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symptoms of heart failure in the elderly, early symptoms and signs of heart failure in the elderly

symptoms of heart failure in the elderly, early symptoms and signs of heart failure in the elderly

Symptoms of heart failure in the elderly

Early symptoms: The early signs of left ventricular dysfunction are fatigue, decreased exercise endurance, increased heart rate by 15 ~ 20 beats/min, and then exertional dyspnea, nocturnal paroxysmal dyspnea, high pillow sleep and so on

Late symptoms: Chen-Shi breathing may occur in patients with severe heart failure, suggesting poor prognosis. In addition to the original signs of heart disease, physical examination can also find that the left ventricle is enlarged, the pulse intensity alternates, and the lung rales can be heard by auscultation.

Related symptoms: emaciation, cachexia, loss of appetite, anxiety and irritability

Symptoms of heart failure in the elderly

Because of the lack of specificity of symptoms and signs, it is difficult to make early diagnosis of heart failure in the elderly based on clinical manifestations alone. Therefore, it is necessary to carry out objective instrument examination, such as radionuclide ventricular function examination, echocardiography, cardiac catheterization, etc., and comprehensively analyze to get a correct diagnosis.

The cardiac function grade of asymptomatic heart failure is close to normal, Patients with low left ventricular function often have the following characteristics: they have a history of coronary heart disease and myocardial infarction in the past, but their heart function has not recovered to the original physiological level. Because patients gradually reduce their exercise or activity of life, or have not recovered to the original physical activity, they may have no sense of cardiac function restriction.

Atypical symptoms: Often complain of discomfort, fatigue, fatigue, mild chest tightness after activities, or chronic cough, but deny other typical symptoms of heart failure, without obvious dyspnea, orthopnea, edema, chest and ascites.

Symptoms: When heart failure, the symptoms and signs of clinical manifestations are different due to the difference between right heart failure mainly caused by systemic circulation congestion and left heart failure mainly caused by pulmonary circulation congestion. No matter which side of heart failure occurs, if it is not corrected in time, the other side will fail sooner or later. Left heart failure and right heart failure are described as follows.

1. Left heart failure

The pathophysiological basis of left heart failure is mainly pulmonary circulation congestion, which leads to a series of clinical symptoms and signs because of pulmonary circulation congestion, increased pulmonary venous pressure, decreased vital capacity, decreased pulmonary elasticity and decreased pulmonary compliance, and pulmonary congestion also hinders capillary gas exchange.

Symptoms:

(1) Fatigue and fatigue:

It can appear in the early stage of heart failure. At ordinary times, I feel weak limbs, which is further aggravated after activities.

(2) Dyspnea:

Dyspnea is not only a conscious symptom of patients, but also a comprehensive manifestation of labored breathing and shortness of breath. Patients with severe dyspnea show chest tightness and shortness of breath. Assist respiratory muscles to participate in breathing movements, as well as nose flapping, etc. Cardiogenic dyspnea must be distinguished from neurogenic dyspnea, which is also called sigh breathing. It often feels comfortable after a deep breath, and few people breathe faster. Cardiogenic dyspnea also needs to be distinguished from acidosis dyspnea, which deepens breathing, but the patient himself does not find breathing particularly laborious.

① Labor dyspnea:

Exercise dyspnea is one of the early symptoms of patients with left heart failure. This is dyspnea that occurs with the patient's physical activity, which can be alleviated or disappeared after rest. The causes of exertional dyspnea are:

A. During physical activity, the aerobic demand of the body increases, but the failed left heart cannot provide the corresponding cardiac output, and the hypoxia of the body intensifies, and CO2 is stored, which stimulates the respiratory center to produce "shortness of breath" symptoms.

B. During physical activity, the heart rate is accelerated and the diastolic period is shortened. On the one hand, the coronary perfusion is insufficient, which aggravates myocardial hypoxia; On the other hand, the decrease of left ventricular filling aggravates pulmonary congestion.

C. During physical activity, the return blood volume increases, lung congestion aggravates, lung compliance decreases, ventilation work increases, and patients feel dyspnea.

② Paroxysmal dyspnea at night:

Paroxysmal dyspnea at night is a typical manifestation of left heart failure. Patients have no dyspnea when they are engaged in general activities during the day, and they can take a supine position when they first fall asleep at night. However, they suddenly wake up due to dyspnea during sleep, and they must sit up for a moment before their symptoms gradually ease. Severe cases have difficulty breathing, obvious asthma, wheezing breathing, repeated cough, and bloody mucus-like sputum or foam sputum. After sitting up for a long time, asthma can gradually subside. If the patient falls asleep during the day, paroxysmal dyspnea can also occur during the day. Paroxysmal dyspnea occurs after falling asleep because:

A. Edema fluid stored in lower limbs or abdominal cavity is transferred to circulating blood volume in lying position, which increases venous reflux and aggravates pulmonary congestion.

B. During sleep, the response of nervous system to afferent information is weakened, so pulmonary congestion is not achievedTo a considerable extent, it is not enough to wake up the patient.

③ Orthopaedic breathing:

Orthopnea is a characteristic manifestation of left heart failure. In mild cases, only 1 ~ 2 pillows need to be added to relieve dyspnea. In severe cases, patients can avoid dyspnea in a half-lying position or sitting position. In the most serious cases, patients need to sit on the bed or chair, with drooping feet, upper body leaning forward, and hands clasping the edge of the bed or chair to assist breathing and relieve symptoms. This is a typical position for orthopaedic breathing. Orthopaedic breathing suggests that patients have severe heart failure. After secondary right heart failure, pulmonary congestion can be relatively reduced due to the decrease of right heart output, so dyspnea can be alleviated. The main causes of orthopnea are the aggravation of pulmonary congestion, the decrease of vital capacity and the decrease of effective volume of chest cavity in supine position.

A. Postural changes in pulmonary blood volume: The pulmonary blood volume in supine position increases (up to 500ml) compared with that in upright position, while the blood volume in upper part of the body may be partially transferred (up to 15%) to abdominal viscera and lower limbs during upright position, which reduces the return blood volume, thus reducing the congestion of pulmonary circulation.

B. Changes of postural vital capacity: When normal people lie down, the vital capacity is only reduced by 5%, while in patients with left heart failure, due to pulmonary congestion and decreased compliance, the vital capacity can be significantly reduced by 25% on average when lying down, and the vital capacity can be increased by 10% ~ 20% when sitting up.

C. Influence of diaphragm position: When the patient has liver enlargement, ascites or flatulence, the supine position can make the diaphragm position rise more obviously, hinder diaphragm movement, reduce the effective volume of abdominal cavity, and thus aggravate dyspnea. Orthopaedic posture can reduce lung congestion, thus reducing the patient's dyspnea, because:

A. When sitting upright, part of the blood is transferred to the lower half of the body due to gravity, which reduces lung congestion.

B. When sitting, the diaphragm position moves down relatively, the thoracic volume increases, and the vital capacity increases; Especially when heart failure is accompanied by ascites and hepatosplenomegaly, sitting posture relieves the squeezed chest cavity and improves ventilation.

C. When lying down, the absorption of edema fluid in the lower half of the body increases, while sitting upright can reduce the absorption of edema fluid and reduce pulmonary congestion.

(3) Cough, expectoration and hoarseness:

During heart failure, pulmonary congestion, tracheal and bronchial mucosa are also congested and edematous, and respiratory secretion increases, which can cause reflex cough and expectoration increase, and sometimes become the main symptoms before the attack of heart failure. Cough is usually aggravated when you are tired or lying down at night, and it is accompanied by cough or foam sputum. Frequent cough can increase pulmonary circulation pressure and affect venous return, induce paroxysmal dyspnea and aggravate shortness of breath, and also aggravate right ventricular load. Acute pulmonary edema can cough up a large amount of pink foam sputum, especially in supine position. Enlargement of left atrium or dilation of common pulmonary artery and aortic aneurysm in mitral stenosis can compress trachea or bronchus, causing cough, expectoration and hoarseness. Pulmonary infarction and pulmonary congestion are easy to be complicated with bronchitis or bronchopneumonia, which can cause cough and expectoration.

(4) Hemoptysis:

In heart failure, when the pulmonary vein pressure rises, it can be transmitted to the submucosal vein of bronchus and dilate it. When the submucosal dilated vein breaks, it can cause hemoptysis, and when the congested pulmonary capillaries break, it can also cause hemoptysis. The amount of hemoptysis is uncertain and bright red. Mitral stenosis may have massive hemoptysis (rupture of bronchial venules or pulmonary venous hemorrhage). Pulmonary edema or pulmonary infarction may have hemoptysis or cough pink foamy sputum.

(5) Cyanosis:

The face of patients with severe heart failure, such as lips, earlobes and extremities, may appear dark color, that is, cyanosis. Cyanosis caused by mitral stenosis is obvious in zygomatic region on both sides, forming mitral valve face. Significant peripheral cyanosis can occur in acute pulmonary edema. Cyanosis is mainly caused by pulmonary congestion, pulmonary interstitial and/or alveolar edema, which affects pulmonary ventilation and gas exchange, makes hemoglobin oxygenation insufficient, and increases reduced hemoglobin in blood.

(6) Increased nocturia:

Increased nocturia is a common and early symptom of heart failure. The ratio of nocturnal urine to daytime urine in normal people is 1: 3, and the amount of urine during the day is more than that at night. The nocturia in patients with heart failure increased, and the ratio of nocturia to daytime urine was inverted to 2 ~ 3: 1. Its occurrence mechanism may be related to the following aspects:

(1) Cardiac function is improved, cardiac output is increased, and subcutaneous edema fluid is partially absorbed during supine rest at night, which is related to the increase of renal perfusion blood flow.

② Sympathetic nerve excitability decreased, renal vascular resistance decreased and renal filtration rate increased during sleep. Normal renal vascular resistance is regulated by sympathetic nerve and renin angiotensin system activity, The increase of renal vascular resistance in upright position and exercise decreased renal water-sodium filtration rate, while the decrease of renal vascular resistance in supine position increased renal water-sodium filtration rate. This change of postural regulation was not obvious in normal people, but became particularly obvious in patients with heart failure due to the increase of circulating norepinephrine concentration and plasma renin activity.

(7) Chest pain:

Some patients may have angina-like chest pain, and about half of patients with primary dilated cardiomyopathy may have chest pain, which may be related to subendocardial ischemia of dilated and hypertrophic heart.

(8) Symptoms of central nervous system:

Manifestations include insomnia, anxiety, nightmare, hallucination and delirium in severe cases, and the latter is accompanied by time, place and person's orientation disorder, which further develops into slow response and coma. If it is caused by heart failure alone, it often indicates the end stage of the disease.

(9) Arterial embolism symptoms:

4% of patients with primary dilated cardiomyopathy had a history of systemic embolism at the time of diagnosis. Follow-up observation shows that 18% of patients with heart failure without anticoagulation will have systemic circulation embolism, and 85% of patients with cardiogenic systemic circulation embolism are located in brain or retina.

2. Right heart failure

Right heart failure is mainly manifested as increased systemic circulation pressure and congestion, which leads to dysfunction and abnormality of various organs, with obvious signs and relatively few symptoms.

(1) Symptoms:【小于】 /p>The symptoms of right heart failure are mainly caused by congestion in gastrointestinal tract, kidney and liver.

① Gastrointestinal symptoms:

Gastrointestinal congestion can lead to loss of appetite, oil aversion, nausea, vomiting, abdominal distension, constipation and epigastric distension and pain. Pain is often dull or accompanied by heavy feeling, which can be aggravated by palpation of upper abdomen or liver. Usually, chronic congestion does not cause pain, but when acute exacerbation of chronic congestion, patients can produce obvious epigastric distension and pain. Nausea, vomiting and oil aversion should be distinguished from the side effects caused by cardiac drugs such as digitalis, quinidine and amiodarone. When heart failure worsens, oil aversion can lead to cardiogenic cachexia, which is a sign of poor prognosis and usually indicates the end stage of the disease.

② Liver pain:

Swelling of liver congestion and swelling of liver capsule stimulate visceral nerve and cause pain. In the early stage, I mainly felt fullness and discomfort or heaviness in the right upper abdomen. With the aggravation of chronic congestion, I gradually felt dull pain and discomfort in the liver area. If it is acute liver swelling or acute exacerbation of chronic congestion, the pain in liver area is obvious, and sometimes it can be misdiagnosed as acute abdomen, such as acute hepatitis and cholecystitis. Deep inhalation, fatigue, tight belt and liver palpation can aggravate pain.

③ Increased nocturia:

Chronic renal congestion can cause renal hypofunction, relative increase of renal blood flow and absorption of subcutaneous edema fluid in lying position, increase of nocturia with increased urine specific gravity (mostly 1.025 ~ 1.030), which can contain a small amount of protein, transparent or granular tube, a small number of red blood cells, and slightly increase of plasma urea nitrogen. After effective anti-heart failure treatment, the above symptoms and laboratory indexes can be alleviated or returned to normal.

④ Dyspnea:

If right heart failure is secondary to left heart failure, after right heart failure, ventricular output is reduced and pulmonary congestion is reduced, which can alleviate dyspnea of left heart failure. However, if ventricular failure is aggravated by a significant decrease in cardiac output (which can be regarded as the end-stage manifestation of heart failure or secondary pulmonary hypertension), dyspnea will become very serious. Isolated patients with right heart failure may also have different degrees of dyspnea. Its mechanism may be related to the following factors:

A. The pressure of right atrium and superior vena cava is increased, which can stimulate baroreceptors and reflex the respiratory center.

B. The acidic metabolites produced by the decrease of blood oxygen content and the relative increase of anaerobic metabolism can stimulate the excitement of respiratory center.

C. Pleural effusion, ascites and swollen liver will affect respiratory movement.

⑤ Others:

A few patients with severe right ventricular failure may also have central nervous system symptoms, such as headache, dizziness, fatigue, irritability, lethargy, delirium, etc., due to cerebral circulation congestion, hypoxia or imbalance of water and electrolyte induced by diuretics. If the right ventricular outflow tract is severely blocked (such as severe pulmonary hypertension and pulmonary artery stenosis), the right ventricular stroke volume cannot increase with the demand, and dizziness can be aggravated during activity, and even syncope symptoms similar to left ventricular outflow tract obstruction may appear. Patients with right heart failure may have low fever due to increased heat production and slow blood flow, and their body temperature is generally less than 38.5 ℃, which will reduce fever when heart failure is compensated. High fever suggests infection or lung infarction.

(2) Physical signs:

Heart failure in the elderly has few signs and no specificity. Common signs are wet rales in the lungs, slight sunken edema in the ankle, tachycardia and so on. Old people often have chronic bronchitis, senile or obstructive emphysema, and wet rales in auscultation of lungs. Long-term bedridden or debilitated elderly people with heart failure are more likely to have edema in sacrum than lower limbs. Normal elderly people can have tachycardia when they are slightly tired, but they do not necessarily have heart failure. Typical signs include alternating veins, third or fourth heart sounds, jugular vein enlargement, heart murmur, enlargement of heart boundary, hepatoma, ascites and so on. The typical signs of left and right heart failure are as follows:

(1) Signs other than the original signs of heart disease:

A. Heart enlargement: Generally, left heart failure, especially in chronic process, has heart enlargement, Left ventricular enlargement is the main factor, The apical beat shifts to the left and down, and the heart enlargement includes tensogenic enlargement and myogenic enlargement. In the early stage of heart failure, in a certain range, with the elongation of myocardial fibers, the contraction force and stroke volume of myocardium increase correspondingly. At this time, the heart enlargement belongs to tensogenic enlargement, which is an effective compensatory way that can play an immediate role. However, in the late stage of heart failure, the myocardial fibers are further elongated beyond a certain limit, but the effective power of contraction decreases, thus losing the compensatory significance. At this time, cardiac enlargement is called myogenic enlargement. Heart enlargement is not necessary before heart failure. Heart failure can occur before heart enlargement in some chronic constrictive pericarditis, restrictive cardiomyopathy, acute myocardial infarction, sudden aggravation of rapid or slow arrhythmia, and rupture of valve or chordae tendineae.

B. Diastolic galloping rhythm: It is not necessary for left heart failure, but the appearance of this sign is an important evidence for the diagnosis of left heart failure, especially for newly appeared ones. Combined with clinical symptoms, it is of greater significance for judging left heart failure, so some people call it "heart cry for help". According to the different time and mechanism of its occurrence, it can be divided into the following types:

A. Early diastolic galloping law: also known as the third heart sound galloping law. In essence, it is an enhanced pathological third heart sound. It occurs in the early stage of ventricular filling, located 0.13 ~ 0.16 s after the second heart sound, with low pitch, in the apical area or its medial side, especially when the patient lies on the left side at the end of deep exhalation. When the heart rate increases more than 100 beats/min, the pathological third heart sound, together with the first and second heart sounds, forms a three-tone rhythm, which is like a running horseshoe sound. Because it occurs in the early diastole, it is called the galloping rhythm in the early diastole. It is suggested that ventricular diastolic overload is an important sign of common myocardial failure or acute left ventricular enlargement. Physiological third heart sound can be heard in healthy adolescents, but rarely occurs in adults after 40 years old, but can occur in patients with heart failure at any age, so it is necessary to judge its significance in combination with clinical practice.

B. Late diastolic galloping rhythm: also known as the fourth heart sound galloping rhythm. It is composed of pathological fourth heart sound and first and second heartA triple melody composed of tones. It occurs in the late diastole, before the first heart sound, with low frequency, low amplitude and low tone. It is easy to hear in the apical area or its medial side with a bell stethoscope, and it is the loudest in the left lateral position and during exhalation, which has the characteristics of frequent changes. Functional changes appear and disappear at will. Normal atrial contraction can be recorded on phonocardiogram, but auscultation is generally difficult to hear, and can only be heard when left ventricular compliance declines. However, it often disappears when accompanied by atrial fibrillation, mitral stenosis, etc., which makes left atrial contraction weak or blood flow into left ventricle limited.

C. Four-tone rhythm and overlapping galloping rhythm: Four-tone rhythm, also known as locomotive galloping rhythm, refers to the simultaneous occurrence of pathological third heart sound and fourth heart sound, that is, there are two extra heart sounds in diastole, which form four-tone rhythm together with the first and second heart sounds. If the heart rate is 100 ~ 110 beats/min, it is easy to hear, and its rhythm is like the sound of wheels colliding with rails when a train runs, so it is also called locomotive running horse law. If the heart rate increases further to 120 ~ 130 beats/min, Diastolic period is shortened, and pathological third and fourth heart sounds are nearly overlapping. Especially when combined with first-degree atrioventricular block (P-R interval is prolonged), atrial contraction falls in the rapid ventricular filling period, which accelerates the rapid ventricular filling, makes the fourth heart sound and the third heart sound overlap and become loud, and a very loud single sound appears in the middle diastolic period, which is called overlapping running horse law. If the heart rate is slowed by pressing the carotid sinus, the overlapping galloping rhythm will be separated again, and the four-tone rhythm will be restored.

C. Hyperactivity of second heart sound in pulmonary valve area in patients with heart failure often indicates increased pulmonary circulation resistance and pulmonary hypertension. When left heart failure occurs, the pressure of pulmonary veins and pulmonary capillaries increases and dilates congestion, and pulmonary arterioles often have protective contraction and spasm, so as to reduce pulmonary congestion and prevent pulmonary edema. On the other hand, the contraction and spasm of pulmonary arterioles further cause the increase of pulmonary artery pressure. Long-term spasm can make pulmonary arteriole wall hardening and lumen narrowing, resulting in more obvious pulmonary hypertension and hyperactivity of the second heart sound in pulmonary valve area. When the left heart failure is further aggravated and the contractile force is obviously weakened, The left ventricular emptying time is prolonged, and the closure of aortic valve can lag behind that of pulmonary valve (the closure component of pulmonary valve of second heart sound is later than that of aortic valve in normal times). As a result, the reverse division of second heart sound can be produced, which is more obvious when exhaling, and can be alleviated or not obvious when inhaling.

D. Systolic murmur in precordial region: In some patients with heart failure, mitral regurgitation is caused by enlarging atrioventricular annulus or shifting papillary muscles due to left ventricular dilatation, resulting in systolic reflux murmur. Most murmurs are blowing murmurs in the whole systole, with loudness above Grade II, located in the precordial area or the inner side of the apex, and conducted to the left armpit.

E. Alternating pulse: Alternating pulse can appear in some patients with heart failure. Palpating peripheral artery can feel normal pulse rhythm but alternating strength. Some can only be found when measuring blood pressure. When the air is gradually deflated during pressure measurement, when the systolic blood pressure is 0.66 ~ 4.0 kPa (5 ~ 30mmHg), only half of the arterial pulsation sounds or the intensity of arterial pulsation appears alternately. It is easy to find alternating veins when the patient takes the sitting position and holds the wrist high to shoulder level. The appearance of alternating veins often indicates severe cardiomyopathy, such as primary cardiomyopathy, left ventricular outflow tract obstruction, coronary heart disease and severe hypertension. Most patients are accompanied by the third heart sound and tachycardia, which are mostly persistent. It can also be paroxysmal. After heart failure is corrected, alternating veins may disappear. The mechanism of alternating veins may be related to the different filling degree of ventricle during diastole. When the ventricular diastolic filling is more, the cardiac output is also more and the pulse is strong and powerful; When ventricular diastolic filling is insufficient, pulse may alternate between strong and weak.

Alternating pulses need to be distinguished from frequent premature pulses. Weak pulses of alternating pulses do not appear early, but can be slightly delayed. Pulse alternation caused by premature pulses often appears early.

F. Wet rales at the floor of the lung: Typical signs of wet rales at the floor of the lung often appear in patients with left heart failure. Usually, when inhaling, stethoscope can be used to hear wet rales at the bottom of both lungs. If wet rales occur only on one side of the patient, it is often more common on the right side. However, the wet rales in most patients with heart failure occur on both sides, that is, they are symmetrical. If rales are confined to the left side during heart failure, care should be taken to exclude the possibility of left lung infarction.

The occurrence of wet rales on the left or right side may also be related to the patient's habit of liking the left or right lateral position. When the duration of left heart failure is prolonged or aggravated, moist rales can also develop upward from the lung floor. When examining patients, it is of certain reference value to record the range and degree of wet rales for observing the progress of disease and judging the curative effect.

G. Pleural effusion: About 1/4 patients with left heart failure can have pleural effusion.

H. Chen-Shi breathing: also known as tidal breathing or periodic breathing. Chen-Shi breathing can occur in patients with severe heart failure, which is characterized by periodic changes of gradual enhancement and gradual weakening of patients' breathing, that is, from gradual weakening to stopping, then gradually strengthening and deepening, reaching the peak, then gradually slowing down and becoming shallow, until stopping again, lasting 30 ~ 60s, and then resuming the next cycle. Its mechanism is due to prolonged blood circulation time in severe heart failure, cerebral hypoxia and cerebral edema caused by pulmonary congestion and hypoxemia, and periodic breathing caused by brain dysfunction. When the carbon dioxide retention time is prolonged, The ventilation response to stimulate the respiratory center is enhanced, Hyperventilation is caused, but apnea after hyperventilation occurs due to the decrease of sensitivity of forebrain (nerve cell cluster in cerebral cortex and thalamus) to ventilation stimulation. During apnea, carbon dioxide retention increases arterial blood carbon dioxide partial pressure until it exceeds the stimulation threshold of respiratory center, and then hyperrespiration begins again.

Chen-Shi breathing can occasionally occur during normal sleep, but persistent Chen-Shi breathing often indicates severe heart failure and, or, nervous system diseases. Metabolic brain dysfunction caused by hypertensive encephalopathy can damage the reflex mechanism of respiratory nerve and cause periodic breathing.

② For patients with right heart failure, in addition to the original signs of heart disease, there can also be:

A. HeartVisceral enlargement: When the right heart fails simply, the right ventricle and/or right atrium enlarge. However, right heart failure is mostly secondary to left heart failure, so the heart is mostly enlarged wholeheartedly. When the right ventricle is enlarged with hypertrophy, obvious pulsation can be seen under the xiphoid process, and lifting pulsation can be found in palpation of precordial area. If there is obvious pulmonary hypertension with enhanced right ventricular activity, the oscillation of pulmonary artery closure can be felt between the 2nd and 3rd costals at the left edge of sternum, and the right ventricular diastolic galloping rhythm can be heard at the left lower edge of sternum and under the xiphoid process or in the precordial area (when the right ventricle is enlarged), which is enhanced when inhaling. If the right ventricle is obviously enlarged, it can cause relative tricuspid insufficiency. Systolic blowing murmur can be heard in the auscultation area of tricuspid valve, which is enhanced when inhaling, and conducted in Lang and apical areas, but not more than the left axillary front line. The murmur is weakened after heart failure control. In addition, when tricuspid regurgitation is obvious, a large amount of blood flow reflows to the right atrium during recontraction, which aggravates systemic circulation congestion and causes jugular vein and superior vena cava pulsation and liver dilation pulsation in late contraction. And sinus tachycardia caused by reflex due to decreased cardiac output.

B. Venous filling, irritation and pulsation: Abnormal filling or irritation of superficial veins such as external jugular vein is an important sign of right heart failure, and severe cases may be accompanied by pulsation. Its mechanism lies in systemic circulation congestion. When the right heart fails, the cardiac output decreases, the right ventricular end-diastolic pressure increases, and the right atrial pressure also increases. There is no valve between the vena cava and the right atrium, so the increase of the right atrial pressure reversibly spreads into the vena cava system, causing the increase of the superior and inferior vena cava pressure, resulting in the filling or irritation of superficial veins such as external jugular vein, dorsal hand vein and sublingual vein. The pulsation of jugular vein and superficial vein of extremity may appear in cases of severe right heart failure, but in supine position, the pulsation is not obvious due to the extreme filling of jugular vein. Generally, patients should be observed in 45 half lying position. The filling degree of jugular vein can reflect the pressure of right atrium, which is of certain value in judging the severity and prognosis of right heart failure.

C. Hepatomegaly, tenderness and hepatic jugular vein reflux sign are positive: Hepatomegaly and tenderness are one of the earliest and most important signs in patients with right heart failure, and hepatomegaly and tenderness can occur in patients with right heart failure. The faster the hepatomegaly, the more obvious the tenderness. The liver is larger than that under the xiphoid process, and sometimes the right costal margin is not satisfactory or unpalpable. Hepatic palpation should be combined with percussion at the liver boundary, because when the liver is prolapsed, the subhepatic pole can extend below the costal margin of the right clavicle midline, but the distance from the upper boundary to the lower boundary of the liver is still 9 ~ 11cm at the clavicle midline. Liver texture is related to the time of liver congestion and enlargement. Patients with long-term chronic right heart failure can cause cardiogenic cirrhosis, which makes the liver hard and sharp, while patients with acute right heart failure cause acute congestion and enlargement of the liver, which is soft and blunt.

Liver enlargement usually occurs before subcutaneous edema, but it recovers slowly, even after other symptoms and signs disappear. In patients with chronic right heart failure, when the right heart failure is compensated, the liver can be relieved but cannot return to normal.

Compressing the congested and swollen liver with the palm for half a minute can increase the blood volume returning to the inferior vena cava and right atrium. However, due to the failure of the right heart, the blood volume returning to the heart cannot be compensated, which further increases the venous pressure and shows more obvious jugular vein filling, which is called positive hepatic jugular vein reflux sign. This is also one of the main signs of right heart failure, but it can also be seen in exudative or constrictive pericarditis. In addition, this kind of hepatic jugular vein reflux is useful for distinguishing the pulsation of arteries or veins in the neck, but it is not necessarily reliable for potential heart failure, because it can only be qualitative and not quantitative compared with normal; Furthermore, jugular vein pressure can change with the change of intrathoracic pressure.

D. Low droop edema: Low droop edema is a typical sign of right heart failure, which occurs after jugular vein filling and liver enlargement. Most cases occur in secondary right heart failure, while isolated right heart failure and subcutaneous edema can be the first sign. Before heart failure causes peripheral sunken edema, there must be a large amount of extracellular fluid accumulation. It is generally believed that before edema occurs, the body weight has increased by about 10%, that is, edema occurs when the body fluid retention exceeds 5kg. The moisture in the tissue space of normal adults is about 7kg, but it can increase to 15 ~ 20kg in heart failure. In heart failure, water mainly remained in extracellular space, extracellular space and space cavity, while circulating blood volume and intracellular water only increased slightly.

Edema fluid is easy to accumulate in the part where hydrostatic pressure is the highest, that is, the low-hanging part of the body. In upright position, sunken edema often appears first in front of feet, ankles and tibia, which is obvious in the afternoon and recovers at night. With the aggravation of the disease, extracellular fluid expands and edema develops gradually. In bedridden patients, sacrococcygeal and medial thigh edema is more obvious. In patients without orthopnea, because they can lie down, edema can occur in the upper arms and hands, but rarely involve the face, except in infants and young children. Systemic edema can occur in the late stage of untreated patients with chronic heart failure. Edema can affect genitals, thoracic cavity, limbs and head, but rarely has fluid retention exceeding 45kg. Chronic edema can lead to erythema, induration and pigmentation in the lower skin, especially in the front of ankle bone. These patients are also prone to subcutaneous cellulitis.

E. Pleural effusion: Pleural effusion can occur in heart failure caused by any reason, most of which occur in patients with whole heart failure, and pleural effusion is often bilateral. Unilateral pleural effusion is more common on the right side, while bilateral pleural effusion often has more fluid on the right side. The protein content of pleural effusion (about 2%) is higher than that of subcutaneous edema fluid (0.2% ~ 0.5%), which is difficult to distinguish from pleural effusion caused by exudative pleurisy, but the number of cells caused by heart failure is less or normal.

F. Ascites: Ascites can be seen in advanced patients with chronic right heart failure or whole heart failure. The composition of ascites is basically the same as that of pleural effusion. In some patients with right heart failure, there may be obvious ascites but no obvious peripheral edema. The reason may be that the lateral pressure (lateral pressure refers to the pressure of venous blood volume on venous wall) decreases after peripheral vasoconstriction, while the lateral pressure increases due to visceral vasodilation, which is beneficial to fluid extravasation. Ascites caused by constrictive pericarditis appears earlier and persistently, with significant ascites volume and slight peripheral edema, often complicated with cardiogenic cirrhosis.

G. Pericardial effusion:It mainly occurs in patients with long-term and severe right heart failure. Inherent heart failure leads to the increase of systemic venous pressure, which affects the physiological fluid in pericardial cavity flowing back to the right heart through lymphatic vessels or veins, thus causing pericardial effusion, which is generally small and medium, and rarely reaches the degree of pericardial tamponade.

H. Cyanosis: Most patients with right heart failure have different degrees of cyanosis, especially in patients with cor pulmonale and congenital heart disease with right-to-left shunt. Cyanosis is more obvious in patients with right heart failure than asthma, while asthma is more obvious in patients with left heart failure. After right heart failure is secondary to left heart failure, dyspnea can be alleviated, but cyanosis can be aggravated. Cyanosis of right heart failure is mostly peripheral. The local temperature is low at the fingers (toes) of limbs, cheeks and earlobes, and cyanosis can disappear after massage or heating. Cyanosis is mixed in whole heart failure, which can also involve mucosa (oral mucosa) and trunk skin.

I. Odd pulse: Some patients with dilated cardiomyopathy have heart failure accompanied by pericardial effusion of different degrees, and the return blood volume of vena cava and right ventricular stroke volume do not increase obviously when inhaling. In addition, the chest cavity is negative pressure when inhaling, and the pulmonary vascular volume increases, which reduces the return blood volume of pulmonary vein and left ventricular stroke volume, resulting in weakened pulse when inhaling; When exhaling, the volume of pulmonary blood vessels decreases, which makes more blood flow into the left heart from pulmonary blood vessels, resulting in increased blood discharge from the left ventricle and stronger pulse, thus producing odd pulse. At this time, attention should be paid to distinguish it from the odd pulse of pericardial tamponade. During pericardial tamponade, the venous pressure rises because the return blood volume cannot increase when inhaling, while the chest cavity of patients with heart failure is negative when inhaling, which is beneficial to venous reflux, so the venous pressure decreases. Therefore, observing the changes of venous pressure during inhalation is helpful for identification.

J. Others: Some severe cases of right heart failure, anorexia caused by mental anxiety, gastrointestinal congestion, protein absorption disorder, water and electrolyte imbalance and excessive use of diuretics, etc., will lead to emaciation and cardiogenic cachexia.

3. Classification according to the development process of heart failure

(1) Acute heart failure:

The disease progresses rapidly, and the cardiac output drops sharply or even loses in a short time. When acute heart failure occurs, the heart function is often too late to compensate. It is more common in: ① acute diffuse severe myocardial damage; ② Acute cardiac bleeding or filling obstruction; Acute increased cardiac volume load; Severe arrhythmia; ⑤ Acute deterioration of chronic heart failure. Clinical manifestations are often acute pulmonary edema, cardiogenic shock, syncope and cardiac arrest, which are urgent and severe cases that need emergency treatment by clinicians.

(2) Chronic heart failure:

The disease progresses slowly and often goes through two stages:

① Compensatory period:

By using various compensatory mechanisms, the heart can still meet or basically meet the needs of metabolism. Therefore, under normal circumstances, patients can have no symptoms of heart failure for a long time.

② Decompensation period:

After the compensatory period, even if various compensatory mechanisms are used, the cardiac output can not meet the needs of metabolism, and the clinical manifestations of heart failure may appear at this time.

4. Classification by site of heart failure

(1) Left heart failure:

Left heart failure refers to heart failure caused by compensatory insufficiency of left ventricle, which is common in clinic and characterized by pulmonary congestion.

(2) Right heart failure:

Simple right heart failure is mainly seen in pulmonary heart disease and some congenital heart diseases, with systemic circulation congestion as the main manifestation.

(3) Bilateral heart failure:

That is, the combination of left heart failure and right heart failure, also known as bilateral heart failure.

This is the most common type of heart failure in clinic. Left heart failure and right heart failure can occur at the same time. For example, when acute and chronic diffuse myocarditis occurs, the left and right hearts are damaged at the same time, and extensive myocardial infarction involving left and right ventricles occurs; It can also occur successively, such as pulmonary circulation congestion and pressure increase when left heart failure, which can eventually lead to right heart failure; On the one hand, the pressure rises due to systemic congestion, and at the same time, the decrease of right ventricular output can also affect the left ventricular function, resulting in left ventricular failure. Therefore, heart failure seen clinically is often total heart failure.

5. Classification according to the changes of myocardial mechanical properties in heart failure

(1) Systolic heart failure:

It is mainly due to heart failure caused by hyposystolic function of myocardium and insufficient ejection of heart. Myocardial systolic dysfunction is the main cause of heart failure caused by most heart diseases in clinic, and systolic heart failure accounts for about 70% of all heart failure.

(2) Diastolic heart failure:

It mainly refers to heart failure caused by abnormal myocardial diastolic function, insufficient ventricular filling and/or disorder in diastole. Diseases that affect ventricular relaxation performance, such as hypertension and hypertrophic cardiomyopathy, and diseases that affect ventricular compliance performance, such as myocardial amyloidosis and restrictive cardiomyopathy, can lead to diastolic heart failure. It is reported that simple diastolic heart failure accounts for about 30% of all heart failure. Heart failure with diastolic insufficiency often has the following characteristics: ① There are basic causes such as hypertension, coronary heart disease (including angina pectoris and myocardial infarction), hypertrophic cardiomyopathy and aortic stenosis; ② The heart size is normal or slightly enlarged with signs of pulmonary congestion or pulmonary edema; ③ LVEF > 45%; The left ventricle was normal (LVDD 3.0 ~ 5.0 cm) and the wall thickness was normal or thickened on echocardiography in heart failure with left atrial dilatation first; ⑤ T wave inversion on electrocardiogram; ⑥ Regular anti-heart failure treatment is ineffective. It must be noted that most congestive heart failure has both systolic and diastolic dysfunction.

(3) Mixed heart failure (mixed heart failure)RT failure):

It refers to heart failure caused by the coexistence of myocardial systolic and diastolic dysfunction. It should be said that most of the heart failure seen in clinic is mixed heart failure, but the degree of systolic and diastolic dysfunction is different in mixed heart failure, especially the so-called simple systolic heart failure may also have different degrees of diastolic dysfunction. Therefore, it is difficult to distinguish between simple systolic heart failure and simple diastolic heart failure clinically.

6. Classification of cardiac function

At present, the classification system of heart failure degree widely used in clinic is the classification standard of heart failure adopted by New York Heart Association in 1964, also known as New York Heart Function Classification (NYHA Classification), which is based on the degree of limited movement of patients. Symptomatic heart failure is divided into 3 degrees or mild, moderate and severe in China. The corresponding relationship with YHA-like heart function classification is that first-degree heart failure is equivalent to grade II, second-degree heart failure is equivalent to grade III and third-degree heart failure is equivalent to grade IV. This classification method is concise and practical, but it has some limitations, such as it excludes asymptomatic heart failure with grade I heart function. Using NYHA cardiac function classification to mark the degree of heart failure basically includes asymptomatic heart failure, which is widely used.

7. Classification and diagnostic criteria of heart failure

(1) Cardiac function classification:

New York Heart Association (NYHA) Grading Method:

Grade I: General physical activity is not restricted, and there are no symptoms such as fatigue, fatigue, palpitation, dyspnea and angina pectoris, and no signs of heart failure.

Grade II: Physical activity is slightly limited, and there are no symptoms during rest, but symptoms such as fatigue, palpitation, dyspnea and angina pectoris and signs of heart failure such as increased heart rate and mild liver enlargement appear during general physical activity (such as walking at normal speed for 3 ~ 4km, going up the third floor and uphill, etc.).

Grade III: Physical activity is obviously limited, and there are no symptoms during rest. Slight physical activity (such as walking 1 ~ 2km at normal speed, going to the second floor, etc.) means symptoms such as palpitation, dyspnea or angina pectoris, and signs such as liver enlargement and edema.

Grade IV: Incompetent for any physical activity, there are still symptoms such as fatigue, palpitation, dyspnea or angina pectoris during rest, and signs such as visceral congestion and obvious edema. Patients with long illness may have cardiogenic cirrhosis.

The grading method is simple and easy to use, but it is greatly influenced by subjective factors and drug treatment. In 1994, the Standards Committee of American Heart Association revised the above classification, and added objective laboratory evaluation, including electrocardiogram, echocardiography, radionuclide angiocardiography, exercise test and so on. According to laboratory examination, it is divided into four levels: A, B, C and D; A: There is no abnormality in objective examination; B: Mild abnormality; C: Moderate abnormality; D: Severe abnormality.

(2) Pump failure classification (slightly supplemented by Killip classification):

Acute myocardial infarction pump failure is divided into 5 grades:

Grade I: There is no sign of heart failure, but PCWP can be increased, and the mortality rate is 0% ~ 5%.

Grade II: Mild to moderate heart failure, the range of lung rales is less than 50% of the two lung fields, the third heart sound, galloping horse rhythm, persistent sinus tachycardia or other arrhythmia, elevated venous pressure, X-ray signs of pulmonary congestion, and the mortality rate is 10% ~ 20%.

Grade III: Severe heart failure, the range of lung rales is larger than 50% of the two lung fields, and acute pulmonary edema may occur, with a mortality rate of 35% ~ 40%.

Grade ⅳ: cardiogenic shock, blood pressure【小于】90mmHg (12.0 kPa), oliguria (<20ml/h),皮肤湿冷,发绀,呼吸加速,脉率>100/min, the fatality rate was 85% ~ 95%.

Grade V: Cardiogenic shock and acute pulmonary edema occurred, and the mortality was extremely high.

(3) Diagnostic criteria of heart failure:

The diagnostic criteria for heart failure recommended by the American Heart Association are as follows:

① Left ventricular failure: Diagnostic basis:

A. X-ray revealed sudden enlargement of left ventricle, pulmonary congestion and/or butterfly cloud shadow in both hilums.

B. When adults have no mitral regurgitation, the third heart sound or galloping horse rhythm is heard in the left ventricular area, or alternating veins are touched.

C. When there is no aortic or mitral valve disease, left ventricular dilatation occurs in angiocardiography, and the cardiac index is less than 2.6 L/(min m2) when resting in supine position (or basic state).

D. When there is no aortic or mitral valve disease, or when there is no obvious hypertrophy of the left ventricle, the following changes occur:

A. Left ventricular end diastolic pressure (LV EDP) > 1.3 kPa (10mmHg) at rest, or left atrial mean pressure or pulmonary capillary wedge pressure (PCWP) > 1.7 kPa (13mmHg). Cardiac index (C ⅰ) at rest was【小于】2.6 L/(min m2).

B. When the lower limbs are properly exercised in supine position, the left ventricular end diastolic pressure (left atrial average pressure or pulmonary capillary wedge pressure) rises by more than 1.8 kPa (14mmHg), and the oxygen consumption increases by 100ml, while the cardiac output does not increase by more than 800ml, or the cardiac stroke does not increase.

C. Left ventricular enlargement with pulmonary congestion and pulmonary edema.

D. When aortic valve stenosis or insufficiency occurs, the size of left ventricle changes suddenly by X-ray examination, which indicates that when exercising and resting, the involvement of valve itself can reduce circulating blood flow, and ventricular hypertrophy causes ventricular end diastolic pressure to increase. Digitalis can reverse these physiological abnormalities and can be used as the basis for the diagnosis of left heart failure.

E. When mitral valve stenosis or insufficiency occurs, the left ventricular end-diastolic pressure rises, which indicates that during rest or exercise, the left atrial pressure or pulmonary capillary wedge pressure rises and the systemic blood flow decreases due to the damage of the valve itself. Similarly, in mitral stenosis, even if the left atrium is enlarged, pulmonary congestion cannot be used as the left heartDiagnostic criteria of ventricular failure. However, left ventricular failure can be diagnosed when galloping horse law or alternating pulse occurs.

All patients with one of the above conditions can be diagnosed as left ventricular failure.

② Right ventricular failure:

A. X-ray showed sudden enlargement of right ventricle and (or) dilatation and abnormal pulsation of superior vena cava.

B. The third heart sound or galloping horse rhythm is heard in the right ventricular area of adults, which is enhanced when inhaling.

C. Alternating veins in the pulmonary artery.

D. When there is no pulmonary valve or tricuspid valve disease, the cardiac index is less than 2.6 L/(min m2) when the angiocardiography has right ventricular dilatation, recumbent rest or basic state.

E. The following changes occur when there is no pulmonary valve or tricuspid valve damage or no obvious hypertrophy of the right ventricle:

A. When the patient was resting in supine position and in basic state, the right ventricular end diastolic pressure (or right atrial mean pressure) increased by more than 5mmHg (0.7 kPa) and the cardiac index was less than 2.6 L/(min m2).

B. When lower limb exercise is properly performed in supine position, the right ventricular end diastolic pressure (or right atrial average pressure) rises by more than (0.7 kPa) 5mmHg, and for every 100ml increase in oxygen consumption, the cardiac output does not increase by more than 800ml, or the cardiac output does not increase.

C. When the right ventricle is enlarged, systemic circulation congestion is found, such as jugular vein distention, hepatic enlargement, liver pulsation in late contraction, positive hepatic jugular vein reflux sign, edema of lower limbs or whole body, etc.

F. When tricuspid valve stenosis or insufficiency occurs, the right ventricular end-diastolic pressure rises, indicating that during rest or exercise, the right atrial pressure rises and blood flow decreases due to the pathological changes of the valve itself.

G. When pulmonary valve stenosis or insufficiency occurs, the right ventricle is dilated by angiocardiography or suddenly enlarged by X-ray examination.

It should be pointed out that during rest and exercise, the increase of right ventricular end diastolic pressure and the decrease of pulmonary blood flow are only caused by valve damage and myocardial hypertrophy caused by valve damage, not simply caused by ventricular failure.

Those who meet one of the above conditions can be diagnosed.

8. Diagnostic criteria for heart failure with left ventricular diastolic dysfunction

Standards revised by the Third National Conference on Heart Failure in Dalian in May 1995;

(1) Diagnostic basis:

① There are definite clinical manifestations of left ventricular CHF: accompanied by heart diseases that are easy to cause diastolic dysfunction, such as hypertension, coronary heart disease, hypertrophic cardiomyopathy, aortic stenosis, myocardial amyloidosis, etc.; However, there was no valvular regurgitation and abnormal intracardiac shunt.

② Physical examination did not enlarge the heart boundary or only slightly increased.

③ Chest X-ray examination showed clear pulmonary congestion and normal or slightly larger heart shadow.

④ Electrocardiogram examination: A. Systolic function index is normal; B. Abnormal diastolic function index; Left ventricular isovolumic diastolic period (ⅰ RP) was prolonged (> 100ms) and rapid filling period (REP) was shortened (<110ms),缓慢充盈期(SFP)延长(>250ms).

⑤ Echocardiography: M-mode or two-dimensional echocardiography showed that the left ventricular end diastolic diameter (LV EDD) did not increase or slightly, the ventricular wall thickened or normal, the left ventricular ejection fraction (LVEF) was normal (> 50%), the shortening rate of left ventricular diameter was > 25%, and the slope of mitral valve EF decreased.

⑥ Doppler echocardiography: A. Left ventricular systolic function parameters were normal. B. The ratio of rapid left ventricular diastolic filling to left atrial systolic flow velocity through mitral valve orifice, that is, E/A【小于】1, and other diastolic filling parameters are abnormal.

⑦ Radionuclide angiocardiography: Left ventricular ejection fraction (LVEF) was normal, peak ejection rate (PER) was normal (> 2.5 ED ⅴ/s), peak filling rate (PER) decreased, peak filling time (TPFR) prolonged, and first 1/3 filling rate (1/3 FR) decreased.

8 Cardiac catheterization and angiocardiography: A. Left ventricular ejection fraction is normal; B. The rate of diastolic left ventricular pressure drop (-dP/dt) slowed down, and the relationship between diastolic left ventricular volume and pressure (P/AV) increased.

(2) Judgment method:

① Those who meet the first 6 items can make clinical diagnosis (in primary medical units, those who meet the first 5 items can also make clinical diagnosis).

② If it accords with the first 6 items plus any one of 7 or 8 items, the diagnosis can be confirmed.

If there are 1 ~ 5 diagnostic criteria and E/A > 1, the diagnosis of heart failure with left ventricular diastolic dysfunction cannot be ruled out. It must be comprehensively judged according to age, clinical manifestations, left ventricular anterior and posterior load, mitral valve structure and function and other diastolic filling parameters, especially the normalization of E/A ratio of severe left ventricular diastolic dysfunction.

Clinical practice shows that it is not enough to diagnose heart failure, but also to diagnose the etiology. Heart failure is often multi-etiological, such as coronary heart disease, hypertension, cor pulmonale, diabetes, degenerative heart disease and other common diseases, which can occur at the same time and become the cause of heart failure.

The heart is damaged by various cardiovascular diseases or other pathogenic factors, but it can be compensated within certain limits, and often leads to heart failure under the action of some inducing factors. Therefore, it is necessary to diagnose the inducement of patients with heart failure for effective treatment.

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