Classification and Forms
Based on the rate of onset, heart failure is classified as acute (occurring over minutes and hours) or chronic.
Depending on the triggering factor, HF is divided into:
- Primary (cardiogenic): intrinsic myocardial contractility decreases despite normal venous return (e.g., in cardiomyopathies).
- Secondary (non-cardiogenic): initial contractility is normal, but venous return drops sharply (massive blood loss, cardiac tamponade, circulatory collapse).
Additionally, HF is categorized as myocardial (direct cellular damage), overload (volume or pressure overload with a healthy myocardium), or mixed. Based on the anatomical site of involvement, it can be left ventricular (myocardial infarction, aortic stenosis), right ventricular (pulmonary hypertension), or biventricular (total).
Immediate Compensatory Mechanisms
To maintain circulation during overload or injury, the body activates interrelated emergency mechanisms:
- Heterometric (Frank-Starling law): the greater the myocardial fiber is stretched during diastole, the greater the force of the subsequent contraction.
- Homeometric: the force of contraction increases in response to increased afterload (resistance).
- Chronoinotropic (Bowditch effect): contractility increases following an increase in heart rate.
- Sympathoadrenal: activation of the sympathetic nervous system.
The net result of these processes is compensatory hyperfunction. The heart beats faster, stronger, and relaxes more rapidly.
Transition from Compensation to Pathology
Prolonged hyperfunction leads to an increase in myocardial mass, but this growth is disproportionate, leading to critical disparities:
- Vascular: microvessels fail to keep pace with muscle mass growth, resulting in relative coronary insufficiency (ischemia).
- Energy: mitochondrial biogenesis lags behind myofibrillar mass, leading to ATP depletion.
- Enzymatic: myosin ATPase activity is insufficient, resulting in decreased contractile force.
- Plastic/Structural: synthesis of cellular structures lags behind metabolic demand, leading to structural dystrophy.
At the cellular level, ionic imbalances, membrane damage, and neurotransmitter depletion occur. A key role is played by decreased norepinephrine content in cardiac tissues.
Clinical Manifestations and Treatment Principles
Impaired pumping function leads to decreased stroke volume and cardiac output. Blood pools: residual volume and end-diastolic pressure rise within the ventricles. Pressure increases in the venous system, leading to venous congestion.
Clinically, chronic HF presents with dyspnea (initially on exertion, later at rest) and generalized edema. The extreme manifestation of acute failure is cardiogenic shock, which occurs during a precipitous drop in cardiac output.
Treatment of the syndrome is always multimodal. It includes etiotropic therapy (addressing the underlying cause), pathogenetic therapy (interrupting the chain of pathological mechanisms), sanogenetic therapy (enhancing adaptation), and symptomatic therapy (relieving patient symptoms, normalizing blood pressure, analgesia).