauma, blood transfusions

Diagnosis

Clinical examination:

Auscultation remains the mainstay of bedside assessment in all patients with respiratory symptoms.

Laboratory diagnosis:

  • Cardiac biomarkers: BNP, troponin
  • Hypoalbuminemia (≤3.4 g/dL): Independent marker of increased in-hospital and post-discharge mortality for patients presenting in acute decompensated heart failure
  • Serum electrolytes, renal function, serum osmolarity, toxicology screening
  • Acute pancreatitis: Lipase, amylase

Radiography:

  • Cardiogenic pulmonary edema: Central edema, pleural effusions, Kerley B septal lines, peribronchial cuffing, and enlarged heart size
  • Noncardiogenic pulmonary edema: Patchy and peripheral edema pattern, presence of ground-glass opacities and consolidations with air bronchograms

Lung Ultrasound:

Newer technique to detect accumulation of extravascular lung water (EVLW) ahead of the clinical manifestations
Different etiologies of interstitial syndrome by lung ultrasound (LUS)
Different etiologies of interstitial syndrome by lung ultrasound (LUS) | Gargani, L. Lung ultrasound: a new tool for the cardiologist. Cardiovasc Ultrasound 9, 6 (2011). https://doi.org/10.1186/1476-7120-9-6

Pulmonary artery catheterization:

GOLD STANDARD in determination of etiology of pulmonary edema
  • Pulmonary artery occlusion pressure > 18 mm: Cardiogenic pulmonary edema

Transpulmonary thermodilution:

Invasive testing modality performed in patients undergoing major cardiac, vascular, or thoracic surgeries

Management

Medical management:

  • Diuretics (IV furosemide): Mainstay of treatment
  • Vasodilators (IV nitroglycerin (NTG)): Adjuvant therapy to diuretics when sBP > 110 mm Hg
  • Inotropes (dobutamine and dopamine): Management of pulmonary congestion associated with low sBP and signs of tissue hypoperfusion
  • Morphine (reduces systemic vascular resistance and acts as an analgesic and anxiolytic): Management of pulmonary edema secondary to acute coronary syndrome
  • Nifedipine: Prophylaxis and treatment of high altitude pulmonary edema (HAPE)
  • Newer drugs:
    • Nesiritide: Recombinant BNP with vasodilatory properties
    • Serelaxin: Recombinant form of relaxin with vasodilatory action
    • Clevidipine: Ultra-short-acting CCB

Ventilatory support:

Improve oxygenation, direct alveolar and interstitial fluids back into the capillaries, improve hypercarbia and hence reverse respiratory acidosis, and lastly, tissue oxygenation
Working algorithm for the management of acute pulmonary oedema in the pre-hospital setting
Working algorithm for the management of acute pulmonary oedema in the pre-hospital setting | Purvey, M., & Allen, G. (2017). Managing acute pulmonary oedema. Australian prescriber, 40(2), 59–63. https://doi.org/10.18773/austprescr.2017.012

Case study:

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