Pathogenesis of heart failure

This article is about chronic heart failure. This is because, strictly speaking, acute heart failure without a previous long-term heart disease is not very common in clinical practice. An example of such a condition may probably be acute myocarditis of rheumatic and non-rheumatic genesis. Most often, acute heart failure occurs as a complication of chronic, possibly against the background of some intercurrent disease and is characterized by the rapid development and severity of individual symptoms of heart failure, thereby demonstrating decompensation.

At early stages of cardiac dysfunction or heart failure, peripheral circulation remains adequate to tissue needs. This is facilitated by the activation of primary adaptation mechanisms already at early, preclinical stages of cardiac failure, when there are no obvious complaints yet and only a careful examination allows us to establish the presence of this syndrome.

Adaptation mechanisms in heart failure

A decrease in myocardial contractile function triggers primary adaptation mechanisms to ensure adequate cardiac output.

Cardiac output is the volume of blood expelled (ejected) by the ventricles during one systolic contraction.

The implementation of adaptation mechanisms has its own clinical manifestations; upon careful examination, one can suspect a pathological condition caused by latent chronic heart failure.

Thus, in pathological conditions characterized hemodynamically by ventricular volume overload, the Frank-Starling mechanism is activated to maintain adequate cardiac output: with an increase in myocardial stretching during diastole, its tension increases during systole.

An increase in end-diastolic pressure in the ventricle leads to an increase in cardiac output: in healthy individuals, it facilitates ventricular adaptation to physical activity, and in heart failure, it becomes one of the most important compensation factors. A clinical example of volumetric diastolic overload of the left ventricle is aortic insufficiency, in which during diastole, regurgitation of part of the blood from the aorta into the left ventricle and blood flow from the left atrium into the left ventricle occur almost simultaneously. Significant diastolic (volume) overload of the left ventricle occurs, and in response to it, tension increases during systole, which ensures adequate cardiac output. This is accompanied by an increase in area and an increase in the apical impulse; over time, a left-sided "heart hump" is formed.

A clinical example of right ventricular volume overload is a large ventricular septal defect. Increased right ventricular volume overload results in a pathological cardiac impulse. Frequently, a chest deformity is formed in the form of a bisternal "heart hump".

The Frank-Starling mechanism has certain physiological limits. An increase in cardiac output with an unchanged myocardium occurs with myocardial overstretching to 146-150%. With a greater load, an increase in cardiac output does not occur, and clinical signs of heart failure become manifest.

Another mechanism of primary adaptation in heart failure is hyperactivation of local or tissue neurohormones, when the sympathetic-adrenal system and its effectors are activated: norepinephrine, adrenaline, the renin-angiotensin-aldosterone system and its effectors - angiotensin II and aldosterone, as well as the natriuretic factor system. This mechanism of primary adaptation works in pathological conditions accompanied by myocardial damage. Clinical conditions in which the content of catecholamines increases are some cardiac myopathies: acute and chronic myocarditis, congestive cardiomyopathy. The clinical implementation of an increase in the content of catecholamines is an increase in the number of heart contractions, which up to a certain time helps maintain cardiac output at an adequate level. However, tachycardia is an unfavorable operating mode for the heart, since it always leads to myocardial fatigue and decompensation. One of the resolving factors in this case is the depletion of coronary blood flow due to the shortening of diastole (coronary blood flow is provided in the diastole phase). It is noted that tachycardia as an adaptive mechanism in cardiac decompensation is already connected at stage I of heart failure. The increase in rhythm is also accompanied by an increase in oxygen consumption by the myocardium.

Exhaustion of this compensatory mechanism occurs with an increase in the heart rate to 180 per minute in young children and more than 150 per minute in older children; the minute volume decreases following a decrease in the stroke volume of the heart, which is associated with a decrease in the filling of its cavities due to a significant shortening of diastole. Therefore, an increase in the activity of the sympathetic-adrenal system as heart failure increases becomes a pathological factor that aggravates myocardial fatigue. Thus, chronic hyperactivation of neurohormones is an irreversible process leading to the development of clinical symptoms of chronic heart failure in one or both circulatory systems.

Myocardial hypertrophy as a factor of primary compensation is included in conditions accompanied by pressure overload of the ventricular myocardium. According to the Laplace law, pressure overload is uniformly distributed over the entire surface of the ventricle, which is accompanied by an increase in intramyocardial tension and becomes one of the main triggers of myocardial hypertrophy. In this case, the rate of myocardial relaxation decreases, while the rate of contraction does not decrease significantly. Thus, tachycardia does not occur when using this mechanism of primary adaptation. Clinical examples of such a situation are aortic stenosis and arterial hypertension (hypertension). In both cases, concentric myocardial hypertrophy is formed in response to the need to overcome an obstacle, in the first case - mechanical, in the second - high arterial pressure. Most often, hypertrophy is concentric in nature with a decrease in the cavity of the left ventricle. However, the increase in muscle mass occurs to a greater extent than its contractility increases, therefore the level of myocardial functioning per unit of its mass is lower than normal. Myocardial hypertrophy at a certain clinical stage is considered as a favorable compensatory-adaptive mechanism that prevents a decrease in cardiac output, although this leads to an increased need for oxygen in the heart. However, myogenic dilation subsequently increases, which leads to increased heart rate and manifestation of other clinical manifestations of heart failure.

The right ventricle rarely forms hypertrophy of this nature (for example, in pulmonary artery stenosis and primary pulmonary hypertension), since the energetic capabilities of the right ventricle are weaker. Therefore, in such situations, dilation of the right ventricle cavity increases.

It should not be forgotten that with an increase in myocardial mass, a relative deficit in coronary blood flow occurs, which significantly worsens the condition of the damaged myocardium.

It should be noted, however, that in some clinical situations myocardial hypertrophy is considered a relatively favorable factor, for example in myocarditis, when hypertrophy, as an outcome of the process, is called damage hypertrophy. In this case, the life prognosis in myocarditis improves, since myocardial hypertrophy allows maintaining cardiac output at a relatively adequate level.

When the primary compensatory mechanisms are exhausted, cardiac output decreases and congestion occurs, as a result of which peripheral circulatory disorders increase. Thus, when the cardiac output of the left ventricle decreases, the end-diastolic pressure in it increases, which becomes an obstacle to the complete emptying of the left atrium and leads to an increase, in turn, in the pressure in the pulmonary veins and the pulmonary circulation, and then retrogradely - in the pulmonary artery. An increase in pressure in the pulmonary circulation leads to the release of fluid from the bloodstream into the interstitial space, and from the interstitial space - into the alveolar cavity, which is accompanied by a decrease in the vital capacity of the lungs and hypoxia. In addition, mixing in the alveolar cavity, the liquid part of the blood and air foam, which is clinically auscultated by the presence of moist wheezing of different sizes. The condition is accompanied by a wet cough, in adults - with abundant sputum, sometimes with streaks of blood ("cardiac asthma"), and in children - only a wet cough, sputum is most often not released due to an insufficiently expressed cough reflex. The result of increasing hypoxia is an increase in the content of lactic and pyruvic acids, the acid-base balance shifts towards acidosis. Acidosis contributes to the narrowing of the pulmonary vessels and leads to an even greater increase in pressure in the pulmonary circulation. Reflex spasm of the pulmonary vessels with an increase in pressure in the left atrium, as a realization of the Kitaev reflex, also worsens the condition of the pulmonary circulation.

Increased pressure in the vessels of the pulmonary circulation leads to the occurrence of small hemorrhages, and is also accompanied by the release of red blood cells per diapedesim into the lung tissue. This contributes to the deposition of hemosiderin and the development of brown induration of the lungs. Long-term venous congestion and capillary spasm cause the proliferation of connective tissue and the development of the sclerotic form of pulmonary hypertension, which is irreversible.

Lactic acid has a weak hypnotic (narcotic) effect, which explains increased drowsiness. A decrease in reserve alkalinity with the development of decompensated acidosis and oxygen debt lead to the appearance of one of the first clinical symptoms - dyspnea. This symptom is most pronounced at night, since at this time the inhibitory effect of the cerebral cortex on the vagus nerve is removed and physiological narrowing of the coronary vessels occurs, which in pathological conditions further aggravates the decrease in myocardial contractility.

Increased pressure in the pulmonary artery becomes an obstacle to the full emptying of the right ventricle during systole, which leads to hemodynamic (volume) overload of the right ventricle, and then the right atrium. Accordingly, with an increase in pressure in the right atrium, a regrograde increase in pressure in the veins of the systemic circulation (v. cava superior, v. cava inferior) occurs, which leads to a violation of the functional state and the occurrence of morphological changes in the internal organs. Stretching of the mouths of the vena cava due to a violation of the "pumping" of blood by the heart from the venous system through sympathetic innervation leads reflexively to tachycardia. Tachycardia gradually turns from a compensatory reaction into one that interferes with the work of the heart due to the shortening of the "rest period" (diastole) and the occurrence of myocardial fatigue. The immediate result of weakening the right ventricle is an enlarged liver, since the hepatic veins open into the inferior vena cava close to the right side of the heart. Congestion also affects the spleen to some extent; in heart failure, it can be enlarged in patients with a large and dense liver. The kidneys are also subject to congestive changes: diuresis decreases (nighttime can sometimes prevail over daytime), urine has a high specific gravity, and may contain some protein and erythrocytes.

Due to the fact that the content of reduced hemoglobin (gray-red color) increases against the background of hypoxia, the skin becomes bluish (cyanotic). A sharp degree of cyanosis in disorders at the level of the pulmonary circulation sometimes gives patients an almost black color, for example, in severe forms of Fallot's tetrad.

In addition to arterial cyanosis, which depends on a decrease in the content of oxyhemoglobin in arterial blood, there is central or peripheral cyanosis (tip of the nose, ears, lips, cheeks, fingers and toes): it is caused by a slowdown in blood flow and depletion of venous blood of oxyhemoglobin due to increased utilization of oxygen by tissues.

Congestion in the portal vein causes stagnant plethora in the vascular system of the stomach and intestines, which leads to various digestive disorders - diarrhea, constipation, heaviness in the epigastric region, sometimes - to nausea, vomiting. The last two symptoms are often the first manifest signs of congestive heart failure in children.

Edema and dropsy of the cavities, as a manifestation of right ventricular failure, appear later. The causes of the edematous syndrome are the following changes.

• Decreased renal blood flow.
• Redistribution of intrarenal blood flow.
• Increased tone of capacitive vessels.
• Increased secretion of renin by direct stimulating effect on receptors of renal tubules, etc.

Increased permeability of the vascular wall as a result of hypoxia also contributes to the development of peripheral edema. A decrease in cardiac output associated with the depletion of primary compensation mechanisms contributes to the inclusion of secondary compensation mechanisms aimed at ensuring normal arterial pressure and adequate blood supply to vital organs.

Secondary compensation mechanisms also include increased vasomotor tone and increased circulating blood volume. Increased circulating blood volume is the result of emptying blood depots and a direct consequence of increased hematopoiesis. Both should be considered as compensatory reactions to insufficient tissue oxygen supply, a reaction that is expressed in increased replenishment of blood with new oxygen carriers.

An increase in blood mass can play a positive role only at first, later it becomes an extra burden for blood circulation, when the heart weakens, the circulation of the increased blood mass becomes even slower. An increase in total peripheral resistance is clinically reflected by an increase in diastolic arterial pressure, which, together with a decrease in systolic arterial pressure (due to a decrease in cardiac output), leads to a significant decrease in pulse pressure. Small values of pulse pressure are always a demonstration of a limitation of the range of adaptive mechanisms, when external and internal causes can cause serious shifts in hemodynamics. Possible consequences of these changes are disturbances in the vascular wall, which leads to changes in the rheological properties of the blood and, ultimately, to one of the severe complications caused by an increase in the activity of the hemostasis system - thromboembolic syndrome.

Changes in water-electrolyte metabolism in heart failure occur due to disturbances in renal hemodynamics. Thus, as a result of a decrease in cardiac output, renal blood flow decreases and glomerular filtration decreases. Against the background of chronic activation of neurohormones, renal vessels narrow.

When cardiac output decreases, organ blood flow is redistributed: blood flow increases in vital organs (brain, heart) and decreases not only in the kidneys, but also in the skin.

The result of the presented complex disorders is, among other things, an increase in the excretion of aldosterone. In turn, an increase in the excretion of aldosterone leads to an increase in the reabsorption of sodium in the distal tubules, which also aggravates the severity of the edema syndrome.

In the late stages of heart failure, one of the causes of edema development is liver dysfunction, when albumin synthesis decreases, which is accompanied by a decrease in the colloid-oncotic properties of plasma. There are still many intermediate and additional links of primary and secondary adaptation in heart failure. Thus, an increase in the volume of circulating blood and an increase in venous pressure due to fluid retention leads to an increase in pressure in the ventricles and an increase in cardiac output (the Frank-Starling mechanism), but with hypervolemia, this mechanism is ineffective and leads to an increase in cardiac overload - an increase in heart failure, and with sodium and water retention in the body - to the formation of edema.

Thus, all the described adaptation mechanisms are aimed at maintaining adequate cardiac output, but with a pronounced degree of decompensation, “good intentions” trigger a “vicious circle”, further aggravating and worsening the clinical situation.

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