Extracardiac mechanisms of heart failure compensation, effects and pathogenetic characteristics. Compensatory mechanisms in heart failure
Hemodynamic compensation mechanisms in heart failure
A healthy body has a variety of mechanisms that ensure timely unloading of the vascular bed from excess fluid. With heart failure, compensatory mechanisms are “turned on” aimed at maintaining normal hemodynamics. These mechanisms in conditions of acute and chronic circulatory insufficiency have much in common, however, there are significant differences between them.
As in acute and chronic heart failure, all endogenous mechanisms for compensating hemodynamic disorders can be divided into intracardiac: compensatory hyperfunction of the heart (Frank-Starling mechanism, homeometric hyperfunction), myocardial hypertrophy and extracardiac: unloading reflexes of Bainbridge, Parin, Kitaev, activation of the excretory function of the kidneys, deposition of blood in the liver and spleen, sweating, evaporation of water from the walls of the pulmonary alveoli, activation of erythropoiesis, etc. This division is somewhat arbitrary, since the implementation of both intra- and extracardiac mechanisms is under the control of neurohumoral regulatory systems.
Compensation mechanisms for hemodynamic disorders in acute heart failure. At the initial stage of systolic dysfunction of the ventricles of the heart, intracardiac factors for compensating for heart failure are activated, the most important of which is Frank-Starling mechanism (heterometric compensation mechanism, heterometric hyperfunction of the heart). Its implementation can be represented as follows. Violation of the contractile function of the heart entails a decrease in stroke volume and hypoperfusion of the kidneys. This contributes to the activation of the RAAS, causing water retention in the body and an increase in circulating blood volume. Under conditions of hypervolemia, there is an increased inflow of venous blood to the heart, an increase in diastolic blood filling of the ventricles, stretching of myofibrils of the myocardium and a compensatory increase in the force of contraction of the heart muscle, which provides an increase in stroke volume. However, if the end-diastolic pressure rises by more than 18-22 mm Hg, there is excessive overstretching of the myofibrils. In this case, the Frank-Starling compensatory mechanism ceases to operate, and a further increase in end-diastolic volume or pressure causes no longer an increase, but a decrease in stroke volume.
Along with intracardiac compensation mechanisms in acute left ventricular failure, unloading extracardiac reflexes that contribute to the occurrence of tachycardia and an increase in the minute volume of blood (MOC). One of the most important cardiovascular reflexes providing an increase in the IOC is The Bainbridge reflex is an increase in heart rate in response to an increase in blood volume. This reflex is realized upon stimulation of mechanoreceptors localized at the mouth of the hollow and pulmonary veins. Their irritation is transmitted to the central sympathetic nuclei of the medulla oblongata, resulting in an increase in the tonic activity of the sympathetic link of the autonomic nervous system, and reflex tachycardia develops. The Bainbridge reflex is aimed at increasing the minute volume of blood.
The Bezold-Jarish reflex is a reflex expansion of the arterioles of the systemic circulation in response to the stimulation of mechano- and chemoreceptors localized in the ventricles and atria.
As a result, hypotension occurs, which is accompanied by
dycardia and temporary respiratory arrest. Afferent and efferent fibers take part in the implementation of this reflex. n. vagus. This reflex is aimed at unloading the left ventricle.
Among the compensatory mechanisms in acute heart failure is increased activity of the sympathoadrenal system, one of the links of which is the release of norepinephrine from the endings of the sympathetic nerves that innervate the heart and kidneys. The observed excitement β -adrenergic receptors of the myocardium leads to the development of tachycardia, and stimulation of such receptors in JGA cells causes increased secretion of renin. Another stimulus for renin secretion is a decrease in renal blood flow as a result of catecholamine-induced constriction of the glomerular arterioles. Compensatory in nature, the increase in the adrenergic effect on the myocardium in conditions of acute heart failure is aimed at increasing the stroke and minute blood volumes. Angiotensin-II also has a positive inotropic effect. However, these compensatory mechanisms can aggravate heart failure if the increased activity of the adrenergic system and RAAS persists for a sufficiently long time (more than 24 hours).
All that has been said about the mechanisms of compensation for cardiac activity equally applies to both left and right ventricular failure. The exception is the Parin reflex, the action of which is realized only when the right ventricle is overloaded, observed in pulmonary embolism.
The Larin reflex is a drop in blood pressure caused by the expansion of the arteries of the systemic circulation, a decrease in the minute volume of blood as a result of the resulting bradycardia and a decrease in the volume of circulating blood due to the deposition of blood in the liver and spleen. In addition, the Parin reflex is characterized by the appearance of shortness of breath associated with the upcoming hypoxia of the brain. It is believed that the Parin reflex is realized due to the strengthening of the tonic influence n.vagus on the cardiovascular system in pulmonary embolism.
Compensation mechanisms for hemodynamic disorders in chronic heart failure. The main link in the pathogenesis of chronic heart failure is, as is known, a gradually increasing decrease in the contractile function of the mi-
ocardium and a fall in cardiac output. The resulting decrease in blood flow to organs and tissues causes hypoxia of the latter, which can initially be compensated by increased tissue oxygen utilization, stimulation of erythropoiesis, etc. However, this is not enough for normal oxygen supply to organs and tissues, and increasing hypoxia becomes a trigger mechanism for compensatory changes in hemodynamics.
Intracardiac mechanisms of cardiac function compensation. These include compensatory hyperfunction and hypertrophy of the heart. These mechanisms are integral components of most adaptive reactions of the cardiovascular system of a healthy organism, but under pathological conditions they can turn into a link in the pathogenesis of chronic heart failure.
Compensatory hyperfunction of the heart acts as an important compensation factor for heart defects, arterial hypertension, anemia, hypertension of the small circle and other diseases. Unlike physiological hyperfunction, it is long-term and, what is essential, continuous. Despite the continuity, compensatory hyperfunction of the heart can persist for many years without obvious signs of decompensation of the pumping function of the heart.
An increase in the external work of the heart associated with an increase in pressure in the aorta (homeometric hyperfunction), leads to a more pronounced increase in myocardial oxygen demand than myocardial overload caused by an increase in circulating blood volume (heterometric hyperfunction). In other words, to carry out work under pressure load, the heart muscle uses much more energy than to perform the same work associated with a volume load, and therefore, with persistent arterial hypertension, cardiac hypertrophy develops faster than with an increase in circulating blood volume. For example, during physical work, high-altitude hypoxia, all types of valvular insufficiency, arteriovenous fistulas, anemia, myocardial hyperfunction is provided by increasing the cardiac output. At the same time, systolic tension of the myocardium and pressure in the ventricles increase slightly, and hypertrophy develops slowly. At the same time, in hypertension, pulmonary hypertension, stenosis
The development of hyperfunction is associated with an increase in myocardial tension with a slightly changed amplitude of contractions. In this case, hypertrophy progresses quite quickly.
Myocardial hypertrophy- This is an increase in the mass of the heart due to an increase in the size of cardiomyocytes. There are three stages of compensatory hypertrophy of the heart.
First, emergency, stage It is characterized, first of all, by an increase in the intensity of the functioning of myocardial structures and, in fact, is a compensatory hyperfunction of the not yet hypertrophied heart. The intensity of functioning of structures is the mechanical work per unit mass of the myocardium. An increase in the intensity of functioning of structures naturally entails the simultaneous activation of energy production, the synthesis of nucleic acids and proteins. This activation of protein synthesis occurs in such a way that at first the mass of energy-forming structures (mitochondria) increases, and then the mass of functioning structures (myofibrils). In general, an increase in the mass of the myocardium leads to the fact that the intensity of the functioning of the structures gradually returns to a normal level.
Second stage - stage of completed hypertrophy- characterized by a normal intensity of functioning of myocardial structures and, accordingly, a normal level of energy production and synthesis of nucleic acids and proteins in the tissue of the heart muscle. At the same time, oxygen consumption per unit mass of the myocardium remains within the normal range, and oxygen consumption by the heart muscle as a whole is increased in proportion to the increase in heart mass. An increase in myocardial mass in conditions of chronic heart failure occurs due to the activation of the synthesis of nucleic acids and proteins. The trigger mechanism for this activation is not well understood. It is believed that the strengthening of the trophic influence of the sympathoadrenal system plays a decisive role here. This stage of the process coincides with a long period of clinical compensation. The content of ATP and glycogen in cardiomyocytes is also within the normal range. Such circumstances give relative stability to hyperfunction, but at the same time they do not prevent metabolic and myocardial structure disorders gradually developing at this stage. The earliest signs of such disorders are
a significant increase in the concentration of lactate in the myocardium, as well as moderately severe cardiosclerosis.
Third stage progressive cardiosclerosis and decompensation characterized by a violation of the synthesis of proteins and nucleic acids in the myocardium. As a result of a violation of the synthesis of RNA, DNA and protein in cardiomyocytes, a relative decrease in the mass of mitochondria is observed, which leads to inhibition of ATP synthesis per unit mass of tissue, a decrease in the pumping function of the heart and the progression of chronic heart failure. The situation is aggravated by the development of dystrophic and sclerotic processes, which contributes to the appearance of signs of decompensation and total heart failure, culminating in the death of the patient. Compensatory hyperfunction, hypertrophy and subsequent decompensation of the heart are links in a single process.
The mechanism of decompensation of hypertrophied myocardium includes the following links:
1. The process of hypertrophy does not extend to the coronary vessels, therefore the number of capillaries per unit volume of the myocardium in the hypertrophied heart decreases (Fig. 15-11). Consequently, the blood supply to the hypertrophied heart muscle is insufficient to perform mechanical work.
2. Due to an increase in the volume of hypertrophied muscle fibers, the specific surface of cells decreases, due to
Rice. 5-11. Myocardial hypertrophy: 1 - myocardium of a healthy adult; 2 - hypertrophied myocardium of an adult (weight 540 g); 3 - hypertrophied adult myocardium (weight 960 g)
this worsens the conditions for the entry of nutrients into the cells and the release of metabolic products from cardiomyocytes.
3. In a hypertrophied heart, the ratio between the volumes of intracellular structures is disturbed. Thus, the increase in the mass of mitochondria and the sarcoplasmic reticulum (SPR) lags behind the increase in the size of myofibrils, which contributes to the deterioration of the energy supply of cardiomyocytes and is accompanied by impaired accumulation of Ca 2 + in the SPR. There is a Ca 2 + overload of cardiomyocytes, which ensures the formation of contracture of the heart and contributes to a decrease in stroke volume. In addition, Ca 2 + overload of myocardial cells increases the likelihood of arrhythmias.
4. The conduction system of the heart and the autonomic nerve fibers innervating the myocardium do not undergo hypertrophy, which also contributes to the dysfunction of the hypertrophied heart.
5. Apoptosis of individual cardiomyocytes is activated, which contributes to the gradual replacement of muscle fibers with connective tissue (cardiosclerosis).
Ultimately, hypertrophy loses its adaptive value and ceases to be beneficial for the body. The weakening of the contractility of the hypertrophied heart occurs the sooner, the more pronounced hypertrophy and morphological changes in the myocardium.
Extracardiac mechanisms of cardiac function compensation. In contrast to acute heart failure, the role of reflex mechanisms of emergency regulation of the pumping function of the heart in chronic heart failure is relatively small, since hemodynamic disorders develop gradually over several years. More or less definitely, one can speak of Bainbridge reflex, which "turns on" already at the stage of sufficiently pronounced hypervolemia.
A special place among the "unloading" extracardiac reflexes is occupied by the Kitaev reflex, which is "launched" in mitral stenosis. The fact is that in most cases, manifestations of right ventricular failure are associated with congestion in the systemic circulation, and left ventricular failure - in the small one. The exception is mitral valve stenosis, in which congestion in the pulmonary vessels is not caused by left ventricular decompensation, but by obstruction of blood flow through
the left atrioventricular opening - the so-called "first (anatomical) barrier." At the same time, stagnation of blood in the lungs contributes to the development of right ventricular failure, in the genesis of which the Kitaev reflex plays an important role.
The Kitaev reflex is a reflex spasm of the pulmonary arterioles in response to an increase in pressure in the left atrium. As a result, a “second (functional) barrier” appears, which initially plays a protective role, protecting the pulmonary capillaries from excessive overflow with blood. However, then this reflex leads to a pronounced increase in pressure in the pulmonary artery - acute pulmonary hypertension develops. The afferent link of this reflex is represented by n. vagus, a efferent - the sympathetic link of the autonomic nervous system. The negative side of this adaptive reaction is an increase in pressure in the pulmonary artery, leading to an increase in the load on the right heart.
However, the leading role in the genesis of long-term compensation and decompensation of impaired cardiac function is played not by reflex, but by neurohumoral mechanisms, the most important of which is the activation of the sympathoadrenal system and the RAAS. Speaking about the activation of the sympathoadrenal system in patients with chronic heart failure, one cannot fail to point out that in most of them the level of catecholamines in the blood and urine is within the normal range. This distinguishes chronic heart failure from acute heart failure.
Chapter 2
Anatomy, physiology and pathophysiology of occlusive diseases of the branches of the aortic arch
COMPENSATION OF BLOOD CIRCULATION IN DISEASES OF BRAIN VESSELS
The defeat of one or several main arteries of the brain leads to the immediate activation of the mechanisms for compensating blood circulation. First, there is an increase in blood flow through other vessels. It has been proven that when the CCA is clamped, the blood flow in the opposite carotid artery increases by 13-38%. Secondly, blood flow compensation can be achieved by increasing the cardiac output.
So, the works of V.S. Rabotnikov proved that in patients with occlusive lesions of the brachiocephalic arteries, a number of changes in general hemodynamics are noted in the form of an increase in circulating blood volume (CBV), stroke index (SI), minute volume (MI) due to an increase in ventricular contractility.
One of the important factors that ensure normal blood circulation in the brain is systemic blood pressure. Arterial hypertension, as an adaptive reaction of the body, occurs in 20-30% of patients with cerebrovascular insufficiency. In addition, when the reactivity of the carotid sinus changes (with atherosclerosis, arteritis), its depressor function is activated, which also leads to an increase in blood pressure.
A significant role in the regulation of cerebral blood flow is also played by the content of carbon dioxide (CO2) in the blood. In arterial blood, only 1.3-1.7% causes expansion of cerebral vessels, while for musculoskeletal vessels, the threshold value of Co 2 blood is 3%.
The works of E.V. Schmidt, Bove revealed adaptive changes in metabolism under conditions of ischemia (an increase in the partial pressure of CO 2 (Pco 2), a decrease in blood pH), which are aimed at reducing the peripheral resistance of cerebral vessels, thereby improving cerebral blood flow. At the same time, Holdt-Rasmussen found that patients with cerebrovascular accident have a perverted reaction of cerebral vessels to inhalation of CO 2 . Fieschi using radioactive albumin noted, in some patients, the absence of changes in cerebral blood flow during inhalation of CO 2 with acute disorders of cerebral circulation.
The most important factor determining the compensation of cerebral circulation in occlusive lesions of the brachiocephalic arteries is the state of the collateral vascular bed, or rather the rate of its development at the time of the cerebral accident. Its insufficient development leads to impaired cerebral circulation. With an adequate condition, clinical manifestations of occlusive lesions of the brachiocephalic arteries may be absent.
The process of formation of collateral circulation has temporal characteristics, and the clinical manifestations of damage to the main arteries of the brain will depend primarily on the rate of formation of adequate collateral circulation.
The level and degree of effectiveness of collateral circulation depend on a number of factors. These include: the state of general hemodynamics, the rate of development and localization of the occlusive lesion, as well as the state of the vessels that provide collateral circulation.
When the main trunk of the main artery is damaged, a compensatory expansion of the terminal branches in the pool of this artery occurs, both due to the occurrence of a drop in intravascular pressure and due to a drop in O 2 voltage in the brain tissue, as a result of which aerobic oxidation of glucose is disturbed and carbon dioxide and carbon dioxide accumulate. lactic acid.
B.N. Klosovsky proposed to distinguish 4 levels of collateral circulation of the brain. The first is the level of the circle of Willis, the second is the level of collateral circulation on the surface of the brain in the subarachnoid space. In these zones, the bulk of the largest anastomoses between the branches of the anterior and middle, middle and posterior, anterior and posterior cerebral arteries is concentrated. The third level of collateral circulation are anastomoses within some area, such as the cerebral hemispheres. The fourth level is the intracerebral capillary network. E.V. Schmidt, in addition, distinguishes the extracranial level of collateral circulation due to the anastomosis of the internal carotid artery and vertebral artery with the pool of the external carotid artery.
We consider it sufficient to assess blood circulation (main, collateral and tissue) division into 2 levels: the first - to the level (and including it) of anatomically determined and formed collaterals (the level of the circle of Willis), the second - from the level (excluding it) of anatomically determined and formed collaterals. Fundamentally, this division is similar to the division into proximal and distal lesions of the arteries.
The main way of compensation is blood flow through the PSA. Normally, all three paths of collateral circulation are in hemodynamic balance with each other, complementing and replacing each other. When the ICA is damaged, the opposite ICA is activated first of all through the PCA, which is involved in the formation of the anterior part of the circle of Willis. The level of blood flow through this artery mainly depends on the state of the contralateral (in relation to the affected) ICA, as if being a trigger mechanism for turning on the remaining pathways. So, with an insufficient degree of development of the flow through the anterior communicating artery due to its underdevelopment, atherosclerotic lesion, or damage to the contralateral ICA, collateral circulation develops through the ophthalmic anastomosis from the system of the ipsi- or contralateral carotid artery, and/or collateral circulation develops through the PCA.
With an occlusive lesion of the ICA, the anatomical structure of the circle of Willis is important in the implementation of all types of circulatory compensation. However, the functional state of all departments of the circle of Willis is no less important.
Occlusion of the artery, its stenosis or tortuosity cause the development of collateral blood flow, primarily due to a drop in varying degrees of perfusion pressure distal to the lesion. In this case, the degree of compensation may be different, and in a fairly large number of cases (up to 25-35%), the perfusion pressure in the distal parts approaches or reaches the norm (for example, the presence of antegrade blood flow through the ophthalmic anastomosis with isolated occlusion of the internal carotid artery). However, this does not mean complete compensation of blood circulation. Since the brain in some cases, for normal functioning, it is necessary to increase the total cerebral blood flow by 40-60%, another important indicator will be the potential ability to compensate for the increase in blood consumption. In other words, the two main indicators of the degree of compensation of cerebral blood flow will be the level of blood flow at rest and the degree of increase in blood flow during a dosed load (functional test) in relation to the level of blood flow at rest.
The combination of lesions of the main arteries of the brain with different hemodynamic significance does not mean a simple summation of these values. The total deficit of cerebral blood flow depends not only on the volume of the lesion, but also on the state of the patient's homeostasis. Mutual influence of lesions also plays an important role in the violation of blood flow. It is much easier to explain this mutual influence with some examples. Patient X., previously completely asymptomatic neurologically with minor stenosis ("hemodynamically insignificant") of both carotid arteries, develops an ischemic stroke after the detection of pathology and prescription of treatment (aspirin). At first glance, the mechanism of stroke development is unclear. However, from the point of view of hemodynamics, the following happened - before the appointment of treatment, the patient had a relatively high blood viscosity. The Reynolds number (determining the transition from laminar to turbulent blood flow), inversely proportional to blood viscosity, was low, and the percentage of turbulence in the area of stenosis was negligible. Therefore, during this period, the carotid arteries provided both sufficient blood flow and sufficient potential for increased blood flow (reactivity). A decrease in blood viscosity led to a decrease in volumetric blood flow through the carotid arteries due to the formation of a highly turbulent flow distal to the stenosis. The disruption of blood flow in one carotid artery causes a compensatory increase in systemic pressure and an increase in volumetric blood flow in the opposite carotid artery, which entails a similar restriction of blood flow.
It is necessary to dwell separately on the external carotid artery, to determine its hemodynamic role in the blood supply to the brain during ICA occlusions, as a source of collateral circulation.
Normally, the ECA does not participate in the blood supply to the brain, but in case of occlusion of the internal carotid arteries, an extensive collateral network of ECA branches anastomosing with the intracranial branches of the internal carotid and vertebral arteries is included in the cerebral blood supply.
When analyzing the frequency of occlusive lesions of the branches of the aortic arch, it was found that the bifurcation of the common and proximal internal carotid arteries is most often affected. The growth of an atherosclerotic plaque leads to occlusion (in 9-34% of cases of occlusive lesions of the branches of the aortic arch) of the internal and (in 3-6% of cases) of the common carotid arteries. The ECA is affected much less frequently than the ICA. Hemodynamically significant damage to the ECA with occlusion of the ICA occurs in 26.9-52.2%. According to our data, 36.8% of patients with ICA occlusion have hemodynamically significant stenosis of the external carotid artery.
A number of authors argue that the role of the ECA in the implementation of intracranial circulation is doubtful, but a large group of specialists, such as Yu.L. Grozovsky, F.F. Barnett, A.D. Callow et al. note the important role of the ECA in cerebral hemodynamics in ICA occlusion. According to Fields W.S. (1976), F.F. Barnett (1978), McGuiness (1988), with occlusion of the internal carotid arteries, the ECA takes up to 30% of cerebral blood flow. Restoration of adequate, main blood flow through the ECA with its stenosis or occlusion of the CCA and ICA in patients with cerebrovascular insufficiency leads to an improvement in the blood supply to the brain through systemic anastomoses, which in turn leads to a decrease in the manifestations of cerebrovascular accident.
However, this work does not aim to show the significance of NCA in cerebral hemodynamics. We consider the external carotid artery as a donor for the formation of EICMA. The state of the ECA determines the adequacy of the microanastomosis. Depending on the degree of narrowing, three types of lesions of the ECA are distinguished (
1 - no ECA lesion, 2 - ECA stenosis, 3 - ECA orifice occlusion with CCA and ICA occlusion "> Fig. 9):
- no damage to the NSA,
- stenosis of the NCA,
- occlusion of the mouth of the ECA with occlusion of the CCA and ICA.
The state of the ECA is determined using ultrasound research methods, duplex scanning and radiopaque angiography. Measurement of blood pressure in the temporal arteries is mandatory included in the protocol for examining patients. This study is highly informative and in patients with ECA stenosis is the main one for determining indications for staging for surgical interventions.
Of particular interest is the situation when both the ICA and the CCA are occluded – respectively, the main blood flow through the ECA also stops. In these patients, brain revascularization using long shunts is possible - subclavian-cortical shunting ended in shunt thrombosis in almost 100% of cases.
Maintaining the patency of the ECA behind its first branch made it possible to use the ECA branches as a donor after restoration of the main blood flow by subclavian-ECA prosthetics.
With occlusion of the ICA and CCA, the ECA remains passable distally to the first branch, blood circulation is maintained through anastomoses between the branches of the ECA, which prevents the spread of thrombosis.
Subclavian-external carotid shunting or prosthetics creates the following hemodynamic situation: blood from the shunt is discharged into the ECA where it is distributed between its branches, due to the high ability to receive blood, the volume flow of blood through the shunt increases, which is the prevention of its thrombosis.
In case of ICA occlusion, the cause of repeated disorders of cerebral circulation can be both hemodynamic factors caused by the ICA occlusion itself, stenosis of the ECA, and embologenic factors, which can be caused by microembolism from ulcerated plaques in the ECA or from the ICA stump.
Microemboli can pass through the HA, and most often there is a violation of the retinal circulation. This fact is confirmed by reports of direct visual observation of the passage of emboli through the vessels of the retina during direct ophthalmoscopy. Barnet F.F. The cause of TIA in the territory of the occluded ICA with normal hemodynamics in some cases is considered to be microembolism through the ophthalmic anastomosis.
Ringelstein E.B. et al showed that in patients with ICA occlusion, repeated cerebrovascular accidents were caused in 41% of cases by hemodynamic factors, in 40% by embologenic factors, and in 19% of cases they were of a mixed nature.
The first operations on the NSA began in the 60s. The fact is that when performing endarterectomy (EAE) from the ECA, resection of the ICA stump is performed, that is, the source of microembolism is eliminated.
To identify the pressure gradient between the branches of the ECA - donor arteries and the intracranial branches of the ICA, in particular the cortical branches of the MCA, we used the method of measuring blood pressure in the superficial temporal artery using the original cuff and determining the pressure in the central retinal artery as a characteristic of pressure in the MCA and its branches.
As the MCA divides, the pressure in its terminal arteries must decrease somewhat, otherwise there would be no blood flow along the pressure gradient and the work of the blood flow against the forces of gravity. This factor is useful as it reduces the pressure in the recipient artery. The parietal and temporal arteries, which can be used as donor arteries, are 2nd order branches of the ECA, therefore, the pressure drop in them will be less than in the cortical branches of the MCA, which are 3rd order arteries. That is, optimal hemodynamic conditions are created that are necessary for the operation of EICMA.
Their inclusion is aimed at restoring the correspondence of blood circulation with the capabilities of the heart.
Adaptive cardiovascular reflexes.
With an increase in pressure in the cavity of the left ventricle, for example, with stenosis of the aortic mouth, the arterioles and veins of the systemic circulation expand, and bradycardia occurs. As a result, the pumping of blood from the left ventricle to the aorta is facilitated and blood flow to the right atrium decreases, and myocardial nutrition improves.
With reduced pressure in the left ventricle and aorta, a reflex constriction of arterial and venous vessels and tachycardia occur. As a result, blood pressure increases.
With increased pressure in the left atrium and pulmonary veins, small arteries and arterioles of the small circle narrow (Kitaev's reflex). The inclusion of the Kitaev reflex helps to reduce the blood filling of the capillaries and reduces the risk of developing pulmonary edema.
With an increase in pressure in the pulmonary arteries and the right ventricle, Parin's unloading reflex is activated. That is, there is an expansion of the arteries and veins of the systemic circulation, bradycardia occurs. This reduces the risk of developing pulmonary edema.
Diuresis changes also referred to as extracardiac compensation mechanisms.
BUT). With a decrease in arterial blood volume, salt and water are retained by the kidneys. As a result, there is an increase in the volume of circulating blood, venous blood flow and cardiac output.
B). With an increase in the volume and pressure of blood in the atria, the secretion of atrial natriuretic factor occurs. It acts on the kidneys, causing an increase in diuresis, thereby lowering high blood pressure.
3. Extracardiac compensatory mechanisms include all those that are activated during hypoxia(see the lecture on the topic "Pathology of breathing").
Peculiarities of hemodynamics and mechanisms of compensation in case of heart defects.
AORTIC VALVE INSUFFICIENCY.
With this type of defect, the semilunar leaflets of the aortic valve do not completely close the aortic opening during ventricular diastole. Therefore, some of the blood ejected into the aorta during systole returns back to the left ventricle during diastole. The blood pressure in the aorta decreases sharply. The return of blood back is called regurgitation or reverse reset, vicious blood flow. The movement of blood in the normal direction is called the effective or translational volume. The sum of these blood volumes is called the total or total volume.
Thus, with aortic valve insufficiency during diastole, the left ventricle is filled with blood flowing from both the left atrium and the aorta. Its diastolic filling increases and, according to the Frank-Starling law, systole increases. Expansion of the cavity of the heart, accompanied by an increase in the force of its contraction, is called tonogenic dilation. It should be distinguished from myogenic dilatation, in which there is a weakening of the strength of systole. Thus, due to tonogenic dilatation and increased systole, the volume of blood entering the aorta increases. And, despite blood regurgitation, effective, forward volume will be normal.
The constant performance of increased work leads to left ventricular hypertrophy. Hypertrophy, which occurs as a result of increased work of volume (that is, on the basis of tonogenic dilation), when the degree of thickening is proportional to the increase in the cavity of the heart, is called eccentric.
Thus, compensation is carried out mainly due to tonogenic dilatation and eccentric hypertrophy of the left ventricle. Reflex tachycardia also has a compensatory value, with this type of defect, since diastole is predominantly shortened, during which blood regurgitation occurs. A more complete emptying of the left ventricle is also facilitated by a decrease in the peripheral resistance of the vessels of the systemic circulation.
STENOSIS OF THE AURTIC STATE.
When narrowing the mouth of the aorta, the passage of blood from the left ventricle to the aorta is difficult. Overcoming resistance, the left ventricle increases systolic tension. There is hypertrophy, which develops without an increase in the cavity of the heart. Such hypertrophy is called concentric. With concentric hypertrophy, the heart consumes more oxygen than with eccentric hypertrophy.
Compensation for the defect is carried out due to concentric hypertrophy of the left ventricle, a reflex decrease in the tone of the peripheral vessels of the systemic circulation and reflex bradycardia.
In the compensation phase, the pulmonary circulation in these two types of heart disease does not suffer.
INSUFFICIENCY OF THE LEFT ATRIOVENTRICULAR
(MITRAL, DOUBLE) VALVE.
This is the most common heart defect. During left ventricular systole, part of the blood returns to the left atrium. As a result, the volume of blood in the left atrium increases and tonogenic dilation occurs. During diastole, it also fills with a large volume of blood. Thanks to the Frank-Starling mechanism, the total systolic volume is increased by the volume of regurgitation and effective blood flow is maintained.
Thus, compensation for this defect is carried out due to tonogenic dilatation of the left atrium and ventricle, eccentric hypertrophy of the left atrium and ventricle.
As with the previously analyzed defects, if, due to an increase in perversity or weakening of the myocardium, the compensation mechanisms turn out to be insufficient and the pressure in the left atrium increases significantly, the right ventricle will be connected to the compensation.
STENOSIS OF THE LEFT ATRIOVENTRICULAR HOLE.
With a decrease in the area of the mitral orifice, systolic pressure in the left atrium increases, which hypertrophies concentrically. However, even the hypertrophied atrial myocardium is not able to compensate for the growing obstruction to blood flow for a long time. It should be noted that during atrial systole, only about 20% of the blood is transported to the ventricle. The rest goes by gravity through the atrium from the pulmonary veins into the ventricle. The pressure in the left atrium begins to rise. Reflex tachycardia joins. In this case, atrial systoles account for about 40% of the blood volume. This creates additional opportunities for compensation. But when the pressure in the left atrium reaches 25-30 mm. rt. column, its complete decompensation occurs. And all the blood flows from the pulmonary veins into the left ventricle during its diastole through the myogenically dilated (dilated) atrium. An increase in blood pressure in the left atrium leads to an increase in pressure in the pulmonary veins, and then in the pulmonary arteries. From this moment, the compensation of stenosis is entirely carried out by the right ventricle, which hypertrophies concentrically.
With an increase in pressure in the left atrium and pulmonary veins, the Kitaev reflex is activated. The narrowing of the small arteries and arterioles of the pulmonary circulation unloads the pulmonary capillaries. And the threat of developing pulmonary edema is reduced. But, on the other hand, arterial spasm dramatically increases the load on the relatively weak right ventricle. It is obvious that the unloading of capillaries simultaneously reduces the pressure of blood in the area of stenosis, reducing the minute volume of the heart.
Parin's unloading reflex, which follows this, is also of relative importance.
Thus, as stenosis increases, capillary pressure in the lungs steadily increases. If, when the atrioventricular opening is narrowed by 3-4 times, the pressure rises only during physical exertion, then when the opening is narrowed by 5-10 times, the capillary pressure becomes critical - about 35 mm. mercury column. Above this level, pulmonary edema develops. With such pressure, the patient suffers from excruciating shortness of breath, and even a slight physical or emotional stress can destroy him.
Right heart valve defects develop similarly, but the pressure will increase in the veins of the systemic circulation.
Heart failure (HF) is a condition in which:
1. The heart cannot fully provide the proper minute volume of blood (MO), i.e. perfusion of organs and tissues, adequate to their metabolic needs at rest or during exercise.
2. Or a relatively normal level of cardiac output and tissue perfusion is achieved due to excessive tension of intracardiac and neuroendocrine compensatory mechanisms, primarily due to an increase in the filling pressure of the heart cavities and
activation of the SAS, renin-angiotensin and other body systems.
In most cases, we are talking about a combination of both signs of heart failure - an absolute or relative decrease in MO and a pronounced tension of compensatory mechanisms. HF occurs in 1–2% of the population, and its prevalence increases with age. In persons older than 75 years, HF occurs in 10% of cases. Almost all diseases of the cardiovascular system can be complicated by HF, which is the most common cause of hospitalization, disability and death of patients.
ETIOLOGY
Depending on the predominance of certain mechanisms of HF formation, the following causes of the development of this pathological syndrome are distinguished.
I. Damage to the heart muscle (myocardial insufficiency).
1. Primary:
myocarditis;
2. Secondary:
acute myocardial infarction (MI);
chronic ischemia of the heart muscle;
postinfarction and atherosclerotic cardiosclerosis;
hypo- or hyperthyroidism;
heart damage in systemic connective tissue diseases;
toxic-allergic lesions of the myocardium.
II. Hemodynamic overload of the ventricles of the heart.
1. Increasing resistance to ejection (increasing afterload):
systemic arterial hypertension (AH);
pulmonary arterial hypertension;
stenosis of the aortic mouth;
stenosis of the pulmonary artery.
2. Increased filling of the chambers of the heart (increased preload):
valvular insufficiency
congenital heart defects
III. Violation of the filling of the ventricles of the heart.
IV. Increasing the metabolic needs of tissues (HF with high MO).
1. Hypoxic conditions:
chronic cor pulmonale.
2. Increase metabolism:
hyperthyroidism.
3. Pregnancy.
The most common causes of heart failure are:
IHD, including acute myocardial infarction and postinfarction cardiosclerosis;
arterial hypertension, including in combination with ischemic heart disease;
valvular heart disease.
The variety of causes of heart failure explains the existence of various clinical and pathophysiological forms of this pathological syndrome, each of which is dominated by the predominant lesion of certain parts of the heart and the action of various mechanisms of compensation and decompensation. In most cases (about 70–75%), we are talking about a predominant violation of the systolic function of the heart, which is determined by the degree of shortening of the heart muscle and the magnitude of cardiac output (MO).
At the final stages of the development of systolic dysfunction, the most characteristic sequence of hemodynamic changes can be represented as follows: a decrease in SV, MO and EF, which is accompanied by an increase in the end-systolic volume (ESV) of the ventricle, as well as hypoperfusion of peripheral organs and tissues; an increase in end-diastolic pressure (end-diastolic pressure) in the ventricle, i.e. ventricular filling pressure; myogenic dilatation of the ventricle - an increase in the end-diastolic volume (end-diastolic volume) of the ventricle; stagnation of blood in the venous bed of a small or large circle of blood circulation. The last hemodynamic sign of HF is accompanied by the most “bright” and clearly defined clinical manifestations of HF (dyspnea, edema, hepatomegaly, etc.) and determines the clinical picture of its two forms. With left ventricular heart failure, stagnation of blood develops in the pulmonary circulation, and with right ventricular heart failure - in the venous bed of a large circle. The rapid development of systolic ventricular dysfunction leads to acute HF (left or right ventricular). The prolonged existence of hemodynamic volume or resistance overload (rheumatic heart disease) or a gradual progressive decrease in ventricular myocardial contractility (for example, during its remodeling after myocardial infarction or prolonged existence of chronic ischemia of the heart muscle) is accompanied by the formation of chronic heart failure (CHF).
In about 25–30% of cases, the development of HF is based on impaired diastolic ventricular function. Diastolic dysfunction develops in heart diseases accompanied by impaired relaxation and filling of the ventricles. Violation of the distensibility of the ventricular myocardium leads to the fact that in order to ensure sufficient diastolic filling of the ventricle with blood and maintain normal SV and MO, a significantly higher filling pressure is needed, corresponding to a higher end-diastolic ventricular pressure. In addition, a slowdown in ventricular relaxation leads to a redistribution of diastolic filling in favor of the atrial component, and a significant part of diastolic blood flow occurs not during the phase of rapid ventricular filling, as is normal, but during active atrial systole. These changes contribute to an increase in pressure and size of the atrium, increasing the risk of blood stasis in the venous bed of the pulmonary or systemic circulation. In other words, diastolic ventricular dysfunction may be accompanied by clinical signs of CHF with normal myocardial contractility and preserved cardiac output. In this case, the cavity of the ventricle usually remains unexpanded, since the ratio of the end diastolic pressure and the end diastolic volume of the ventricle is disturbed.
It should be noted that in many cases of CHF there is a combination of systolic and diastolic ventricular dysfunction, which must be taken into account when choosing the appropriate drug therapy. From the above definition of heart failure, it follows that this pathological syndrome can develop not only as a result of a decrease in the pumping (systolic) function of the heart or its diastolic dysfunction, but also with a significant increase in the metabolic needs of organs and tissues (hyperthyroidism, pregnancy, etc.) or with a decrease in the oxygen transport function of the blood (anemia). In these cases, MO may even be elevated (HF with “high MO”), which is usually associated with a compensatory increase in BCC. According to modern concepts, the formation of systolic or diastolic HF is closely associated with the activation of numerous cardiac and extracardiac (neurohormonal) compensatory mechanisms. With systolic ventricular dysfunction, such activation is initially adaptive in nature and is aimed primarily at maintaining the MO and systemic blood pressure at the proper level. In diastolic dysfunction, the end result of the activation of compensatory mechanisms is an increase in ventricular filling pressure, which ensures sufficient diastolic blood flow to the heart. However, in the future, almost all compensatory mechanisms are transformed into pathogenetic factors that contribute to an even greater disruption of the systolic and diastolic function of the heart and the formation of significant hemodynamic changes characteristic of HF.
Cardiac compensation mechanisms:
Among the most important cardiac adaptation mechanisms are myocardial hypertrophy and the Starling mechanism.
In the initial stages of the disease, myocardial hypertrophy helps to reduce intramyocardial tension by increasing wall thickness, allowing the ventricle to develop sufficient intraventricular pressure in systole.
Sooner or later, the compensatory response of the heart to hemodynamic overload or damage to the ventricular myocardium is insufficient and a decrease in cardiac output occurs. So, with hypertrophy of the heart muscle, the contractile myocardium “wears out” over time: the processes of protein synthesis and energy supply of cardiomyocytes are depleted, the ratio between the contractile elements and the capillary network is disturbed, the concentration of intracellular Ca 2+ increases, fibrosis of the heart muscle develops, etc. At the same time, there is a decrease in diastolic compliance of the heart chambers and diastolic dysfunction of the hypertrophied myocardium develops. In addition, pronounced disorders of myocardial metabolism are observed:
The ATP-ase activity of myosin, which provides the contractility of myofibrils due to ATP hydrolysis, decreases;
The conjugation of excitation with contraction is broken;
The formation of energy in the process of oxidative phosphorylation is disrupted and the reserves of ATP and creatine phosphate are depleted.
As a result, the contractility of the myocardium, the value of MO decreases, the end diastolic pressure of the ventricle increases and blood stagnation appears in the venous bed of the small or large circulation.
It is important to remember that the effectiveness of the Starling mechanism, which ensures the preservation of cardiac output due to moderate (“tonogenic”) dilatation of the ventricle, sharply decreases with an increase in end-diastolic pressure in the left ventricle above 18–20 mm Hg. Art. Excessive stretching of the walls of the ventricle (“myogenic” dilatation) is accompanied by only a slight increase or even decrease in the force of contraction, which contributes to a decrease in cardiac output.
In the diastolic form of heart failure, the implementation of the Starling mechanism is generally difficult due to the rigidity and inflexibility of the ventricular wall.
Extracardiac compensation mechanisms
According to modern concepts, the activation of several neuroendocrine systems, the most important of which are:
Sympathetic-adrenal system (SAS)
Renin-angiotensin-aldosterone system (RAAS);
Tissue renin-angiotensin systems (RAS);
Atrial natriuretic peptide;
Endothelial dysfunction, etc.
Hyperactivation of the sympathetic-adrenal system
Hyperactivation of the sympathetic-adrenal system and an increase in the concentration of catecholamines (A and Na) is one of the earliest compensatory factors in the event of systolic or diastolic dysfunction of the heart. Especially important is the activation of the SAS in cases of acute HF. The effects of such activation are realized primarily through a- and b-adrenergic receptors of cell membranes of various organs and tissues. The main consequences of SAS activation are:
Increase in heart rate (stimulation of b 1 -adrenergic receptors) and, accordingly, MO (since MO \u003d UO x heart rate);
Increased myocardial contractility (stimulation of b 1 - and a 1 -receptors);
Systemic vasoconstriction and increased peripheral vascular resistance and blood pressure (stimulation of a 1 receptors);
Increased venous tone (stimulation of a 1 -receptors), which is accompanied by an increase in venous return of blood to the heart and an increase in preload;
Stimulation of the development of compensatory myocardial hypertrophy;
Activation of the RAAS (renal-adrenal) as a result of stimulation of b 1 -adrenergic receptors of juxtaglomerular cells and tissue RAS due to endothelial dysfunction.
Thus, at the initial stages of the development of the disease, an increase in SAS activity contributes to an increase in myocardial contractility, blood flow to the heart, preload and ventricular filling pressure, which ultimately leads to the maintenance of sufficient cardiac output for a certain time. However, long-term hyperactivation of the SAS in patients with chronic HF can have numerous negative consequences, contributing to:
1. A significant increase in preload and afterload (due to excessive vasoconstriction, activation of the RAAS and retention of sodium and water in the body).
2. Increased myocardial oxygen demand (as a result of the positive inotropic effect of SAS activation).
3. A decrease in the density of b-adrenergic receptors on cardiomyocytes, which eventually leads to a weakening of the inotropic effect of catecholamines (a high concentration of catecholamines in the blood is no longer accompanied by an adequate increase in myocardial contractility).
4. Direct cardiotoxic effect of catecholamines (non-coronary necrosis, dystrophic changes in the myocardium).
5. The development of fatal ventricular arrhythmias (ventricular tachycardia and ventricular fibrillation), etc.
Hyperactivation of the renin-angiotensin-aldosterone system
Hyperactivation of the RAAS plays a special role in the formation of heart failure. In this case, not only the renal-adrenal RAAS with circulating neurohormones (renin, angiotensin-II, angiotensin-III and aldosterone) circulating in the blood is important, but also local tissue (including myocardial) renin-angiotensin systems.
Activation of the renal renin-angiotensin system, which occurs with any slight decrease in perfusion pressure in the kidneys, is accompanied by the release of renin by JGA cells of the kidneys, which cleaves angiotensinogen with the formation of a peptide - angiotensin I (AI). The latter, under the action of angiotensin-converting enzyme (ACE), is transformed into angiotensin II, which is the main and most powerful RAAS effector. Characteristically, the key enzyme of this reaction - ACE - is localized on the membranes of endothelial cells of the vessels of the lungs, proximal tubules of the kidneys, in the myocardium, plasma, where the formation of AII occurs. Its action is mediated by specific angiotensin receptors (AT 1 and AT 2), which are located in the kidneys, heart, arteries, adrenal glands, etc. It is important that, upon activation of tissue RAS, there are other ways (besides ACE) for the conversion of AI to AI: under the action of chymase, chymase-like enzyme (CAGE), cathepsin G, tissue plasminogen activator (TPA), etc.
Finally, the effect of AII on the AT 2 receptors of the glomerular zone of the adrenal cortex leads to the formation of aldosterone, the main effect of which is the retention of sodium and water in the body, which contributes to an increase in BCC.
In general, activation of the RAAS is accompanied by the following effects:
Severe vasoconstriction, increased blood pressure;
Delay in the body of sodium and water and an increase in BCC;
Increased myocardial contractility (positive inotropic effect);
Initiation of the development of hypertrophy and remodeling of the heart;
Activation of the formation of connective tissue (collagen) in the myocardium;
Increased sensitivity of the myocardium to the toxic effects of catecholamines.
Activation of the RAAS in acute HF and at the initial stages of the development of chronic HF has a compensatory value and is aimed at maintaining normal levels of blood pressure, bcc, perfusion pressure in the kidneys, an increase in pre- and afterload, and an increase in myocardial contractility. However, as a result of prolonged hyperactivation of the RAAS, a number of negative effects develop:
1. an increase in peripheral vascular resistance and a decrease in perfusion of organs and tissues;
2. excessive increase in afterload on the heart;
3. significant fluid retention in the body, which contributes to the formation of edematous syndrome and increased preload;
4. initiation of heart and vascular remodeling processes, including myocardial hypertrophy and smooth muscle cell hyperplasia;
5. stimulation of collagen synthesis and the development of fibrosis of the heart muscle;
6. development of necrosis of cardiomyocytes and progressive myocardial damage with the formation of myogenic dilatation of the ventricles;
7. increased sensitivity of the heart muscle to catecholamines, which is accompanied by an increased risk of fatal ventricular arrhythmias in patients with heart failure.
Arginine-vasopressin system (antidiuretic hormone)
Antidiuretic hormone (ADH), secreted by the posterior pituitary gland, is involved in the regulation of water permeability of the distal tubules of the kidneys and collecting ducts. For example, when there is a lack of water in the body and tissue dehydration there is a decrease in the volume of circulating blood (BCC) and an increase in the osmotic pressure of the blood (ODC). As a result of irritation of the osmo- and volumic receptors, the secretion of ADH by the posterior pituitary gland increases. Under the influence of ADH, the water permeability of the distal tubules and collecting ducts increases, and, accordingly, facultative reabsorption of water in these sections increases. As a result, little urine is excreted with a high content of osmotically active substances and a high specific gravity of the urine.
Conversely, with an excess of water in the body and tissue hyperhydration as a result of an increase in BCC and a decrease in the osmotic pressure of the blood, irritation of the osmo- and volumic receptors occurs, and the secretion of ADH decreases sharply or even stops. As a result, water reabsorption in the distal tubules and collecting ducts is reduced, while Na + continues to be reabsorbed in these sections. Therefore, a lot of urine is excreted with a low concentration of osmotically active substances and a low specific gravity.
Violation of the functioning of this mechanism in heart failure can contribute to water retention in the body and the formation of edematous syndrome. The lower the cardiac output, the greater the stimulation of osmo- and volumic receptors, which leads to an increase in the secretion of ADH and, accordingly, fluid retention.
Atrial natriuretic peptide
Atrial natriuretic peptide (ANUP) is a kind of antagonist of the body's vasoconstrictor systems (SAS, RAAS, ADH, and others). It is produced by atrial myocytes and released into the bloodstream when they are stretched. Atrial natriuretic peptide causes vasodilatory, natriuretic and diuretic effects, inhibits the secretion of renin and aldosterone.
The secretion of PNUP is one of the earliest compensatory mechanisms that prevent excessive vasoconstriction, Na + and water retention in the body, as well as an increase in pre- and afterload.
Atrial natriuretic peptide activity increases rapidly as HF progresses. However, despite the high level of circulating atrial natriuretic peptide, the degree of its positive effects in chronic HF is markedly reduced, which is probably due to a decrease in receptor sensitivity and an increase in peptide cleavage. Therefore, the maximum level of circulating atrial natriuretic peptide is associated with an unfavorable course of chronic HF.
Endothelial function disorders
In recent years, endothelial function disorders have been given particular importance in the formation and progression of CHF. endothelial dysfunction that occurs under the influence of various damaging factors (hypoxia, excessive concentration of catecholamines, angiotensin II, serotonin, high blood pressure, accelerated blood flow, etc.), is characterized by a predominance of vasoconstrictor endothelium-dependent influences and is naturally accompanied by an increase in the tone of the vascular wall, acceleration of platelet aggregation and processes parietal thrombosis.
Recall that the most important endothelium-dependent vasoconstrictor substances that increase vascular tone, platelet aggregation and blood clotting include endothelin-1 (ET 1), thromboxane A 2 , prostaglandin PGH 2 , angiotensin II (AII), etc.
They have a significant impact not only on vascular tone, leading to severe and persistent vasoconstriction, but also on myocardial contractility, preload and afterload, platelet aggregation, etc. (see chapter 1 for details). The most important property of endothelin-1 is its ability to "start" intracellular mechanisms leading to increased protein synthesis and the development of cardiac muscle hypertrophy. The latter, as you know, is the most important factor that somehow complicates the course of heart failure. In addition, endothelin-1 promotes the formation of collagen in the heart muscle and the development of cardiofibrosis. Vasoconstrictor substances play a significant role in the process of parietal thrombus formation (Fig. 2.6).
It has been shown that in severe and prognostically unfavorable CHF, the level endothelin-1 increased by 2–3 times. Its plasma concentration correlates with the severity of intracardiac hemodynamic disorders, pulmonary artery pressure, and mortality in patients with CHF.
Thus, the described effects of hyperactivation of neurohormonal systems, together with typical hemodynamic disturbances, underlie the characteristic clinical manifestations of HF. Moreover, symptoms acute heart failure It is mainly determined by sudden hemodynamic disorders (a pronounced decrease in cardiac output and an increase in filling pressure), microcirculatory disorders, which are aggravated by the activation of the CAS, RAAS (mainly renal).
In development chronic heart failure Currently, more importance is attached to prolonged hyperactivation of neurohormones and endothelial dysfunction, accompanied by severe sodium and water retention, systemic vasoconstriction, tachycardia, development of hypertrophy, cardiofibrosis, and toxic damage to the myocardium.
CLINICAL FORMS OF HF
Depending on the rate of development of HF symptoms, two clinical forms of HF are distinguished.
Acute and chronic HF. The clinical manifestations of acute HF develop within minutes or hours, while the symptoms of chronic HF develop from several weeks to several years from the onset of the disease. The characteristic clinical features of acute and chronic HF make it quite easy to distinguish between these two forms of cardiac decompensation in almost all cases. However, it should be borne in mind that acute, for example, left ventricular failure (cardiac asthma, pulmonary edema) can occur against the background of long-term chronic heart failure.
CHRONIC HF
In the most common diseases associated with primary damage or chronic overload of the left ventricle (CHD, postinfarction cardiosclerosis, hypertension, etc.), clinical signs of chronic left ventricular failure, pulmonary arterial hypertension and right ventricular failure consistently develop. At certain stages of cardiac decompensation, signs of hypoperfusion of peripheral organs and tissues begin to appear, associated with both hemodynamic disorders and hyperactivation of neurohormonal systems. This is the basis of the clinical picture of biventricular (total) HF, which is the most common in clinical practice. With chronic overload of the right ventricle or primary damage to this part of the heart, isolated right ventricular chronic HF develops (for example, chronic cor pulmonale).
The following is a description of the clinical picture of chronic systolic biventricular (total) HF.
Complaints
shortness of breath ( dyspnea) is one of the earliest symptoms of chronic heart failure. At first, shortness of breath occurs only with physical exertion and disappears after its cessation. As the disease progresses, shortness of breath begins to appear with less and less exertion, and then at rest.
Shortness of breath appears as a result of an increase in end-diastolic pressure and LV filling pressure and indicates the occurrence or aggravation of blood stagnation in the venous bed of the pulmonary circulation. The immediate causes of dyspnea in patients with chronic heart failure are:
Significant violations of ventilation-perfusion ratios in the lungs (slowing of blood flow through normally ventilated or even hyperventilated alveoli);
Swelling of the interstitium and increased rigidity of the lungs, which leads to a decrease in their extensibility;
Violation of the diffusion of gases through the thickened alveolar-capillary membrane.
All three causes lead to a decrease in gas exchange in the lungs and irritation of the respiratory center.
Orthopnea ( orthopnoe) - this is shortness of breath that occurs when the patient is lying down with a low headboard and disappears in an upright position.
Orthopnea occurs as a result of an increase in venous blood flow to the heart, which occurs in the horizontal position of the patient, and an even greater overflow of blood in the pulmonary circulation. The appearance of this type of shortness of breath, as a rule, indicates significant hemodynamic disturbances in the pulmonary circulation and high filling pressure (or “wedge” pressure - see below).
Unproductive dry cough in patients with chronic heart failure, it often accompanies shortness of breath, appearing either in the horizontal position of the patient, or after physical exertion. Cough occurs due to prolonged stagnation of blood in the lungs, swelling of the bronchial mucosa and irritation of the corresponding cough receptors (“cardiac bronchitis”). Unlike cough in bronchopulmonary diseases in patients with chronic heart failure, cough is non-productive and resolves after effective treatment of heart failure.
cardiac asthma(“paroxysmal nocturnal dyspnea”) is an attack of intense shortness of breath, quickly turning into suffocation. After emergency treatment, the attack usually stops, although in severe cases, suffocation continues to progress and pulmonary edema develops.
Cardiac asthma and pulmonary edema are among the manifestations acute heart failure and are caused by a rapid and significant decrease in LV contractility, an increase in venous blood flow to the heart, and stagnation in the pulmonary circulation
Severe muscle weakness, rapid fatigue and heaviness in the lower extremities, appearing even against the background of slight physical exertion, are also early manifestations of chronic heart failure. They are caused by impaired perfusion of skeletal muscles, not only due to a decrease in cardiac output, but also as a result of spastic contraction of arterioles caused by high activity of the CAS, RAAS, endothelin and a decrease in the vasodilatory reserve of blood vessels.
Palpitation. The sensation of palpitations is most often associated with sinus tachycardia, which is characteristic of patients with HF, resulting from the activation of the SAS or with an increase in pulse pressure. Complaints about the heartbeat and interruptions in the work of the heart may indicate the presence of a variety of cardiac arrhythmias in patients, for example, the appearance of atrial fibrillation or frequent extrasystoles.
Edema- one of the most characteristic complaints of patients with chronic heart failure.
nocturia- increased diuresis at night It should be borne in mind that in the terminal stage of chronic heart failure, when cardiac output and renal blood flow are sharply reduced even at rest, there is a significant decrease in daily diuresis - oliguria.
To manifestations chronic right ventricular (or biventricular) HF Patients also complain about pain or a feeling of heaviness in the right hypochondrium, associated with liver enlargement and stretching of the Glisson capsule, as well as on dyspeptic disorders(decreased appetite, nausea, vomiting, flatulence, etc.).
Swelling of the neck veins is an important clinical sign of increased central venous pressure (CVP), i.e. pressure in the right atrium (RA), and stagnation of blood in the venous bed of the systemic circulation (Fig. 2.13, see color insert).
Respiratory examination
Examination of the chest. Count respiratory rate (RR) allows you to tentatively assess the degree of ventilation disorders caused by chronic stagnation of blood in the pulmonary circulation. In many cases, shortness of breath in patients with CHF is tachypnea, without a clear predominance of objective signs of difficulty in inhaling or exhaling. In severe cases, associated with a significant overflow of the lungs with blood, which leads to an increase in the rigidity of the lung tissue, shortness of breath may take on the character inspiratory dyspnea .
In the case of isolated right ventricular failure that has developed against the background of chronic obstructive pulmonary diseases (for example, cor pulmonale), shortness of breath has expiratory character and is accompanied by pulmonary emphysema and other signs of obstructive syndrome (see below for more details).
In the terminal stage of CHF, aperiodic Cheyne–Stokes breathing when short periods of rapid breathing alternate with periods of apnea. The reason for the appearance of this type of breathing is a sharp decrease in the sensitivity of the respiratory center to CO 2 (carbon dioxide), which is associated with severe respiratory failure, metabolic and respiratory acidosis, and impaired cerebral perfusion in patients with CHF.
With a sharp increase in the sensitivity threshold of the respiratory center in patients with CHF, respiratory movements are “initiated” by the respiratory center only at an unusually high concentration of CO 2 in the blood, which is reached only at the end of the 10-15-second period of apnea. Several rapid breaths cause the CO 2 concentration to fall below the threshold, causing the apnea period to repeat.
arterial pulse. Changes in the arterial pulse in patients with CHF depend on the stage of cardiac decompensation, the severity of hemodynamic disorders, and the presence of cardiac arrhythmias and conduction disturbances. In severe cases, the arterial pulse is frequent ( pulsus frequency), often arrhythmic ( pulsus irregularis), weak filling and tension (pulsus parvus and tardus). A decrease in the arterial pulse and its filling, as a rule, indicate a significant decrease in SV and the rate of blood ejection from the LV.
In the presence of atrial fibrillation or frequent extrasystole in patients with CHF, it is important to determine pulse deficit (pulsus deficiens). It is the difference between the number of heartbeats and the arterial pulse rate. Pulse deficiency is more often detected in the tachysystolic form of atrial fibrillation (see Chapter 3) as a result of the fact that part of the heart contractions occurs after a very short diastolic pause, during which there is not sufficient filling of the ventricles with blood. These contractions of the heart occur as if “in vain” and are not accompanied by the expulsion of blood into the arterial bed of the systemic circulation. Therefore, the number of pulse waves is much less than the number of heartbeats. Naturally, with a decrease in cardiac output, the pulse deficit increases, indicating a significant decrease in the functionality of the heart.
Arterial pressure. In those cases when a patient with CHF did not have arterial hypertension (AH) before the onset of symptoms of cardiac decompensation, the level of blood pressure often decreases as HF progresses. In severe cases, systolic blood pressure (SBP) reaches 90–100 mm Hg. Art., and pulse blood pressure - about 20 mm Hg. Art., which is associated with a sharp decrease in cardiac output.
Compensation for circulatory disorders. In the event of any circulatory disorders, its functional compensation usually quickly occurs. Compensation is carried out primarily by the same regulatory mechanisms as in the norm. In the early stages of K.'s disturbances, their compensation occurs without any significant shifts in the structure of the cardiovascular system. Structural changes in certain parts of the circulatory system (for example, myocardial hypertrophy, development of arterial or venous collateral pathways) usually occur later and are aimed at improving the functioning of compensation mechanisms.
Compensation is possible due to increased myocardial contractions, expansion of the cavities of the heart, as well as hypertrophy of the heart muscle. So, with difficulty in expelling blood from the ventricle, for example, with stenosis At the mouth of the aorta or pulmonary trunk, the reserve power of the contractile apparatus of the myocardium is realized, which contributes to an increase in the force of contraction. With valvular insufficiency, in each subsequent phase of the cardiac cycle, part of the blood returns in the opposite direction. At the same time, dilatation of the cavities of the heart develops, which is compensatory in nature. However, excessive dilatation creates unfavorable conditions for the work of the heart.
An increase in total blood pressure caused by an increase in total peripheral resistance is compensated, in particular, by increasing the work of the heart and creating such a pressure difference between the left ventricle and the aorta that is capable of ejecting the entire systolic blood volume into the aorta.
In a number of organs, especially in the brain, with an increase in the level of general blood pressure, compensatory mechanisms begin to function, thanks to which blood pressure in the vessels of the brain is maintained at a normal level.
With an increase in resistance in individual arteries (due to angiospasm, thrombosis, embolism, etc.), a violation of the blood supply to the corresponding organs or their parts can be compensated for by collateral blood flow. In the brain, collateral pathways are represented as arterial anastomoses in the circle of Willis and in the system of pial arteries on the surface of the cerebral hemispheres. Arterial collaterals are well developed in the heart muscle. In addition to arterial anastomoses, an important role for collateral blood flow is played by their functional dilatation, which significantly reduces blood flow resistance and promotes blood flow to the ischemic area. If in the expanded collateral arteries the blood flow is increased for a long time, then their gradual restructuring occurs, the caliber of the arteries increases, so that in the future they can fully provide the blood supply to the organ to the same extent as the main arterial trunks.
