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Differential diagnosis of heart failure

Table of contents
Differential diagnosis of heart failure
Heart failure at a chronic pulmonary heart
Biventrikulyarny heart failure of an illness of a cardiac muscle
Heart failure at myocarditis
Heart failure at a congestive cardiomyopathy
Heart failure at rare diseases
Heart failure at a heart amyloidosis
Heart failure at a mitral stenosis
Heart failure at defect of an interatrial partition
Heart failure at a myxoma of the left auricle
Heart failure at mitral insufficiency
Heart failure at an aortal stenosis
Heart failure at aortal insufficiency
Reasons and types of heart failure

Diagnostic work at the patient's bed with chronic heart failure is recommended to be begun with clarification of sequence of emergence of its most easily defined signs: hypostases, asthma, asthma, hepatomegalia. It is better to estimate the collected facts according to the scheme stated in the annex providing allocation of 3 types of heart failure: right ventricular, biventrikulyarny and left ventricular. Each of the specified types of heart failure is caused only by several diseases that facilitates the solution of the main diagnostic objective, establishment of the only reason of its development.

Heart failure at an ischemic disease and valve heart diseases begins, as a rule, with the asthma arising at physical efforts. Soon asthma attacks at night, increase in a liver, hypostases join it. Heart failure becomes biventrikulyarny.

The isolated right ventricular insufficiency meets seldom. It begins with increase in a liver and hypostases. The majority of its cases is caused by diseases of a parenchyma of easy, pulmonary vessels, a thorax, alveolar hypoventilation. Sometimes tumors and some inborn diseases are the reason of its development. Diffusion heart troubles begin usually a picture of a biventrikulyarny circulatory unefficiency with approximately simultaneous development of symptoms and signs of left ventricular and right ventricular failure.

Right ventricular insufficiency

Inborn valve pulmonic insufficiency. Inborn pulmonic insufficiency which arises owing to an underdevelopment, an union or windowing of petals of the valve belongs to number of the rare reasons causing insufficiency of a right ventricle of heart. The isolated inborn pulmonic insufficiency was for the first time is intravital is diagnosed in 1955 for the 24-year-old student of medical institute. Inborn valve pulmonic insufficiency at it proceeded asymptomatically, and he did not show any complaints.

Pulmonic insufficiency cannot be referred to harmless anomalies of development. Sometimes after several decades of normal life carriers of this defect have signs of insufficiency of a right ventricle of heart which progressing leads to a failure. We managed to find detailed data on 4 proved cases of the isolated insufficiency of the pulmonic valve in available literature. One patient died at the age of 64 flyings of heart failure. On opening the bikuspidalny valve of a pulmonary artery was found in it. Heart failure at 3 patients came at the age of 21, 34 and 54 years. Insufficiency of the kvadrikuspidalny valve of a pulmonary artery was recognized as its only reason.

Valve defect in itself is only one of the reasons of development of right ventricular insufficiency. It remains compensated until there is a pulmonary hypertension under the influence of which blood regurgitation volume in a right ventricle increases, and easy pulmonic insufficiency gradually becomes heavy. The operational load increases by a right ventricle as, except an overload pressure, he tests also all the accruing overload blood volume.
Inborn pulmonic insufficiency is found usually accidentally at inspection of healthy faces. Its main diagnostic characters are diastolic noise and expansion of a pulmonary artery. Diastolichesky noise is best of all heard about a breast in the second and third left intercostal spaces. On FKG it is possible to define that it has the spindle-shaped form and occupies only the middle of a diastole. The first cardiac sound is not changed, the second tone is weakened and consists of only one aortal component. Except diastolic, also systolic noise which has the rhomboid form and occupies the middle of a systole often is defined. The increased volume of systolic emission in a pulmonary artery leads to emergence of systolic noise, and in more hard cases — and to the strengthened pulsation of a pulmonary artery in the second mezhreberye at a breast.
The ECG at easy pulmonic insufficiency remains normal, and in cases of the expressed regurgitation on it signs of an overload of a right ventricle are found.

X-ray inspection allows to reveal one of the main signs of inborn pulmonic insufficiency, expansion of the main trunk and leading branchs of a pulmonary artery. Peripheral vessels of lungs have a normal appearance.
Inborn valve pulmonic insufficiency on clinical manifestations most of all reminds relative pulmonic insufficiency which develops as complication of a pulmonary hypertension and inborn expansion of a pulmonary artery.

The pulmonary hypertension (primary or secondary) with the sufficient duration and expressiveness leads to expansion of a valve ring of a pulmonary artery, there is a relative pulmonic insufficiency. Diastolic noise is one of its main diagnostic characters. It begins at once after the second tone of a pulmonary artery, occupies all or almost all diastole. Its intensity at the beginning of a diastole maximum and considerably decreases to the middle of a diastole. At the end of a diastole Noise stops. As it is already noted, noise at inborn valve pulmonic insufficiency occupies only the middle of a diastole. The second tone over a pulmonary artery at inborn valve pulmonic insufficiency is weakened, and at a pulmonary hypertension with relative pulmonic insufficiency it either is well heard, or is increased.
Expansion of a pulmonary artery at a pulmonary hypertension contrasts with depletion of vascular drawing on the periphery of a lung. When the pulmonary hypertension leads to development of relative pulmonic insufficiency, vascular drawing often is not defined on peripheries of lungs at all. Vascular drawing on the periphery of lungs at inborn valve pulmonic insufficiency does not undergo changes.

Diastolic noise at inborn valve pulmonic insufficiency is listened irrespective of symptoms of heart failure, and at a pulmonary hypertension it appears usually together with it. Successful therapy is followed by easing or disappearance of diastolic noise of relative pulmonic insufficiency and does not influence its intensity at inborn insufficiency of the valve of a pulmonary artery.

The differential diagnosis is facilitated also by existence of symptoms of the main illness which led to development of a pulmonary hypertension and relative pulmonic insufficiency. Inborn valve pulmonic insufficiency can be taken by mistake for inborn expansion of a pulmonary artery at which diastolic noise sometimes appears. It is easy to carry out the differential diagnosis of these diseases as valve pulmonic insufficiency always proceeds with a hypertrophy of a right ventricle, and sometimes and is complicated by heart failure. The hypertrophy of a right ventricle never meets at inborn expansion of a pulmonary artery. Blood regurgitation in a right ventricle at this illness is extremely insignificant and never leads to development of right ventricular insufficiency.

Right ventricular insufficiency can be caused by a pulmonic stenosis. Infundibulyarny and subinfundibulyarny stenoses of a pulmonary artery are always combined with defect of an interventricular partition. Heart failure at these options of a pulmonic stenosis proceeds with temporary or constant cyanosis. Valve and nadklapanny stenoses often meet in the form of the isolated defeat, and the last option of a stenosis is among exclusively rare diseases. Patients with these options of a pulmonic stenosis of an atsianotichna.
The isolated valve stenosis of a pulmonary artery can proceed a long time asymptomatically. Depending on weight of a stenosis the first complaints appear at the age of 10 — 40. Before everything an asthma at physical efforts develops and increased fatigue. Right ventricular insufficiency arises, as a rule, suddenly and accepts uncontrollably progressing current. The clinical picture of right ventricular insufficiency consists of the signs characteristic of a pulmonic stenosis and tricuspid insufficiency. Under supervision of the therapist get usually sick with a lung or moderately expressed stenosis. Carriers of this defect sometimes live till 70 flyings.

Compensation of defect at a pulmonic stenosis is reached at the expense of a hypertrophy of a right ventricle which strengthened pulsation can be defined in the third mezhreberye at the left edge of a breast. The first cardiac sound at a valve stenosis remains normal. It to be followed by high-frequency tone of exile which is best of all heard in the second left mezhreberye. The stenosis is heavier, the time interval between the first tone and tone of exile is shorter. At an easy stenosis both sounds are divided by an interval which can be caught an ear. At very heavy stenosis tone of exile disappears and there is only the first tone. Symmetric rhomboid noise at a heavy stenosis continues to an aortal component of the second tone or even for an aortal component of the second tone, muffling it. The noise maximum in similar cases moves in the second half of a systole.
Right ventricular insufficiency at a pulmonic stenosis differs from right ventricular insufficiency at rheumatic heart disease and a cardiosclerosis in character of vascular drawing of lungs. A characteristic sign of a valve pulmonic stenosis are: gradual expansion of the main trunk of a pulmonary artery. Extent of this expansion well correlates with weight of a stenosis. Especially sharply the left branch of a pulmonary artery extends. Aneurism of the left branch of a pulmonary artery is sometimes formed. Walls of this aneurism can be exposed to calcification. The expressed dilatation of a pulmonary artery at a pulmonic stenosis is combined with normal or even the grown poor vascular drawing of lungs.
The ECG in cases of an easy stenosis remains normal. In more hard cases signs of a hypertrophy of the right auricle and a right ventricle of heart are always found. Expressiveness of these signs well correlates with weight of a stenosis. Height of a tooth P in the I chest assignment well reflects the level of a blood pressure in a right ventricle of heart.

The diagnosis of a pulmonic stenosis is finalized by results of sounding of cavities of the right heart. Increase of pressure of blood in a right ventricle and the low systolic pressure of blood in a pulmonary artery is characteristic of a pulmonic stenosis. The same method is applicable for identification of infundibulyarny stenoses of a pulmonary artery.
The Nadklapanny stenosis of a pulmonary artery is among not progressing inborn heart diseases. Weight of a stenosis does not increase with age. Heart failure at these patients usually does not develop.
Heart failure at a pulmonic stenosis differs in an adverse current. The condition of the patient under the influence of medical actions improves usually for a while. The death occurs in 1 — 2 years after emergence of hypostases. Right ventricular insufficiency at a pulmonic stenosis develops separately. Left ventricular failure signs at it are never observed. The characteristic X-ray pattern of a pulmonic stenosis does not meet at one of other diseases.
Right ventricular insufficiency is included as an obligatory syndrome into anomaly of Ebstein at whom maldevelopment of the three-leaved valve usually in combination with not fusion of an oval window or defect of an interatrial partition is noted. Shutters of the valve are deformed and displaced towards a top of a right ventricle. Papillary muscles are underdeveloped, deformed and shortened. The fibrous ring is always expanded. Departments of a left heart remain normal. Aorta and pulmonary artery of a gipoplazirovana.

Approximately it is not found in 20% of patients of defect of an interatrial partition, they have no cyanosis, they can lead a usual life and even to carry out for many years a hard physical activity. As a rule, patients die of right ventricular insufficiency usually 4 — 20 years later after its emergence. The death can occur suddenly for no apparent reason. Patients with Ebstein's anomaly are inclined to development of paroxysmal arrhythmias. In illness cases with defect of an interatrial partition cyanosis develops for the first time usually during an attack of a ciliary arrhythmia or a Bouveret's disease.
Tricuspid insufficiency is among obligatory signs of anomaly of Ebstein. It would seem that in each case of this illness the positive venous pulse has to be defined, however pulse on a jugular vein can be normal. The systolic nulsation of the increased right ventricle at rheumatic heart diseases best of all is defined at edge of a breast in the fourth mezhreberye, and at Ebstein's anomaly the systolic pulsation of a right ventricle is absent. The pulsation of an output path of a right ventricle which is located in the third mezhreberye usually is found in these patients. In all cases of an illness the obtusion to the right of a breast caused by increase in the right auricle is defined.
Ebstein's anomaly differs from other defects of the three-leaved valve as well by results of heart auscultation. Systolic noise of tricuspid insufficiency is listened almost in all cases of anomaly of Ebstein. Usually this rough scraping noise occupies all or almost all systole. The maximum of noise is located between a breast and a top of heart. Though this noise and tricuspid, but during a breath it amplifies as the weak right ventricle cannot strengthen the systole during a breath.

The first cardiac sound at Ebstein's anomaly is often split because of the blockade of the right leg of a gisov of a bunch which is almost constantly found at it. The combination of the specified disturbances leads to the fact that in all cases of anomaly of Ebstein the third or fourth cardiac sound is listened. Summing of the third and fourth cardiac sounds can make impression of diastolic noise. Sometimes on FKG the presystolic noise caused probably by a functional stenosis of the right venous opening is registered.
Approximately in 95% of cases of an illness blockade of the right leg of a gisov of a bunch which in many cases is combined with delay of atrioventricular conductivity is found. Not less important diagnostic significance is attached to changes of a tooth R. R. P. Zubarev (1975) found increase in a tooth P in 70% of the cases of anomaly of Ebstein investigated by it. It was especially well-marked in I, II and V: assignments. At asymptomatic disease atrial teeth can remain normal.
In hard cases of anomaly of Ebstein heart sharply increases at the expense of the right auricle and a right ventricle. Its right border is formed by an expanded right auricle and atrial part of a right ventricle, left — a right ventricle. In cases of anomaly of Ebstein with signs of right ventricular insufficiency the shape of heart approaches spherical. The left ventricle, as a rule, remains invariable.
Ebstein's anomaly without cyanosis often is accepted to an exudative pericardis or to a kongestivny cardiomyopathy. The expressed cardiomegaly and weakening of a heartbeat are the general symptom of all three diseases. Ebstein's anomaly differs from a pericardis in the expressed dysfunction of the right auricle. Electrocardiographic signs of a hypertrophy of the right auricle in combination with disturbances of atrioventricular conductivity are among the most characteristic signs of anomaly of Ebstein and do not meet at a pericardis. Not less important differential and diagnostic significance should be attached to nature of tones and noise of heart. Diagnostic difficulties often happen nevertheless are so big that they manage to be overcome only after angiokardio-graphic research and a ventrikulografiya.

It is much easier to distinguish Ebstein's anomaly from the valve heart diseases of a rheumatic origin proceeding in combination with tricuspid insufficiency with relative or organic insufficiency of the three-leaved valve. Right ventricular insufficiency at rheumatic valve heart diseases and at cardiomyopathies proceeds is more good-quality, than at Ebstein's anomaly. Characteristic disturbances of a water and electrolytic exchange often are reversible. In many cases they completely disappear under the influence of long and persistent therapy. Patients with Ebstein's anomaly die usually still before they form ascites and a hydrothorax. The death at them occurs suddenly usually in connection with attacks of terminal disturbances of a cordial rhythm.

The tricuspid stenosis is in most cases combined with defects of other valves. Joining other heart diseases, it leads to additional disturbances of a hemodynamics. New conditions of blood circulation before everything affect a liver which increase appears the first clinical sign of the coming heart failure.
Diastolic pressure of blood in the right auricle is put on average upon 5 — 7 mm above, than in a ventricle. It leads to expansion of the right auricle. On the perednezadny roentgenogram the arch of the right auricle at the healthy person comes for the right edge of a backbone no more than on 2 cm. The pressure in the right auricle is higher, especially the arch eminates it to the right pulmonary field and the more sharply there is a corner between the right auricle and a diaphragm.

The described shape of heart with sharp expansion of its shadow at the expense of the right departments received the name of tricuspid. It meets quite seldom as tricuspid heart disease always joins a mitral stenosis or mitral aortally heart disease at which increase in either a right ventricle, or the right and left departments of heart is observed. Simultaneous increase in both auricles and ventricles leads to a cardiomegaly. The shape of heart at the same time in a perednezadny projection becomes spherical.

Considerable protrusion of heart to the right pulmonary field is a constant radiological symptom of tricuspid heart disease, but it meets also at other defects. On M. A. Ivanitskaya's (1963) supervision, the lower arch of the right contour of heart can act to the right pulmonary field on 5 — 7 cm not only at tricuspid heart disease, but also at the isolated mitral stenosis. Therefore, expansion of a shadow of heart allows to think of possible defeat of the tricuspid valve only to the right.

Increase in the right auricle (as well as a right ventricle) best of all can be estimated on the roentgenograms removed in the second slanting situation. The increased right auricle in this position narrows retrosternal space, especially in his upper part. Even more convincing signs of increase in the right auricle can be found on rentgenokimogramma.
In healthy heart the right lower contour of heart is formed by atrial teeth and only over a diaphragm throughout 1 — 2 strips teeth of ventricular type are defined. The zone of double-peak teeth of the right auricle at a tricuspid stenosis extends to 6 — 8 strips. Complication of a tricuspid stenosis a ciliary arrhythmia leads to "ventrikulization" of atrial teeth of a rentgenokimogramma. The tricuspid stenosis in these cases becomes indistinguishable from tricuspid insufficiency.
The intravenous angiocardiography allows to reveal a characteristic sign of a tricuspid stenosis — formation of the differentiating line between cavities of the right auricle and right ventricle. A contrast agent at a sharp tricuspid stenosis is late in the right auricle during 20 — 26 pages. The delay of its less specified term is observed also in cases of the expressed tricuspid insufficiency. Time of contrasting of the right auricle depends as well on a condition of sokratitelny function of heart. The heart failure, the more slowly a blood stream and the big duration of contrasting of the right auricle is heavier.

Accuracy of diagnosis of a tricuspid stenosis has great practical value especially for cardiosurgeons therefore when results of use of the listed methods of its diagnosis are insufficiently convincing, resort to a ventrikulografiya. During a systole of heart of a cavity of the right auricle and a right ventricle at the healthy person are completely isolated from each other therefore the contrast agent entered into a cavity of a right ventricle cannot get to the right auricle. The pelting of a contrast agent from a ventricle in an auricle is a reliable sign of tricuspid insufficiency.
Malignant and benign tumors lead to development of chronic heart failure or by means of a direct adverse effect on a myocardium sokratitelnost, or thanks to creation of the conditions complicating normal action of the heart as the pump. Specific mechanisms of heart failure include a heart overload pressure or volume of the blood proceeding through it which are often combined with disturbance of a cordial rhythm and short-term complete cessation of a blood-groove through heart. The clinical syndromes arising at the same time can differ markedly from each other on mechanisms and rates of development.

Achievements of modern medicine allowed to reconsider opinion on the adverse forecast of heart failure at heart tumors. Now some of these diseases are completely curable therefore the correct and timely diagnosis has them value which goes beyond the academic interest.
Chronic heart failure meets both at primary, and at metastatic tumors of a myocardium. Heart failure at primary tumor of a myocardium is caused by its adverse influence on contractility and a heart rhythm. Sarcoma is the most frequent malignant tumor of a myocardium. His most frequent benign primary tumors are the myxoma and a rhabdomyoma (Abrikosov's tumor). Much less often fibroma, a lipoma, a leiomyoma meets.
Malignant tumors of other bodies can lead to development of heart failure too. Extensive metastasises of a malignant tumor in lungs result in right ventricular insufficiency which arises owing to quickly increasing resistance to a blood-groove in a small circle of blood circulation. On the development mechanism this heart failure is similar that at a pulmonary heart. The overload of a right ventricle is followed by its hypertrophy which is expressed, as a rule, unsharply as because of subacute disease the death of the patient occurs 1 — 2 month later after emergence of signs of right ventricular insufficiency.

The subacute course of heart failure most often meets development of a moderate hypertrophy of a right ventricle at a carcinoma of the stomach. Increase of venous pressure, increase in a liver, emergence of hypostases lower extremities, and sometimes and ascites at these patients appears one of reliable signs of extensive innidiation of cancer in lungs. Pathoanatomical confirmation of this diagnosis is the muscat liver and unsharply expressed hypertrophy of a right ventricle of heart. Tumor metastasises in a peritoneum and in the portal fissures arising along with metastasises in lungs can lead to development of ascites. Gipoproteinemichesky hypostases are observed at cancer patients also. The liver in similar cases has a dense consistence, sometimes it is uneven. At heart failure the liver increases evenly, at metastasises of a tumor increase in any one its share is noted. On opening the atrophy and a degeneration of a liver and myocardium is found.

Heart failure at metastasises of a malignant tumor vashokard in one cases develops at a normal heart rhythm, in others — in combination with arrhythmias. Metastasises in a myocardium especially often meet at a cancer of a lung and chest gland. The clinical picture of heart failure in these cases, as well as a picture of heart failure at primary sarcoma of heart, is defined by localization of a tumor and rates of its growth. The diagnosis of a metastasis of a tumor in a myocardium can be assumed on emergence of electrocardiographic signs of focal damage of a myocardium and on complication of the main illness a picture of subacute heart failure. The diagnosis of primary sarcoma "hearts is submitted extremely difficult. The illness is diagnosed usually only after opening.
Chronic heart failure is among late displays of a carcinoid tumor (argentofinoma). Depending on localization of primary tumor either the right, or left heart is surprised.
The carcinoid tumor meets in all departments of a digestive tract, beginning from a stomach and finishing a rectum. The worm-shaped shoot is surprised much more often than other departments of a digestive tract. Slightly less often the carcinoid tumor develops in an ovary and is absolutely rare — in a gall bladder and bronchial tubes.
The carcinoid tumor allocates in blood 5-gidroksitriptamin (serotonin) and probably other humoral substances under the influence of which the picture of carcinoid damage of heart develops. Pulmonary monoaminoxidase is capable to inactivate serotonin with formation of 5-hydroxyindolacetic acid. If the tumor is located in an abdominal cavity, then the humoral substances produced by it get into the right heart in the beginning, causing its damage, and only after it are affected by pulmonary monoaminoxidase. Defeat of a left heart meets in cases when the tumor comes from bronchial tubes, and the substances produced by it come to a left heart in not changed look.
Under the influence of these substances diffusion fibrosis of valve structures develops. Free edges of valves, tendinous chords and tops of papillary muscles are especially sharply thickened. The subsequent shortening of shutters, tendinous chords, papillary muscles results in insufficiency of the valve, unions on lines of commissures lead to narrowing of valve openings. Focal thickenings of an endocardium are often formed over tumor metastasises in a heart muscle.
Heart failure at a carcinoid tumor always develops gradually and only at patients with a characteristic picture of a carcinoid syndrome. In most cases in the beginning signs of right ventricular insufficiency appear. By results of clinical trial she is called by tricuspid insufficiency, pure or in combination with a tricuspid stenosis more often. These openings specify that the pulmonic stenosis is not less frequent reason of heart failure at a carcinoid syndrome.
The specified discrepancy between clinical and pathoanatomical data is explained by the fact that at measurement of diameter of openings it is easier for prosector to find the initial phenomena of a pulmonic stenosis, than tricuspid insufficiency. Also the fact that heart failure at pulmonic insufficiency always right ventricular matters.

In the beginning the pulmonic stenosis leads to a hypertrophy, and then and to dilatation of a right ventricle. Expansion of a valve ring is followed by disturbance of normal space ratios between separate morphological structures of the valve. Owing to these disturbances there is a relative tricuspid insufficiency which anatomic signs it is difficult for prosector whereas it is easy for clinical physician to hear and write down its auskultativny signs on FKG to find.
If heart failure is among late complications of a carcinoid tumor, then time of emergence of valve defeats still remains obscure. More or less expressed signs of tricuspid insufficiency sometimes are found at the first inspection of patients concerning recently appeared signs of a carcinoid syndrome. Duration of existence of a tumor in cases of this sort remains to the unknown.
The oncotomy before formation of metastasises leads to disappearance of a carcinoid syndrome, but symptoms of valve heart disease at the same time remain. Moreover, over time symptoms of heart disease become more expressed owing to the continuing growth of fibrous fabric. Gradually the patient has clinical, electrocardiographic and radiological signs of a hypertrophy of a right ventricle, increase of venous pressure, increase in a liver, hypostases, ascites" Use of heart glucosides and diuretics is followed by short-term improvement. Longevity after emergence of symptoms of heart failure averages 5 years.

Heart failure at a carcinoid syndrome happens short-term. After an oncotomy it can disappear. Assume that right ventricular insufficiency in similar cases develops under the influence of a pulmonary hypertension which in turn is a consequence of konstriktorny effect of serotonin on arterioles of lungs. After an oncotomy secretion of excess amounts of serotonin stops, there passes the pulmonary hypertension, and with it and an overload of a right ventricle. Disappearance of right ventricular insufficiency is a consequence. With pas serotonin influence function of lungs is explained also by asthma attacks at a carcinoid syndrome.
Subendocardial growth of fibrous fabric leads to various disturbances of a rhythm and conductivity. The venous hypertension of lungs, asthma attacks, temporary or constant heart failure in these cases can be a consequence: a ciliary arrhythmia and not to consist in relationship of cause and effect with serotonin. The specified mechanism can have independent value, obviously, only at patients with a remote carcinoid tumor and with normal excretion of 5-hydroxyindolacetic acid with urine.

The fibrous myocarditis arising under the influence of the substances emitted by a carcinoid tumor can lead to defeat of the valve device of heart with formation of a syndrome of insufficiency of the valve or a stenosis of an opening and to become a basic reason of development and progressing of heart failure. The death at a carcinoid tumor occurs or from effects of heart failure, or from the cachexia coming under the influence of tumor metastasises in other bodies. Except the academic interest, ability to find out the reason of the developed clinical displays of an illness can prolong life of the patient and reduce his sufferings.
Disturbances of a water and electrolytic exchange at a carcinoid tumor can be caused by both heart failure, and other reasons. Tumor metastasises in portal fissures lead sometimes to development of a portal hypertension with its consequences: ascites and hypostases of the lower extremities.
Development of the isolated syndromes of tricuspid insufficiency or a tricuspid stenosis whereas the most widespread syndromes of tricuspid insufficiency and a tricuspid stenosis of a rheumatic origin meet, as a rule, along with a mitral stenosis is characteristic of heart failure at a carcinoid tumor.
The inborn isolated defects three-leaved and pulmonic valves differ from the corresponding defects at a carcinoid tumor according to the anamnesis and character of a current. Noise in heart at patients with inborn defects are listened since the childhood whereas tricuspid heart disease and a pulmonic stenosis develop at patients with a carcinoid tumor not earlier than other clinical signs of a syndrome.
Right ventricular insufficiency is caused sometimes by a myxoma of the right auricle. The tumor during each systole gets into the right atrioventricular opening. Hemodynamic effects of it depend not so much on the tumor size how many from as far as it complicates a blood stream through the right atrioventricular opening and as far as interferes with inflow of blood from venas cava to the right auricle.
Clinical signs of a myxoma of the right auricle in many respects remind signs of a tricuspid stenosis. At an auskultaliya also diastolic noise which differ from the noise of a tricuspid stenosis corresponding to them in the variability are listened systolic. Especially variability of duration and intensity of diastolic noise attracts attention. The right ventricle of heart sometimes increases. Moderate increase in the right auricle is noted in all cases of an illness.
Signs of right ventricular insufficiency at a myxoma of the right auricle differ from its signs developing at a decompensation of tricuspid heart disease a little. Sharply expressed increase of venous pressure which is found already in the onset of the illness is considered especially characteristic. The tumor in similar cases is located near the mouth of an upper vena cava and interferes with inflow of blood to the right auricle. Thereof the picture of right ventricular insufficiency at a myxoma of the right auricle can sometimes remind a chronic cardial compression picture.

The embolism of lungs particles of a tumor or the blood clots located on its surface leads to a repeated blood spitting and heart attacks of lungs. These repeated thromboembolisms of lungs in combination with right ventricular insufficiency, subfebrile condition or moderate fever, with the increased content of globulins in blood give the grounds to assume at the patient rheumatic heart disease with recurrence of a rheumatic carditis.
Making the diagnostic decision, it must be kept in mind that rheumatic defect of the tricuspid valve, as a rule, meets in combination with a mitral stenosis whereas the myxoma of the right auricle proceeds always without pulmonary hypertension, without increase in the left auricle and other signs of a mitral stenosis. Characteristic symptoms of heart failure at a myxoma of the right auricle are: faints, heartbeat, collapses, frequent complications by heart attacks of lungs and uncontrollably progressing current. Hypostases of hypodermic cellulose and ascites are expressed usually unsharply. Heart failure at rheumatic heart diseases has usually wavy current, in her clinical picture into the forefront the general weakness and hypostases, but not faints and collapses act.
The listed differential diagnostic characters not always happen rather expressed, and it is not always reasonable to wait before full clarification of features of a clinical course of heart failure. Identification of an endocardiac tumor, as well as an exception of other reasons of right ventricular insufficiency, can be reached by use of special methods of research (an echocardiography, catheterization of heart and angiocardiography).



 
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