18th February 2025

Predisposing and precipitating factors of cardiogenic pulmonary oedema

Predisposing factors are the chronic underlying primary conditions that lead to the development of heart failure. Precipitating events are the triggers that cause decompensation and result in episodes of pulmonary oedema.

This section will not cover all the details and causes of heart failure, but examples of predisposing factors include:

• Left ventricular systolic dysfunction, e.g. from coronary artery disease, valvular heart disease, hypertension or a dilated cardiomyopathy
• Left ventricular diastolic dysfunction, e.g. from left ventricular hypertrophy, hypertrophic or restrictive cardiomyopathies or acute hypertensive crisis
• Left ventricular outflow obstruction, e.g. in aortic stenosis or hypertrophic cardiomyopathy with obstruction
• Valvular disease, e.g. mitral stenosis

Precipitating events can be split into those that increase preload, decrease cardiac contractility or increase afterload:

• Increased preload
  • Volume overload: chronic liver disease, chronic kidney disease, nephrotic syndrome, high dietary sodium load, iatrogenic intravenous fluid, blood transfusion
  • Acute aortic regurgitation: infective endocarditis, aortic dissection
  • Acute mitral regurgitation: chordal rupture, papillary muscle rupture from ischaemia
• Decreased contractility
  • Myocardial ischaemia or infarction
  • Arrhythmias: atrial fibrillation/flutter, ventricular tachyarrhythmias
  • Non-ischaemic: cardiomyopathy dilated cardiomyopathy, Takotsubo cardiomyopathy
  • High-output cardiac failure: anaemia, sepsis
• Increased afterload
  • Hypertensive crisis
  • Left ventricular outflow tract obstruction: progressive aortic stenosis, atrial myxoma or thrombus

These precipitating factors lead to decreased ventricular emptying and cardiac output resulting in increased end-diastolic volume and pressure, increased left atrial pressure and increased pulmonary vascular pressure. This, in turn, causes hydrostatic pressure to exceed oncotic pressure in the pulmonary vasculature, resulting in fluid transudating into the pulmonary interstitium and alveoli. Fluid accumulates once the rate of leakage surpasses the speed of lymphatic drainage. Fluid accumulation leads to impaired gas exchange and hypoxaemia.

These downstream effects precipitate further physiological responses that feed back into a vicious cycle and worsen pulmonary oedema. Hypoxaemia triggers release of catecholamines, increasing systemic vascular resistance and increasing afterload. There is also activation of the renin-angiotensin-aldosterone system, leading to increased salt and water retention, causing increased overall fluid and an increase in pre- and afterload and increases cardiac strain and demand. All these lead back to decreased ventricular emptying, ventricular relaxation and cardiac output, the factors that started the cycle.