HUMAN MEDICAL BIOLOGY, ANATOMY, PHYSIOLOGY AND PATHOLOGY - Ya.I. Fedonyuk 2010

ANATOMY, PHYSIOLOGY, PATHOLOGY

CHAPTER 5. BLOOD AND LYMPH CIRCULATION PROCESSES AND THEIR PATHOLOGY

CARDIOVASCULAR SYSTEM DISEASES

HEART FAILURE

2. CHRONIC CIRCULATORY FAILURE

Chronic circulatory failure develops in various diseases that lead to cardiac damage and impairment of its pumping function.

The primary trigger mechanism of Heart Failure is a decrease in Cardiac Output, which results in reduced Blood supply to Organs in the outflow tract. Simultaneously, due to The Heart's inability to pump all the blood returning to it, congestion develops in the inflow tract, namely in the Veins. Since the capacity of the venous bed is approximately 10 times greater than that of the arterial bed, a significant volume of blood accumulates in the veins.

When the function of one cardiac ventricle is impaired, circulatory failure acquires specific features and is accordingly classified as left-ventricular or right-ventricular failure. Left-ventricular failure leads to congestion in the Pulmonary Circulation, which can result in pulmonary edema. In right-ventricular failure, congestion predominates in the systemic circulation, accompanied by

enlargement of the Liver, peripheral edema in the lower extremities, and fluid accumulation in the Abdominal cavity (ascites).

The heart is capable of rapidly adapting to increased workload and, by performing enhanced work, temporarily compensates for Circulatory Disorders.

A compensatory mechanism may involve an acceleration of heart contractions, known as tachycardia. From an energetic standpoint, this is the least favorable mechanism of compensation because, firstly, it is accompanied by high oxygen consumption and, secondly, a significant shortening of diastole—the period of myocardial recovery and rest.

Myocardial hypertrophy serves as an adaptive phenomenon aimed at sustaining increased workload without a proportional increase in stress per unit of Muscle mass.

In a hypertrophied heart, the range of adaptive capabilities—that is, the capacity to adjust to changing loads—is significantly diminished.

Pathological changes also arise in other organs and systems. Circulatory disorders in the Lungs lead to an elevated level of deoxygenated Hemoglobin in the blood, giving the Skin and mucous membranes a characteristic bluish discoloration (cyanosis). Due to slowed BLOOD FLOW IN the systemic circulation, Tissues receive insufficient oxygen, resulting in Hypoxia. This triggers the accumulation of under-oxidized metabolic products and carbon dioxide, leading to acidosis. Acidosis and hypoxia disrupt respiratory regulation, causing dyspnea. To compensate for hypoxia, erythropoiesis is stimulated; however, this increases blood viscosity and impairs its hemodynamic properties.

Elevated capillary pressure leads to tissue edema.

These phenomena are characteristic of the terminal stage of circulatory failure. Combined with severe gastrointestinal dysfunction, progressive circulatory failure leads to profound physical wasting, known as cardiac cachexia.

In clinical practice today, the Classification of circulatory failure proposed by M.D. Strazhesko and V.H. Vasylenko is widely used. According to this classification, there are three stages:

Stage I (Initial): latent circulatory failure manifested by dyspnea, palpitations, and fatigue appearing only during physical exertion. These symptoms disappear at rest. Hemodynamics at rest remain undisturbed.

Stage II - Period A: signs of circulatory failure at rest are moderately expressed, and Physical Exercise tolerance is reduced. There are moderate signs of hemodynamic impairment in either the systemic or pulmonary circulation; Period B: pronounced signs of heart failure at rest, with severe hemodynamic disorders in both the SYSTEMIC AND PULMONARY circulations.

Stage III (Terminal): a dystrophic stage characterized by pronounced hemodynamic disturbances, Metabolic Disorders, and irreversible structural changes in organs and tissues.