Definition and causes of acute heart failure
Heart failure as a whole is a clinical syndrome in which the heart fails to supply tissues with an adequate amount of blood (impaired perfusion) or does so only at the cost of pathologically elevated pressure within its chambers.
The acute form (AHF) is characterized by its sudden onset. Myocardial contractility drops sharply, causing a rapid collapse of hemodynamics.
The most frequent cause of this catastrophic scenario is myocardial infarction. Much less commonly, AHF develops paradoxically in the setting of high-output cardiac states (for example, in extremely severe anemia).
Cardiac asthma: a harbinger of catastrophe
In acute left ventricular failure, the output of blood into the systemic circulation is impaired, causing blood to rapidly pool in the pulmonary circulation (the lungs). Clinically, this manifests as cardiac asthma—episodes of severe dyspnea.
A typical attack develops at night while the person is sleeping in a horizontal position. Contributing factors include:
- Redistribution of blood from vascular reservoirs and an increase in circulating blood volume, which raises the workload on the myocardium.
- Physiological nocturnal decrease in myocardial contractility.
- Decreased pulmonary ventilation and a drop in the sensitivity of the respiratory center.
The patient wakes up with air hunger, dyspnea, and cough. On auscultation, the physician initially hears only harsh breathing, but as congestion worsens, moist rales begin to appear.
Pulmonary edema: stages and symptoms
If a cardiac asthma attack is prolonged, it progresses to pulmonary edema. This process has two distinct stages:
- Interstitial edema: fluid (transudate) permeates the pulmonary interstitium but has not yet entered the alveoles themselves. On auscultation, breathing is diminished and dry rales are heard.
- Alveolar edema: transudate penetrates into the alveolar lumen. Fine moist rales appear (initially in the lower lung fields, then spreading throughout all lung fields).
The patient's appearance is characteristic: they assume a forced sitting position (orthopnea), breathing noisily with the use of accessory muscles. The skin is cold, clammy (diaphoretic), and bluish (cyanosis). A cough appears with abundant pink frothy sputum (the pink color is due to erythrocyte admixture). Without emergency care, clinical death ensues following an agonal state with Cheyne-Stokes respiration.
Principles of emergency care
Treatment of acute left ventricular failure (asthma and pulmonary edema) requires immediate action. The basic medication therapy algorithm includes three components:
- Morphine: reduces the excitability of the respiratory center and suppresses the sympathetic nervous system, which decreases vascular spasm.
- Furosemide: administered IV bolus for rapid fluid removal (diuretic effect).
- Nitroglycerin: administered IV infusion. As a potent vasodilator, it effectively reduces both preload and afterload on the myocardium.
Briefly: answers to topical questions
What causes the development of acute heart failure?
Acute heart failure arises from conditions that cause a sudden drop in cardiac output or develops in the setting of its pathological increase.
The main causes include:
- Myocardial infarction — damage to a large volume of the left ventricle, rupture of the interventricular septum or papillary muscles.
- Decompensation — acute exacerbation of chronic heart failure of any etiology.
- Valvular defects — acutely developed mitral, tricuspid, or aortic valve regurgitation.
- Hemodynamic shifts — a sudden, sharp rise in systemic blood pressure (hypertensive crisis).
- Arrhythmias — paroxysmal tachycardias, atrial fibrillation, sudden bradyarrhythmias (SA and AV blocks).
- High-output cardiac states — a rare variant developing, for example, in severe anemia.
Class and exam questions
Can heart failure be diagnosed based solely on ultrasound data (reduced ejection fraction)?
No. Heart failure is primarily a clinical syndrome (dyspnea, fluid retention, reduced exercise tolerance). The ejection fraction helps assess the degree of dysfunction but does not replace clinical evaluation. There is no reliable instrumental "gold standard."
Why do cardiac asthma attacks most commonly occur at night?
In the supine position, blood from vascular reservoirs returns to the circulation, increasing the workload on the heart. Additionally, during sleep, myocardial contractility, pulmonary ventilation, and the sensitivity of the respiratory center physiologically decrease.
How does interstitial pulmonary edema differ from alveolar edema?
In interstitial edema, fluid accumulates only in the lung tissue, and dry rales are heard on auscultation. In alveolar edema, transudate transudates into the alveoli, and fine moist rales and frothy pink sputum appear.
What else to study on this topic
- Chronic heart failure: clinical course and compensatory mechanisms
- Differences between systolic and diastolic heart failure
- Acute right ventricular failure and its systemic manifestations
- Cardiogenic shock: pathogenesis and differences from pulmonary edema
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