Heart failure is the normal venous return and cardiac output decrease due to primary heart damage caused by a syndrome can not meet the needs of tissue metabolism. Clinical and (or) due to systemic congestion and tissue blood perfusion deficiency as the main feature, also known as congestive heart failure (congestiveheartfai1ure), often of various etiologies of heart disease end stage pulmonary circulation.
Congestive heart failure and cardiac dysfunction the (cardiacdysfunction) concept is basically the same, but the latter meaning is broader, including already reduced cardiac output but has not yet appeared at this stage of the clinical symptoms. Often from a variety of diseases caused by diminished myocardial contractility, thereby reducing the heart's blood output, is insufficient to meet the needs of the body, and the resulting series of signs and symptoms. Heart valve disease, coronary artery disease, hypertension, endocrine disorders, bacterial toxins, acute pulmonary embolism, emphysema or other chronic lung disorders can cause heart disease and heart failure performance. Pregnancy, fatigue, intravenous rapid and massive fluid etc. may increase the burden on the heart sick, induced heart failure.
Heart failure - clinical classificationHeart failure (a) heart failure the speed of development can be divided into two kinds of acute and chronic, mostly to chronic. Acute left heart failure is more common, mainly as acute pulmonary edema.
(B) According to the site of heart failure can be divided into the left heart, right heart and heart failure. Left heart failure is characterized by congestion of the pulmonary circulation; right heart failure as the main manifestation of systemic congestion.
(C) caused by contraction or diastolic heart failure due to systolic dysfunction caused by systolic emptying weakened heart failure systolic heart failure. The clinical characteristics of the chambers of the heart to expand, and end-systolic volume increased and reduced ejection fraction. The vast majority of heart failure have systolic dysfunction. The importance of diastolic dysfunction in congestive heart failure, have received increasing attention in recent years. With systolic dysfunction at the same time, can also stand alone. Diastolic heart failure is due to diastolic ventricular active relaxation ability to damage and reduce ventricular compliance resulting in ventricular diastolic filling impairment, ventricular pressure - volume curve to the left shift, and thus reduce stroke volume, left ventricular end-diastolic pressure increased and heart failure, which represents the contractile function of normal ejection fraction. The mechanism of diastolic heart failure: ① The impaired left ventricular relaxation. Particular, such as myocardial ischemia, cardiac sarcoplasmic reticulum uptake of Ca2 ability to weaken, reduce the level of intracellular Ca2 slow take the initiative to impaired relaxation, causing; ② cardiac hypertrophy and myocardial stiffness increased (accompanied by myocardial fibrosis), diastolic myocardial expansion diminished capacity (reduced compliance). Pure diastolic heart failure have significant myocardial hypertrophy, cardiac chamber size of normal and increased heart rate, heart disease such as hypertension and concentric hypertrophy of; aortic stenosis; hypertrophic cardiomyopathy and ischemic cardiomyopathy.(D) the symptoms are no divided into asymptomatic (asymptomatic) heart failure and congestive heart failure. Asymptomatic heart failure is left ventricular existing dysfunction, ejection fraction decreased to normal (<50%) and no symptoms of heart failure at this stage. May last for several months to several years. It has been proved, this stage has been the neuroendocrine activation. Once the symptoms of congestive heart failure, heart function can be divided into four (in 1928 the New York Heart Association [NYHA] classification, the Standards Committee of the American Heart Association [AHA], revised in 1994).
Class I: unrestricted physical activity. Daily activities do not cause fatigue, palpitation, dyspnea or angina. II level: mild limitation of physical activity. Asymptomatic at rest, daily activities can cause fatigue, palpitation, dyspnea or angina. Grade Ⅲ: physical activity is significantly limited. Asymptomatic at rest, light daily activities can cause these symptoms. Class IV: You can not engage in any physical activity. Symptoms at rest also, after the increase in physical activity.
AHAl994 revised standard grading standards of objective assessment and classification, divided into A, B, C, D, four based on the objective examination of the ECG, exercise test, X-ray and ultrasound echocardiography. Class A: No objective evidence of cardiovascular disease. Class B: objective evidence of mild cardiovascular disease. Grade C: objective evidence of moderate cardiovascular disease. Grade D: objective evidence of severe cardiovascular disease. For example, asymptomatic patients, but across the aortic valve pressure gradient great, the penalty is as follows: cardiac function in Class I, Level D objective assessment.Closely related to the clinical manifestations of heart failure and how lateral ventricular or atrial involvement. The clinical features of left heart failure was mainly due to the left atrium and (or) right ventricular failure caused by pulmonary congestion, pulmonary edema; the clinical features of right heart failure is due to the right atrium and (or) right ventricular failure caused by the circulation of venous stasis and water and sodium retention. Left heart failure, right heart often have occurred dysfunction, eventually leading to heart failure. Of right heart failure, left heart failure symptoms can be eased.
Left ventricular failure(A) difficulty in breathing is the earliest and most common symptoms of left heart failure. Mainly due to reduce acute or chronic lung congestion and vital capacity. The light only in heavy manual labor, difficulty in breathing, quickly disappear after the break, it is known as exertional dyspnea. Labor induce the huixin blood increase in right ventricular function is normal, but also to promote the sake of pulmonary bleeding heavier. With the progress of the disease, mild physical activity, a sense of difficulty in breathing, severe cases also a sense of dyspnea at rest, so was forced to take the semi-supine or sitting position, called orthopnea (forced to sit breathing). The influence of gravity allows blood due to the seat by more than accumulate in lowered parts such as lower limb and abdomen, Rhodobryum, compared with supine reduce pulmonary congestion relief, the seat when the diaphragm to drop, increase lung capacity, so that dyspnea. Paroxysmal nocturnal dyspnea is a manifestation of left heart failure, patients are asleep in the arousal, there is a sense of suffocation, forced to sit up, cough frequent, severe breathing difficulties. The light and sat up after a few minutes, the symptoms ceased to exist, severe cases, seizures, cyanosis, cold sweat, the lungs can hear the wheezing sound, known as cardiac asthma. In severe cases can develop into pulmonary edema, slightly foamy bloody sputum, lungs covered with wet rales, blood pressure can be reduced, or even shock.(B) cough and hemoptysis is a common symptom of left heart failure. Due to the congestion of the alveolar and bronchial mucosa, with breathing difficulties coexist, hemoptysis color foamy or bloody sputum.(C), fatigue, weakness, insomnia, palpitations. Chen Steinmann breathing, drowsiness, dizziness, loss of consciousness, convulsions and other severe cerebral hypoxia can occur.(D) signs in addition to the original heart disease signs, the apex may have diastolic gallop, pulmonary valve auscultation area hyperthyroidism second heart sound, the lungs can be heard at the bottom covered with wet Luo scattered moist rales, severe lungs The tone and accompanied by wheezing, often alternating pulse.
Heart failure Right heart failure(A) upper abdominal fullness are the early symptoms of right heart failure. Often accompanied by loss of appetite, nausea, vomiting and upper abdominal pain, this is more than the liver, spleen and gastrointestinal tract congestion. Liver congestion, swelling and tenderness, enlargement by acute right heart failure, acute hepatic congestion, abdominal pain sharp, can be misdiagnosed as acute abdomen. Chronic hepatic congestion and hypoxia can cause liver cell degeneration, necrosis, and ultimately the development of cardiac cirrhosis, liver function showing normal or jaundice. If so, tricuspid regurgitation coexist, and palpation of the liver can feel the throb of expansionary.(B) of the jugular vein engorgement is a more obvious signs of right heart failure. Often compared with subcutaneous edema or hepatomegaly earlier, while visible sublingual abnormal filling of superficial veins of the arm such as jugular vein distention is more obvious oppression of congestive enlargement of the liver, that liver a jugular vein reflux and positive signs .(C) edema and right heart failure early edema, when the body first, sodium and water retention, so before edema appeared before weight gain, fluid retention of more than five kilograms. Edema of heart failure more than the first seen in the lower limbs, ambulatory patients often waist, back and sacral falls parts obviously, was pitting edema, severe, can affect the body, lower extremity edema than in the evening or aggravate the rest for a night can reduce or disappear, often accompanied by the increase of urine at night, this rest because of the night when Rhodobryum less activity than during the day, the heart can still pump out the blood of the venous return, significantly reduced ventricular end systolic residual blood, veins and increased capillary pressure were reduced, and thus the edema subsided.Small number of patients with pleural effusion and ascites. Pleural effusion can be seen in the left and right sides of the chest, but more to the right side, the reason is unclear, because the venous return to the vena cava of parietal pleura, visceral pleura, venous return to the pulmonary vein, thus pleural effusion common in heart failure . Ascites tends to occur late, mostly due to cardiac cirrhosis caused.(D) more than cyanosis, right heart failure who have varying degrees of cyanosis, was first seen in the fingertip, lips and ear, left heart failure significantly. The reason for addition to the lung oxygenation dysfunction hemoglobin in the blood, often due to slow blood flow, tissue from the capillaries in the intake more oxygen leaving the blood reduced hemoglobin increase (peripheral cyanosis). Severe anemia, cyanosis is not obvious.(E) of the nervous system symptoms may include nervousness, insomnia, lethargy and other symptoms. Severe cases, mental disorder, this may be due to a brain haemorrhage, hypoxia, or electrolyte imbalance causes.(F) cardiac signs the performance of existing heart disease, right heart failure is often secondary to left heart failure, and thus the left and right heart can be expanded. Right ventricular enlargement caused by tricuspid regurgitation can hear the hair of the systolic murmur in the tricuspid valve auscultation. Symptoms of pulmonary congestion caused by left ventricular failure and pulmonary valve of the second heart sound hyperthyroidism may be due to the emergence of right heart failure and reduced.
Heart failureCan co-exist to the left and right heart failure, clinical manifestations, can also be left or right heart failure clinical performance-based.
Heart Failure - diagnosisThe diagnosis of heart failure is the cause of comprehensive, medical history, symptoms, signs and objective examination. Should first be clear diagnosis of structural heart disease. The signs and symptoms of heart failure is an important basis for diagnosis of heart failure. Fatigue, weakness and other symptoms of cardiac output decrease non-specific, the diagnosis of little value, left heart failure, pulmonary congestion caused by the different degree of difficulty in breathing, circulation congestion of right heart failure caused by jugular vein distention, hepatomegaly , edema is an important basis for diagnosis of heart failure.Typical of chronic heart failure diagnosis is not difficult. Existing heart disease or the occurrence of heart failure based on the patient, such as signs and symptoms of congestion of the pulmonary circulation, it is not difficult to diagnosis of left heart failure; such as congestive symptoms and signs of circulation, it is not difficult to diagnose right heart failure. X-ray examination, venous pressure measurement, and can often provide the diagnosis is based on.Diagnosis based on: (a) left ventricular failure: early pulmonary venous congestion stage X-ray examination showed upper lobe vein dilation. Interstitial pulmonary edema stage, the increase in pulmonary vascular shadow thickening, lymphangiectasia, obscure and lobe between the characteristic Kerley, line B. To the stage of alveolar pulmonary edema, the lungs show a cloudy shadow, hilar was Butterfly. In addition, yet may show a pleural effusion and pleural thickening (or). (B) right heart failure: the X-ray examination showed the right atrium and right ventricle increases, the superior vena cava widened lung fields clear. Secondary to left heart failure the heart increases with markings increase. Venous pressure test showed significantly higher (normally not more than 1.37kPa), the oppression of the liver increased more significantly.Laboratory tests: (a) X-ray examination: 1. Cardiac size and shape to provide important reference information for the diagnosis of the cause of heart disease, according to the degree of enlargement of the heart and the dynamic changes indirectly reflect the state of the heart function. Two. The presence or absence of pulmonary congestion and the extent of a direct reflection of the heart function. (B) echocardiography: 1. Provide more accurate than X-ray of the heart chamber size changes and the heart valve structure and function. Two. Estimated cardiac function. (C) of the radionuclide: Radionuclide blood pool imaging, in addition to help determine the size of the ventricular chamber in order to shrink the difference of the end of ventricular end-diastolic images to calculate the EF value, while activity by recording radiation - time curve calculation of left ventricular peak filling rate to reflect the diastolic function. (D) of the heart - lung oxygen exercise test: Determination of the amount of patients with exercise tolerance in the state of the campaign, is better able to explain the functional status of the heart. This test applies only to patients with chronic stable heart failure. (E) invasive hemodynamic examination: at the bedside of patients with heart failure is the use of floating catheter, pressure and blood oxygen content of the various parts of the venous catheter until the small pulmonary arteries were measured to calculate the cardiac index ( CI) and pulmonary artery wedge pressure (the PCWP), a direct reflection of left ventricular function, normal CI> 2.5L / (min · m2); PCWP12mmHg.
Heart failure - etiology and pathologyCause ofFirst, the basic cause of heart failure caused by many reasons, to reduce the number of myocardial cells and ventricular systolic and diastolic dysfunction results from the pathophysiological basis, primary myocardial damage or myocardial systolic or diastolic overload.(A) primary myocardial damageA segmental or diffuse myocardial damage segmental myocardial damage such as myocardial infarction, myocardial ischemia. Diffuse myocardial damage such as myocarditis, dilated cardiomyopathy, hypertrophic and restrictive cardiomyopathy, as well as connective tissue disease, myocardial damage.Myocardial primary or secondary metabolic disorders, such as lack of vitamin Bl, diabetic cardiomyopathy, cardiac amyloidosis.
(B) ventricular overloading of ventricular afterload (pressure load) and preload (volume overload) overweightPressure overload seen in hypertension, aortic stenosis; pulmonary hypertension, pulmonary valve stenosis, left and right ventricular systolic ejection impedance increased.(2) volume overload following three conditions:① valve regurgitation disease: such as mitral regurgitation, aortic regurgitation, tricuspid regurgitation;(2) heart inside and outside the shunt diseases: such as atrial septal defect, ventricular septal defect, patent ductus arteriosus;③ systemic blood volume increased: double room capacity, such as hyperthyroidism, chronic anemia, arteriovenous fistulas, beriberi, etc. often overloaded. Whether primary myocardial damage or ventricular overloading ultimately lead to changes in myocardial structure and function and lead to heart failure.Second, the incentives appear or worsen heart failure symptoms often can be induced by certain factors, known as the incentive. Common are:Infections, especially respiratory infections, followed by infection, such as the heart and systemic infection;(2) arrhythmias especially atrial fibrillation, and tachyarrhythmia.Water and electrolyte disorders, too much sodium infusion too much too fast.(4) physical fatigue, mental stress, overweight, emotional.5 environment, the climate changed dramatically.The increased cardiac load, such as pregnancy, childbirth and so on.Improper treatment: such as digitalis dosage or excessive diuresis excessive.8 with hyperthyroidism, anemia, pulmonary embolism.
The development of heart failure of ① heart failure from the adaptation to maladaptation, resulting in progressive deterioration. ② heart tissue next to the autocrine secretion of activation, and myocardial energy depletion resulting decrease in the number of myocardial cells, myocardial cells consisting of a qualitative change resulting in myocardial cells shorten the life span of the hemodynamic abnormalities is the result of heart failure, correct the hemodynamic abnormalities can not be change the prognosis of heart failure and thus the modern heart failure treatment can not just focus on organ dysfunction (cardiac pump dysfunction should still take into account the neuroendocrine activation, and myocardial energy consumption growth-promoting or inhibiting the growth and so should be organ, cellular and molecular level to consider.First, the hemodynamic abnormalitiesHemodynamic abnormalities in patients with heart failure to produce the pathophysiological basis of the clinical "congestive" symptoms of right ventricular dysfunction caused by cardiac output (CO) reduction and left ventricular end-diastolic pressure (LV-EDP) increased, the former lead to inadequate perfusion of tissues and organs, the latter may cause increased pulmonary vascular wedge pressure (PCWP) when approved PCWP> 2.4 kPa (18mmhg) the pulmonary circulation congestion syndrome; right ventricular end-diastolic pressure and right atrial pressure caused by central venous> Stone only * 2 t), with the reduction of cardiac output, systemic vascular congestion syndrome, the activation of a variety of neuroendocrine regulation mechanism, increase in peripheral blood redistribution, kidney and skeletal muscle blood decreased peripheral vascular resistance, lead to the end Therefore the exception of the end organ, heart failure, hemodynamic characteristics: the central pump dysfunction of CO ↓, the LVEDP ↑); increase in peripheral vascular resistance and end-organ abnormalities; and pulmonary circulation and systemic circulation gal disease, however, hemodynamic abnormalities only is the result of heart failure.Second, the circulating endocrine and heart tissue autocrine. Paracrine activation of circulating endocrine results show that heart failure [including the sympathetic nervous system (the SNS renin-angiotensin system (RAS) and vasopressin) activation, can accelerate the deterioration of heart failure. Endogenous atrial natriuretic peptide also activated but not enough to offset the SNS and RAS. Recent studies further indicate that the organization of local autocrine and paracrine important role in the development of heart failure. "Autocrine" role of the local secretion own cells; local paracrine secretion, acting on the adjacent tissue. Circulatory endocrine myocardial damage after the initial rapid activation (the SNS, the RAS in the factors of pressure and atrial natriuretic peptide person but when the damage recovery, circulatory endocrine cardiovascular obtain compensatory to restore normal or only slightly elevated at this time that into adaptive or compensatory phase until the last significant heart failure, into maladaptive or decompensated stage, circulating endocrine re-activate the adaptive stage in this too long, many Asian clinical pathological physiological processes including cardiovascular remodeling in progress, and heart tissue of endocrine and paracrine played an important role in myocardial and microvascular within the endocrine and paracrine more important than the circulating endocrine role. However, heart tissue from autocrine and paracrine sustained activation will eventually damage the myocardium, into maladaptive stage heart failure occurs, the circulating endocrine re-activated, so the formation of the vasoconstrictor role of the vicious cycle of under normal circumstances, the positive inotropic effect autocrine and paracrine growth-promoting effect, and has a negative inotropic effect of vasodilators and inhibition of growth in an autocrine and paracrine in the heart, vascular system is in equilibrium state. In fact most of the vasoconstrictor agent at the same time positive inotropic and growth promoting effect, such as angiotensin and endothelin, the same majority of vasodilator agents also have negative inotropic and inhibition of growth, such as derived relaxing factor, atrial natriuretic peptide and prostacyclin elements of these has the relative role of endocrine imbalance, such as heart failure, IMS and SNS activation of short-term role in the performance of vascular tone and cardiac contraction force changes in the vasoconstriction and positive inotropic effect; long-term activation leads to changes in cardiac structure, ie, cardiac hypertrophy , followed by ventricular enlargement, and ultimately accelerate myocardial failure.Third, the left ventricular remodelingInitial myocardial injury, cardiac hypertrophy, followed by ventricular enlargement, ventricular remodeling process of ventricular remodeling and heart Ingredients: cardiac myocyte hypertrophy; the amount and composition of the extracellular matrix collagen network changes and microvascular density increase. Primary myocardial damage and cardiac overload the weight caused by the increase in wall stress may be the initiating mechanism of ventricular remodeling and various growth factors played an important role, in which angiotensin II may be the core of a series of biochemical reactions.How to develop cardiac hypertrophy to ventricular enlargement, the mechanism is not clear lengthening of the myocardial fibers, the sliding of the bracket of the collagen network damage caused by myocardial cells may be involved in the process of ventricular enlargement. Hypertrophy of myocardial systolic velocity drop; contraction time; relaxation delay muscle fiber shortening and ventricular emptying does not diminish, therefore, if the myocardial appropriate hypertrophy sufficient to overcome the wall stress, ventricular function is still able to maintain, is the effort failure to adapt to the stage; when cardiac hypertrophy is not sufficient to overcome the wall stress, that is, into the maladaptive stage of left ventricular sexual expand with dysfunction and, ultimately, to irreversible myocardial damage in the end not stage. Ventricular remodeling is caused by the leading cause of heart failure and death.Heart failure how to adapt to change maladaptive may be related to the following two aspects: (1) the number of myocardial cells to reduce: energy consumption of the muscle fibers of the hypertrophied myocardium increase in the number; mitochondria decrease in the number of generated energy; In addition, the muscle cell biochemical abnormalities obstacles, leading to energy generated thereby hypertrophied myocardium is energy hungry, persistent to reduce the number of myocardial cells, so that heart failure progressive deterioration of the of ② myocardial cytoplasmic changes (composition and function): hypertrophic myocardial contractile protein gene expression abnormalities. similar to the fetal phenotype, thus shortening the life of hypertrophic myocardial cells of adult cardiac myocytes can not divide, normal protein synthesis is very slow, when the heart is in overload state, many newly synthesized proteins into the fetal type of the same protein, so to accelerate protein synthesis rate. Such fetal protein, however, the myocardial cells in the failure, thus also participated in a role in the process of worsening heart failure In addition, abnormal extracellular matrix in a cell of the bracket of the heart is also very important.
Heart Failure - pathology
Pathophysiological mechanisms of heart failure congestive heart failure is very complex, the main characteristics of the following three aspects:
First, the blood flow dynamics exception from any cause, heart failure, the basic problem is poor ventricular function curve to shift to the right. In any particular left ventricular end-diastolic pressure, stroke volume is lower than normal. Ventricular function curve reflects the cardiac output relationship between blood volume and ventricular filling pressure. According to the Frank-Starling law, with the increase in ventricular filling pressure and end-diastolic myocardial fiber length increases, stroke volume can be a corresponding increase, showing the rise of the ventricular function curve. However, this increase of stroke volume there is a limit, when the left ventricular end diastolic pressure up to 2.0 ~ 2.4kPa (15 ~ 18mmHg), the Frank-Starling, mechanism of effect, the stroke volume is no longer increase, and even but reduced, is the plateau of the ventricular function curve and the subsequent decline. Signs and symptoms of low cardiac output when cardiac index <of 2.2L/min · m2. Left ventricular end diastolic pressure increased subsequently left atrial pressure, pulmonary venous pressure and pulmonary capillary wedge pressure increased. When the latter more than 2.4kPa (18mmHg), that is, the signs and symptoms of congestion of the pulmonary circulation. When the right ventricular end-diastolic pressure and right atrial pressure caused by central venous pressure> 1.6kPa (12mmHg), ie the circulation congestion levy. With the lack of reduction in cardiac output and arterial blood filling, the activation of various neuroendocrine regulation mechanism, especially the sympathetic nervous system activation, increased peripheral vascular resistance and redistribution of peripheral blood, kidney and skeletal muscle blood flow decreased , leading to end-organ (endorgan) exception. Therefore, congestive heart failure, hemodynamic abnormalities characterized by: the central pump dysfunction (cardiac output decreased ventricular end-diastolic pressure); increased peripheral vascular resistance and end-organ abnormalities.
Second, the neuroendocrine activation congestive heart failure, the sympathetic nervous system (sympatheticnervoussystem SNS), renin - angiotensin system (renninangiotensionsystem, activity of the RAS) and vasopressin levels were higher. The neuroendocrine activation can enhance myocardial contractility leaving the cardiac output to increase; peripheral vasoconstriction to maintain arterial blood pressure and to ensure that blood flow to the vital organs, from the short-term support effect of the cycle. However, the long-term activity increased but its adverse effect. Peripheral vascular resistance increases and sodium and water retention to increase the heart, the first load further inhibition of left ventricular function. A large number of catecholamines on the myocardium direct toxic. Heart failure, atrial natriuretic peptide secretion was also increased. Atrial natriuretic peptide has natriuretic, dilate blood vessels and inhibition of renin and aldosterone. Heart failure, endogenous atrial natriuretic peptide is often not enough to offset the strong role of activation of the SNS and RAS. A large number of studies have shown that cardiac dysfunction occurred the development process, there is always the neuroendocrine activation, and that such activated earlier than the clinical symptoms of heart failure appear. Previously thought to play an important adaptive regulation of neuroendocrine mechanisms in heart failure. In the 1980s, this concept is a major change. Think of heart failure, the activation of neuroendocrine often the case over in turn harmful to the cardiovascular system. Long-term neuroendocrine activity increased not only increase the hemodynamic disturbances, but also directly damage the myocardium, exacerbating the deterioration of heart failure, and its activity level is directly related to the prognosis of patients.Third, the myocardial damage and ventricular remodeling (remodeling) overloading the primary myocardial damage and heart wall stress increases, leading to ventricular response hypertrophy and enlargement of the composition of the myocardial cells and extracellular matrix - collagen network have changed. This is the process of ventricular remodeling. Hypertrophy of myocardial contraction slowed down; prolonged contraction time; relaxation delay, but the muscle fiber shortening capacity and ventricular emptying does not diminish. If myocardial appropriate hypertrophy sufficient to overcome the wall stress, ventricular function is still able to maintain, do not produce clinical symptoms of congestive heart failure. Thus, cardiac hypertrophy at an early stage can play a useful role in compensatory Hypertrophy in the heart of how the development of progressive ventricular enlargement and heart failure, in which the mechanism is not yet clear, energy depletion is one of the main factors. Myocardial hypertrophy in the energy hungry, myocardial ischemia, myocardial cell death, followed by fibrosis, leaving the survival of cardiac load is further aggravated, myocardial hypertrophy with further progressive fibrosis, and so a vicious cycle. When cardiac hypertrophy is not sufficient to overcome the wall stress, left ventricular sexual expand with the dysfunction, and finally to irreversible myocardial damage in the terminal stage. The above three are interrelated and reinforce each other. Hemodynamic abnormalities activate the neuroendocrine aggravate myocardial damage; the neuroendocrine sustained activation can directly damage the myocardium and aggravate the hemodynamic abnormalities; and myocardial damage, left ventricular sexual expand and failure results has led to an increase in hemodynamic and neuroendocrine activation.
Heart failure mechanisms wereA, low cardiac output, Cardiac failure, coronary heart disease, acute myocardial infarction, ventricular aneurysm, diffuse myocarditis (rheumatic, viral, toxic infectious), Keshan disease, dilated cardiomyopathy perinatal cardiomyopathy. Alcoholic cardiomyopathy, hypothyroidism and acromegaly, Cushing's syndrome, cardiac amyloidosis, sarcoidosis, hemochromatosis, glycogen accumulation disease, diabetes, uremia, systemic lupus erythematosus scleroderma, skin-muscle inflammation, multiple arteritis rheumatoid arthritis, ankylosing spondylitis, polymyositis, muscular dystrophy, atrophic myotonia, work type of hereditary ataxia swing polysaccharide disease, metastatic cardiac tumors, leukemia left hypoplastic heart syndrome, excessive hypertrophy, senile heart to change the radioactive drug-induced the poison ischemic heart disease, acute or chronic pulmonary heart disease, mountain sickness hyperthyroidism, vitamin Bl deficiency.2, after the load excessive aortic valve stenosis, tricuspid regurgitation, thick obstructive cardiomyopathy chest thick aortic valve stenosis with essential hypertension, renal hypertension, aortic stenosis with pulmonary valve stenosis, three mitral regurgitation, hypertrophic obstructive cardiomyopathy, hypertrophic subaortic stenosis, hypertension, renal hypertension and coarctation of the aorta, primary pulmonary hypertension, Barnheim syndrome, toxemia of pregnancy, Ai Sen Mange syndrome.3, excessive pre-load aortic regurgitation, mitral regurgitation, papillary muscle dysfunction, atrial septal defect, patent ductus arteriosus, three-chamber heart of the main pulmonary septal defect, acute glomerulonephritis, acute renal failure, intravenous blood transfusion, infusion of too much too fast, and and hyperandrogenism enter the sodium salt of sodium or pig ventricular septal defect, congenital arteriovenous repeated, anemia, pregnancy, chronic pulmonary heart disease.4, preload mitral stenosis, atrial myxoma, left atrial ball thrombus restrictive cardiomyopathy, pericardial tamponade, constrictive pericarditis and acute pulmonary embolism, barrel chest with the heart of the shift.Arrhythmia atrial fibrillation, atrial flutter, paroxysmal atrial or ventricular tachycardia, atrioventricular block, sick sinus syndrome.Second, high cardiac outputHyperthyroidism, anemia, heart disease, toxemia of pregnancy, beriberi, lung, heart disease, mountain sickness, the arteriovenous thin abnormal atrioventricular canal, the primary hyperdynamic circulatory state, polycythemia vera polycythemia carcinoid syndrome, severe liver disease, Paget's disease of Stryker-Halbisom syndrome, heat stroke, high fever, evil, pain qualityThird, the left heart, right heart and heart failure, a common cause of1, left heart failure, coronary heart disease, hypertension, aortic stenosis aortic valve close the failure of hypertrophic obstructive cardiomyopathy, mitral regurgitation, acute glomerulonephritis, acute renal failure, transfusion too much too fast.2, right heart failure, acute pulmonary embolism, chronic pulmonary heart disease, congenital pulmonary valve stenosis defect large atrial septal defect and patent ductus arteriosus with a large number of left to right shunt pulmonary hypertension, restrictive cardiomyopathy, constrictive pericarditis and obstructive right ventricular failure syndrome, primary pulmonary hypertension.3, heart failure, acute rheumatic myocarditis, beriberi heart disease, ischemic heart disease idiopathic dilated cardiomyopathy. Large pericardial effusion, left ventricular failure with advanced.
Heart failure - differential diagnosisA determination of cardiac function and grading(A) functional classificationCardiac function classification of labor identification and treatment are certain guiding significance1, NYHA classification method: the New York Heart Association (NYHA) in 1964 based on induced heart failure symptoms (fatigue, palpitations, shortness of breath or angina), the required amount of activity of cardiac function is divided into l-Level 4 standard in clinical still widely used. The classification method is as follows:Cardiac function a (decompensation of cardiac function) asymptomatic physical activity without restriction.Cardiac function two (once the heart function insufficiency) heavy physical activity, symptoms of physical activity is slightly restricted.Cardiac function three (the second cardiac insufficiency) minor physical activity that is slightly mitigate after the rest of the obvious symptoms, physical activity greatly restricted.Cardiac function four (three degrees of heart function insufficiency) Even if any of the quiet resting state have obvious symptoms of physical activity completely restricted.
1994 American Heart Association NYHA standard complement in the original level 1-4 heart function, according to the ECG for Cardiovascular Angiography and objective examination results for each level of cardiac function divided AB, C, D, four sub-level objective no abnormal A mild exception of Class B, moderate abnormality of Grade D Grade C Severely abnormal. However necessary to recognize the subjective nature of such classification merely reflects the hemodynamic changes in symptoms does not apply to isolated diastolic heart failure and right heart failure.
2, exercise tolerance, determination ① they use a treadmill or a treadmill graded exercise test to limit the maximal heart rate limit the strength of the secondary amount of movement endpoint symptoms. ECG radionuclide angiocardiography, echocardiography, or continuous determination of the terminal gas oxygen and carbon dioxide concentrations, to measure the patients response to exercise stress ② OUTCOME MEASURES: total movement time, the amount of movement acting metabolic equivalents (MET) to measure IMET is the resting oxygen consumption is equivalent to 3.5ml • min-1kg movement when the left ventricular ejection fraction (LVEF) increased the degree of movement when the maximum oxygen intake (VO2 max) and anaerobic metabolism threshold (AT ) sports the total time must be combined with the exercise program is converted into MET in order to reflect the exercise tolerance, but using the same program can be used for the comparison of the treatment before and after exercise. (3) assessment standards: normal: Sports for the power of 6-10 MEIS, exercise LVEF increased> 5% during exercise maximal oxygen intake> 20ml • min-1kg, the AT> 14ml min-1kg. Reduce the degree of Weber cardiac function is divided into A, B, CD, four press VO2max and AT.
Killip class: to determine the status of cardiac function due to acute myocardial infarction in patients on bed rest, can not be used NYHA standard, should be used Killip class Ⅰ level without heart failure, grade II mild to moderate heart failure, can be Wen and a third heart sound and the back half lung field rales III level of severe pulmonary edema with heart failure class IV cardiogenic shock. Forrester type is derived on the basis of the relationship between cardiac index and pulmonary artery wedge pressure in acute myocardial infarction in patients with hemodynamic monitoring should be noted that regardless of calendar commander classification and the Forrester typing only for acute myocardial infarction patients can not be used for the judgment of old myocardial infarction or other heart function of patients with heart disease.
(B) ventricular systolic function determinationVentricular systolic function parameters commonly used in ejection fraction and the average peripheral shortening fraction (mvcf), load change in the ejection phase parameters susceptible to influence, if used properly still help to evaluate and compare different patients with left ventricular systolic function. The lower limit of normal left ventricular EF was 50% lower limit of normal exercise test at least higher 5% mvcf, 1.1 weeks / s, lower than the above values are prompted to left ventricular systolic dysfunction.
(C) Ventricular Diastolic FunctionMost of the observed indicators include echocardiography Figure mitral and radionuclide ventriculography Technical former isovolumic relaxation time, early and late diastolic filling velocity and the ratio of (E, A and E / A) early diastolic filling deceleration time atrial systolic pulmonary venous flow in the reverse flow velocity (AR), left ventricular outflow tract before the inner chamber systolic flow velocity (Ar) and A-of Ar time limit. Left ventricular relaxation decrease the performance of the eight peaks higher, lower peak E and E / A decreased IVRT extend the left ventricular myocardial stiffness increased (or decreased compliance), E peak eight peak at low E / A increased IVRT shortened. Left ventricular relaxation to reduce the combined stiffness increased when these changes and shortened mitral spectrum "false normalization" must be simultaneous detection of AR and A-Ar, the AR increased (> 20cm / s) and A Ar (<45ms) prompt ventricular dysfunction. Peak filling rate by radionuclide ventriculography Diastolic Function indicators to reduce and extend the peak filling time to reflect diastolic dysfunction.
(4) cardiac function to determine the classification method evaluationPlays an important role in the NYHA functional classification method simple heart function in the assessment of cardiac function of patients with heart disease to evaluate the therapeutic effect, contrast different clinical trials of candidate objects, as well as the treatment of different functions graded subgroup. Susceptible patients with noninvasive method to accept, and can repeatedly and quantitative imaging or imaging techniques, respectively, subject to the restrictions of its own technical errors, it is difficult to determine the clinical significance of mildly abnormal measurement results. For example, the clinical significance of the determination of indicators of left ventricular diastolic function E / A ratio of mild changes so far uncertain. Exercise test, the subjective enthusiasm of patients and medical personnel can significantly affect the movement of the total time and sports power the amount of these indicators may also review when patients are familiar with the inspection procedures and improved, so as to be mistaken for the treatment.
Heart failure two, acute heart failureAcute heart failure refers to a sharp decline or even loss of the ejection function in the short-term cardiac output. Severe acute myocarditis, myocardial infarction, ventricular outflow tract obstruction, atrial ball valve-like thrombosis or a liquid tumor incarcerated, pulmonary trunk or large branch infarction; Jiqi of volume overload such as trauma, infective endocarditis , myocardial infarction caused by valve perforation and damage to chordae rupture, ventricular papillary muscle dysfunction, ventricular septal perforation aortic sinus aneurysm ruptured heart chamber, the infusion of too much or too fast; Jiqi ventricular diastolic limited, such as acute pericardial plot of blood or fluid fast ectopic rhythm, severe arrhythmias such as ventricular fibrillation, ventricular standstill significant bradycardia.
Cardiac blood dysfunction, the degree of speed and duration of the compensatory function of the difference, the following performance: Syncope: refers to the reduced cardiac output caused by brain ischemia occurs a brief loss of consciousness if sustained for a few seconds more than occurrence of the limbs, convulsions, apnea, cyanosis, heart sounds disappeared or the corresponding arrhythmia (A Adams syndrome). Seizures were short, the onset of consciousness often be resumed immediately after shock. Cardiac arrest. Acute pulmonary edema: acute left heart failure performance typical of often sudden onset of a high degree of shortness of breath, rapid shallow breathing (30-40 times / min) orthopnea. Cough, cough white or pink foamy sputum pale gray, lips and extremities, cyanosis, sweating irritability, palpitations, fatigue and other signs, including the lungs extensive blistering tone and (or) wheezing, fast heart rate, apex gallop to expand under the law and the systolic murmur left heart border, arrhythmias, or alternating pulse, different heart disease, there are visible signs and symptoms of X-ray inspection hilar butterfly-shaped mass of shadow and around the extension and expansion of the heart border, the apex pulse weakened and other ECG revealed sinus tachycardia, or a variety of arrhythmias, myocardial injury, left atrioventricular hypertrophy.
Third, congestive heart failureCongestive heart failure, also known as chronic heart failure or chronic cardiac insufficiency, it is a long period of pressure and (or) volume overload state due to pathogenic factors to the heart, resulting in depletion of cardiac reserve force, compensatory loss of function of cardiac output absolute or relative, unable to maintain the body metabolic needs of the circulatory disturbance syndrome. Congestive heart failure, circulatory disorders, mainly body. Hypoperfusion of the pulmonary circulation congestion and arterial system. Can be divided into the left heart failure, right heart failure and heart failure congestive heart failure first occurs mainly in the side.
(A) left ventricular failureLeft heart failure is the most important of the most common type of heart failure. It refers to the left heart can not be fully discharged the pulmonary venous blood, causing pulmonary congestion and arterial ischemic hypoperfusion of vital organs. Failure can be divided into the left atrium (eg, mitral stenosis, left atrial myxoma caused by left ventricular filling obstructed left atrial congestion, expand, and even failure) and left ventricular failure, which is common in hypertension, coronary heart disease, myocarditis, cardiomyopathy, artery stenosis and (or) regurgitation, mitral insufficiency Keshan disease, acute glomerulonephritis, and ventricular septal defect, patent ductus arteriosus, coarctation of the aorta and other congenital heart disease.
Clinical manifestations: (1) difficulty in breathing is the most important clinical symptoms according to severity by exertional dyspnea, until the rest also difficulty in breathing, and even orthopnea or paroxysmal nocturnal dyspnea. In addition, cough, hemoptysis, cough, white or pink foamy sputum (acute pulmonary edema into fatigue, cyanosis, palpitations and other symptoms. In severe cases, Cheyne-in Stoke respiratory system severe brain ischemia, induced by hypoxia; ② different causes heart disease, there may be special symptoms, such as coronary heart disease patients may have angina, cardiopulmonary death in the performance of thick triceps insufficiency, mitral stenosis may have a hoarse voice, and hypertrophic heart disease may be a history of syncope [J]; left heart failure are often the heart dullness to the left to expand the apex was the lifting of the pulse, heart rate acceleration, the first heart sound weakened a variety of arrhythmias, the apex systolic murmur (left ventricular enlargement; the mitral relatively regurgitation) often the third, fourth heart sound or gallop may have alternating pulse. In addition, different heart disease can still be the corresponding signs of mitral regurgitation 3/6 systolic murmur at the apex, aortic valve disease in the main aortic valve area noise and other small blisters that may be associated with wheeze in the lung bases signs of pleural effusion in some patients with mitral stenosis and left atrial a liquid is the most common tumor in the left atrial failure clinical pulmonary edema signs, the first heart sound hyperthyroidism apical diastolic murmur in the former there are mitral valve to open the valve sound, the latter, there may be tumor Park off the sound and the pulmonary valve second heart sound, hyperactivity and other signs of laboratories and equipment check: (1) X ray examination often left ventricle and (or) left atrial enlargement, pulmonary congestion or pulmonary edema levy, Kerley, line B appears thicker due to (pulmonary lymphatic deposition in the lung lobules interval) there are different X-ray findings in the different causes, such as aortic valve disease heart often has boot-shaped heart, the aorta widened elongation, mitral stenosis was pear-shaped heart, esophagus barium swallow often the limitations of left atrial pressure trace, etc.; ② The electrocardiogram showed left atrial and (or) left ventricular hypertrophy disorders, negative V1 ECG P-wave terminal force (Ptf V1) increased the-0.02mm • S ≤ (mm • sec); ③ echocardiography to display valvular disease, they can still detect heart size and ventricular wall activity is quite helpful in determining the etiology of left ventricular failure; the degree of of ④ left ventricular failure, left heart catheterization, right heart floating catheter and cardiac radionuclide scanning methods give the assessment.
(B) right heart failureRight heart failure, right heart venous return blood can not be fully discharge caused by venous congestion and arterial insufficiency. Often secondary to left heart failure caused by pulmonary hypertension, can also be due to pulmonary heart disease with pulmonary stenosis or regurgitation, primary pulmonary hypertension, atrial septal defect with tetralogy of Fallot, aortic sinus aneurysm ruptured into the right heart, disease caused by myocarditis, cardiomyopathy, hyperthyroidism and heart disease.Clinical manifestations: (1) often oliguria, nocturia, gastrointestinal tract congestion symptoms such as nausea, vomiting, anorexia, palpitations, shortness of breath, fatigue and other symptoms; the ② circulation congestion signs such as sagging edema, pleural effusion, ascites, jugular vein engorgement and pulsatile, hepatic jugular reflux and positive signs, cyanosis, abdominal distension, hepatomegaly, jaundice, heart and even cirrhosis; ③ The corresponding signs of heart disease, due to right heart failure secondary to left heart failure based on, so often about ventricular enlargement the precordial lifting beats, liver the expansionary beat systolic murmur, and mitral valve area (the tricuspid valve is relatively regurgitation), right ventricular third heart sound or gallop.
Laboratory and instrumental examinations: (1) X-ray examination may have the right heart or left ventricular enlargement of the superior vena cava and azygos vein expansion, may be associated with two working parents or unilateral pleural effusion; ② The electrocardiogram showed right atrial and ventricular hypertrophy strain, right axis deviation ; (3) venous pressure was significantly increased venous pressure in the normal 0.294-1.37 kPa (3-14 cmH2O)], average 0.98kPa (9.9 cmH2O and); the ④ severe right heart failure may have abnormal liver and kidney function; ⑤ echocardiography, the right atrioventricular hypertrophy, right ventricular outflow tract widened and heart disease change.
(C) heart failureThe pathological changes in heart failure is most of the congestion but also the body of both the pulmonary circulation loop congestion is left heart failure development due. Also be found in myocarditis, cardiomyopathy clinical manifestations of left heart and right heart failure in the performance of integrated, but the extent may vary, often to the side of the main.
Fourth, asymptomatic heart failureAsymptomatic heart failure, also known as asymptomatic ventricular dysfunction, it refers to the clinical symptoms of congestive heart failure, but there are left ventricular dysfunction, resting ejection fraction decreased asymptomatic heart failure is congestive heart failure before a stage, which lasted for several months to several years.Heart failure is the heart in the case of pathological complete loss of reserve force loss of the compensatory ability of a stage, so that heart failure can be divided into three stages of asymptomatic, congestive refractory.
Five simple diastolic heart failureVentricle when the diastolic blood filling the left ventricular diastolic dysfunction to accept a reduced ability to only high filling pressure (left atrial pressure) to accept the normal amount of blood filling in order to maintain normal stroke volume, severe diastolic dysfunction, left atrial pressure increased by more than 2.6kPa (20mmHg) caused by liver congestion, so diastolic D power failure in anisotropic heart failure.Clinical manifestations: (1) congestive heart failure manifestations (pulmonary congestion); (2) small left ventricular wall of left ventricle are mostly thickening, left atrial enlargement; ③ The normal left ventricular EF (≥ 50%), diastolic dysfunction; ④ responded poorly to medication digitalis.Simple diastolic heart failure seen in the following diseases: ① hypertensive left ventricular hypertrophy; the ② hypertrophic cardiomyopathy; ③ aortic stenosis and left ventricular hypertrophy; ④ The ischemic heart disease, myocardial ischemia caused by the first diastolic dysfunction, lack of blood area can cause lung congestion; ⑤ The limit cardiomyopathy such as endomyocardial fibrosis of cardiac amyloidosis.
Pericardial diseases such as constrictive pericarditis and pericardial tamponade, major changes also the relaxation is limited, but unlike the above, muscle disease treatment also completely different, it is not listed in the people within the context ofCommonly used clinical indicators of diastolic function: ① The peak filling rate (PFR) and peak filling time (TPER) and other (radionuclide angiocardiography method); 2 E / A <(echocardiography method). These are load-dependent index is well received by the load before and after impact to the influence of age by heart rate, so to obtain the measured value is diastolic function, preload and afterload and heart rate factors combined effect results only rule out the load, heart rate and other factors after the impact, in order to move the change of ventricular diastolic function in to be careful so the diagnosis of diastolic dysfunction, diastolic dysfunction without clinical symptoms can not be diagnosed with diastolic heart failure.Severe systolic heart failure is often accompanied by diastolic dysfunction with improvement of systolic heart failure, diastolic function can be restored, and the nature of the above-mentioned problems.
Heart failure six with refractory heart failureRefractory heart failure, congestive heart failure symptoms and the clinical status of cardiac function III - IV level in patients with congestive heart failure with appropriate and complete diuretics and digitalis preparations vascular Zhang agent treatment and the elimination of complications and incentives has not improved or even deteriorated, be referred to as refractory congestive heart failureRefractory heart failure may have been heart disease end-stage performance, but a substantial part is due to ill-considered, ineffective or inappropriate treatment due to be deep to explore its causes. Appropriate analysis and evaluation should normally be first on the following factors: ① the original heart of the state changes and increase the lowered cardiac dysfunction, such as rheumatic heart valve patients with active rheumatism; (2) co-infection, especially lung infection, and endocarditis, increased cardiac load leaving the heart function state of deterioration. Patients with congestive heart failure, lung infections, its clinical manifestations often not obvious, resulting in the clinical diagnosis is more difficult; (3) associated with diseases such as hypertension, anemia, pulmonary embolism, and renal dysfunction, may increase the heart load, resulting in congestion heart failure increase; ④ The sodium intake of excessive sodium intake in the Food and Drug not the role of appropriate restrictions to enable the body fluid retention aggravating, and may weaken the diuretic; ⑤ electrolyte and acid-base balance disorders such as low blood potassium, low blood magnesium and for any reason caused by the acid-base balance disorders can affect cardiac function resulting in deterioration of cardiac dysfunction.
Seven, the clinical features of elderly heart failureThe elderly With the aging cardiovascular system and other systems are a series of changes in the morphology and function of the so-called "physiological aging". At the same time, the elderly and often multi-system environment in vivo stability of multi-organ disease occurrence change. Disease resistance. The functional reserve of various organs were reduced, the elderly, not only susceptible to heart failure, and clinical manifestations of complex treatment of contradictions, poor efficacy and high incidence of drug interaction deal with difficulties to the elderly heart failure. Physiological characteristics of the elderly cardiovascular system: (1) myocardial contractility decreased cardiac output is reduced; ② cardiac reserve function decline diminished left ventricular compliance, increased peripheral vascular resistance.Clinical features: Etiology: (1) cause for the older people are often also suffering from several diseases, coronary heart disease, pulmonary heart disease, hypertensive heart disease, diabetes, degenerative valvular heart disease ischemic heart disease and other. One of the main reason for others to participate and aggravated avoid heart failure disease complicated; the high incidence of ② iatrogenic heart failure. Elderly cardiac reserve capacity decreased intake of sodium excess and other factors can be sudden heart failure due to fast a lot of fluids. Incentives: elderly patients with acute heart failure a predisposing factor to respiratory tract infections (especially pneumonia), acute myocardial ischemia is the most common followed by arrhythmia, such as atrial fibrillation, paroxysmal supraventricular tachycardia and other incentives, including the commonly used dose general case lol, adrenal cortex hormones, pulmonary infarction, renal failure, fatigue, emotional meal.
Symptoms and signs of: ① elderly heart failure symptoms are atypical in some patients in the moderate heart failure can be completely asymptomatic, once subject to certain factors induced, can occur with severe left heart failure and life-threatening. The elderly with acute left ventricular failure due to decreased cardiac output, cerebral insufficiency, and more symptoms of cerebral ischemia; The ② elderly often have a variety of diseases coexist and influence each other to cover up or aggravate the symptoms and signs of heart disease, leading to diagnosis difficult. The following cases to support left ventricular failure were: cough and shortness of breath suddenly appear or worsen; night paroxysmal dyspnea dyspnea, abnormal lung wet Jun sound increased, and with postural changes; symptoms after application of vasodilators or diuretics quickly ease. ③ Evaluation of elderly heart failure is relatively difficult to be combined with obstacles to the comprehensive judgment of history, signs, auxiliary examination data (4) elderly heart failure is easily complicated by other organ function, such as renal failure, metabolic acidosis, cerebral circulation, hypoxemia , electrolyte imbalance and arrhythmia.
Acute myocardial infarction complicated by congestive heart failureThe reasons for acute myocardial infarction complicated by congestive heart failure as follows: ① The left ventricular infarct necrosis, decreased myocardial contractility and decreased left ventricular compliance caused by left atrial pressure increased; ② The small number of mechanical complications of acute myocardial infarction; ③ the right ventricle infarction. Clinical manifestations: (1) acute myocardial infarction complicated by congestive heart failure clinical manifestations of left heart failure were right; failure has less to see, if the inferior wall, posterior wall myocardial infarction associated with right heart failure, suggesting the possibility of right ventricular infarction; 2 chest X-ray shows the upper lobe pulmonary venous congestion in the lungs, caused by pulmonary interstitial and alveolar edema and serious hilar cloudy shadow outward expansion; ③ The Swan-Ganz floating catheterization to measure pulmonary capillary wedge pressure (PCWP) thermal dilution method cardiac output (CO) or cardiac index (CI). PCWP can be indirect estimation of left ventricular filling pressure (LVFP), CO / the PCWP can be estimated as an index of systolic function to the PC the WP> 2.4kPa (18mmHg), left ventricular systolic function in pulmonary congestion, peripheral hypoperfusion, CI, <2.2L min -1 • m-2.
Pump dysfunction classification: 1 Killip class method: Killip class method is based on clinical symptoms and signs to determine the level I: heart failure signs; grade II: mild to moderate heart failure, apical diastolic gallop law, less than 50% of lobes wet Jun tone; grade Ⅲ: severe heart failure more than 50% of the lobe wet very sound or pulmonary edema; IV level: cardiogenic shock. This classification does not include acute right ventricular infarction complicated by right heart failure, and should pay attention to the elderly serving identify bronchitis lung infection caused by pulmonary rales. ② According to the hemodynamic examination type (modified Forrester classification) the right to guide treatment. Type Ⅰ: the PCWP ≤ 2.4 kPa (18mmHg) CI> 2.2 L • min-1 m-2, patients without pulmonary congestion and the surrounding tissue hypoperfusion; type II: the PCWP> 2.4 kPa (18mmHg) CI > 2.2 L • min-1 m-2, patients without pulmonary congestion and peripheral tissue perfusion is inadequate; type III: the PCWP ≤ 2.4 kPa (18mmHg) CI <2.2 L • min-1 • m-2 Clinical hypotension and peripheral tissue perfusion is inadequate; without pulmonary congestion. Surrounding tissue hypoperfusion, pulmonary congestion this type of increased right ventricular diastolic pressure (right atrial pressure) can be divided into AB two subtypes; III Type A: right ventricular end diastolic pressure <0.66kPa (5mmHg) as the absolute or relative hypovolemia see. : Right ventricular end diastolic pressure> 1.33kPa.Conclusion (100mmHg) for right ventricular infarction.
Etiology and pathology diagnosis1, age: heart failure, age and etiology closely related. Newborns or infants with congenital vascular malformations more common. Endocardial elastic fibers, increased disease viral myocarditis, neonatal respiratory distress syndrome, severe asphyxia neonates with severe hemolysis psychosis or during the neonatal period heart failure. Severe pneumonia or bronchiolitis, infection, toxic myocarditis fluid or blood transfusion too much too fast, in fact often the infant of heart failure. Children 5-15 years old with heart failure, rheumatic fever with rheumatic B myositis, viral myocarditis, Keshan disease and acute glomerulonephritis, a few by the septal defect, patent ductus arteriosus caused by young adults while caused by rheumatic heart valve disease. Power failure, power is the most common, younger age the opportunity to merge myocarditis or rheumatism activities the more patients over the age of 40 are caused mostly by the Board of blood pressure, coronary heart disease or pulmonary heart disease.
Gender: rheumatic heart disease, especially mitral stenosis and connective tissue disease complicated. B heart disease caused by power failure women were more common. Syphilitic heart disease with coronary heart disease, cardiomyopathy, heart failure caused by aortic stenosis is more common in men.
3 Area: 3000 m above sea level plateau of heart failure should first be wary of mountain sickness. Keshan disease often occurs in certain regions of China (three provinces in Northeast China, Inner Mongolia, Shaanxi and Gansu, Sichuan and Yunnan provinces and autonomous regions) in rural areas.
History: often the cause of diagnostic provide important clues. Before the prevalence of streptococcal infection may suggest acute glomerulonephritis or rheumatic myocarditis. History of past or recent relevant section pain arthritis prompt rheumatic myocarditis, or heart valve disease. Years of history of hypertension, blood pressure levels continued to exceed 21/13kPa (160/100mmHg) accompanied by increased left ventricle, left heart failure disease hypertension of chronic cough, accompanied by progressive dyspnea, pulmonary heart disease. possibility. Malnutrition, especially lack of vitamin B1, or alcoholics, beriberi heart disease or cardiomyopathy heart failure in pregnancy should be suspected rheumatic heart valve disease should be considered first, followed by anemia, congenital toxemia of pregnancy and post-natal heart disease.
5, the more obvious signs: cyanosis in the general heart failure. Such as rendering obvious central hair purple and forest-like refers to (toe) in children should consider the congenital hair purple class of heart disease such as large vessels dislocation, double outlet right ventricle and forever artery stem, etc., and their hair purple before heart failure has long exist, such as the original non- cyanosis and heart failure, the more is left to right shunt congenital heart disease, such as septal defect or patent ductus arteriosus is not closed, converted to right to left shunt is the so-called Eisenmenger syndrome in heart failure . Adults with heart failure showed obvious cyanosis Department of chronic pulmonary heart disease.
Found a significant heart murmur or tremor, which is characterized by the difference between congenital cardiovascular malformations, rheumatic heart valve disease, syphilitic heart disease, congenital or acquired arteriovenous epidemic, etc. It must be emphasized accompanied by a remarkable expansion of left and right ventricular function of the mitral or tricuspid systolic murmur is the most common, sometimes rough easily with organic murmur confused. The heart is extremely expand diastolic murmur is not uncommon, attention should be identified.
In the diagnosis of heart failure on the judgment of the following signs should be cited as Note: ① The enlargement of the heart: Generally speaking, enlargement of the heart of heart failure there must be signs, but mitral stenosis, acute myocardial infarction, constrictive pericarditis and restrictive cardiomyopathy heart failure, heart can be significantly expanded; (2) heart rate fast: Most patients with faster heart rate in heart failure, sick sinus syndrome or severe atrioventricular block and heart rate can be unpleasant; (3) pulmonary rales: In majority of patients with left ventricular failure, pulmonary bottom of the Hui tone but is still in the stage of interstitial pulmonary edema in some patients, though already apparent shortness of breath, but the lungs may be time to tone at the bedside radiography to help diagnose; ④ jugular vein distention: chronic obstructive pulmonary emphysema, pulmonary pressure on the vena cava, right heart failure also shows jugular venous distention, hepatic jugular reflux levy data can be identified.
6, X-ray examination can be divided according to the form of cardiac enlargement, aortic and mitral heart, but also contribute to the identification of pericardial effusion and cardiomyopathy. To determine whether pulmonary congestion can be the difference between the pulmonary vascular and lung field change initiative hyperemia or passive congestion. Congestion initiative is important evidence of left to right shunt congenital heart disease, and passive congestion only reflect changes in heart failure.
7 ECG to detect myocardial infarction, myocardial ischemia, ectopic law, block the pathology or etiology of heart failure, atrioventricular hypertrophy with strain to provide an objective basis.
8, ultrasound heart diagram and ultrasound Doppler of mitral stenosis and regurgitation, aortic stenosis and bicuspid aortic valve Month thick obstructive cardiomyopathy, pericardial effusion, atrial a liquid tumor, atrioventricular valve or neoplasm, and congenital cardiovascular malformations of the semilunar specific changes. Diagnosis of heart disease cause of an important means of Doppler ultrasound to selectively observe the chambers of the heart or great vessels of a part of the blood disorder, the nature and extent to diagnosis of valvular lesions, and congenital malformations of the site.
