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Chronic heart failure
Pathogenesis. Basic concepts:
• Preload. This is the degree of diastolic filling of the left ventricle, determined by the venous return of blood to the heart, pressure in the pulmonary circulation. The most appropriate level of preload reflects the final diastolic pressure in the pulmonary artery (KDLA).
• Afterload - systolic myocardial tension required to expel blood. Practically, afterload is judged by the level of intra-aortic pressure, total peripheral resistance.
• Frank-Starling Law: an increase in the diastolic tension of the myocardial fibers (the equivalent is the final diastolic pressure in the cavity of the left ventricle - CEDAW) up to a certain point is accompanied by an increase in its contractility, an increase in cardiac output (ascending knee curve). With further stretching of the heart into the diastole, the ejection remains the same (does not increase) - the plateau of the curve; if the extension into the diastole increases even more, exceeding 150% of the initial length of the muscle fibers, then the cardiac output decreases (the descending knee of the curve). In heart failure, the heart operates in the “plateau” or “descending knee” mode of the Frank-Starling curve.
The main “starting point” of heart failure is a decrease in systolic volume (the equivalent is the ejection fraction of the left ventricle), an increase in the final diastolic pressure in the left ventricle (CEDAW). Further events are illustrated by schemes 6 and 7.
It is seen that the “launch” of the neurohumoral module begins with an increase in pressure in the left atrium and in the pulmonary veins. Stimulation of baroreceptors leads to irritation of the vasomotor center, the release of catecholamines. A decrease in renal blood flow is the reason for the increase in renin secretion. Angiotensin-2 causes vasoconstriction, increased secretion of aldosterone, hypersympathicotonia. Hyperaldosteronism is the cause of Na ° delay and an increase in circulating blood volume. Compensatory factors (see Scheme 6) are powerless before renin-angiotensin-aldosterone (RAA) activity. An increase in post- and preload contributes to a decrease in systolic ejection. This starts a vicious cycle of heart failure.
Based on the leading pathogenetic mechanism, N.M. Mukharlyamov distinguished:
• heart failure due to volume overload (diastolic overload of the left ventricle) with aortic and mitral insufficiency, defects of the heart walls, open ductus arteriosus;
due to resistance overload (hypertension of the large or small circle, stenosis of the aorta, pulmonary artery);
• primary myocardial form in dilated cardiomyopathy, myocarditis, myocardial infarction, post-infarction cardiosclerosis;
• heart failure due to impaired filling of the ventricles with hypertrophic cardiomyopathy, “hypertensive heart” with its expressed hypertrophy without dilatation, pericardial mitral stenosis;
• conditions with high cardiac output, when tissues require a greater amount of oxygen than actually delivered. This situation is possible with thyrotoxicosis, severe anemia, obesity.
Clinic, classification. The leading symptoms of left ventricular heart failure: shortness of breath, tachycardia, weakness; right ventricular failure - swelling of the cervical veins, enlarged liver, swelling of the lower extremities.
Features of additional methods:
• resting ECG clarifies the presence or absence of post-infarction scars, "diffuse" changes, tachycardia, arrhythmias and heart block;
• X-ray examination informs about the size of the heart chambers, helps to clarify the nature of valvular or congenital malformation, the presence and severity of stagnation in the pulmonary circulation;
• echo cardiographic method gives information about the thickness of the myocardium of the atria and ventricles, the main parameters of the violation of the contractile function of the myocardium.
The most important parameter is the ejection fraction of the left ventricle, which normally is 65-80%.
The classification of chronic heart failure is based on patient tolerance of physical activity.
N.D. Strazhesko, V.Kh. Vasilenko (1935) identified three stages:
• 1 stage (initial). At rest, there are no signs of heart failure. With physical exertion, shortness of breath, tachycardia, increased fatigue appear.
• 2 A stage. Dyspnea, tachycardia at rest (with left ventricular left) or enlarged liver, swelling of the legs (with right ventricular failure) - monoventricular heart failure.
• 2 B stage. Shortness of breath, tachycardia at rest; enlarged liver, swelling of the legs, sometimes ascites, hydrothorax. Biventricular heart failure.
• Stage 3 (terminal, dystrophic). Severe biventricular heart failure, irreversible organ changes (cardiogenic cirrhosis, cardiogenic pneumosclerosis, encephalopathy, pluriglandular endocrine insufficiency).
In Europe and America, the classification of the Cardiology Association of New York (NYHA), adopted in 1964, is used.
• 1st functional class (f. Cl.). A patient with heart disease without significant limitation of physical activity. Normal physical activity does not cause premature fatigue, shortness of breath, tachycardia. The diagnosis is made using instrumental research methods using stress tests.
• 2nd f. class A patient with a moderate restriction of physical activity. At rest, there are no complaints, normal physical activity leads to shortness of breath, tachycardia.
• 3rd f. class A patient with a pronounced limitation of physical activity satisfactorily feels at rest. Fatigue, shortness of breath and tachycardia with minimal exertion.
• 4th f. class Symptoms of biventricular heart failure at rest.
A general practitioner and a community therapist can use any of these classifications. It is important that the diagnosis is dynamic and reflects what the doctor managed to achieve during treatment. Chronic heart failure reduces the patient's quality of life (WO Spitzer; PA Li-bis, Ya.I. Kots). The decrease in the quality of life index is due to the need to be treated, the restriction of physical activity, the change in relationships with relatives, friends and colleagues, the restriction of labor activity, the decrease in incomes, demotion, restrictions on leisure activities, decreased activity in everyday life, and restrictions on nutrition and sex life.
Hence the psychological problems that result, depending on the basic structure of the personality, in asthenic, astheno-neurotic, hypochondriacal and other syndromes. A typology of the patient’s attitude to the disease is being formed, which is reflected in the rubric “psychological status”. Knowledge of the social status of the patient is necessary to develop a treatment strategy that is adequate to the capabilities of a particular patient and his family.
• IHD: post-infarction cardiosclerosis.
Chronic heart failure 2 A Art. (3 f. C.) with the transformation into the 1st art. (2 F. cl.). Astheno-neurotic syndrome, moderate.
• Rheumatism, inactive phase. Combined mitral defect with a predominance of stenosis of the left atrioventricular opening. Atrial fibrillation, tachysystolic form. Chronic heart failure 2 B Art. (4 f. Cl.) With transformation into the 2nd A art. (3 f. Cl.). Astheno-depressive syndrome, moderate.
• Dilated cardiomyopathy. Complex disturbance of rhythm and conduction: atrial fibrillation, tachysystolic form, polytopic ventricular extrasystole, blockade of the right bundle branch block. Chronic heart failure 2 B Art. (4 f. Cl.), Refractory. Astheno-hypochondria syndrome.
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Chronic heart failure
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