Heart failure symptoms
The history of the study of heart failure dates back several centuries and is one of the most frequent and very serious complications in cardiovascular diseases. However, until now there is no generally accepted definition of CHF.
V. Kh. Vasilenko in the article "Blood circulation inadequacy" of the second edition of the Great Medical Encyclopedia gives the following definition of circulatory insufficiency: "Circulatory failure is a pathological condition consisting in the inability of the circulatory system to deliver organs and tissues the amount of blood necessary for normal functioning."It should be noted that the term circulatory failure, which has become widespread in our country, is, in fact, synonymous with heart failure. How to treat this ailment with folk remedies, look here.
E. Braunwald believes that CHF can be defined as "a pathophysiological condition in which a violation of the heart's function leads to the inability of the myocardium to pump blood at the rate necessary to meet the metabolic needs of tissues, or these requirements are provided only by a pathological increase in the filling pressure of the heart cavities".
An important position that can be seen in the definition of CHF, given by FI Komarov and LI Olbinskaya, is that, along with the manifest forms of the pathological state( decompensated CHF), the existence of early, latent forms is acknowledged when the metabolic needs of organs and tissuesin rest are provided by mobilization of compensatory mechanisms( compensated CHF): "a pathological condition in which the cardiovascular system is unable to deliver to the organs and tissues the amount of blood necessary fortheir normal functioning alone or upon presentation to the circulatory system of increased requirements( physical or emotional load intercurrent diseases) ".
The authoritative International Guide to Heart Failure states that a modern and accurate definition of CHF should be as follows: "Heart failure is a multi-systemic disease in which a primary impairment of heart function causes a number of hemodynamic, nervous and hormonal adaptive reactions aimed at maintaining blood circulation inaccording to the needs of the body. Shortness of breath, combined with signs of fluid retention or without it, is the most frequent clinical sign of heart failure. The severity of dyspnea does not reflect the degree of left ventricular( LV) dysfunction that causes it, which is the most significant prognostic indicator. In many patients with LV dysfunction, symptoms of the disease are absent, at least at the onset of the disease. Heart failure is a rapidly progressive condition with a clearly poor prognosis. "This definition is not without flaws. First of all, I would like to express doubt about the unambiguous benefits of chronic neurohumoral hyperactivation and hemodynamic changes associated with CHF.Imperfect hemodynamic and neurohumoral mechanisms compensate for impaired cardiac function allow "to maintain blood circulation in accordance with the needs of the body" only for a time after which prolonged excessive neurohormonal activation begins to play a negative role, causing the progression of cardiac decompensation. Fortunately, the possibilities of modern pharmacotherapy of CHF( in particular, neurohumoral unloading of the heart) and cardiac surgery led to the fact that this progression does not always have high rates in all cases.
In the recently published guidelines for the evaluation and treatment of CHF in adults, experts from the American College of Cardiology( ACC) and the American Heart Association( AAK) define CHF as "a complex clinical syndrome that can be caused by any structural or functional heart disease that interferes with the ventricular capacityfill with blood or drive it out. "Undoubtedly, an important point of the presented definition is an indication of the basic mechanisms that ultimately determine the development of CHF( systolic and / or diastolic dysfunction of the myocardium).According to EI Chazov, the need to isolate the variants of CHF depending on the mechanisms that determine the development of heart dysfunction is dictated not by theoretical calculations and ambitions of certain scientists or individual clinical schools, and not even by the desire to unite patients by the nature and degree of pathological changes, andthe desire to build the most effective differentiated therapy and determine the prognosis of the disease.
The authors of all the above definitions combine the view on CHF as the final stage( outcome, complication) of many diseases that affect the heart, that is, as a syndrome, rather than an independent nosological form. At the beginning of the XXI century.leading Russian experts on heart failure presented a reasoned viewpoint on CHF not only as a complex symptom complex complicating the course of a disease of the cardiovascular system, but also as an independent nosological form: "a disease with a complex of characteristic symptoms( dyspnea, decreased physical activity, edema, etc.) that are associated with inadequate perfusion of organs and tissues at rest or under stress and often with fluid retention in the body. The primary cause is deterioration of the ability of the heart to fill or empty due to damage to the myocardium, as well as an imbalance of vasoconstrictive and vasodilating neurohumoral systems. "
Thus, we can agree with the authors of the International Guidelines for Heart Failure: "Heart failure is defined in different ways, but none of the proposed interpretations is completely adequate."
In accordance with the National Recommendations for diagnosis and treatment of CHF, the term "congestive heart failure"( as well as "chronic circulatory failure") should not be used to unify the terminology. Among the other terms in the literature are the following:
There is still no consensus on the clinical suitability of all these definitions. Apparently, there is no threat of wide use in the clinical practice of the last two terms of Russia.
Table. Incidence of heart failure( per 1000 population per year) in different age groups of
Today we observe an increase in the prevalence of CHF, the situation of which resembles a non-infectious epidemic. The impressive successes achieved in recent decades in the treatment of the most common cardiovascular diseases( primarily acute coronary catastrophes) concerned mainly the immediate results of pharmacological and surgical interventions. Thus, a significant reduction in mortality in myocardial infarction( MI), observed in the last three decades in most economically developed countries, was not accompanied by an equivalent reduction in overall cardiovascular mortality. This paradoxical situation, which was referred to as the "ironic failure of success," is explained by an increase in the number of people suffering from CHF.
There are three main reasons for the increase in the incidence of CHF:
The paradoxical situation is that the better we treat patients with underlying cardiovascular diseases, the more patients survive to an older age.
In view of the latest research, Yu. N. Belenkov et al.warn that "you need to be prepared for the fact that in 10-20 years every second or third patient after visiting a cardiologist( or therapist) will leave his office with this diagnosis."
According to the definition of CHF given by experts from ACC and AAK, this "... complex clinical syndrome. .. can be caused by any structural or functional heart disease. .."In the most general form, the main causes of CHF development are presented in Table.
Table. The main causes of the development of CHD
Naturally, the incomplete list of the causes of CHF development listed in Table 1 could be continued( myocarditis, myocardial dystrophy, particularly in patients with diabetes mellitus, heart tumors, etc.) and detailrhythm of the heart, causes of chronic pulmonary heart, cardiotoxic drugs, etc.).
In the etiological structure of CHF, IHD and hypertension predominate. A number of epidemiological studies performed in the Americas show that the most common cause of CHF is hypertension in combination with or without IHD( Table).
Table. Etiology of heart failure( %)
In Europe, on the contrary, in first place is CHD, rather than systemic arterial hypertension( reports of domestic cardiologists are closer to the data of European colleagues).
The direct cause of decompensation of CHF( regardless of the nosological form underlying the lesion of the cardiovascular system) can be different states, many of which usually do not usually lead to CHF.Identification of such an immediate cause of CHF is of fundamental and extremely great importance, since its timely diagnosis and adequate correction often allow saving the patient's life.
Practical physician most often can face the following situations: pulmonary embolism, MI, infection, anemia, thyrotoxicosis, pregnancy, arrhythmias( even simple increase in heart rate), myocarditis, endocarditis, systemic hypertension, physical, emotional, dietary and othersincluding medicamentous) external stresses. Looking ahead, in connection with this, it should be noted that the prognosis in patients with heart failure, the triggering mechanism of which is known and eliminated in some way( including active treatment), is more favorable than in patients whose direct cause could not be established.
Significance of symptoms and clinical signs is extremely high, since it is they that allow the doctor to suspect the presence of CHF in the patient and, consequently, to organize the diagnostic process with maximum purposefulness and concreteness in order to confirm or disprove the diagnostic hypothesis. Intensive development of science and technology contributed to the creation and implementation of numerous informative instrumental and laboratory methods for studying patients with diseases of the cardiovascular system. Nevertheless, direct clinical examination of the patient is the first stage of diagnosis. Unfortunately, it often happens that the clinical examination of a patient is replaced by one or another paraclinical tests. And if such a vicious approach is practiced long enough, it can lead to atrophy of the doctor's skills of so-called "bedside" diagnostics.
Sometimes a patient with complaints indicating a cardiovascular disease( for example, pain in the heart, "irregularities" in the heart, a headache associated with an increase in blood pressure), at which the likelihood of developing CHF is likely to be admitted to a cardiologist or therapist. Nosological diagnosis( in particular, IHD) in such a case, when there are no manifestations of heart failure, "helps" the syndromic diagnosis of the initial stage of heart failure.
Symptoms:
dyspnea as mentioned above, is the most "popular" finding in CHF.In the Great Medical Encyclopaedia( 2nd ed.) N. Savitsky gives the following definition of dyspnea( dyspnoA, from Greek dyspnoia - shortness of breath, shortness of breath) - "shortness of breath characterized by a violation of its frequency, depth and rhythm, accompanied by a complex of unpleasant sensations ina kind of constriction in the chest, a lack of air, which can reach a painful sense of suffocation. "
Inspired inspiratory inspiration ( or, according to James Mackenzie, "thirst for air") in patients with CHF has a complex origin( the significance of each factor is different for different patients and for various diseases of the cardiovascular system), and there are still unsolved questions regardingits genesis. Apparently, in the formation of dyspnea, in addition to stagnation of blood "higher" the weakened heart( LV) with increasing pressure in the pulmonary capillaries, due to which traditionally explains its appearance, other factors not fully understood can also participate. In particular, the perception of shortness of breath depends largely on the diffusion capacity of the lungs( dyspnea is sharper the more pronounced the hypoxemia is), the reactions of the central nervous system to changes in the blood composition( hypoxemia, hypercapnia, acidosis, etc.), peripheral and respiratory musculature and massespatient. Contributes to the appearance of dyspnea fluid accumulation in the pleural and abdominal cavities, which hampers the respiratory excursion of the lungs. It is also possible that this symptom is based on a decrease in the extensibility of the lungs and an increase in intrapleural pressure, which leads to an increase in the work of the respiratory muscles and the auxiliary musculature. To this, it should be added that in patients with long-lasting pulmonary embolism, their stagnant( induc- tive) sclerosis-the brown compaction( induration) of the lungs develops.
The sensitivity, specificity and prognostic significance of dyspnea were discussed already. The main thing to remember is the low specificity of this symptom.
Naturally, in the initial stage of CHF, shortness of breath in rest is absent and appears only with intense muscle tension( climbing stairs or uphill, with fast walking for long distances).Patients move freely around the apartment and can occupy any position convenient for themselves. With the progression of heart failure, shortness of breath is observed even with minor stresses( even during conversation, after eating, while walking around the room), then - becomes permanent. And, finally, the patient gets some relief only in the forced vertical position - the state of orthopnea. In this case, dyspnea becomes for the patient the most serious symptom of heart disease. For severe forms of CHF is characterized by the development of excruciating dyspnea at night( see below "orthopnea" and "cardiac asthma").Very often patients avoid position on the left side, as this causes unpleasant feelings on the side of the heart, which they usually can not describe well, and dyspnea increases( it is assumed that in this position the dilated heart is closer to the anterior chest wall).Many patients with CHF relieve being left in front of an open window.
With the development of central nervous system hypoxia in severe CHF and especially in cases complicated by atherosclerosis of the cerebral arteries, periodic Cheyne-Stokes respiration may occur.
Orthopnea ( orthopnoji from Greek orthos - "direct" and pnore - "breathing" - high degree of dyspnea with involuntary( semi-sitting or sitting) position of the patient.) Orthopnea is not only a highly specific symptom of CHF, but also its objective sign, Patients with severe heart failure often sit in the armchair, on the bed( if they still have the strength to sit down), lowering their legs, leaning forward, leaning on the back of the chair, pulling up the table or reclining, dropping onto the pillows( the high head is created with a few pillows(in cases of untreated or "refractory" heart failure), severe dyspnea causes the patient to spend all the time - day and night( only this way he can forget himself for a short while)He wakes up from a feeling of lack of air if the head slides off the pillows, sleepless nights can last for weeks until the patient is relieved from CHF therapy. This phenomenon is especially characteristic for the failure of the left heart. Orthopnea is explained by the fact that in the vertical position of the patient there is a movement of blood( deposition in the veins of the lower part of the trunk and limbs) with a decrease in the venous return to the right atrium, and, consequently, the small circle of blood circulation becomes less full-blooded. Improvement of respiratory function in the vertical position is facilitated by the creation of better conditions for the movement of the diaphragm, and also for the operation of the auxiliary respiratory muscles. Orthopnea usually disappears( or becomes much less pronounced) with an increase in right ventricular heart failure secondary to left ventricular.
Cardiac asthma ( from the Greek asthma - "choking, heavy breathing") - acute asthma coming from the "heart" patient. The attack of severe cardiogenic dyspnea, reaching the degree of suffocation, indicates an acute left ventricular heart failure( the most striking clinical manifestation of interstitial pulmonary edema), which can develop in the situation of the absence of existing CHF and be the first manifestation of heart dysfunction. Nevertheless, most cardiologists report a high positive predictive value of cardiac asthma in the diagnosis of CHF.Cardiac asthma can occur at any time of the day, but more often develops at night in a horizontal position. In this situation, blood is discharged from the depot, the so-called hidden edema - extracellular fluid accumulated during the day in the tissues of the predominantly lower half of the body, due to an increase in venous pressure, is transferred to the vascular bed, and weakening of the respiratory function, a decrease in gas exchange, an increase in the tone of the vagus nerveand bronchoconstriction. The patient awakens( if before he could fall asleep) usually after nightmarish dreams with a feeling of suffocation, tightness in the chest, fear of death, and forced to sit in bed. He is afraid to move, keeps his hands on the bed, breathes slowly or rapidly( respiratory movements are unimpeded!), Often with a cough with serous sputum. If a simple inspiratory dyspnea in a patient with CHF may decrease after the patient occupies an upright position on the edge of the bed, lowering his legs, then in the case of acute left ventricular congestion, severe shortness of breath and cough often persist in this position. The main cause of cardiac asthma is the discrepancy between LV dysfunction and a satisfactory right-ventricular "pump" function in the pulmonary circuit with the inconsistency of Kitaev's reflex. If active therapy of heart disease is not carried out, then once started, attacks of cardiac asthma tend to recur. With the weakening of the contractility of the right ventricle, the adherence of the insufficiency of the tricuspid valve( this gave reason to call it the "safety valve of the heart") and with the development of chronic stasis morphological changes in the lungs, as well as sclerosis of the branches of the pulmonary artery, when the inconsistency of the Kitaev's reflex loses its clinical significance, relapses of cardiac asthma usually cease or their frequency is reduced. Among doctors, it is common to erroneously imagine that cardiac asthma is one of the criteria for stage IIB of CHF, whereas in the progression of heart failure from stage IIA to stage II, the urgency of asthma attacks( acute heart failure!) Becomes less.
Cough ( tussis).Dyspnoea in patients with chronic left ventricular heart failure often accompanies( especially at night) a cough, dry or unproductive with mucus difficult to separate sputum( in patients with acute left ventricular heart failure sputum is usually not viscous, easily excreted as a liquid, foamy liquid).Cough( this reflex act) is due to swelling of the mucous membrane of the "stagnant" bronchi( bronchitis cyanotica) or irritation of the recurrent nerve, an enlarged left atrium. Blood overflow of small vessels of the lung can be accompanied by diapedesis of erythrocytes or even a small hemorrhage and the appearance of hemoptysis( impurity of blood in the sputum).At a microscopy in such sputum besides erythrocytes the so-called "cells of cardiac defects"( hemosiderophages) can be found out.
Rapid fatigue, according to the IMPROVEMENT study, is the second after a shortness of breath for the sensitivity symptom of heart failure, which is found in most patients even with initial CHF events. Nevertheless, in many guidelines for physicians of weakness or increased fatigue in patients with CHF, unfair attention is paid little attention. Sometimes even this symptom is not referred to the main complaints of a patient with CHF, but to "general"( along with sweating, dizziness, irritability).There is no precise data on the specificity of the symptom under discussion, but it seems to be small, since it can be observed in many other diseases. As with the dyspnea of the pathophysiology of rapid fatigue, there is no trivial explanation. It should be noted that dyspnoea caused by stagnation in a small circle of blood circulation is often an early sign of diastolic CHF, and increased fatigue, which is associated with impaired blood supply to skeletal muscles, is most common in systolic CHF.Despite the fact that, traditionally, the central role in the development of heart failure plays a central role in the development of CHF, the peripheral blood flow disorder( in this case, skeletal muscle) is becoming increasingly important in its pathophysiology.
Heart palpitations ( palpitatio cordis) is the third most common symptom of CHF, which is expressed in the feeling of sickness of each contraction of one's heart. More often the palpitation is felt at a tachycardia( from here a synonym - warm "race"), but can be and at normal frequency of intimate or cardiac reductions and even a bradycardia. Apparently, not only the frequency of heart contractions, but also their nature and the state of the nervous system( persons with increased nervous excitability of the nervous system complain about heartbeat more often) is important for the palpitation. It is known that under normal conditions a person does not feel the activity of his heart as the motor activity of other internal organs, since most of the reflexes from the somatic organs close in the reflex arcs of the regions of the central nervous system located below the cortex of the cerebral hemispheres and, therefore,sensory perception. The change in the strength and quality of these reflexes in diseases of the cardiovascular system leads to the fact that they reach the cerebral cortex. However, sometimes with severe heart lesions, rapid and severe contractions, which are evident from the concussion of the chest wall, there are no complaints about the heart beat.
In the initial stages of CHF, the heart rate at rest does not deviate from the norm, and tachycardia occurs only with physical exertion, but unlike the physiological increase in heart rate in patients with heart failure, it normalizes not after termination of the load, but 10 minutes later. With the progression of heart failure, palpitations and tachycardia are noted and at rest. Tachycardia is a compensatory hemodynamic reaction aimed at maintaining a sufficient shock level( the mechanism of Boudich) and a minute blood volume, the effectiveness of which is given by most researchers to a low score( with the exception of situations with insufficient heart valves) - quickly becomes untenable, leading to an even more fatigue of the myocardium. In patients with CHF, tachycardia is explained by humoral( activation of the sympathoadrenal system, etc.), reflex( by the Bainbridge reflex with proliferating hollow veins) effects on the heart, but can sometimes be associated with taking medications( for example, nitrates or short-acting calcium antagonists dihydropyridinenumber), abuse of strong coffee, tea, tobacco smoking.
Patients with CHF can also experience "interruptions" in the heart, heart failure with its subsequent strong impact, sudden increase in the heart rate and other subjective manifestations of rhythm and conduction disorders.
Edemas ( from the Greek oidax - "pukhnu" in the Latin oedema - "swelling, edema"), detected by patients with CHF, indicate that the volume of extracellular fluid is increased by more than 5 liters.and the stage of "hidden edema" has already been passed. Hidden swelling can be detected by weighing or by McClure-Aldrich test to increase the rate( normally 40-60 min) of 0.2 ml saline solution( in the classical version 0.8% NaCl solution), injected intracutaneously with a thin needle into the most superficial layer of the epidermis( the tip of the needle should be visible!) with the formation of a "lemon peel" usually on the volar surface of the forearm. Also about hidden swelling is indicated by a sharp increase in diuresis after the use of diuretics or cardiac glycosides.
There is a pronounced dependence of edema on the position of the body: they propagate from the bottom up. Cardiac edema is localized first only in the sheltered places - symmetrically, in the areas located most low. In the early stages with the patient in a vertical position( the debilitated swelling of the patient lying on the back), there is only swelling of the dorsal surface of the feet, which appears in the evening and disappears by morning( a characteristic complaint is that "the shoes become tight by evening").As they develop, they spread to the ankle joints( in the condyles), then ascend to the lower leg and up, grab the arms and genitals. In the future, swelling of the legs becomes permanent and they spread to the lower abdomen and waist up to the anasarca( on the face, neck and chest edema usually does not happen!).If the patient is transferred to bed rest after already developed persistent edema of the legs, then they can significantly decrease and even disappear, but they appear or increase( move) in the lumbosacral region. With the prolonged existence of edema, trophic skin changes occur, cracks( with massive swelling, the skin often bursts and fluid leaks out of the ruptures), dermatitis.
The pathogenesis of edema in patients with CHF can be satisfactorily explained on the basis of the hydrodynamic views of Starling. However, the mechanical( hydrodynamic) factor is not unique, and sometimes, apparently, the main one. The causes of edema in these patients are very diverse - a whole complex of neurohumoral, hemodynamic and metabolic factors is important.
Edema is traditionally associated with a deficiency of the right ventricle, but they can also be with decreasing left ventricular contractility. Edema, caused mainly by right ventricular failure and venous congestion, usually appear later than the liver increases, they are vast, dense to the touch, the skin over them is thinned, cyanotic, with trophic changes. Edema with left ventricular dysfunction occurs earlier than venous stasis, small, soft, shiftable, located on the remote parts of the body, the skin above them is pale. If the first kind of edema depends on venous congestion, edema of the second kind is the result of hypoxemic disorders, the porosity of the walls of the capillaries as a result of slowing blood circulation.
Edema( both in anamnesis and according to the physical examination) is a low-sensitivity sign of CHF and can be associated with impaired local venous or lymphatic outflow( in particular, varicose veins with venous insufficiency II-III degree), liver and kidney diseases, etc. Therefore, the cardiac genesis of edema is established only on the basis of a comprehensive examination of the patient.
The severity of ( with slow stagnation) or pain( with rapidly developing congestion) in the right upper quadrant in patients with right ventricular heart failure usually precedes the appearance of edema, since the liver is the first to respond to the failure of the right side of the heart. These symptoms are caused by the proliferation of the liver capsule with blood overflow of the liver veins and capillaries( with a rapid increase in the liver, the stretching of the glisson capsule is accompanied by a rather intense pain in the right hypochondrium).With the progression of CHF, prolonged stagnation( "nutmeg liver", cardiac cirrhosis), symptoms of a violation of the liver function - icterism of the skin and mucous membranes. There is portal hypertension - at the initial stage of the patient is worried about the feeling of bloating and overflow of the abdomen, then he notices the increase in the abdomen in the volume( due to the accumulation of ascitic fluid).In this case, extremely rarely complaints of a patient with CHF may be supplemented with a feeling of heaviness in the left hypochondrium( due to an increase in the spleen).
Nausea, vomiting, decreased appetite, constipation, flatulence and other symptoms of gastric and intestinal dyspepsia are almost constant companions of congestive heart failure. The functions of the gastrointestinal tract in CHF are always violated to a greater or lesser degree due to both hypoxia and reflex effects. Often, dyspeptic disorders are a manifestation of side effects of drugs used to treat heart disease( in particular, aspirin, cardiac glycosides).
Decrease in diuresis ( naturally not during the period of convergence of edema) and nocturia. Impaired renal function is due to a significant( almost double) decrease in renal blood flow, reflex spasm of renal arterioles and increased renal vein pressure( the mechanism of these phenomena was discussed above).As a result of a simultaneous( but not uniform) decrease in glomerular filtration and an increase in tubular reabsorption of sodium and water, the daily amount of urine decreases, and urine becomes concentrated with a high relative density. Urine is excreted mainly at night due to some improvement in the blood supply of the kidneys at rest and horizontal position, the exit of the edematous fluid into the blood at this time. In addition, the central disturbance of the regulation of the rhythm of diuresis seems to be important.
Changes in body weight. Sudden gain in weight( sometimes 2 kg or more in 2-3 days) is a sign of increasing decompensation of cardiac activity. The multiple changes in metabolism in patients with CHF, barely noticeable at the beginning, in the III stage lead to exceptionally severe malnutrition of all tissues and organs - a progressive decrease in body weight occurs( so-called cardiac cachexia develops, which for some time is masked by the presence of edema).
Complaints of patients with CHF on decrease in mental performance and mood, irritability, sleeplessness at night, and then drowsiness during the day , are associated with early changes in the functional state of the central nervous system following a circulatory disorder.
The study of the mechanisms of the progression of CHF is a subject of intensive scientific searches all over the world. The available knowledge about the role of chronic activation of neurohormonal systems, endothelial dysfunction, disturbed cardiomyocyte status, etc., provide the key to solving many practical questions of treatment of patients with CHF.Now it is rare to trace the natural course of CHF, since pathogenetic pharmacotherapy largely changes it. As a result, there appears a new syndrome-treated heart failure, which differs significantly from the syndrome of untreated heart failure. However, unfortunately, often and the heart failure is progressing. If the doctor can clearly present the mechanisms of progression of heart failure in a specific clinical situation, it provides him invaluable help in individual therapy and prevention of CHF.
Basic mechanisms of progression of heart failure:
1. Continuing myocardial damage:
2. Myocardial remodeling:
3. Accompanying arrhythmias:
4. Medications:
The rate of progression of CHF depends on the nature of the pathological process - whether it is possible to establish its nature and effecton it, whether it is represented by a single lesion( as in viral myocarditis) or repeated( as in alcoholic cardiomyopathy).However, in all cases of CHF with severe LV dysfunction, the clinical condition of the patient may worsen and without the influence of any additional factor that causes damage to the myocardium.
Background. Attempts to make a meaningful classification of CHF go back to the distant past. Even Jean Nicolas Corvizar, when he measured heart sizes( using percussion), divided heart failure into two types: with the presence of heart dilatation( including aneurysms) and with the absence of dilatation. However, only recently has a thorough differentiation of HF started taking into account the mechanisms of its development. Basically, this is due to the wide introduction in clinical practice of the latest informative ultrasound, radionuclide, radiopaque test methods and magnetic resonance imaging.
The first classification of CHF in our country( in fairness, it should be noted that it dealt with chronic circulatory failure) was proposed by ND Strazhesko and V. Kh. Vasilenko and approved at the 12th All-Union Congress of Physicians in 1935. Thisclassification, which covers the manifestation of CHF in the dynamics, the degree of disturbance of the general state of the organism and the initial site of the lesion of the cardiovascular system, has been showing its viability for almost 70 years( Table).
Traditionally, in accordance with this classification of stages of CHF to a patient who has a heart failure syndrome in the first day of hospitalization, corresponding to Stage II, in the diagnosis and after discharge from the hospital, the stage of CHF that he had initially showed is exposed, even if against a background of complex treatment of the patient alreadyhas formal signs of heart failure not II B, and IIA or I stage.
This "rigidity" of the classification of CHF ND Strazhesko and V. Kh. Vasilenko often served as the subject of criticism of leading experts in heart failure, as it creates difficulties in assessing the severity of the disease and determining the degree of the patient's ability to work.
Table. Classification of chronic circulatory insufficiency
Indeed, a patient with an ansarca hospitalized for the provision of qualified or specialized care should be prescribed with the diagnosis of "CHF IIB stage", even if during the treatment the patient at rest was able to eliminate all without exception symptoms and clinical signs of heart failure,since such a diagnosis is the most solid justification for active combination therapy. But at the outpatient stage there will inevitably be a need to "rest" CHF in order to be able to correctly assess the severity and prognosis of the disease, looking for a clinical diagnosis( and not for an outpatient card), determine the actual work capacity and prescribe the appropriate treatment( it is clear thata patient with Stage I CHF to control symptoms of the disease requires less activity of treatment than a decompensated patient).It is even more difficult to understand why a boy with a rheumatic mitral malformation, weighed down by left ventricular heart failure, and after an effective surgical treatment that allows us to actually talk about recovery, the end of life in medical documents should be CHF IIA stage.
Table. Classification of
Table. Classification of heart failure
Table. Stages of heart failure
CH - heart failure.
In our country, the classification of CHF, which takes into account the division into stages and functional classes, was different: with the repeatedly updated classification of stages of CHF ND Strazhesko and V. Kh. Vasilenko are well acquainted with several generations of doctors who applied it in their everyday practicalactivities. Functional classes of CHF were isolated with rare exception only by clinicians in scientific research institutes and medical universities. The situation changed when experts from the Society of Heart Failure Specialists proposed a combined classification for discussion( Table).In the official commentary of the Society of Heart Failure Specialists, the classification under consideration is drawn attention to the continuity of this edition of the classification with the classifications of ND Strazhesko and V. Kh. Vasilenko adopted in Russia( the classification "lost" all the additions to the classical version of the 1935 classification,which were made for its long history, but it introduced new concepts - "adaptive remodeling of the heart and blood vessels", "disadaptive remodeling of the heart and blood vessels", etc.), and NYHA, which usesEntire world( and its changes affected).
Table. Classification of CHD
The classification is divided into two parts: the right one - functional and the left one - structural( morphological), which are specially arranged in the form of steps to emphasize the originality and independent significance of each part. In this case, the stages are located below the corresponding functional classes, since, according to the authors of the classification, "functional" disorders occur somewhat earlier than "structural" ones.
There are two opposing views on the diagnosis of CHF.Supporters of the former proceed from the proposition that heart failure is a clinical syndrome. In this regard, in their opinion, a detailed assessment of the history of the disease and a complete clinical examination are of major importance in the diagnosis of CHF.It is believed that CHF syndrome is diagnosed fairly well on the basis of clinical data only and, therefore, it is not necessary to use the entire arsenal of additional tests and studies when diagnosing.
The clinical stage of diagnosis is undoubtedly very important( necessary) in the recognition of CHF.
Table. Symptoms most typical for patients with CHF
The results of the Russian study indicate that the most frequent symptom of heart failure in real practice is shortness of breath - 98.4%, the second and third most frequent symptoms are fatigue - 94.3% and palpitation - 80.4%, and not swelling or wheezing, whichthey take on a much more modest position in the list of symptoms.
Table. Sensitivity, specificity and prognostic significance of clinical signs and symptoms in the diagnosis of CHD
The same can be said for another "popular" finding in CHF - fatigue. Often, dyspnoea and fatigue during exercise are taken as manifestations of CHF, while similar complaints can be made by patients with obesity, respiratory diseases, anemia, hypo- and hyperthyroidism, asthenia after infection and many other diseases. Finally, the same symptoms with sufficient physical effort can be observed in healthy, but untrained people, especially older streets. In addition, it should be recalled that many of the symptoms of heart failure are highly subjective.
The results of a physical examination should also not be overestimated, since the signs of CHF that are detected while possessing a rather high specificity are not sensitive( see Table) - during examination, palpation, percussion and auscultation, the doctor may not reveal any significant changes( especially at rest) until the disease reaches a certain degree of severity.
Thus, the results of numerous studies indicate that the accuracy of clinical diagnosis of CHF leaves much to be desired. There is reason to believe that the results of the Framingham study will facilitate the clinical diagnosis, during which a number of criteria( primary and additional) of CHF were formulated( Table).The presence of two main criteria, or one basic and one or two additional ones, allows one to assume with sufficient confidence that CHF is present in the patient.
However, since on the basis of complaints, the history( if the patient does not have a detailed extract from the clinic with a high level of diagnosis) and a general examination, the diagnosis of CHF can only be taken into consideration, but do not put it with certainty - in most cases an extended examination is required.
The International Manual on HF states: "It should be a rule not to be limited to clinical evaluation of signs and symptoms of heart failure, but to try in one way or another, for example, by echocardiography, to investigate. .. LV function before diagnosing heart failure... ".
Table. Diagnostic criteria of CHF
According to the recent Recommendations of the European Society of Cardiology, as well as the National Recommendations for the diagnosis and treatment of CHF, the determination of CHF is possible on the basis of three key criteria:
Table. Definition of CHF
Presence of criteria 1 and 2 is mandatory in all cases of the heart must necessarily be detected at rest! This is due to the fact that, for example, a low ejection fraction or a change in the diastolic function of LV during exercise may be signs of not coronary heart failure, but coronary insufficiency. In the latter case, it is a case of a load-induced acute ischemic dysfunction.
Details of the main criteria used in the determination of CHF are presented in Table.
Only positive dynamics of the patient's condition during treatment with drugs used to treat
Table. Criteria used in the determination of CHF
Note. ECG - electrocardiography;DZLA - pulmonary artery wedge pressure;MNP is a brain natriuretic peptide.
CHF is not enough to diagnose this syndrome, however, the diagnosis becomes more reliable if, on the background of such treatment( for example, the appointment of diuretics), it is possible to achieve a sufficiently rapid weakening of symptoms and / or signs of heart failure. In most cases, do not start therapy until there is sufficient confidence in the correctness of the diagnosis.
Anamnesis collection( all of its types) is an important part of the examination of a patient with a cardiovascular disease. At the same time, they reveal: risk factors or anamnesis of IHD;presence of arterial hypertension, diabetes, valvular pathology;family history of cardiomyopathy;the presence of a recent pregnancy, a viral( "cold") disease, risk factors for AIDS and associated diseases;thyroid gland diseases and other systemic diseases;the presence and extent of alcohol dependence. When collecting a clinical history, it is important to find out the features and sequence of the appearance of symptoms in this patient. It is always important to determine the time of occurrence of each symptom and its relation to the estimated time of heart disease, the likely provoking factors of the first manifestation and exacerbations of CHF, indications of therapeutic interventions and their effectiveness.
If possible, the laboratory and instrumental and other clinical studies that were conducted in the patient during the present illness, extracts from old case histories, copies of analyzes, electrocardiograms, etc. should be clarified. Obtained information often becomes one of the keys to the recognition of CHF and largely determines the starting choice of medical actions.
It is necessary to ask the patient about physical and intellectual development, the transferred diseases, bad habits, living conditions, unfavorable professional factors. It is important to get information about the parents of the patient, relatives of the I, II degree of kinship, to find out their age, diseases, and if they died, then what and at what age.
The objective survey data can be varied.
At general examination of a patient with a moderate CHF at rest, to identify any signs of heart disease, as a rule, fails. When examining a patient with a manifestation of CHF, the following signs can be found:
1. Forced position of the patient( dyspnea, orthopnea).
2. Cyanosis( Latin cyanosis - "cyanosis" from the Greek kyaneos - "dark blue") - cyanotic staining of the skin is a frequent sign of CHF.Nevertheless, we are not aware of qualitative studies in which the sensitivity and specificity of this clinical feature were accurately established. The appearance of cyanosis in patients with CHF is associated with a decrease in blood flow velocity and an increase in oxygen uptake in tissues, as well as with insufficient blood arterialization in the pulmonary capillaries, as a result of which the content of reduced hemoglobin in the blood increases( it has a blue color).The degree of severity of cyanosis and its character also depend on the functional and organic changes in small arteries( angiospasm, obliterating endarteritis, etc.), the diameter of small venules, the activity of arterio-venous anastomoses( the phenomenon of "short circuit").The first manifestations of cyanosis in patients with CHF are called acrocyanosis( from the Greek asporus, the limb + kyaneos - dark blue), that is, the cyanosis of the parts of the body most distant from the heart( the tip of the nose, earlobes, lips, fingernails).The occurrence of acrocyanosis is mainly due to a slowing of the blood flow and therefore it is peripheral( it is often called peripheral cyanosis).To distinguish peripheral cyanosis from the central respiratory disease caused by the disease( it is necessary to remember the functional and structural changes in the lungs in patients with chronic left ventricular failure leading to a violation of oxygen saturation, which significantly complicates the differential diagnosis), can be achieved by two methods:
With increasing heart weakness and oxygen deficiency, cyanosis increases( from subtle cyanosis to dark blue color) and becomes widespread( all skin and mucous membranes acquire a bluish tinge) - central cyanosis, when arterial oxygen saturation drops to 80% and lower. According to its pathophysiological nature( violation of arterialization of the blood) and clinical manifestations, the latter is very close to that observed in patients with respiratory diseases. Especially sharp central cyanosis is observed in patients with congenital heart defects in the presence of arteriovenous communication( "black heart patients").To the so-called vices of the "blue type" is the tetralogy of Fallot( stenosis of the output part of the pulmonary artery, defect of the interventricular septum, dextroposition of the aorta, right ventricular hypertrophy), Eisenmenger complex( subaortic defect of the interventricular septum, "sitting" above this aorta defect, hypertrophy and enlargementright ventricle, normal or enlarged pulmonary artery), Ebstein's disease( dysplasia and displacement of the tricuspid valve in the right ventricular cavity), pulmonary artery stenosis, general arterial( artopulmonalny) trunk, atresia of the tricuspid valve, embodiments transposition of the great vessels, defective interatrial and interventricular septum. Cyanosis can also occur when poisoning with substances forming methemoglobin, sulfamoglobin( sulfanilamides, phenacetin, aniline, nitrobenzene, bertholets salt, arsenic hydrogen, nitrates and nitrites, etc.).
3. Pale skin and mucous membranes in patients with CHF can be combined with cyanosis( the so-called "pale cyanosis") with aortic heart defects( stenosis of the aortic aorta, aortic valve failure), collapse, heavy bleeding, infective endocarditis. With stenosis of the mitral orifice, paleness is combined with a purple-red "blush" on the cheeks - "mitral butterfly."
4. Jaundice( Greek icteros).Jaundice staining of the skin and mucous membranes( primarily sclera) in patients with severe chronic right ventricular heart failure is due to the development of congestive fibrosis( "cardiac cirrhosis") in the liver. Jaundice in patients with CHF usually expressed slightly( rarely up to 68-85 μmol / l).However, sometimes against a background of chronic stagnation in the liver, jaundice quickly and significantly increases - "bilirubinemic crisis".The latter is associated with paroxysmal deterioration of intrahepatic circulation, which develops after decompensation of cardiac activity. With infective endocarditis, the yellowness of the skin is combined with its pallor, and then the color resembles the color of "coffee with milk."In such cases, petechiae with a pale center( the Lukin-Liebman symptom) can be found on the skin and especially on the conjunctiva of the lower eyelid.
5. "The face of Corvizar"( Jean Nicolas Corvisart) is typical for a significant untreated or refractory CHF.It is swollen, flabby, yellowish-pale with a bluish tinge, its expression is apathetic, indifferent, drowsy, eyes sticking together, dull, mouth - always half open, lips - cyanotic.
6. Fingertip "fingers" [Pierre Marie-Bamberger syndrome of hypertrophic osteoarthropathy] occurs with CHF, which develops in patients with infective endocarditis, with some congenital heart defects.
7. Edema in patients with CHF can be so pronounced that it is already determined by general examination. However, even before the appearance of pronounced edematous edema appears, palpability( from Latin pastosus - doughy, flabby) of tissues( especially in the region of the ankles, on the back of the foot, legs) can be noted by touching -2 min) disappearing fossa, which is only palpable. Massive, widespread edema of the subcutaneous fat of the trunk and extremities, usually accompanied by ascites and hydrothorax, is called anasarka( from Greek and paña, up, + sane, sarcos - meat).Skin with edema, especially the lower extremities, pale, smooth and tense. With long-lasting swelling, it becomes rigid, maloelastic and acquires a brown tint due to diapedesis of red blood cells from stagnant capillaries. With pronounced swelling in the subcutaneous tissue of the abdomen, linear gaps resembling scars after pregnancy can appear. Comparison of the sensitivity and specificity of edema, detected by the patient's complaints, and those established by physical examination, is presented in Table.
8. Cardiac cachexia( from the Greek cachexia - exhaustion).Significant weight loss and development of cachexia are observed in the far-advanced stage of CHF and in the case of treated cardiac decompensation usually indicates a final( irreversible) stage of the development of the disease. A patient with an anasarka as it were "dries up" - a "dry dystrophic type" according to V. Kh. Vasilenko. At the same time muscle atrophy is combined with a significantly increased( due to ascites) stomach. Cachexia is a consequence of:
9. Swelling and pulsation of the cervical veins, an enlargement of the veins of the hands that do not subside when the arm rises. In a healthy person, the veins of the neck can be seen only if it is in a recumbent position. If the overflow and expansion of the cervical veins is also noticeable in the vertical position, then there is a general( right ventricular heart failure, as well as diseases that increase the pressure in the chest and obstruct the outflow of venous blood through the hollow veins) or local( compression of the veins from the outside -scars, etc., or its clogging with a thrombus) venous congestion. And if in severe diseases of the respiratory system cervical veins swell only when exhaled, due to increased intrathoracic pressure and difficulty in the flow of blood to the heart, then with CHF swelling of the cervical veins is constantly observed. The Austrian pathologist G. Gertner proposed for clinical practice the simple reception of an approximate determination of the level of pressure in the right atrium - the higher it is necessary to raise the hand so that the superficial veins of the hands fall, the higher the pressure in the right atrium( the height the arm rises fromthe level of the right atrium, expressed in millimeters, approximately corresponds to the value of venous pressure).
Patients with CHF in the neck can see pulsation of the jugular veins - a viral pulse. Swelling and decay of the jugular veins during one cardiac cycle is due to the dynamics of outflow of blood to the right atrium in different phases of the systole and diastole of the heart( slowing of the blood flow in the jugular vein and its some swelling during the systole of the atria and acceleration during the systole of the ventricles with its collapse)207, 213].In healthy people, a physiological negative venous pulse is usually not visualized and can be analyzed only when it is graphically recorded. In case of obstruction of the outflow of venous blood into the right atrium, the pulse of the pulse is detected during a routine examination - a pathological vascular pulse. The pulsation of the jugular veins coinciding with the systole of the ventricles( carotid artery pulsates outside of the jugular veins) is called a positive venous pulse and usually indicates a failure of the tricuspid valve - the 1st symptom of Bamberger I.Nevertheless, the cause of a noticeable pulsation of the cervical veins may be hypertrophy and left ventricular failure, even in the absence of deficiency of the right chambers, due to the transfer of pressure through the interventricular septum.
To determine the nature of the pulse, the jugular vein should be pressed with a finger. If the vein ripple is retained below the compression site, the vein pulse is positive, if not, negative.
10. Symptom Plesh( Plesh) - swelling of the jugular veins with pressure on the liver in the direction from the bottom up( hepatic-lobular reflux), which is observed with severe right ventricular heart failure( in particular, when the tricuspid valve is inadequate).
11. Palpation and percussion of the heart in patients with CHF make it possible to detect signs of cardiomegaly - displacement of the apical impulse( normally located in the 5th intercostal space by 1-1.5 cm medial to the left mid-clavicular line) to the outside of the left mid-clavicular line andbelow the fifth intercostal space;diffuse( more than 2 cm2) character of apical impulse( with concentric hypertrophy of LV - "lifting", with eccentric hypertrophy - "domed");the so-called cardiac shock( pulsation of the enlarged right ventricle to the left of the sternum, extending to the epigastric region);expansion of the boundaries of relative dullness of the heart. To determine the proper maximum heart size, the patient's height is divided by 10 and subtracted 3 cm for the longus and 4 cm for the diameter. With the development of heart disease in childhood, signs of cardiomegaly can be detected even when examining the heart area - bulging chest( "heart hump"),
12. Tachycardia, arrhythmia, weakening of the sonority of heart sounds( it is necessary to exclude the hydropericardium) and the proto-diastolic rhythm of the gallop caused by a pathological( significantly strengthened) III tone are often heard in CHF, not being specific for it. It is worth noting that pathological III tone often occurs in patients with a reduced systolic function, whereas IV tone can be determined if the ventricular wall compliance( diastolic dysfunction) is compromised. With auscultation, it is also possible to detect "direct" and additional signs of impaired valvular heart apparatus. Listening to heart sounds may be a key issue in the diagnosis of heart disease underlying CHF, or may indicate the presence of functional( relative) mitral and tricuspid insufficiency as a result of dilatation of the ventricles and / or atria( hence, the valve ring in the area of the atrioventricular junction);or dysfunction of papillary muscles.
13. Systemic arterial pressure is increased in patients who are in a state of acute decompensation, or in poorly controlled arterial hypertension, but for a late stage of the disease, low blood pressure with low pulse pressure is more characteristic. There is an opinion that arterial pressure with prevalence of left ventricular heart failure decreases, and with prevalence of right ventricular heart failure may slightly increase( "congestive hypertension").Nevertheless, the validity of such a judgment is not always confirmed in clinical practice.
Symptom Katzenstein( M. Katzenstein) - after compression of the femoral artery, the blood pressure in a healthy person rises, and in the presence of weakness of the heart muscle - decreases.
14. Physical examination of respiratory organs in patients with CHF may reveal signs of pulmonary congestion with wet and dry wheezing, as well as the presence of fluid in the pleural cavity.
The appearance of silent damp wheezing, mainly in the inspiratory and / or crepitating phase( crepitatio-crack), is associated with high pressure in the pulmonary veins, capillaries and accumulation above the basal parts( especially on the side of the patient) of the lungs in patients with left ventricular heart failurea small amount of secretion in the lumen of small bronchi( small bubbling rales) or alveoli( crepitation).In patients with extremely severe left ventricular decompensation and cardiac asthma, in addition to wet wheezing( up to "rattling" wheezing in the later phase of pulmonary edema), which are heard over all pulmonary fields, dry rales of high tonality due to the fullness of bronchial mucosa andaccumulation in the lumen of bronchi viscous transudate. At the same time, such wheezing can be caused not only by left ventricular failure( to exclude obstructive bronchial diseases!).
The increase in pleural capillary pressure in CHF and the penetration of fluid into the pleural cavities lead to the accumulation of pleural effusion( in the right pleural cavity more often than in the left one), which can be established with the help of known physical diagnostic techniques( lagging of the "sick" half of the chest in the actrespiration, a sharp weakening or lack of vocal tremor over the area of fluid accumulation, percussion is determined by a dull sound or absolute dullness, with auscultation, breathing and bronhophonia abruptly weakenedene or absent).It is common knowledge that since the pleural veins are draining into the veins of both the large and small circles of the circulation, hydrothorax develops in both left ventricular and right ventricular heart failure. However, AG Chuchalin( 215) believes that patients with pulmonary hypertension with signs of right ventricular heart failure do not accumulate fluid in the pleural cavity, and hydrothorax is associated with left ventricular dysfunction!
15. Hepatomegaly is the first symptom of congestive liver and represents a classic manifestation of right ventricular failure.
The liver is called a "reservoir" for stagnant blood and a right atrial manometer. Elevated central venous pressure is transmitted to the hepatic veins and interferes with the blood flow to the central part of the lobule - central portal hypertension develops. The latter is associated with hypoxia, which eventually causes atrophy and even necrosis of hepatocytes with replacement fibrosis and a violation of liver architectonics( up to the development of cardiac cirrhosis of the liver).
In the initial period of right ventricular heart failure, the liver( painful on palpation!) Only protrudes slightly from under the costal arch, its edge is rounded, smooth, the surface is soft. Characteristic variability of its dimensions, associated with the state of hemodynamics and the effectiveness of treatment. Subsequently, the organ can reach enormous sizes, "drop" below the scallop of the ilium. Plesh's symptom is determined. The edge of the liver is sharpened, the surface becomes dense. At the same time, the intensity of pain in palpation may decrease. Cardiologists and hepatologists note the variety of clinical manifestations of the stagnant liver: a clinical situation with severe CHF, manifested by an ansarca and ascites and a slight increase in the liver, and, on the contrary, pronounced hepatomegaly with poorly expressed other phenomena of stagnation is possible.
With prolonged right ventricular heart failure, as for example in patients with tricuspid valve disease or chronic constrictive pericarditis, splenomegaly can develop simultaneously with hepatomegaly.
Systemic venous hypertension may also be manifested by pulsation of the liver. The true venous( for example, in patients with a deficiency of the right atrioventricular valve) or coincident with the apical push of the arterial( for example, in the absence of aortic valves), the pulsation of the liver itself should be distinguished from the so-called transfer pulsation in cases of cardiac contraction.
16. Ascites( Latin ascites - abdominal hydrocrack from Greek ascos - a leather bag for wine or water) in a patient with right ventricular heart failure develops as a result of fluid exudation from the veins of the liver and peritoneum, the pressure in which is increased. As a rule, massive ascites is diagnosed in patients with lesion of the tricuspid valve or chronic constrictive pericarditis. Ascites that develop after a long period of edema in patients with cardiac cirrhosis are often refractory to digitalis-diuretic therapy.
During the examination in the upright position of the patient, the abdomen with pronounced ascites looks saggy;in the horizontal position the stomach is spread out, and the lateral sections of it bulge( "frog stomach").With the so-called intense ascites, the shape of the abdomen depends little on the position of the patient( the fluid in the cavity of the peritoneum is so large that it does not move).The navel in the upright position of the patient makes it possible to distinguish the enlarged abdomen in ascites from that with significant obesity.
Symptom Conn( N. Conn) - a sign of pronounced edema of the scrotum in patients with ascites: the patient lies on his back with widely diverted legs.
Detection of a large amount of free fluid in the abdominal cavity( more than 1.5 liters) does not cause difficulties. A percussion examination of the patient's abdomen, which is in a horizontal position on the back, reveals dullness over the lateral areas, and in the middle - intestinal tympanitis. Moving the patient to the left side causes the blunt sound to move downwards, and it is determined over the left half of the abdominal cavity, and in the right flank - tympanic sound. To identify a small amount of fluid, percussion is applied in the standing position of the patient: in ascites, a blunt or blunted sound appears in the lower abdomen, disappearing in the clinostatic position.
Symptom of Pitfield I( R.L. Pitfield) is a sign of ascites: if a sitting patient with one hand produces percussion of a square muscle of the waist, the second arm, palpating the anterior abdominal wall, perceives weak oscillations.
The Journal of Heart Failure( №2, 2003) presents a modified V. Yu. Mareyev scale of assessing the clinical state of CHF, which consists of 10 categories and can be a good alternative to the test of a six-minute walk in the objectification of the functional class of CHF in the absence of opportunity forany reason to perform the last one:
I. Dyspnea: 0 - no;1 - under load;2 - at rest.
II.Has the weight changed during the last week: 0 - no;1 - increased.
III.Complaints about interruptions in the work of the heart: 0 - no;1 - is.
IV.In what position is in bed: 0 - horizontally;1 - with a raised head end( + 2 pillows);2 - 1 + night suffocation;3 - sitting.
V. Swollen cervical veins: 0 - no;1 - lying down;2 - standing.
VI.The wheezing in the lungs: 0 - no;1 - lower departments( up to 1/3);2 - up to the blades( up to 2/3);3 - above the entire surface of the lungs.
VII.Presence of a gallop rhythm: 0 - no;1 - is.
VIII.Liver: 0 - not enlarged;1 - up to 5 cm;2 - more than 5 cm.
IX.Edema: 0 - no;1 - pastosity;2 - edema;3 - anasarca.
X. The level of ADA: 0 - & gt;120 mm Hg.p.1-100-120 mm Hg.p.2 - & lt;120 mm. Art.
During the interview and examination of the patient, the doctor evaluates the clinical status for all 10 categories of the scale. Mathematical processing of the results of the study consists in counting the sum of scores corresponding to the severity of the clinical manifestations of CHF.In total, the maximum patient can score 20 points( "critical" CHF).0 points indicates complete absence of signs of CHF.The results obtained are evaluated as follows:
Etiological treatment and elimination of immediate causes of cardiac decompensation. Primary prevention of symptomatic chronic heart failure in the development of individual treatment tactics should take into account the etiological heterogeneity of the group of patients with CHF.Correctly selected treatment of the underlying disease underlying CHF, in many cases can significantly reduce the severity of manifestations of cardiac decompensation, and sometimes allows to completely rid them of the patient( for example, after a successful surgical correction of heart disease).First of all, we are talking about the treatment of ischemia and acute myocardial infarction, the prevention of reinfarctions, the careful identification and active treatment of people with arterial hypertension, the elimination of the causes of specific myocardial damage, timely correction of the pathology of the valves and heart defects.
In the clinical situation, when due to the presence of severe circulatory failure, radical treatment of the underlying disease is impossible, therapy should be aimed at reducing the clinical manifestations of CHF and creating conditions that would allow us to return to the issue of etiotropic treatment.
Unfortunately, despite the understanding that without influencing the underlying cause of CHF in many cases it is difficult to count on positive results of treatment, the format of this publication does not allow us, at least briefly, to dwell on the treatment of the main nosological forms leading to the development of heart failure. Let us just make recommendations of ACC / AAC on the prevention of manifest cardiac insufficiency in patients with various cardiovascular diseases, since it was prescribed in a timely manner to patients with a high risk of developing heart failure and asymptomatic stage of CHF( stages A and B according to the ACC / AAC classification, 2001) competent etiotropic and pathogenetic therapy, if it does not prevent the development of cardiac decompensation in 100% of cases, at least to a large extent pushes back its debut. In other words, given the fact that there are effective methods for treating many potential causes of myocardial damage and reducing the severity of damage, the main task should be not so much the treatment of existing CHF, but the prevention of its development.
The recommendations of the ACC / AAC experts are as follows:
The data on which the recommendations of the ACC / AAC experts on the level of evidence are based are ranked as follows: evidence level A - data obtained in several randomized clinical trials;Evidence level B - data obtained in one randomized clinical trial or in non-randomized trials;level of evidence C - the main source of recommendations is the agreed opinion of experts. Naturally, the recommendations based on the coincident results of several randomized, controlled clinical trials can be trusted to the maximum extent. Meanwhile, many of those "fundamental clinicians" who constantly talk about medical practice based on evidence( the so-called "evidence-based medicine"), in fact, are more likely to trust the opinion of an authoritative expert, sometimes known only to them. The rather low adherence of physicians of all links to modern principles of CHF therapy, the effectiveness of which has been proven in large controlled trials, is noted in the Recommendations of the European Society of Cardiology, which requires even greater educational efforts.
Recommendations for patients at high risk for CHF( stage A).Considering the main risk factors, at the stage A to reduce the risk of development of CHF, ACC / AAC experts offer the following main areas of prevention: 1) treatment of hypertension;2) encouraging cessation of smoking;3) treatment of lipid metabolism disorders;4) encourage regular exercise;5) preventing the consumption of alcoholic beverages, the use of narcotic drugs;6) application( according to indications) of ACE inhibitors. Recommendations have the following format:
Class I
Class III
Recommendations concerning patients with asymptomatic LV dysfunction( stage B).At Stage B of CHF, ACC / AAC experts recommend all the activities proposed for patients at high risk for CHF.Especially emphasizing the advisability of using in patients with asymptomatic LV dysfunction ACEI and [3-adrenoblockers. Recommendations have the following format:
Class I
Class IIa
Long-term therapy with systemic vasodilators in patients with severe aortic regurgitation( level of evidence B).
Class III
No less important than etiotropic therapy, have therapeutic measures aimed at eliminating some provoking factors - immediate causes of worsening of patients with CHF.Recall that among the most frequent of them are: non-compliance with patients prescribed regime( regarding the consumption of salt, liquid, physical activity, drug regimens, etc.);infection;alcohol consumption;acute coronary syndrome;pulmonary embolism;disorders of electrolyte metabolism( hypokalemia, hypophosphatemia, hypocalcemia, etc.);pregnancy and childbirth;the occurrence of paroxysms or a constant form of atrial fibrillation;dysfunction of the thyroid gland( including, caused by the reception of amiodarone);anemia;impaired renal function( eg, due to the use of a large number of diuretics);the appearance or growth of mitral or tricuspid insufficiency. In all cases, it is necessary to carefully study the pharmacological anamnesis, purposefully revealing the facts of the use of drugs that cause sodium and water retention( estrogens, androgens, chlorpropamide, glucocorticoids, etc.), which have a negative inotropic effect( verapamil, diltiazem, antiarrhythmic drugs I class, β-adrenoblockers in inadequately high doses), inhibiting the formation of vasodilating prostaglandins and endothelial factors( nonsteroidal anti-inflammatory drugs, glucocorticoids), prleading to an excessive decrease in preload( large doses of diuretics, ACE inhibitors, etc.).