1、Heart Failure,Shifang Ding , MD,Dep . of Cardiovascular Diseases Wuhan General Hospital,DEFINETION,Physiologically，heart failure is defined as the inability of the heart to match its output to the metabolic needs of the body (determined as O2 consumption) even though filling pressures of the heart a
2、re adequate,The biochemical features are not as certain as the hemodynamic, but appear to involve defective conversion by the heart muscle of chemical energy to mechanical Work,GENERAL OVERVIEW,Heart failure is predicted to be the major worldwide cardiovascular problem. The increase in prevalence of
3、 heart failure is due in part to the general aging of populations throughout the world,and to improved treatment of myocardial infarction so that many patients survive the acute event but with a damaged heart,More than 400,000 new cases of congestive heart failure are diagnosed each year in the U.S.
4、A. and it is estimated that 2 to 3 million Americans have congestive heart failure. The annual mortality rate approaches 200,000, and congestive heart failure is the leading diagnosis at hospital dismissal for patients older than 65 years. The annual health care cost of congestive heart failure exce
5、eds $10 billion,CATEGORIES OF HEART FAILURE,In the clinic, the type of heart failure is generally identified by its duration (acute or chronic), initiating mechanisms, the ventricle that is primarily affected, the characteristic clinical syndrome, and the underlying physiologic derangements,1. Acute
6、 vs chronic heart failure 2. Left vs right heart failure 3. Backward vs forward heart failure 4. Low vs high output heart failure 5. Systolic vs diastolic heart failure,New York Heart Association Functional Classification for Congestive Heart Failure,Patients with cardiac disease but without resulti
7、ng limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain,Class ,Patients with cardiac disease resulting in slight limitations of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue，
8、palpitation, dyspnea, or anginal pain,Class ,Class ,Patients with cardiac disease resulting in marked limitations of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain,Class ,Patients with cardiac disease result
9、ing in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of anginal syndrome may be present even at rest. If any physic alactivity is undertaken , discomfort is increased,CLINICAL MANIFESTATIONS OF HEART FAILURE,The signs and symptoms of heart failu
10、re depend on the ventricle that has failed and the duration of the failure. The clinical syndrome of left ventricular failure is dominated by symptoms of pulmonary congestion and edema. In contrast, right ventricular failure is dominated by signs of systemic venous congestion and peripheral edema. F
11、atigue and weakness are common in both types of heart failure,Left Ventricular Failure,Complaints of respiratoty discomfort or distress dominate the symptoms of left ventricular failure. They vary with postion, stress, and activity. They are often associated with physical signs of disturbances in th
12、e lungs or in respiratory control mechanisms,Sysptoms,DYSPNEA,Like pain or anxiety, dyspnea is subjective and difficult to quantify. Because breathing is ordinarily automatic and effortless except after strenuous exertion, the complaint of breathlessness may signify anything from awareness to distre
13、ss. Dyspnea during modest exertion is usually the first symptom of left heart failure. Usually dyspnea is associated with increased rate breathing (tachypnea),Although precise mechanisms for dyspnea remain uncertina，its occurrence in left heart failure clearly depends on the increase in the blood an
14、d water content of the lungs at the expense of the air volume. Ventilation increases as the air volume is progressively encroached upon, and as the minute ventilation approaches the maximal ventilatory capacity, the likelihood of dyspnea increases,PAROXYSMAL NOCTURNAL DYSPNEA,A bout of urgent respir
15、atory distress, verging on suffocation, may rouse the patient unexpectedly from sleep and cause him to seek relief desperately, either by sitting up or by rushing to the open window to breathe “fresh air.” Respiration may be labored and wheezing, hence the designation “ cardiac asthma ”,The episodes
16、 represent intolerable aggravation of pulmonary congestion and edema during sleep in the supine position. A combination of dulling of the respiratory center to sensory input from the lungs during sleep and increase in venous return to the lungs makes it possible for pulmonary venous congestion and e
17、dema to accumulate to the point of precipitating the frightening episode of breathlessness,ORTHOPNEA,Progressive, and often urgent, dyspnea that occurs soon after lying flat is designated as orthopnea; it is relieved by sitting up. The physiologic basis for orthopnea is the augmented venous return f
18、rom the lower extremities and splanchnic bed to the lungs that results from redistribution of gravitational forces in the supine position and the reabsorption of diurnal edema,In the patient with heart disease, orthopnea is reliable evidence of left ventricular failure. In contrast, the dyspnea of c
19、hronic lung disease of musculoskeletal disorders is rarely aggravated by lying flat,The patient learns to avoid respiratory distress at night by supporting head and thorax by two or more pillows. In severe heart failure, orthopnea may force the patient to sleep upright in a chair rather than in bed.
20、 In some patients with extensive coronary artery disease and left ventricular failure, orthopnea occurs only in the left lateral position; the mechanism for this is unclear,Cough and expectoration are common in left heart failure, presumably a consequence of reflexes from the congested lungs and bro
21、nchi. The patient may also manifest an orthopneic cough which has the same significance as orthopnea, and is presumably the consequence of venous congestion and edema of the tracheobronchial walls,In some patients, precordial distress may substitute for breathlessness in the supine position. This “n
22、octurnal angina” is also somehow related to the mobilization of water from the tissues to the circulation when the patient goes to bed,ACUTE PULMONARY EDEMA,In an acute episode of left ventricular failure, such as that which follows myocardial infarction, the inability of the left ventricular myocar
23、dium to handle the blood that the competent right ventricle is delivering to it may result in an abrupt increase in pulmonary venous and capillary pressure, followed by flooding of the interstitial spaces and alveoli,If the edema is confined to the interstitial spaces of the lungs, an increase in re
24、spiratory frequency because of stiff lungs would be expected to produce alveolar hyperventilation and respiratory alkalosis; conversely, once free fluid enters the terminal bronchioles and mounts the respiratory tree, respiratory acidosis may occur because of imbalances between alveolar ventilation
25、and alveolar blood flow (ventilation-perfusion inhomogeneities),Pulmonary edema may begin with a cough, with wheezing, or with breathlessness. Often there is a sense of oppression in the chest. At first, except for the abnormal breathing pattern and the evidences of heart disease, there may be few p
26、hysical signs,In time, as free fluid enters the distal airways, rales become audible, most marked in the dependent parts of the lungs, but extending upward as the attack worsens. In a severe attack, the patient is pale, sweating, cyanotic, obviously gasping for breath, and usually producing frothy s
27、putum which may be blood tinged,In addition to being breathless, the patient is generally pale, a bit dusky, and sweaty. His handshake is cold because of peripheral vasoconstriction. The heart rate is rapid and the pulse pressure is narrow, with a modest increase in diastolic blood pressure. If only
28、 the left ventricle has failed, the neck veins are not distended,Physical Sings,THE HEART,Enlargement of the heart is usually evident to inspection and palpation of the apical impulse and is confirmed by roentgenologic and radiographic examination. Angina pectoris is not a manifestation of heart fai
29、lure, nor is palpitation common unless overzealous administration of digitalis and diuretics has occasioned digitalis toxicity,As the left ventricle fails and pulmonary venous pressure increases, pulmonary arterial pressure also increases, and the heart sound attributable to pulmonary valve closure
30、increases in intensity. Also, as the left ventricle dilates, the mitral valve leaflets fail to appose properly, resulting in mild mitral incompetence,THE LUNGS,A characteristic consequence of interstitial edema and pulmonary venous congestion is tachypnea. As left heart failure progresses, interstit
31、ial edema is succeeded by alveolar edema and fluid in the terminal bronchioles, particularly at the lung bases. Accordingly, bilateral basal rales are common in moderate failure of the left ventricle,Abnormalities in the electrocardiogram arise from the underlying cardiac disorder and from therapeut
32、ic agents, e.g. , digitalis and diuretics, rather than from heart failure perse,Electrocardiogram,The x-ray can be exceedingly helpful in the diagnosis of left ventricular failure. Typically, the cardiac silhouette is enlarged, often assuming telltale configurations that are determined by the underl
33、ying disorder,Radiologic Aspects,In contrast to the normal, in which pulmonary arteries are prominent in the lower lung fields, pulmonary vasculature is prominent at the apices, reflecting pulmonary venous hypertension and redistribution of blood flow because of edema and fibrosis at the bases. Enla
34、rged hilar shadows accompany the prominent pulmonary veins in the upper lung fields,Prominent septal lines, particularly near the costophrenic angles (kerleys lines), indicate the presence of interstitial edema. The advent of alveolar edema is signaled by a generalized clouding of the lung fields. P
35、leural effusion may occasionally occur in left heart failure, but is much more apt to occur in biventricular heart failure,Evidence of interstitial and alveolar edema often lessens or disappears when right ventricular failure supervenes. However, hydrothorax generally persists. A widened shadow of t
36、he superior vena cava may provide reliable evidence of right ventricular failure and systemic venous congestion,Right Ventricular Failure,Isolated failure of the right ventricle is uncommon, generally a consequence of corpulmonale secondary to intrinsic lung disease,Clinical Manifestations,More ofte
37、n, right ventricular failure is a sequel to left ventricular failure. In right ventricular failure, neck veins are distended and fill from below; the engorged liver may be tender to gentle pressure, and compression causes a surge of blood into the neck veins (hepatojugular reflux),In time, when both
38、 ventricles have failed, evidence of right ventricular failure may dominate the scene; but continuing dyspnea and rales attest to the persistence of left ventricular failure, and the continuing low cardiac output is manifested by signs of increased sympathetic nervous activity and of organ hypoperfu
39、sion,Weakness may be marked and is occasionally associated with anorexia, weight loss, and malnutrition (“cardiac cachexia”). Not only severe heart failure but also digitalis, diuretics, and electrolyte disturbances are generally involved in the genesis of this cachectic state,ABNORMAL HEART AND LUN
40、GS,Although the breathlessness of the left ventricular failure may be somewhat relieved by right heart failure, usually some dyspnea persists along with tachypnea and basal rales. Severe right heart failure (and dilatation ) may produce tricuspid valvular insufficiency, thereby contributing to syste
41、mic venous engorgement,The murmur of tricuspid insufficiency is distinguished from that of mitral insufficiency by its location (lower left border of sternum) and by its tendency to increase during inspiration. Hydrothorax, generally unilateral, is more common than in isolated left ventricular failu
42、re,LIVER,The liver is usually enlarged and palpable in right heart failure, often in association with mild abdominal discomfort, and generally somewhat tender to compression. In severe right heart failure, particularly if the onset is acute, constraint of the swollen liver by its tight capsule may c
43、ause right upper quadrant pain,Tricuspid insufficiency accompanying right ventricular dilatation may cause synchronous pulsations in neck veins and liver. Splenomegaly is uncommon except in prolonged congestion of the liver. Rarely is the enlarged spleen tender from congestion per se,SUBCUTANEOUS ED
44、EMA,Dependent edema, manifested as swelling of feet of ankles, developing gradually during the day and subsiding by morning, is a characteristic feature of right heart failure. Invariably, it is anteceded by systemic venous congestion, but after diuresis subcutaneous edema may linger even though sys
45、temic venous hypertension has been relieved by the reduction in venous blood volume,Usually a gain in weight precedes clinical evidence of edema. If edema is allowed to persist, complications such as low-grade cellulites may occur. The combination of edema and slowed venous flow predisposes to throm
46、bosis and to pulmonary embolism,The massive pitting edema of the lower extremities that was commonly seen before the advent of potent diuretics is now rarely encountered except in instances of gross neglect,HYDROTHORAX,It is so uncommon for hydrothorax to complicate isolated failure of the right ven
47、tricle, that the association of pleural effusion and cor pulmonale should lead to search for an independent mechanism for the pleural effusion, e.g., pulmonary infarction. On the other hand, as indicated previously, it is quite common in combined heart failure(right and left),The pathogenesis of hyd
48、rothorax involves impaired removal of water from the pleural space because of high venous pressures in both the pulmonary and systemic circulations, thereby not only compromising transcapillary exchange of water in the pleural but also impeding lymphatic drainage,Hydrothorax contributed to dyspnea n
49、ot only by encroaching on the air volume but also reflexly, probably by stimuli from lungs and chest wall. Pulmonary infarction may cause pleural effusion in tow days: by direct contiguity of the infarcted area of the lung and the pleural space, or by aggravation of heart failure,ASCITES,Clinically
50、evident excess of free fluid in the abdominal cavity is designated as ascites. It is a late manifestation of right heart failure, generally associated with marked systemic venous hypertension, evere peripheral edema, and hydrothorax. It occurs most frequently in patients with tricuspid valvular disease (or with constrictive pericarditis ),
