Pathogenesis of heart failure

In this article we are talking about chronic heart failure. This is due to the fact that, strictly speaking, acute heart failure without a previous long-term heart disease is not often met in clinical practice. An example of such a state may be, probably, acute myocarditis of rheumatic and non-rheumatic origin. More often, acute heart failure occurs as a complication of chronic, perhaps against a background of some intercurrent disease and is characterized by the rapid development and severity of certain symptoms of heart failure, thereby demonstrating decompensation.

In the early stages of impaired cardiac function or heart failure, peripheral circulation remains adequate to the needs of the tissues. This is facilitated by the connection of primary adaptation mechanisms already at early, preclinical stages of heart failure, when there are still no obvious complaints and only an attentive examination makes it possible to ascertain the presence of this syndrome.

Mechanisms of adaptation in heart failure

Reduction of the contractile function of the myocardium activates the primary mechanisms of adaptation to ensure adequate cardiac output.

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

The implementation of the mechanisms of adaptation has its clinical manifestations, with careful examination it is possible to suspect a pathological condition caused by latent chronic heart failure.

Thus, in pathological conditions, hemodynamically characterized by an overload of the ventricles with volume, the action of the Frank-Starling mechanism is connected to maintain an adequate cardiac output: with increasing myocardial tension during diastole, its stress increases during the systole period.

An increase in end-diastolic pressure in the ventricle leads to an increase in cardiac output: in healthy individuals, by facilitating the adaptation of the ventricles to physical exertion, and in case of heart failure, becoming one of the most important factors of compensation. A clinical example of volume diastolic overload of the left ventricle is aortic insufficiency, during which, at the same time, a part of blood from the aorta to the left ventricle and the flow of blood from the left atrium into the left ventricle occur regurgitating. There is a significant diastolic (volume) overload of the left ventricle, in response to it, the stress increases during the systole period, which provides an adequate cardiac output. This is accompanied by an increase in area and an increase in apical impulse, with time a left-sided "heart hump" is formed.

A clinical example of volume overload of the right ventricle is a defect of the interventricular septum with a large discharge. Increased volume overload of the right ventricle leads to the appearance of a pathological heartbeat. Often a deformity of the chest in the form of a bisternal "heart hump" is formed.

The Frank-Starling mechanism has definite physiological limits. Increase in cardiac output with unchanged myocardium occurs with myocardial overstretch up to 146-150%. With a larger load, no increase in cardiac output occurs, and clinical signs of heart failure become manifest.

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

The depletion of this compensatory mechanism occurs when the number of cardiac contractions increases to 180 per minute in infants and more than 150 per minute in older children; minute volume decreases after 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 the diastole. Therefore, the increase in activity of the sympatho-adrenal system as the heart failure increases becomes a pathological factor exacerbating the overfatigue of the myocardium. So, chronic hyperactivation of neurohormones is an irreversible process, leading to the development of clinical symptoms of chronic heart failure in one or both circles of the circulation.

Hypertrophy of the myocardium as a factor of primary compensation is included in conditions accompanied by pressure overload of the ventricular myocardium. According to Laplace's 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 relaxation of the myocardium decreases, while the rate of contraction does not decrease significantly. Thus, using this mechanism of primary adaptation, there is no tachycardia. Clinical examples of such a situation are aortic stenosis and hypertension (hypertension). In both cases, concentric hypertrophy of the myocardium is formed in response to the need to overcome the obstacle, in the first case - mechanical, in the second - high blood pressure. More often than not, hypertrophy has a concentric character with a decrease in the cavity of the left ventricle. However, the increase in muscle mass occurs to a greater extent than increases its contractility, so the level of functioning of the myocardium per unit of its mass is lower than normal. Hypertrophy of the myocardium at a certain clinical stage is considered as a favorable compensatory-adaptive mechanism, which prevents a decrease in cardiac output, although this leads to an increased need of the heart in oxygen. However, in the subsequent, myogenic dilatation increases, which leads to an increase in heart rate and manifestation of other clinical manifestations of heart failure.

The right ventricle rarely forms hypertrophy of this nature (for example, with pulmonary artery stenosis and primary pulmonary hypertension), since the right ventricular energy capacity is weaker. Therefore, in such situations, the dilatation of the right ventricular cavity increases.

Do not forget that with an increase in the mass of the myocardium there is a relative deficit of coronary blood flow, 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 the outcome of a process, is called damage hypertrophy. In this case, the life expectancy for myocarditis improves, since myocardial hypertrophy allows to maintain cardiac output at a relatively adequate level.

With the depletion of primary compensatory mechanisms, cardiac output decreases and stagnation occurs, and peripheral circulation disorders also increase. Thus, with a decrease in cardiac output, the left ventricle increases the end-diastolic pressure in it, which becomes an obstacle to complete emptying of the left atrium and leads to an increase in pressure in the pulmonary veins and a small circulation, and then retrograde - and in the pulmonary arteries. Increase in pressure in a small circle of blood circulation leads to the release of fluid from the bloodstream into the interstitial space, and from the interstitial space into the cavity of the alveoli, which is accompanied by a decrease in the vital capacity of the lungs and hypoxia. In addition, mixing in the cavity of the alveoli, the liquid part of the blood and air foam, which is clinically auscultatory manifested by the presence of moist variously-different rhonchuses. The condition is accompanied by a wet cough, in adults - with abundant sputum, sometimes with blood veins ("cardiac asthma"), and in children - only with a wet cough, sputum is not usually allocated due to an insufficiently expressed cough reflex. The result of an increase in hypoxia is an increase in the content of lactic and pyruvic acids, the acid-base state shifts toward acidosis. Acidosis promotes narrowing of the vessels of the lungs and leads to an even greater increase in pressure in a small circle of blood circulation. Reflex spasm of the lung vessels with increasing pressure in the left atrium, as the implementation of Kitaev's reflex, also worsens the condition of the small circle of the circulation.

Increased pressure in the vessels of the small circle of blood circulation leads to the appearance of small hemorrhages, and is accompanied by the release of red blood cells per diapedesim into the pulmonary tissue. This contributes to the deposition of hemosiderin and the development of brown lung induration. Prolonged venous congestion and spasm of capillaries cause the proliferation of connective tissue and the development of a sclerotic form of pulmonary hypertension, which is irreversible.

Lactic acid has a weak hypnotic (narcotic) effect, which explains the increased drowsiness. Lowering 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 takes place, in pathological conditions, the aggravating decrease in myocardial contractility is taking place.

An increase in 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 to the right atrium. Accordingly, when the pressure in the right atrium increases, the pressure in the veins of the large circulation increases vigorously (v. Cava superior, v. Cava inferior), which leads to a disruption in the functional state and the appearance of morphological changes in the internal organs. Stretching of the mouths of the hollow veins in violation of the "pumping out" of the blood by the heart from the venous system through sympathetic innervation leads reflexively to tachycardia. Tachycardia from the compensatory reaction gradually turns into interfering work of the heart due to the shortening of the "rest period" (diastole) and the occurrence of overfatigue of the myocardium. The immediate result of weakening the activity of the right ventricle is an increase in the liver, since the hepatic veins open into the inferior vena cava close to the right heart. Stagnation affects to some extent and on the spleen, with heart failure, it can be increased in patients with a large and dense liver. Changes in the stagnation of the kidneys: diuresis decreases (night may sometimes predominate over daytime), urine has a high specific gravity, may contain some amount of protein and red blood cells.

In connection with the fact that against the background of hypoxia the content of reduced hemoglobin (gray-red color) increases, the integuments become cyanotic (cyanotic). A sharp degree of cyanosis with violations at the level of the small circle of blood circulation gives the patients sometimes almost black color, for example, in severe forms of the tetralogy of Fallot.

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

Stagnation in the portal vein causes congestion 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 edema of the cavities, as a manifestation of right ventricular failure, appear later. The reasons for the appearance of edematous syndrome are the following changes.

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

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

The secondary mechanisms of compensation include also increased vasomotor tone and an increase in the volume of circulating blood. An increase in the volume of circulating blood is the result of emptying of blood depots and a direct consequence of increased hematopoiesis. Both should be considered as a compensatory response to the lack of supply of tissues with oxygen, a reaction expressed in the enhancement of blood replenishment with new oxygen carriers.

The increase in the mass of blood can play a positive role only at first, in the future it becomes an extra burden for blood circulation, with the weakening of the heart, the circulation of the increased blood mass becomes even slower. The increase in total peripheral resistance is clinically reflected by an increase in diastolic atrial pressure, which together with a decrease in systolic blood 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 the 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 hemostatic system - thromboembolic syndrome.

Changes in water-electrolyte metabolism in heart failure occur in disorders of renal hemodynamics. Thus, as a result of a decrease in cardiac output, there is a decrease in renal blood flow and a decrease in glomerular filtration. Against the backdrop of chronic activation of neurohormones, narrowing of the kidney vessels takes place.

With a decrease in cardiac output, there is a redistribution of the organ blood flow: an increase in blood flow in vital organs (brain, heart) and a decrease in blood flow 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 aldosterone excretion leads to an increase in sodium reabsorption in the distal tubules, which also exacerbates the severity of the edematous syndrome.

In the late stages of heart failure, one of the reasons for the development of edema is a violation of liver function, when the synthesis of albumins decreases, which is accompanied by a decrease in the colloidal-oncotic properties of the plasma. There are many more 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 ventricular pressure and an increase in cardiac output (the Frank-Starling mechanism), but in hypervolaemia, this mechanism is ineffective and leads to an increase in heart overload-an increase in heart failure, and with the delay of sodium and water in the body - to the formation of edema.

So, all described mechanisms of adaptation are aimed at maintaining an adequate cardiac output, but with a pronounced degree of decompensation, "good intentions" launch a "vicious circle" that aggravates and worsens the clinical situation even more.

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