Etiology and Main Causes
AHF most commonly develops in conditions that sharply reduce cardiac output. The most frequent cause is myocardial infarction, especially with extensive myocardial damage, wall rupture, or acute mitral regurgitation.
Low-output causes are divided into two groups:
- Direct myocardial injury: ischemic heart disease, myocarditis, cardiomyopathies, toxic agents (e.g., alcohol), infiltrative disorders (sarcoidosis, amyloidosis), and vitamin B1 deficiency.
- Myocardial overload and flow obstruction: hypertension, valvular heart disease (aortic and mitral stenosis), valvular regurgitation, arrhythmias, thrombi, and tumors. This category also includes massive pulmonary embolism, cor pulmonale, hypertensive emergency, and cardiac tamponade.
Notably, AHF can also occur with a relatively high cardiac output. This is seen in severe anemia, thyrotoxicosis, arteriovenous shunting, and acute glomerulonephritis with hypertension.
Pathogenesis: The Hemodynamic Vicious Cycle
Reduced blood flow triggers neurohormonal mechanisms. Initially compensatory, they rapidly become pathogenetic drivers.
- Effect on the heart. The sympathoadrenal system is activated, causing tachycardia and peripheral vasoconstriction. Vasospasm increases peripheral resistance, which raises afterload—the resistance the ventricle must overcome during ejection.
- Effect on the kidneys. Decreased renal perfusion activates the renin-angiotensin-aldosterone system (RAAS), elevating renin and angiotensin II. Angiotensin II causes potent vasoconstriction (worsening afterload) and stimulates aldosterone and antidiuretic hormone (ADH) release.
- Fluid retention. Aldosterone retains Na+ and water, while ADH enhances water reabsorption. Circulating blood volume increases, leading to edema. The net result is a marked increase in preload—the blood volume that stretches the ventricle in diastole.
Clinical Presentations and Pulmonary Hypertension
In conditions such as hypertrophic cardiomyopathy, cardiac amyloidosis, or constrictive pericarditis, left ventricular compliance and filling are impaired. This leads to increased left ventricular end-diastolic pressure (LVEDP) and decreased cardiac output. Pressure retrogradely rises in the left atrium and pulmonary vasculature, causing pulmonary hypertension and congestion.
There are two main clinical presentations:
- Cardiac asthma. Manifests as acute dyspnea and paroxysmal nocturnal dyspnea. Pathogenetically, this results from a rapid pressure spike in the pulmonary circulation and the development of interstitial pulmonary edema.
- Cardiogenic pulmonary edema. May present predominantly in an interstitial form (clinically resembling cardiac asthma) or progress to severe alveolar pulmonary edema. As pulmonary hypertension progresses, right ventricular failure may supervene.
Principles of Pharmacotherapy
Timely treatment can achieve long-term hemodynamic stabilization. Therapy is divided into two main approaches:
1. Etiological Approach Aiming to reduce cardiac workload:
- Reducing afterload (decreasing vascular tone): vasodilators, beta-blockers, sympatholytics, and ACE inhibitors.
- Reducing preload (decreasing venous return): venodilators and diuretics.
2. Pathogenetic Approach Aiming to correct intracellular disturbances:
- Increasing contractility: catecholamine precursors, cardiac glycosides, phosphodiesterase inhibitors.
- Improving energy metabolism: antihypoxants, antioxidants, coronary vasodilators.
- Cardioprotection: agents with membrane-stabilizing effects.
- Correcting fluid and ion balance: potassium-sparing agents, calcium channel blockers, magnesium supplements.
- Receptor regulation: sympatholytics, cholinomimetics, and positive inotropes.