Classification and forms
Depending on the rate of development, acute (measured in minutes and hours) and chronic failure are distinguished.
Depending on the triggering factor, HF is divided into:
- Primary (cardiogenic): contractility itself drops with normal venous return (e.g., in cardiomyopathies).
- Secondary (non-cardiogenic): contractility is initially normal, but venous return drops sharply (massive blood loss, tamponade, collapse).
There are also myocardial (direct cell damage), overload (volume or pressure overload with a healthy myocardium), and mixed forms. By localization, failure is classified as left ventricular (infarction, aortic stenosis), right ventricular (pulmonary hypertension), and total.
How the heart attempts to cope (emergency compensation)
To maintain circulation during overload or damage, the body activates interrelated emergency mechanisms:
- Heterometric (Frank-Starling law): the more the muscle fiber is stretched, the stronger it contracts.
- Homeometric: contraction force increases in response to increased resistance (afterload).
- Chronoinotropic (Bowditch phenomenon): contractility increases following an increase in heart rate.
- Sympathoadrenal: activation of the sympathetic nervous system.
The outcome of these processes is compensatory hyperfunction. The heart beats faster, harder, and relaxes more quickly.
Why compensation turns into pathology
Prolonged hyperfunction leads to an increase in myocardial mass, but this growth is disproportionate. Critical disparities arise:
- 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 deficiency.
- Enzymatic: myosin ATPase activity is insufficient, causing contraction force to drop.
- Plastic: structural synthesis lags behind demands, leading to dystrophy.
At the cellular level, ion imbalance, membrane damage, and depletion of neurotransmitters occur. A key role is played by the decrease in norepinephrine content in cardiac tissues.
Clinical manifestations and treatment principles
A drop in pumping function leads to decreased stroke volume and cardiac output. Blood stagnates: residual volume and end-diastolic pressure increase in the ventricles. Pressure rises in the afferent vessels, causing venous congestion.
Clinically, the chronic form manifests as dyspnea (initially upon exertion, then at rest) and extensive edema. The extreme degree of acute failure is cardiogenic shock, which occurs with a sharp drop in cardiac output.
Syndrome treatment is always comprehensive. It includes etiotropic therapy (eliminating the cause), pathogenetic (breaking the chain of disorders), sanogenetic (enhancing adaptation), and symptomatic (relieving patient condition, blood pressure normalization, analgesia).
Briefly: answers to topical questions
What are the main etiological factors in the development of right ventricular heart failure?
The main causes of right ventricular heart failure explicitly stated in the sources include: right ventricular overload; pulmonary valve stenosis; increased pressure in the pulmonary artery (pulmonary hypertension). Massive thromboembolism of the main pulmonary artery or its large branches is also indicated for acute right ventricular failure.
What are the pathogenetic mechanisms of edema formation in chronic heart failure?
The primary triggering mechanism of edema formation in heart failure is decreased cardiac output. Cardiac edema forms as a result of the combined action of the following interrelated pathogenetic factors:
- Hemodynamic factor — blood congestion and a direct increase in capillary hydrostatic pressure.
- Hypervolemic factor — water and sodium retention in the body.
- Osmotic factor — tissue hyperosmolarity due to impaired outflow of osmotically active substances (metabolites).
- Lymphogenic factor — mechanical lymphatic insufficiency due to impaired lymph drainage.
- Oncotic and membranogenic factors — complement and enhance the action of other mechanisms.
Which pharmacological drug groups are used for the pathogenetic treatment of chronic heart failure?
For the pathogenetically substantiated treatment of CHF, the sources list the following drug groups. In early forms of DCM and asymptomatic LV dysfunction, first-line therapy may include: ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists. For symptomatic CHF with low LVEF (≤40%), baseline therapy includes 4 classes: ACE inhibitors or Sacubitril/Valsartan; beta-blockers; aldosterone antagonists; sodium-glucose cotransporter 2 (SGLT2) inhibitors, e.g., Dapagliflozin.
The four factors of hypertrophied heart exhaustion are easily remembered by the acronym SEFP: Vascular (Sosudisty), Energy (Energetichesky), Enzymatic (Fermentativny), Plastic (Plastichesky).
Class and exam questions
What is the difference between systolic and diastolic heart failure?
In systolic failure, contractile function itself and cardiac output drop. In diastolic failure, relaxation and filling of the left ventricle are impaired (due to hypertrophy or fibrosis), leading to an increase in end-diastolic pressure.
Why does the level of norepinephrine drop in heart failure?
This occurs due to the suppression of the tyrosine hydroxylase enzyme (reduced synthesis), impaired reuptake of the neurotransmitter by nerve endings, and a drop in receptor sensitivity to it.
How does parasympathetic regulation change in this pathology?
The effects of acetylcholine on M-cholinergic receptors are enhanced. This inhibits cAMP production, stimulates cGMP, and blocks calcium channels, reducing heart rate. These mechanisms are more resistant to damage than sympathetic ones.
What else to study on this topic
- Molecular mechanisms of cardiomyocyte membrane damage
- The role of ion imbalance in reduced myocardial contractility
- Pathogenesis of cardiogenic shock in myocardial infarction
- Mechanisms of dyspnea and edema development in chronic heart failure
- Sanogenetic and symptomatic therapy: sites of action
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