HEART FAILURE

From Big Medical Encyclopedia

HEART FAILURE — the morbid condition caused by inability of heart to provide adequate blood supply of bodies and fabrics.

Heart failure is a component of insufficiency blood circulations (see). The term «circulatory unefficiency» accepted at the XII congress of therapists (1935) includes concepts of heart and vascular failure. In a wedge, practice quite often concepts of a circulatory unefficiency and S. of N are differentiated not quite clearly and one term is substituted for another. Meanwhile in the classification developed by G. F. Lang, N. D. Strazhesko and V. of X. Vasilenko (1935), is accurately allocated as an acute heart failure — cardiac asthma (see), fluid lungs (see), acute right ventricular insufficiency, and chronic S. of N; chronic S.'s types of N on preferential localization of developments of stagnation (left ventricular, right ventricular) and its stages are allocated. N divide chronic S. into three stages. The I stage (initial) is shown by short wind, tachycardia, fatigue etc. only at an exercise stress; at rest hemodynamics (see) and function of bodies are not broken. The II stage is characterized by the signs of stagnation in a small and big circle of blood circulation and dysfunction of bodies remaining a long time. In it allocate IIA a stage, at a cut these disturbances are expressed unsharply, and PB a stage when disturbances of a hemodynamics and water and electrolytic exchange are expressed sharply and keep at rest. The III stage (final, or dystrophic) is characterized by heavy disturbances of a hemodynamics, metabolism and functions of all bodies with development in them irreversible morfol. changes.

The American association of cardiologists developed S.'s classification N, in a cut 4 classes (stage) are allocated. The I class is characterized by the minimum extent of dysfunction of a myocardium, its hypertrophy, norm the lny minute volume of heart, lack of circulator frustration. Dysfunctions of a myocardium at preservation of normal minute volume at the expense of reserve mechanisms are referred to the II class that leads to increase in end diastolic, pulmonary and system venous pressure; at physical activity increase in these parameters, emergence of fatigue, an asthma, insufficient increase in minute volume is observed. III and IV classes are characterized by further increase of hemodynamic disturbances and a wedge, manifestations of a decompensation. Most of researchers distinguish also latent (latent) heart failure, at a cut inadequacy of function of heart comes to light only against the background of extraordinary loadings or only tool methods.

The etiology and a pathogeny

the Fundamental «starting» unit of S. of N is decrease in propulsive ability of heart, to-rogo its overload pressure can be the cause at stenoses of mitral, three-leaved valves, mouths of an aorta or a pulmonary artery (see. acquired ), an overload volume at insufficiency of valves of heart and existence of endocardiac shunts, the combined overload pressure and volume and actually insufficiency of a myocardium as a result of its defeats, as primary at myocardites (see), cardiomyopathies (see), and secondary at atherosclerotic and postinfarction cardiosclerosis (see), different types myocardial dystrophies (see).

Normal regulation of reduction and relaxation of fibers of a myocardium (see. Heart, physiology ) occurs with direct participation of ions of Ca 2+ also it is provided with energy of makroergichesky phosphorus compound — ATP (see. Adenosine triphosphoric acid ), developed in mitochondrions and coming to a sarcoplasmic reticulum in the form of creatine phosphate. At rest ion concentration of Sa 2+ in cells of a myocardium it is approximately equal to 10-7 mol that excludes a possibility of interaction between sokratitelny proteins actin and a myosin (see. Muscular tissue ). At excitement of a cell there is an ionic yield To + from cells and receipt of ions of Na + in a cell on a concentration gradient that is followed by an ionic yield of Sa 2+ from a sarcoplasmic reticulum in a sarcoplasm. Concentration of Sa 2+ raises to 10 - 5 — 10 - 6 the mol, i.e. to level, at Krom occurs interaction of actin and a myosin and reduction of a myocardium. After reduction happened, ions of Ca 2+ by means of Ca 2+ - activated-Mg-dependent ATP-ase come to a sarcoplasmic reticulum against a concentration gradient again; then they can leave from a cell or at the next depolarization to leave in a sarcoplasm again and to catalyze reaction of reduction. Removal from cells of ions of Na + and the return receipt in a cell of ions of K+ is implemented so-called sodium potassium pump due to energy of ATP. Transport through a cellular membrane of ions of Ca 2+ it is connected with transport of ions of Na + and it is carried out by means of Na — Sa-obmennogo of the mechanism, power to-rogo depends on the Na function — the K-pump (see. Membranes biological , Transport of ions ).

At S. of N the power of Na — the K-pump decreases, ion concentration of Na + in cells of a myocardium increases also through accumulation in cells of ions of Ca 2+ will mobilize contractility; along with it deceleration of power of Na — the Sa-obmeniy mechanism and increase in maintenance of ions of Ca 2+ in a sarcoplasm of myocytes lead to disturbance of full diastolic relaxation, dissociation of reduction and relaxation of fibers of a myocardium. Besides, the power of the mitochondrions which are carrying out at the same time power supply of processes of removal of a sarcoplasm of ions of Ca 2+ and resynthesis of ATP, providing as a result reduction, there is a deficit of high-energy phosphorus compounds (see. Vysokoergichesky connections ). Processes are at the same time activated glycolysis (see), the maintenance of a lactate and hydrogen ions increases (N +), to-rye competitively force out ions of Ca 2+ from a troponin of myofibrils also promote increase in their capture by a sarcoplasmic reticulum. It leads to the progressing decrease in contractility of fibers of a myocardium and, as a result, to decrease in pumping function of heart.

Adequate cordial emission at S. of N is supported till a certain moment thanks to operation of the law of Starlinga (see. Starlinga law ), but at achievement of critical degree of compensatory dilatation of heart this earlier compensatory mechanism becomes pathological and cordial emission decreases, despite much supertension of filling of ventricles of heart. In response to decrease in cordial emission there is an activation sympathoadrenal system (see), directed to maintenance of the ABP adequate level in a big circle of blood circulation at reduced emission. Catecholamines (more noradrenaline) stimulate narrowing of peripheral arterioles of all bodies, except for vessels of heart and brain. Narrowing of arterioles of kidneys against the background of the lowered cordial emission leads to reduction of a renal blood-groove and inclusion of a renal link in the mechanism C. of N. At the same time, first, there is an activation of system a renin — angiotensin — Aldosteronum. Increase in formation of angiotensin II (see. Angiotenzin ), being the powerful vasopressor agent, stimulates a spasm of peripheral arterioles and venules, and also the increased development with bark of adrenal glands even more Aldosteronum (see). Secondly, there is a switching of a renal blood-groove to the yukstamedullyarny nephrons having the increased ability to detain sodium that in combination with impact of the increased quantity of Aldosteronum on distal renal tubules leads to the sharp growth of a reabsorption of Na+.

The delay in an organism of ions of Na + increases osmolarity of plasma and due to activation of osmoreceptors of vessels strengthens development by a back share of a hypophysis of vasopressin (see). Vasopressin along with noradrenaline (see) and angiotensin II strengthens narrowing of peripheral arterioles and venules and, besides, detains in an organism osmotically free water, edges, being added to water, reabsorbiruyushcheysya on a concentration gradient after Na+, leads to significant increase in volume to the circulating blood and a delay of liquid in bodies and body tissues. The arising hypostases are the mechanical factor which is also stimulating narrowing of peripheral venules. In combination with the increased volume of the circulating blood it leads to disproportionate increase of venous return of blood to heart, an overload of a small circle of blood circulation, further increase of pressure of filling of ventricles of heart, their excessive dilatation and the progressing decrease in cordial emission.

The important place in S.'s pathophysiology of N is taken by damage of a liver. The mechanism of development of a congestive liver consists of two highlights: reduction of a hepatic arterial blood-groove as a result of decrease in cordial emission and narrowing of hepatic arterioles, and also retrograde venous stagnation owing to sharp increase of pressure in the right auricle and the lower vena cava. There is an increase of pressure in the central veins of hepatic segments and sinusoids that can lead to hemorrhages in hepatic segments, to a centrolobular necrosis and development of so-called cardial cirrhosis (see). Disturbance of process of neutralization of slags is followed by the phenomena of intoxication; the insufficient inactivation of angiotensin II and especially Aldosteronum promotes development of secondary hyper aldosteronism (see), stimulating a delay of liquid in an organism; decrease and disturbance of protein synthesis, to-rogo is caused dominance of globulins over albumine, leads to formation of hypooncotic hypostasis (see). Gradual development of portal hypertensia (see) promotes formation of persistent hypostases of the lower extremities and ascites (see).

A long overload of vessels of a small circle of blood circulation, substantial increase of pressure in pulmonary venules and capillaries, and at a row patol. states and in pulmonary arterioles lead to a gradual thickening of alveolar capillary membranes, fibrosis of intersticial fabric, time to drink of hypostasis of iyeribronkhialny fabric (sometimes and a mucous membrane of bronchial tubes), and further to dysfunction of breath at patients with S. N (see. Respiratory insufficiency ). The first compensatory mechanism is the hyperventilation (see. Lung ventilation), however along with it irregularity of lung ventilation, decrease in maximal ventilation of lungs and an oxygen utilization quotient is noted. With S.'s progressing the N worsens alveolar and capillary diffusion and there is a further decrease in saturation of blood oxygen aggravating a hypoxia of bodies and body tissues (see the Hypoxia). These disturbances are supported as a result of deterioration in bronchial passability and elasticity of lungs.

A part in S.'s pathogeny of N is played by also secondary changes of an electrolytic profile and acid-base equilibrium (see). In distal tubules of kidneys ions of Na + are competitors in relation to ions of K+ and and Н^. At S. of N the raised reabsorption of ions of Na + is followed by the increased removal from an organism of ions of K+ and H+ that leads, on the one hand, to decrease in the general exchange potassium of an organism and the maintenance of ions of K+ in cells, and with another — to development of a metabolic alkalosis (see), expressiveness to-rogo, as a rule, increases in process of S.'s progressing N Besides, at a number of patients the hypomagnesiemia and a hypocalcemia since removal of ions of Mg2 + and Ca can be noted 2+ from an organism increases at a secondary hyper aldosteronism. The hypopotassemia (see), and especially decrease in content of potassium in fabrics, increases electric instability of a myocardium at patients with S. of N and can promote development of various disturbances of a heart rhythm (see. Arrhythmias of heart ). Changes of acid-base equilibrium at S. of N are rather variable. Along with a metabolic alkalosis at most of patients the noncompensated respiratory alkalosis is noted owing to a hyperventilation. However at a part of patients the hypoxia of bodies and fabrics is followed by gradual accumulation in an organism of nedookislenny decomposition products and the phenomena of a metabolic acidosis (see), and at patients with frequent attacks of a left ventricular failure the respiratory acidosis can develop. The N helps to choose definition of acid-base equilibrium at S. correctly to lay down. tactics.

Pathological anatomy

At left ventricular S. the N observe developments of stagnation in the left auricle and a small circle of blood circulation therefore pressure in capillaries of lungs increases, there is transudation of a blood plasma in alveoluses and the fluid lungs develops. Right ventricular S. of N is characterized by development of developments of stagnation in system top and bottom venas cava. The combined forms C. of N meet — with signs levozhet ud-point and right ventricular insufficiency.

At acute S. N on opening, along with signs of damage of heart (ischemia, a myocardial infarction), find a large amount of blood in cardial cavities, large arteries and veins, including intraorganic, a venous plethora of internals without signs of selective deposition of blood in separate vascular systems, lack of signs of a hypovolemia. At the same time the uniform venous plethora of internals, signs of increase in capillary permeability with plasmatic treatment and hypostasis, staza in capillaries and multiple diapedetic hemorrhages (see), dystrophic and necrotic changes in parenchymatous bodies histologically come to light. In covers and tissue of a brain, a liver, a myocardium the picture of perivascular hypostasis is expressed, in a brain and lungs perivascular hemorrhages, in an epithelium of renal tubules — dystrophic and necrotic changes, and in a liver — centrolobular hemorrhages and necroses are found. In a myocardium zones of dystrophic changes and sites of a necrosis against the background of microcircus-lyatornykh of disturbances come to light (cm. Micro circulation). However they not always are morfol. acute S.'s manifestation N, and demonstrate only existence of alterativny shifts in cardiomyocytes. At gistokhy. a research in these zones of a myocardium decrease of the activity of enzymes of oxidizing phosphorylation (see), balance upset between oxidation-reduction processes in cells and glycolysis, increase in quantity of products of an intermediate metabolism is noted.

The N is quite often difficult to distinguish changes in heart at acute S. from the changes caused by the direct mechanism of a cardiac standstill (fibrillation of ventricles, an asystolia). So, at fibrillation of ventricles of heart (see) kontrakturny changes of myofibrils of a myocardium are found, in the polarized light sites of fragmentation of muscle fibers clearly are visible.

Electronic and microscopic studying of heart at experimental acute S. of N allowed to reveal a complex of changes in cardiomyocytes and to differentiate nekoronarogenny (calcic), koronarogenny and hypoxemic damages of a myocardium.

At nekoronarogenny damages of a myocardium three types of calcic cellular dystrophy are noted. Primary litiche-sky the type is characterized by early lipidic infiltration, a focal lysis of myofilaments, swelling of mitochondrions and development of waves of excessive reductions grupy sarcomeres. Early configuration changes in a sarcoplasmic reticulum, emergence in mitochondrions of electronic and dense rainfall, reduction of one groups of sarcomeres and pererastyazhe-ny others demonstrate development primary rigornogo like calcic cellular dystrophy. In some cases at acute S. of N against the background of intact sarcomeres and kernels there comes the bystry vacuolation of mitochondrions and a sarcoplasmic reticulum testimonial of development of vacuolar calcic cellular dystrophy.

N subdivide Koronarogenny damages of a myocardium at acute S. on reversible and irreversible. Reversible koronarogenny damages are characterized by an early relaxation of sarcomeres, decrease in maintenance of a glycogen, easy swelling of mitochondrions and a margination of nuclear chromatin (primary and ischemic type of cellular dystrophy). At the same time при^не-обратимых koronarogenny damages of a myocardium (primary and ischemic type of cellular death) swelling of mitochondrions progresses, in to-rykh there are lipidic inclusions, and the sarcoplasmic reticulum remains intact. Reperfusion it is irreversible an ischemic myocardium leads to a secondary calcic overload (secondary and calcium type of cellular death), at a cut sharp intracellular hypostasis, a peresokra-shcheniye and a break-up of groups of sarcomeres, vacuolation of a sarcoplasmic reticulum and emergence in a matrix of mitochondrions of electronic and dense rainfall of calcium phosphate is noted.

Hypoxemic defeats of cardiomyocytes only in details differ from the changes found at calcic type of cellular dystrophy. So, at hypoxemic option of rigorny type of calcic cellular dystrophy vesiculation of a sarcoplasmic reticulum, a margination of nuclear chromatin, activation of lysosomes, excessive reduction and a relaksirovaniye of groups of sarcomeres, disappearance of cytogranules is noted. Irreversible changes at this type of dystrophy are characterized by education in a myocardium of rigorny complexes with sites of ruptures of sarcomeres, emergence of the bulked-up and condensed mitochondrions, and also vacuolated structures of a sarcoplasmic reticulum.

At hypoxemic option of primary and lytic type of calcic cellular dystrophy there is a focal lysis of myofibrils, vesiculation of a sarcoplasmic reticulum, condensation of electronic and dense material in mitochondrions, and bruises of sarcomeres are absent. Transition of cardiomyocytes to an irreversible state at this type of dystrophy is characterized by swelling of mitochondrions and the progressing lysis of myofibrils. Thus, from the point of view of changes of ultrastructure of a myocardium acute S. of N represents the alterativny reaction of the majority of cardiomyocytes arising at early stages patol. process and caused by a hyperpermeability of sarcolemmas.

Chronic S. of N in a stage of a decompensation of heart is characterized hron. venous stagnation in internals and fabrics. Dominance of insufficiency of a right ventricle leads to stagnation in veins of a big circle of blood circulation. Capacity blood depots (see) much increases. Resulting hron. venous stagnation the fabric hypoxia leads to development of plasmorrhagias (see), hypostasis and hemorrhages, dystrophy and a necrosis, atrophic and sclerous changes in bodies. Growth of connecting fabric in bodies in conditions hron. hypoxias it is caused by strengthening of synthesis by fibroblasts of tropocollagen. In the subsequent connecting fabric forces out elements of a parenchyma, causes congestive consolidation of bodies and fabrics — induration (see).

At chronic S. the N notes cyanosis of skin, expansion and overflow by blood of veins of skin and hypodermic cellulose, hypostasis of a derma and hypodermic cellulose, growth in skin of connecting fabric. The liver is increased, dense, with the rounded edges, gray-yellow color with dark red mottling (a muscat liver); at gistol. a research the plethora of the central departments of hepatic segments with destruction of hepatocytes and the phenomena of their dystrophy (quite often fatty) on the periphery is noted. In lungs against the background of a congestive plethora numerous hemorrhages decide on development hemosiderosis (see) and growth of connecting fabric — brown consolidation of lungs (see). Kidneys at hron. venous stagnation are increased in sizes, dense, cyanochroic (a tsianotichesky induration of kidneys). The sharp plethora of veins of marrow and an intermediary zone, the phenomenon are noted lymphostasis (see); against the background of venous stagnation there are dystrophy of an epithelium of tubules of the main departments of nephron and moderate sclerous changes in a parenchyma. The Tsianotichesky induration of a spleen is shown by increase in its sizes and weight (to 300 g); the spleen has dark cherry color and a dense consistence. At it gistol. a research the atrophy limf, follicles and sclerous changes in a red pulp is noted. In tissue of a brain the plethora and hypostasis are observed (see. Swelled also swelling of a brain ). In cross-striped and unstriated muscles sites of destruction come to light. In a pancreas the plethora of vessels, hypostasis, hemorrhages, sometimes extensive, swelling of walls of small vessels and their fibrinferments, often the centers of a fatty necrosis are noted (see. Fatty necroses ), destruction of cells of the excretory device in the form of a diskomplek-sation, a necrosis. In a stomach against the background of a plethora of vessels and hypostasis of a submucosal layer the centers of a necrosis of a mucous membrane of various depth, acute erosion and ulcers owing to sloughing are visible. In adrenal glands the sharp plethora (preferential mesh layer of bark), small hemorrhages, the centers of a necrosis, a focal delipidization of cells of glomerular and mesh layers is noted.

Macroscopic changes in heart at hron. Page of N depending on a stage of the basic patol. process can be expressed by a compensatory hypertrophy of a myocardium or myogenetic dilatation of cardial cavities (see the Hypertrophy, Compensatory processes). At a decompensation the myocardium becomes flabby, on a section has a clay appearance; changes of sclerous character are noted. At gistol. a research in a myocardium it is noted granular, vacuolar, and fatty dystrophy — so-called tiger heart is more often (see. Vacuolar dystrophy , Fatty dystrophy ). Depending on the disease which caused development hron. Page of N, in a myocardium it is possible to reveal sclerous changes, sites of inflammatory infiltration and a necrosis, an atrophy and a hypertrophy of muscle fibers.

At electronic microscopic examination of a myocardium the disturbance of processes of intracellular regeneration which is characterized by decrease in a reproduction of ultrastructures of cardiomyocytes, slow growth of mitochondrions and sni-zheniyekhm power security and consequently, and kontraktilny ability of myofibrils is noted. Insufficient power security of myofibrils at the time of reduction leads to reduction of force of a systole. The diastolic weakness noted at hron. The page of N, is a consequence of a lack of energy, to-ry test volatile calcic pumps of a sarcoplasmic reticulum during a diastole. A consequence of the broken metabolism of cells at hron. Pages of N are in various degree the expressed changes in sarcomeres, a sarcoplasmic reticulum, mitochondrions, cytogranules, lysosomes.

The clinical picture

the Acute heart failure is shown cardiac asthma (see), fluid lungs (see). The main wedge, manifestations hron. Pages of N are tachycardia (see), cyanosis (see), asthma (see), hypostases (see. Swelled ), increase in a liver, swelling and pulsation of cervical veins, dysfunction of different bodies and systems.

Tachycardia in an initial stage of S. of N arises at an exercise stress, however pulse is returned to initial level not earlier, than in 10 min. At S.'s progressing N tachycardia is observed also at rest. It arises owing to a Bainbridge reflex from the stretching mouths of venas cava (see. Reflexogenic zones ) also it is directed to compensation of an insufficient stroke output and maintenance up to standard of minute volume. Further this compensatory reaction becomes insolvent and leads to a bigger overfatigue of a myocardium.

Cyanosis of skin and mucous membranes is expressed more on the periphery (fingers of hands and legs, lobes of ears) — where the speed of a blood-groove small. Developing of cyanosis is connected with excess absorption fabrics of oxygen of blood and increase in content in blood of the recovered hemoglobin, and also with insufficient saturation of blood oxygen in pulmonary capillaries.

An asthma — the most frequent and early symptom of S. of N (as a rule, left ventricular) — is shown by the speeded-up, shallow breathing with involvement in the act of breath of auxiliary muscles, often is followed by the cough caused reflex from congestive bronchial tubes or the expanded left auricle connected with irritation of a recurrent nerve. Sometimes find haemo siderophages («heart failure cells») in a phlegm. In an initial stage an asthma arises at an exercise stress, further it progresses and becomes a constant. Emergence of an asthma is connected with accumulation in blood milk, coal to - t and change of pH of blood as a result of its stagnation in vessels of a small circle, and also with reduction of vital capacity of lungs (see), increase in their rigidity, increase in intrapleural pressure, reduction of a peripheral blood-groove and disturbance of a thermolysis. Night attacks of suffocation are characteristic of the expressed S. of N, to-rye can pass into a fluid lungs (see). Attacks of suffocation, as a rule, stop during the weakening of sokratitelny function of a right ventricle, accession of insufficiency of the three-leaved valve and development owing to hron. stagnation of blood of sclerous changes in lungs.

Hypostases — one of characteristic signs of S. of N. At early stages the obscure edemas when the delay in an organism less than 5 l of liquid can not be followed by visible manifestations can be observed. Hypostases develop at first standing, to a waist, then extend and cover all hypodermic cellulose (anasarca). They are especially expressed on extremities, generative organs, in a stomach, on a waist. Transudate accumulates also in serous cavities. The hypostases connected preferential with right ventricular insufficiency and venous stagnation develop later, after increase in a liver. They are extensive, dense to the touch, skin over them is thinned, a tsianotichna, with trophic changes. The hypostases caused by a left ventricular failure develop earlier, than venous staz. They are small, soft, movable, body parts, skin, remote from heart, over them pale cover. These hypostases are a consequence hypoxemic disturbance and the porosity of walls of capillaries caused by delay of a blood-groove.

The increase in a liver (sometimes to the considerable sizes) caused by delay of a peripheral blood-groove and overflow krovyo hepatic veins and capillaries is a classical sign of iravo-ventricular insufficiency (see. Pulmonary heart). The liver is strained, painful at a palpation (at the expense of stretching of the capsule), its edge is rounded; at S.'s progressing N the liver becomes dense, its edge is pointed, signs of dysfunction appear (an ikte-richnost of skin and mucous membranes, a hyperbilirubinemia, an urobilinuria, a disproteinemia, etc.) - Stagnation of blood and development of fibrosis of a liver leads to portal hypertensia (see), to ascites (see), to increase in a spleen (see).

The swelling and a pulsation of cervical veins caused by rise in venous pressure at S. of N have constant character unlike respiratory insufficiency, at a cut cervical veins bulk up only on an exhalation due to increase in vnut-rpgrudny pressure and difficulty of inflow of blood to heart. Pressing on the increased liver can lead to strengthening of swelling of cervical veins (a hepatojugular reflux).

Due to the dysfunction went. - kish. a path nausea, a loss of appetite, a meteorism, locks are noted. Owing to a hypoxia the muscle tone of a stomach goes down and the peristaltics is slowed down, absorption in a small bowel is at a loss that aggravates dispeptic frustration, disbolism. Congestive gastritis with an atrophy of gastric glands is noted (see. Gastritis ). In an end-stage of S. of N the cordial cachexia (see) masked to a nek-swarm of degree by hypostases usually develops.

Function of kidneys is significantly broken because of considerable decrease in a renal blood-groove, a reflex spasm of renal arterioles and rise in pressure in renal veins. The daily urine decreases, urine becomes concentrated, with high specific weight, supports squirrels (0,2 — 0,5 °/oo and more), single erythrocytes. The nocturia connected with improvement of blood supply of kidneys in rest and in horizontal position is noted (see the Nocturia).

The diagnosis

the Diagnosis at the expressed S. of N which is followed by tachycardia, short wind, hypostases and other characteristic signs comes easy. He is clinical and does not demand, as a rule, use of special methods of a research. In diagnosis of N by initial S. complaints of patients to heartbeat and an asthma at an exercise stress are of great importance. It is especially important to specify tolerance of the patient to an exercise stress for what find out, e.g., by what floor of the patient can rise, without stopping also without an asthma. At identification of latent and initial stages of S. of N special methods of a research are highly informative, among to-rykh exist invasive and noninvasive.

Invasive methods are based on catheterization of cardial cavities (see Catheterization of heart) and the main vessels, and also studying of their state by means of the entered radiopaque substance. The main indicators characterizing a functional condition of a myocardium and its insufficiency at these researches are the end diastolic pressure, estimated values of indexes of contractility based on the speed of change of pressure and filling in ventricles, fraction of emission of blood. However invasive methods cannot widely be applied in clinic. In recent years there were new, noninvasive methods. The most informative and perspective of them (from the point of view of a possibility of their use in kardiol. departments of BC) — ultrasonic methods, in particular echocardiography (see).

For S.'s diagnosis N (including and its latent form) widely use a research of a hemodynamics at performance by the patient of any loading test (the stationary bicycle iya, test on the tredmil), etc. In the hidden and initial stages of S. of N increase in volumes of a left ventricle (preferential systolic) in response to the dosed exercise stress is very typical for patients with coronary heart disease. Use of loading tests allows to find the hidden S.'s signs of N and in patients with aortal heart diseases. At rather small loading increase in shock emission happens preferential due to reduction of final systolic volume of a left ventricle. Further at increase in degree of loading at patients from latent S. the N is not marked out so considerable gain of shock emission any more, the size of final systolic volume even increases in comparison with the size of this indicator at the previous loading a little. At the same time there is a decrease in size of fraction of emission and speed of circular shortening of fibers of a myocardium.

From other tool diagnostic methods use also a reokardiografiya (see) and the phase analysis of cordial activity (see Polikardiografiya). By means of the last reveal generally so-called syndrome of a hypodynamia of heart, for to-rogo lengthening of a postsphygmic period, shortening of the period of exile and sometimes a mechanical systole is characteristic (isometric contraction + the period of exile). Also complex indicators of phase activity change: the vnutrisisto-lichesky indicator decreases (the relation of the period of exile to a mechanical systole, in %), the index of tension of a myocardium increases (the relation of the period of tension of a myocardium to duration of the general systole, in %); the size of the relation of the period of tension by the period of exile increases, and it is in direct dependence on the size of the fraction of emission characterizing pumping function of a myocardium.

N nek-ry researchers consider one of latent S.'s manifestations delay of auskultativny phenomena in relation to teeth of an ECG (power and dynamic insufficiency of heart, or Hegglin's syndrome).

The complex of researches for identification of early stages of S. of N includes studying of a functional condition of system of external respiration (see), one of the most precursory symptoms of disturbances to-rogo is the hyperventilation not adequate to an exercise stress. Already at early stages of S. of N, despite turning on of compensatory mechanisms, efficiency of ventilation can be even at rest reduced. The important indicator characterizing a functional condition of system of external respiration is degree of irregularity of lung ventilation. At diseases of cardiovascular system this indicator increases even to formation a wedge, S.'s symptoms of N. A precursory symptom of S. of N also reduction of vital capacity of lungs is considered.

The differential diagnosis

Klin, signs characteristic of S. N, separately can meet at many diseases proceeding without S.'s development by N (e.g., tachycardia at a thyrotoxicosis, an asthma at diseases of lungs, hypostases at damage of kidneys, etc.). However assessment a wedge, pictures in general allows to establish or reject in most cases S.'s presence in N. The greatest difficulties are presented by the differential diagnosis cordial and a pulmonary heart (see. Pulmonary heart ).

In the anamnesis at patients with a pulmonary heart cough, frequent catarrhal diseases or repeated pneumonia are for many years noted. An asthma at a pulmonary heart has the nature of the complicated breath with the extended exhalation more often; cyanosis is considerably expressed and is diffusion, at the same time extremities of the patient to the touch remain warm. The patient can low lie. At auscultation of lungs the scattered dry whistling rattles against the background of the extended exhalation are usually listened. Swelling of cervical veins considerably amplifies at an exhalation. A ciliary arrhythmia (see) unlike S. the N develops very seldom.

Patients with S. of N in the anamnesis have instructions on heart diseases; short wind and cough develop at them later, in connection with stagnation in lungs. Breath is usually not complicated, the exhalation is not extended; cyanosis is localized preferential in distal departments of extremities (Crocq's disease), extremities to the touch cold. Patients hold a semi-sitting position in a bed. In lungs wet rattles are listened more often, it is preferential in lower parts; the exhalation is not extended. Swelling of veins of a neck is expressed equally on a breath and on an exhalation. In differential diagnosis use data of an ECG, X-ray analysis and careful studying of function of external respiration.

Treatment

acute S.'s Treatment N is directed to stopping of an attack of cardiac asthma (see), a fluid lungs (see). At treatment of patients hron. Villages of N hold events of the general character: restriction of physical activity and removal of psychological tension (psychotherapy, sedatives), a diet with restriction of sodium chloride (to 3 — 4 g a day) and liquids (to 1,0 — 1,2 l a day). These actions can improve considerably a condition of patients even without medicinal therapy. Extent of restriction of activity of the patient is defined individually, depending on S.'s expressiveness of N. It is necessary if it is possible, to remove origins of S. of N (operational treatment of heart diseases, treatment of active rheumatic process, elimination of disturbances of a heart rhythm, etc.).

The important place in treatment of patients with S. N is taken by medicinal therapy. Remain the main pathogenetic remedy C. for N cardiac glycosides (see). Apply strophanthin, Korglykonum, digoxin, digitoxin, Celanidum more often (a synonym Isolanidum), powder from leaves of a foxglove, lantosidum, drugs of the adonis. High-speed cardiac glycosides with high speed of an inactivation are shown generally in acute S.'s cases of N, and also at decrease in tolerance to glycosides. Strophanthin or Korglykonum at chronic S. of N - can be recommended in an initiation of treatment because of inconvenience of long intravenous administration. At chronic S. N use well soaking up in went. - kish. a path it is also long the operating cardiac glycosides (digitoxin, digoxin, etc.).

There are three methods of a digitalization: bystry speed when saturation by cardiac glycoside of an organism of the patient is aimed to be reached within a day; moderately bystry speed when the same effect occurs within 3 days; slow speed when saturation of a serdechnsha glycosides is carried out during more long term. Digitalization is applied by bystry speed in a crust, time rather seldom that is caused by danger of overdose of cardiac glycosides in connection with different individual sensitivity to them. The greatest distribution was gained by a digitalization moderately bystry speed when in the first days enter 50% of an average therapeutic dose. Drug is appointed fractionally, and the size of each subsequent dose is defined by response to previous. It is the safest to enter each additional dose not earlier than in 1 hour after approach of the maximum effect of the previous dose. Two next days cardiac glycoside is also entered fractionally, selecting an optimum dose of drug. Moderately bystry digitalization is shown to patients with hron. Page of N, proceeding with tachycardia, and also the patient with a supraventricular tachyarrhythmia. Normalization of heart rate is usually rather reliable criterion of an adequate digitalization. It is important to monitor changes of an ECG also. At patients with S.'s signs of N in assessment of therapeutic effect of drug it is possible to be guided also by a positive inotropic effect on the administered drug (increase in a diuresis, reduction of hypostases and the sizes of a congestive liver, subjective improvement of a state, etc.). It is the safest to carry out a digitalization by slow speed. In this case daily enter the fixed dose of a cordial glycoside before obtaining therapeutic effect. At such way of introduction saturation by strophanthin occurs usually for the 5th days, digoxin — on 5 — the 7th days, digitoxin occurs more slowly.

When therapeutic effect of the cordial glycoside entered inside reach, it is necessary under' to take a maintenance dose of drug for prolonged treatment. The supporting daily dose of cardiac glycoside shall correspond approximately to amount of the drug destroyed and removed in 1 days. At achievement of such compliance there comes balance between the glycoside entered and destroyed serdechnsh and its optimum concentration (saturation) can is long to keep. Usually maintenance dose is slightly less than that, on a cut there was an optimum saturation.

At the combined treatment by cardiac glycosides and other pharmaceuticals change (more often reduction) doses of cardiac glycoside can be required (so, at addition of diuretic this dose should be reduced sometimes since the myocardium changes the sensitivity to it in connection with change of the electrolytic balance, decrease in hemodynamic loading; the same can be told concerning quinidine and blockers of beta adrenoceptors).

Sensitivity to cardiac glycosides is defined by a condition of a myocardium and its specific receptors connecting cardiac glycosides and also noncardiac factors (disturbance of electrolytic exchange — a hypopotassemia, a hypomagnesiemia, a hypercalcemia, acid-base equilibrium of any genesis, acute and hron. hypoxia, hypothyroidism, increase in a tone of sympathoadrenal system, use of sympathomimetics, alkaloids of Rauwolfia, etc.).

Under the influence of various pharmaceuticals influencing absorption or breakdown rate of cardiac glycosides, their level in blood can change.

One of the main reasons for the inadequate answer to a long maintenance therapy cardiac glycosides which is shown increase of cordial reductions or increase of signs of a decompensation is considerable expansion of the mode of a physical activity of patients after their extract from a hospital. Therefore already in a hospital it is necessary to pay attention to tolerance of patients to an exercise stress.

Correction of water and electrolytic disturbances at S. of N is reached by inclusion in a complex to lay down. actions of diuretics (see. Diuretics ), increasing a diuresis, the natriuresis reducing the volume of the circulating blood. The fixed diuretic assets reduce a reabsorption of ions of Na + and waters in io-chechny tubules, affecting preferential proximal renal tubules (e.g., osmotic diuretics, inhibitors of a karboangidraza), the ascending part of a nephronic loop (e.g., thiazide diuretics, furosemide, Uregitum), distal renal tubules. Carry to the last kaliysberegayushchy competitive (e.g., veroshpiron, Aldactonum) and non-competitive antagonists of Aldosteronum (Triamterenum, etc.). The diuretics operating on all ascending part (furosemide, Uregitum) or a cortical segment of the ascending part of a nephronic loop are most often applied (hypothiazid, Cyclomethiazidum, gigroton, Brinaldixum), to-rye apply independently or in a combination with the kaliysberegayu-shchy diuretics operating on distal tubules of kidneys.

The patient with heart failure of IIA of a stage with moderate developments of stagnation treatment is recommended to begin hypothiazid of ohms on 50 — 150 mg a day in two steps or Brinaldixum on 20 — 60 mg a day once, in need of a combination with veroshpirony on 150 — 250 mg a day (in the presence of a secondary hyper aldosteronism) or Triamterenum (Pterofenum) on 100 — 200 mg a day. The similar combination allows to achieve an ecuresis and a natriuresis at maintenance of stable level of potassium in blood. Veroshpiron appoint prior to treatment the main diuretic since he begins to act on 3 — the 4th day of use. Therapy by kaliysberegayushchy diuretic drugs is carried out continuously, the main diuretics in a phase of active therapy appoint daily or every other day, and upon transition to a maintenance therapy — one — two times a week under control of body weight and a diuresis. At change in case of need doses of the main diuretic in proportion to it change a daily dose and kaliysberegayushchy drug.

Sometimes in the absence of effect even from high doses of drugs it is reasonable to combine diuretics, and also to combine them with the drugs improving renal blood circulation (an Euphyllinum, theophylline).

During performing complex treatment careful control of a condition of water and electrolytic exchange, acid-base equilibrium and level of crude protein in an organism is necessary.

The most adverse disturbances of water and electrolytic exchange are dehydration leading to a hyponatremia and a hypochloraemia and a hypopotassemia. At hyponatremias (see) it is necessary to cancel temporarily diuretics and to enter to the patient of sodium salt and chlorine; active diuretic therapy is reappointed, having changed doses of diuretics, only after recovery of content of electrolytes in blood. At patients from the expressed S. of N decrease in level of sodium in a blood plasma testifies, as a rule, to dominance of a delay of water in extracellular space of an organism, i.e. to a hyponatremia of cultivation, at a cut correction is not required or administration of salts of potassium is necessary (but not sodium). Hypopotassemia (see), developing under the influence of diuretic means, is an adverse factor since at patients from chronic S. of N the content of potassium in an organism is initially reduced. The raised excretion of potassium leads to falling of level of electrolyte not only in a blood plasma, but also in cells that increases risk of development of disturbances of a rhythm and conductivity at purpose of cardiac glycosides and worsens portability of the last. In these cases appoint drugs of potassium, potassium - saving diuretic or increase their doses. Noted disturbances, and also decrease in level of protein in an organism are observed usually at the expressed heart failure (IIB — III of a stage). Decrease in level of crude protein of blood, and first of all hypoalbuminemia, can be shown by a persistent refrakternost of an organism to diuretics. In such cases inclusion in complex diuretic therapy of osmotic diuretics (Mannitolum, urea) and administration of protein in the form of plasma or albumine is shown. Purpose of osmotic diuretics is shown first of all at acute S. to N at patients with reduced renal filtering; at chronic S. of N the increase in volume of the circulating blood taking place in the first phase of effect of osmotic diuretics can lead to development of an acute left ventricular failure and a fluid lungs.

Metabolic belongs to disturbance of acid-base equilibrium of blood at patients from chronic S. of N alkalosis (see), caused by deficit of potassium or chlorine (is more often owing to use of diuretics). At a metabolic alkalosis the drugs operating on the ascending part of a nephronic loop gradually cease to render the expressed diuretic effect. Reduction of degree of a metabolic alkalosis is reached by purpose of adequate doses of kaliysberegayushchy diuretics, salts of potassium and the prevention of an excessive diuresis. Inclusion in complex therapy of inhibitor of a karboangidraza of Diacarbum (Diamoxum) allows to avoid development of an alkalosis and to achieve an ecuresis.

The maintenance therapy should be continued by diuretics in individually picked up dose constantly in out-patient conditions under control of the district doctor.

At heavy S.'s treatment N apply peripheral Vasodilatum Torah — the means improving a hemodynamics by impact on a tone of peripheral vessels. On localization of preferential action they can be divided into three groups: acting on a tone of veins (nitroglycerine, nitrates of the prolonged action — Nitrosorbidum, Corvotonum); acting on a tone of arterioles (apressine, phentolamine); acting at the same time on a tone of veins and arterioles (Sodium nitroprussidum, Prazozinum).

Drugs of the first group, first of all nitroglycerine and Nitrosorbidum, reducing a tone of venules, reduce venous return of blood to heart, pressure in vessels of a small circle of blood circulation, pressure of filling of a left ventricle and, respectively, sizes of the last. Clinically it is shown by reduction of an asthma and cyanosis. Cordial emission at the same time does not change or decreases slightly. These drugs do not cause essential change of heart rate and the ABP. A lack of use of nitroglycerine sublingual is short duration of its action (up to 30 min.). Use of Nitrosorbidum operating within 4 — 5 hour allows to achieve uniform concentration of drug in blood within a day and lasting clinical and hemodynamic effect. Nitrosorbidum is appointed on 20 mg by each 4 — 5 hours, Corvotonum — on 4 mg of 4 — 6 times a day.

The patient without the expressed developments of stagnation in a small circle of blood circulation, but with considerable decrease in cordial emission (at insufficiency of the mitral or aortal valve) it is reasonable to appoint drugs of the second group, reducing the general peripheric and intra aortal resistance that promotes increase in effective cordial emission and allows to reduce the volume of mitral and (or) aortal regurgitation, and also to achieve decrease in volume of a left ventricle. Apressine in a dose of 50 — 75 mg 3 — 4 times a day moderately increases heart rate and reduces the ABP level, without having significant effect on pressure of filling of a left ventricle.

Drugs of the third group, and first of all nitroprus - Cyd of sodium (Nipridum) who is reducing pressure of filling of a left ventricle and at the same time promoting increase in cordial emission at reduction of the sizes of a left ventricle and left auricle are most effective in treatment by the expressed S. of N. It allows to try to obtain a wedge, effect from a number of patients with S. N, refractory to use of cordial glycosides and diuretics. The drug is administered only intravenously kapelno at a close check behind a condition of a hemodynamics (number of cordial reductions, the ABP, pulmonary pressure or the central venous pressure). Duration of administration of drug, as a rule, 12 hours; however in need of it it is possible to increase till 60 — 72 o'clock. Drug begins to work in 2 — 5 min. after the beginning of introduction that allows to use it for stopping of an acute left ventricular failure. Drug is terminated in 30 min. after the end of introduction. It is possible to apply to maintenance of the reached effect orally Vasodilatum Torahs the Prazozinum having effect, similar to Sodium nitroprussidum, and operating within 4 — 5 hour. Applying a combination of Nitrosorbidum (20 mg) and apressine (75 mg), appointed in each 4 — 6 hours, it is possible to receive the long, though less expressed wedge, effect, similar to action nitropruss Ida of sodium.

All peripheral Vasodilatum Torah due to reduction of volume of a left ventricle and vnutrimiokar-dialny tension reduce the need of a myocardium for oxygen and transfer heart to more «economical» duty.

At a refrakternost to cardiac glycosides, edges it is observed sometimes at patients with the large volume of a left ventricle, reduction of the sizes of the last under the influence of vazodilatator allows to use effectively drugs of a digitalis in adequate doses, and signs of toxic action are not observed.

In recent years in case of inefficiency or impossibility of use of cardiac glycosides use the drugs possessing a positive inotropic effect, not relating to cardiac glycosides — the selection beta-adrenergic agonists (prenalterol, etc.).

For overcoming a refrakternost to cardiac glycosides include in complex treatment also other drugs. So, at S. of N which is followed by a high level of activity simpatiko-adrenalo-howl systems and persistent tachycardia, apply in addition to cardiac glycosides blockers R-adre-nergicheskikh of receptors — inderal (Obsidanum), etc., to-rye allow to lower doses of cardiac glycosides and diuretics. At the same time reduction of the sizes of heart, normalization of heart rate, increase in working capacity, improvement of health of the patient is noted. However in the first days of treatment p-adrenoblockers do not exclude a possibility of temporary strengthening of symptoms of S. of N.

In complex therapy of S. of N try to use also other metabolic active drugs (a stimulator of synthesis of nucleic acids — inosine, etc.).

The forecast and Prevention

the Forecast depends, first of all, on the disease which caused S. of N and also on its stage. At heart failure of the III stage the forecast in all cases adverse. An opportunity to remove S.'s cause for N (e.g., an operative measure at heart diseases) considerably improves the forecast.

Prevention — see articles devoted to various diseases of cardiovascular system (e.g., Myocarditis , acquired , Stenocardia ).



Bibliography: Beskrovnova H. N, etc. About a possibility of definition like cellular death of cardiomyocytes by means of the ultrastructural analysis, Arkh. patol., t. 42, century 3, page 34, 1980; In and - x e r A. M. t and Sh and r about in V. G. O heart failure and its morphological expression, Cardiology, t. 15, No. 10, page 23, 1975; In otchat B. E. and the Slutsk M. E. Cordial glycosides, M., 1973, bibliogr.; Davydovsky I. V. General pathology of the person, page 178, M., 1969; Lang G. F. Diseases of the blood circulatory system, M., 1958; Meerson F. 3. Adaptation, deadaptation and insufficiency of heart, M., 1978, bibliogr.; Mukharlyamov H. M. Early stages of a circulatory unefficiency and mechanisms of its compensation, M., 1978; A. L. Butchers. Internal diseases, M., 1967; Spiders V. S. and Frolov V. A. Elements of the theory of pathology of heart, M., 1982; N. K. Residents of Perm. Bases of resuscitation pathology, page 52, M., 1979; The Guide to cardiology, under the editorship of E. I. Chazova, t. 1, page 330, etc., M., 1982; Sarkisov D. S. and In t yu r and N B. V. Elektronnomikroskopichesky the analysis of increase in endurance of heart, M., 1969; With I eat e with N about in and L. A. and C e l of l and r and - at from Yu. G. Ultrastruktur of muscle cells of heart at focal metabolic damages, Novosibirsk, 1978; With m about l I am N of N and to about in A. V. and Naddach and N and T. A. Questions of pathological anatomy and pathogeny of coronary insufficiency, M., 1963, bibliogr.; Sycheva I. M. and Vinogradov A. V. Chronic circulatory unefficiency, M., 1977; X e x t And. Introduction to experimental bases of modern pathology of a cardiac muscle, the lane with it., M., 1975; Chazov E. I. Molecular bases of heart failure, Cardiology, t. 15, No. 10, page 12, 1975; Arnolds. Century and. lake of Long-term digitalis therapy improves left ventricular function in heart failure, New Engl. J. Med., v. 303, p. 1443, 1980; Cohn J. N. a. Franciosa * J. A. Selection of vasodilator, inotropic or combined therapy for the management of heart failure, Amer. J. Med., v, 65, p. 181, 1978; The concept of heart failure, Cambridge, 1980; H a t t P. Y. e. a. Pathologie myocardique h 1’ Echelon cellulaire, Arch. Mai. Coeur, p. 77, 1972; Jennings R. B., Ganote of Page E. R e i m e r K. A. Ischemic tissue injury, Amer. J. Path., v. 81, p. 179, 1975; Lemberg L. Digitalis in congestive heart failure, Arch, intern. Med., v. 138, p. 451, 1978; M a s o n D. T. a. o. Alterations of hemodynamics and myocardial mechanics in patients with congestive heart failure, pathophysiologic mechanisms and assessment of cardiac function and ventricular contractility, Progr. cardiovasc. Dis., v. 12, p. 507, 1970, bibliogr.; Mechanism of contraction of the normal and failing heart, ed. by E. Braunwald a. o., Boston, 1967; Weber K. T. a. o. Vasodilator and inotropic agents in the treatment of chronic cardiac failure, Amer. Heart J., v. 102, p. 569, 1981, bibliogr.; Z e-1 i s R. F 1 an i m S. F. Alterations in vasomotor tone in congestive heart failure, Progr. cardiovasc. Dis., v. 24, p. 437, 1982, bibliogr.


H. M. Mukharlyamov; V. Yu. Mareev (stalemate. physical.), N. K. Permyakov, G. M. Mogilevsky (stalemate. An.).

Яндекс.Метрика