Etiology and main causes
AHF most commonly develops against the background of conditions that sharply reduce cardiac output. The most frequent cause is myocardial infarction, especially with extensive involvement, wall rupture, or acute mitral regurgitation.
Low-output causes are divided into two groups:
- Direct myocardial damage: coronary artery disease, myocarditis, cardiomyopathies, toxic effects (e.g., alcohol), infiltrative pathologies (sarcoidosis, amyloidosis), and vitamin B1 deficiency.
- Myocardial overload and obstruction to blood flow: arterial hypertension, valvular heart disease (aortic and mitral stenosis), valvular regurgitation, arrhythmias, thrombi, and tumors. This also includes massive pulmonary embolism, cor pulmonale, hypertensive crisis, and cardiac tamponade.
It is important to remember that AHF can also occur with a relatively high cardiac output. This happens in severe anemia, thyrotoxicosis, arteriovenous shunting, and acute glomerulonephritis with arterial hypertension.
Pathogenesis: the hemodynamic vicious circle
The decrease in blood supply triggers neurohumoral mechanisms. Initially, they are compensatory in nature, but quickly become pathogenetic factors.
- Effect on the heart. The sympathoadrenal system is activated, causing tachycardia and peripheral vasoconstriction. Due to vascular spasm, peripheral resistance increases, which means an increase in afterload—the resistance the ventricle must overcome during blood ejection.
- Effect on the kidneys. The drop in renal perfusion activates the renin-angiotensin system. Levels of renin and angiotensin II rise. The latter causes potent vasoconstriction (aggravating afterload) and stimulates the production of aldosterone and antidiuretic hormone (ADH).
- Fluid retention. Aldosterone retains Na+ ions and water, while ADH enhances water reabsorption. The circulating plasma volume increases, and edema appears. The result is a sharp increase in preload—the volume of blood that stretches the ventricle in diastole.
Clinical variants and pulmonary hypertension
In pathologies such as hypertrophic cardiomyopathy, cardiac amyloidosis, or constrictive pericarditis, left ventricular compliance and filling are reduced. This leads to an increase in left ventricular end-diastolic pressure (LVEDP) and a drop in cardiac output. Pressure retrogradely rises in the left atrium and pulmonary vessels, causing pulmonary hypertension and blood stasis.
Two main clinical variants are distinguished:
- Cardiac asthma. Manifests as attacks of suffocation and paroxysmal nocturnal dyspnea. Pathogenetically, this is the result of a rapid pressure surge in the pulmonary circulation and the development of interstitial pulmonary edema.
- Cardiogenic pulmonary edema. Can present predominantly in an interstitial form (which clinically resembles cardiac asthma) or progress to a severe alveolar form. As pulmonary hypertension progresses, right ventricular failure may join the process.
Principles of pharmacotherapy
With timely treatment, long-term hemodynamic normalization can be achieved. Therapy is divided into two directions:
1. Etiological principle Aims at eliminating cardiac overload:
- Reduction of afterload (decreasing vascular tone): vasodilators, beta-blockers, sympatholytics, and ACE inhibitors are used.
- Reduction of preload (decreasing venous return): venous vasodilators and diuretics are used.
2. Pathogenetic principle Aims at correcting intracellular disturbances:
- Increasing contractility: catecholamine precursors, cardiac glycosides, phosphodiesterase inhibitors.
- Improving energy supply: antihypoxants, antioxidants, coronary vasodilators.
- Cardioprotection: drugs with a membranoprotective effect.
- Correction of water-electrolyte balance: potassium-sparing drugs, calcium channel blockers, magnesium preparations.
- Receptor regulation: sympatholytics, cholinomimetics, and agents with positive inotropic effects.
Briefly: answers to topical questions
What is the mechanism of action of phosphodiesterase inhibitors in acute heart failure?
The mechanism of action of drugs in this group consists in the intracellular prevention of the degradation of second messengers in cardiomyocytes, leading to an increase in cardiac contractility.
This is based on the following processes:
- Enzyme inhibition — selective blockade of the phosphodiesterase-III (PDE-III) isoenzyme occurs.
- Accumulation of mediators — since PDE-III normally degrades cAMP to inactive 5'-AMP, inhibition of the enzyme leads to the intracellular accumulation of cAMP.
- Activation of enzyme systems — elevated cAMP levels maintain high protein kinase activity.
- Transmembrane transport — the result of the process is prolonged activation of calcium channels and an increase in calcium ion entry into the cell.
What are the clinical manifestations of a cardiac asthma attack?
Clinically, an attack of cardiac asthma manifests as suffocation and paroxysmal nocturnal dyspnea.
Main manifestations:
- pronounced breathing difficulty;
- cardiac rales that may resemble asthmatic wheezing;
- development of symptoms against the background of pulmonary congestion, which corresponds to interstitial pulmonary edema.
To avoid confusing the types of load, remember: Kidneys and plasma increase preload (volume overload before the heart), while vessels and the sympathetic system increase afterload (resistance after the heart).
Class and exam questions
Can acute heart failure develop with high cardiac output?
Yes, this occurs in conditions requiring increased blood circulation: severe anemia, thyrotoxicosis, arteriovenous shunting, or acute glomerulonephritis.
What is the difference between cardiac asthma and cardiogenic pulmonary edema?
Cardiac asthma is a clinical manifestation of the interstitial stage of pulmonary edema caused by pulmonary congestion. If fluid penetrates further, a more severe alveolar edema develops.
How do the kidneys respond to a decrease in cardiac output?
Due to a drop in perfusion, the kidneys activate the renin-angiotensin system. This leads to the release of angiotensin II, aldosterone, and ADH, which causes vasospasm and fluid retention, overloading the heart.
What else to study on this topic
- Mechanisms of development of right ventricular failure in pulmonary hypertension
- The role of infiltrative diseases (amyloidosis, sarcoidosis) in reducing myocardial compliance
- Differences in the pathogenesis of AHF in myocardial infarction and constrictive pericarditis
- The effect of electrolyte imbalance on cardiomyocyte contractility
- Pathogenesis of cardiogenic shock as an extreme degree of left ventricular failure
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