Heart failure in the elderly

Introduction to heart failure in the elderly Heart failure is a clinically very common pathological manifestation, a syndrome of cardiac dysfunction caused by various heart diseases. It refers to the need for hemodynamics and neuro-humoral activity due to a decrease in myocardial contractility and/or diastolic dysfunction due to a decrease in myocardial contractility and a requirement for absolute or relatively lower than normal systemic tissue metabolism. Abnormalities, clinical symptoms and signs of arterial insufficiency, pulmonary and/or systemic venous congestion, from hemodynamics, due to cardiac systolic dysfunction, the heart chamber pressure is higher than normal (left End diastolic pressure or left ventricular filling pressure >2.4kPa; right ventricular end-diastolic pressure or right ventricular filling pressure >1.3kPa) is heart failure, also known as cardiac dysfunction (cardiacinsufficiency). basic knowledge The proportion of illness: 0.006% Susceptible people: the elderly Mode of infection: non-infectious Complications: coma cardiogenic cirrhosis

The cause of heart failure in the elderly

Primary myocardial systolic and diastolic function is reduced (30%):

1. Diffuse and localized myocardial damage:

(1) Cardiomyopathy: Dilated cardiomyopathy often affects the whole heart, manifesting as extensive myocardial lesions, thinning of the heart wall, enlargement of the heart chamber, and also one-sided lesions or only one lesion in the clinic. The influence of cardiomyopathy on cardiac function often leads to a decrease in systolic and diastolic function, and the systolic function is more pronounced. The main pathological change of hypertrophic cardiomyopathy is cardiac hypertrophy, which limits myocardial relaxation, and the late stage of the disease can also affect myocardial contractile function. Type of cardiomyopathy is mainly due to the limited filling of the ventricle, which makes the heart unable to effectively relax.

(2) Myocarditis: Myocarditis caused by various causes such as viral, rheumatic, bacterial or other connective tissue diseases can cause myocardial localized or diffuse damage, which weakens myocardial systolic and diastolic function.

(3) Myocardial infarction: After myocardial infarction in ischemic heart disease, myocardial systolic and diastolic function is weakened due to the decrease in the number of effective myocardial tissue and the imbalance of myocardial contraction, especially in the large anterior wall infarction.

(4) Myocardial fibrosis: myocardial fibrosis caused by various causes can alleviate myocardial systolic and diminished function. For example, in ischemic heart disease, there is a myocardial fibrotic lesion formed by long-term chronic ischemia. Myocardium hardens, myocardial contraction and diastolic dysfunction.

(5) Myocardial poisoning: various harmful physical factors such as radiotherapy for chest tumors; chemical factors such as anti-tumor drugs, antiarrhythmic drugs and drug use; biological factors such as harmful microbial infections release toxins can cause myocardial limitation Or diffuse damage, resulting in decreased myocardial function.

(6) Abnormal substance deposition: such as myocardial amyloidosis, deposition of abnormal substances such as glycogen and pigment, which can reduce myocardial compliance and affect diastolic function.

2, primary or secondary myocardial metabolic disorders:

(1) ischemia and hypoxia: primary or secondary myocardial ischemia and hypoxia can cause myocardial energy metabolism disorders, affecting myocardial relaxation and contraction.

(2) Vitamin B1, B12 deficiency: When vitamin B1 is deficient, pyruvic acid can not be converted into acetyl-CoA into the tricarboxylic acid cycle through oxidative decarboxylation, which can cause ATP production disorder, energy deficiency and heart failure, vitamin B12 deficiency Severe anemia reduces myocardial oxygen supply, increases stress and induces heart failure.

(3) Electrolyte disorders: Abnormal increase or decrease of important ions in the body such as potassium, sodium, calcium, magnesium, chlorine, etc. can directly affect the electrical, mechanical functions and normal metabolism of the heart, leading to heart failure.

(4) acid-base balance disorders: severe acid-base poisoning can also significantly affect myocardial systolic and diastolic function.

(5) Endocrine disorders: various endocrine diseases such as hyperthyroidism, primary aldosteronism and diabetes can affect myocardial systolic and diastolic function through a variety of different mechanisms, leading to heart failure.

Long-term over-loading of the heart (25%):

1. Excessive pressure overload: A. Common diseases leading to excessive pressure overload in the left heart system: hypertension, aortic stenosis, aortic coarctation, hypertrophic obstructive cardiomyopathy, etc.; B. causing excessive pressure overload in the right heart system Common diseases: pulmonary hypertension, pulmonary stenosis, pulmonary embolism, chronic obstructive pulmonary disease and mitral stenosis. C. Increased blood viscosity in diseases that cause excessive stress on the whole heart system.

2. Excessive capacity load:

(1) Diseases leading to excessive left ventricular volume overload: aortic regurgitation, mitral regurgitation, ventricular aneurysm;

(2) diseases leading to excessive right ventricular volume overload: pulmonary valve insufficiency, tricuspid regurgitation and ventricular septal defect.

(3) causes excessive ventricular volume overload disease: hyperthyroidism, chronic anemia, arteriovenous fistula and the like.

Excessive pressure and volume overload can lead to heart failure.

Diastolic filling is limited (20%):

The disease that restricts the heart during diastolic filling is tamponade, constrictive pericarditis, and barrel chest with heart shift. In most cases, the myocardium itself has no diminished performance, and The cure of the primary disease, the symptoms and signs of heart failure are also controlled, so some people think that these diseases are not the cause of heart failure in the true sense, but they can also reduce the cardiac output due to insufficient ventricular diastolic filling. When the ventricle is dilated, the venous return blood disorder causes the symptoms and signs of heart failure, and the long-term limitation of cardiac activity can also weaken the myocardial contractile function. Therefore, in this sense, such diseases should still belong to The cause of heart failure.

Insufficient venous return (10%):

Acute blood loss or large body fluid loss and blood volume reduction caused by exudation and acute small arteries, venule dilatation (decapitation) can lead to insufficient blood flow to the venous return, decreased cardiac output, and symptoms and signs similar to heart failure.

Arrhythmia (10%):

Rapid arrhythmias such as atrial, ventricular and atrioventricular junction tachycardia, frequent premature beats and ventricular flutter, tremors, etc., and slow arrhythmias such as atrioventricular block, left and right bundle conduction Blocking, etc. can affect heart function to varying degrees due to its speed, severity and duration, and cause heart failure.

Incentive

Most of the elderly heart failure have predisposing factors. The influence of these predisposing factors on heart failure is often greater than the original heart disease. Therefore, correcting or controlling the cause is an important link in the prevention and treatment of heart failure in the elderly.

1, infection: infection is one of the most common factors inducing and aggravating heart failure, especially respiratory infections, accounting for half of all incentives, 9% of the elderly suffering from pneumonia died of heart failure, as well as the urinary system, stomach Intestinal system and biliary system infection, infection is often accompanied by fever, sympathetic nerve excitement during fever, peripheral vasoconstriction, increased cardiac load; infection can cause heart rate to increase, myocardial oxygen consumption increases, diastolic filling time is shortened, myocardial blood Supply reduction, thereby aggravating the contradiction between supply and demand of myocardial oxygen; the toxin released by pathogenic microorganisms during infection can directly damage the myocardium and inhibit myocardial contractility; respiratory infection can also cause contraction and paralysis due to trachea and bronchi, affecting airway ventilation and lung gas Exchange, reduce myocardial oxygen supply, pulmonary vascular bed contraction can increase right heart load; such as hemolytic streptococcal infection may also lead to rheumatic myocarditis and heart valve damage, all of which may induce or aggravate heart failure, due to fever, Fast heart rate, insufficient ventricular filling, decreased blood output, increased pulmonary venous and pulmonary capillary pressure, leading to urgency Sexual left heart failure, respiratory infections are prone to hypoxemia, causing myocardial hypoxia to promote heart failure.

2, overwork and emotional excitement is also a very common factor inducing and aggravating heart failure: overwork can increase the heart load, once the heart's compensatory ability is exceeded, heart failure can be induced; sympathetic nerves are excited when emotional, catecholamines increase Can cause heart rate to accelerate and contraction of peripheral small blood vessels, which in turn induces heart failure.

3, arrhythmia: arrhythmia, especially rapid type such as various tachycardia and frequent premature beats can induce and aggravate heart failure, the mechanism is:

(1) The heart rate is increased and the myocardial oxygen consumption is increased;

(2) The ventricular filling time is shortened, the diastolic filling is reduced, and the cardiac output is reduced;

(3) increased heart rate can also reduce coronary perfusion, affect myocardial blood supply, slow arrhythmia such as severe atrioventricular block, sick sinus syndrome, etc., can also reduce cardiac output due to slow heart rate and room Cardiac failure is induced by the coordinated destruction of the contraction of the ventricular contraction. Arrhythmia can also occur after heart failure. The latter causes heart failure to worsen and the heart is converted from compensatory to decompensated.

(4) Electrolyte disorders and acid-base balance disorders: electrolyte imbalance and acid-base balance disorders are also common predisposing factors for heart failure. They can be induced by mechanisms that affect the electrical and mechanical functions of the heart, interfere with myocardial metabolism or directly inhibit myocardial contractility. Heart failure.

(5) Blood loss and anemia: blood loss can reduce the amount of blood returning to the vein, insufficient ventricular filling, decreased blood output, and reduced blood supply to the heart muscle; blood loss can also cause a reflex heart rate to increase, myocardial oxygen consumption increases, and heart rate increases during anemia. The compensatory increase of circulating blood volume, the increase of cardiac load, and the decrease of oxygen carrying capacity of hemoglobin can cause chronic degenerative changes in the myocardium, which are the mechanisms that induce or aggravate heart failure in blood loss and anemia.

(6) too much blood transfusion infusion: the elderly's heart reserve capacity decreased, infusion or excessive blood transfusion, excessive sodium input, can increase the heart load in a short period of time and induce heart failure.

(7) Drug effects: Digitalis preparations, -blockers and some antiarrhythmic drugs may aggravate or induce heart failure even at normal doses.

(8) Concomitant with other diseases: patients with heart failure are accompanied by other diseases such as lung, liver, kidney, blood, endocrine diseases and tumors, severe hypoxia, malnutrition, etc., or other diseases besides heart failure in the cardiovascular system. Coexistence can make heart failure worse, and the treatment effect is worse.

(9) Anesthesia and surgery: It is not uncommon for patients with heart failure to undergo anesthesia and surgery. Internal medicine such as various diagnostic tests (cardiac catheter, bronchoscopy, colonoscopy, etc.) and therapeutic surgery such as radiofrequency erosion treatment of tachycardia, installation Temporary or permanent cardiac pacemaker, heart valve balloon dilatation, PTCA, etc. can affect cardiac function, induce heart failure, surgical emergency surgery such as trauma treatment, organ rupture repair and elective surgery such as cholecystectomy, tumor removal, etc. Anesthesia is required and the entire surgical procedure is performed. Any factors affecting cardiac activity during anesthesia and surgery may induce or aggravate heart failure.

Pathogenesis

The basic pathophysiological changes of chronic congestive heart failure are the increase of residual ventricular systolic blood volume and the increase of ventricular diastolic pressure caused by myocardial contractility, and the occurrence of clinical manifestations is a recurring compensatory change. Such as venous congestion, increased circulating blood volume and increased extracellular water in the body, cardiomyocytes are the basic unit for performing systolic function. When myocardial ischemia, poisoning and inflammation occur, the cell membrane is first damaged, destroyed, and cytoplasmic contents leak. The cells swell, followed by cell lysis and death.

Cell damage caused by myocardial infarction is an ischemic necrosis. When the ischemic myocardium is reperfused, it is saved from the dead cardiomyocytes. Although the blood supply is restored, its diastolic function cannot be recovered in time. The state of the myocardium is called to suppress the myocardium, and the non-functional state of the myocardium is an important cause of heart failure after coronary artery occlusion.

In addition, when the myocardium is in a state of low perfusion or hypoxia for a long time, the cardiomyocytes reduce their contractile function to near hibernation in order to save energy consumption and avoid death. This is a function of the myocardium in the case of low perfusion. Down-regulation of adaptation, this phenomenon is generally reversible, that is, when the low perfusion correction, its function can still be restored, but the time required is longer, it takes several months or even more than one year, clinically seen in the area caused by insufficient coronary blood supply Hypoxic, showing hibernation in this regional myocardium, called hibernating myocardium, which still preserves life in the cardiomyocytes. The effect on heart function depends mainly on the amount and distribution of hibernating myocardium, such as large amount and distribution in the heart. Under the membrane, the effect is serious. Otherwise, the amount is small or distributed under the epicardium. The effect is light. The degree of heart failure and heart failure depends mainly on the amount of myocardial loss (including loss of function). Generally speaking, when When the myocardial loss exceeds 8% of the left ventricle, left ventricular compliance decreases, >10%, the ejection fraction decreases, >20% to 25%, then heart failure occurs, and if it exceeds 40%, cardiogenic shock occurs. .

How to protect cardiomyocytes, prevent or limit the amount of myocardial loss, is the basic measure to prevent heart failure. In addition, the quality of myocardial ischemia and the destruction of collagen network make the myocardial tissue lose the support of collagen network, and the compliance increases. Loss of high degree of coordination in myocardial contraction, resulting in cardiac ejection dysfunction and diastolic dysfunction, leading to the occurrence and development of heart failure, decreased myocardial contractility, especially the decline of ventricular contractility, is congestive The basic pathophysiological factors of depletion, congestive heart failure refers to the blood that the heart can not normally discharge from the large venous return, that is, the blood discharge function of the heart cannot adapt to the load of the heart, and thus the blood supply is insufficient (weak feeling) in various parts of the body. As well as the accumulation of blood and body fluids (aspiration, edema), only from a clinical point of view, congestive heart failure, can be divided into two categories of left heart failure and right heart failure, but the left heart failure will affect the right heart sooner or later Function, which produces bilateral heart failure, ie, heart failure, but at the beginning of heart failure, often in phase In the long period of time, it may only be manifested as asymptomatic heart failure, that is, only mild or no symptoms at all, but there is already left ventricular dysfunction.

Elderly heart failure prevention

Strengthening tertiary prevention is a fundamental measure to reduce the incidence of cardiovascular disease and mortality in the elderly.

Primary prevention: refers to the prevention of risk factors and fundamentally prevent or reduce the occurrence of diseases, mainly including the whole population strategy and individual strategies of high-risk subjects, reducing the incidence of cardiovascular disease in the elderly, starting from childhood, A good foundation for overall health.

Secondary prevention: Adhere to the regular physical examination and diagnosis and treatment of the elderly, early detection of the disease, early treatment, especially systemic treatment of patients, can reduce the incidence of complications and complications.

Tertiary prevention: It is mainly to reduce the cardiovascular mortality and mortality of the elderly, and actively carry out rehabilitation medical treatment, psychological medical treatment, family medical care, prevent the disease from worsening, reduce sickness, prolong life and improve the quality of life of the elderly.

Risk factors and interventions: The main risk factors for heart failure are high blood pressure (especially systolic blood pressure), diabetes, overweight, left ventricular hypertrophy, heart enlargement, advanced age, coronary heart disease, heart murmur, etc., coronary heart disease, hypertension or heart In patients with valvular disease, the risk of heart failure varies greatly, mainly related to the influence of cardiovascular risk factors on the heart. In the Framingham study, 50% to 60% of heart failure occurs in patients with the above risk factors. Therefore, people who believe that there are high-risk factors should do non-invasive cardiac function and evaluate to see if there is any impairment of heart function.

Complications of heart failure in the elderly Complications, coma, cardiogenic cirrhosis Can be complicated by upper respiratory tract infection, severe cases can occur coma, right heart failure can cause cardiogenic cirrhosis.

Symptoms of heart failure in the elderly Common symptoms: fatigue, exertional dyspnea, shortness of breath after appetite

Because of the lack of specificity of symptoms and signs in the elderly, it is difficult to make early diagnosis based on clinical manifestations. Therefore, it is necessary to carry out objective instrument examinations such as radionuclide ventricular function tests, echocardiography, cardiac catheterization, etc. Comprehensive analysis to arrive at the correct diagnosis.

Asymptomatic heart failure, cardiac function classification is close to normal, left ventricular dysfunction often has the following characteristics: previous coronary heart disease, history of myocardial infarction, and cardiac function did not return to the original physiological level, due to patients gradually reduce their exercise or living activities Ability, or not restored to the original physical activity, so there is no heart function limitation.

Atypical symptoms: often complained of discomfort, fatigue, fatigue, mild chest tightness after activity, or chronic cough, but denied other typical symptoms of heart failure, no obvious breathing difficulties, no breathing, no swelling, chest, ascites.

Symptoms: In heart failure, the right heart failure mainly due to systemic congestion and the left heart failure mainly caused by pulmonary circulation congestion, the symptoms and signs of clinical manifestations are not the same, no matter which side of heart failure occurs, such as failure Corrected in time, the other side will sooner or later fail, and the left heart failure and right heart failure are now described as follows.

1, left heart failure

The pathophysiological basis of left heart failure is mainly pulmonary congestion, due to pulmonary circulation congestion, elevated pulmonary venous pressure, decreased lung capacity, decreased lung elasticity, decreased lung compliance, and pulmonary congestion also impede capillary gas exchange, resulting in a series of Clinical signs and symptoms.

symptom:

(1) Fatigue and fatigue: It can occur in the early stage of heart failure. It usually feels weak limbs and is further aggravated after activities.

(2) Difficulty breathing: Dyspnea is a patient's self-conscious symptom, and it is also a comprehensive manifestation of respiratory effort and shortness of breath. When the patient has severe dyspnea, the patient presents with chest tightness and shortness of breath, assisted respiratory muscles to participate in respiratory movements, and nasal fanning. Dyspnea must be differentiated from neurological dyspnea, which is also known as sigh breathing. It is often comfortable after a deep breath, and there is very little respiratory increase. Cardiac dyspnea also needs to be accompanied by acid-toxic breathing. Difficult identification, the latter's breathing deepens, but the patient itself does not feel particularly difficult to breathe.

1 Labor dyspnea: Labor dyspnea is one of the early symptoms of patients with left heart failure. This is a breathing difficulty that occurs with the physical activity of the patient. It can be alleviated or disappeared after a break. The causes of labor dyspnea are:

A. The body's aerobics increase during physical activity, but the left heart of the exhaustion can not provide the appropriate cardiac output, the body's hypoxia is intensified, CO2 is stored, and the respiratory center is stimulated to produce "urgent" symptoms.

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

C. When physical activity occurs, the amount of blood returning to the heart increases, the pulmonary congestion increases, the lung compliance decreases, the ventilation work increases, and the patient feels difficulty breathing.

2 paroxysmal dyspnea at night: paroxysmal nocturnal dyspnea at night is a typical manifestation of left heart failure. The patient is engaged in general activities during the day and has no dyspnea performance. He can also take a supine position when he falls asleep at night, but suddenly causes difficulty in sleep. Difficult to breathe and wake up, must sit up for a while, the symptoms gradually relieved, severe breathing difficulties, asthma, and wheezing breathing, cough repeatedly, cough with blood mucus or foam, must sit After a long time, the asthma can gradually subside. If the patient falls asleep during the day, paroxysmal dyspnea can also occur in the daytime. The reason why paroxysmal dyspnea occurs after falling asleep is because:

A. Stored in the lower limb or abdominal cavity edema fluid in the supine position, transferred to the circulating blood volume, so that the venous return increased, thereby aggravating pulmonary congestion.

B. The response of the nervous system to the incoming information is weakened during sleep, so when the pulmonary congestion does not reach a certain level, it is not enough to arouse the patient.

3 end sitting breathing: sitting breathing is a characteristic feature of left heart failure, lighter only need to add 1 or 2 pillows to relieve breathing difficulties, in severe cases, patients in semi-recumbent or sitting position to avoid breathing difficulties The most serious patients need to sit on the edge of the bed or on the chair. The two feet are drooping, the upper body is leaning forward, and the hands are tightly gripping the edge of the bed or the side of the chair to assist in breathing. Alleviate the symptoms. This is a typical posture for sitting breathing, sitting breathing. It is suggested that patients with severe heart failure are more severe. After secondary right heart failure, pulmonary congestion can be reduced due to the decrease of right heart discharge, so dyspnea can be alleviated. The main cause of sitting breathing is pulmonary congestion in supine position. Exacerbation, decreased lung capacity and reduced effective volume of the chest.

A. Changes in orthostatic pulmonary blood volume: The blood volume of the lungs in the supine position is increased compared with the erect (up to 500 ml), while the blood volume in the upper part of the body may be partially transferred (up to 15%) to the abdominal viscera and lower limbs. In order to reduce the amount of blood return, thus reducing the congestion of the pulmonary circulation.

B. Changes in orthostatic vital capacity: when the normal person is lying down, the lung capacity is only reduced by 5%, while in patients with left heart failure, due to pulmonary congestion, decreased compliance, etc., the lung capacity can be significantly reduced when lying down, with an average reduction of 25%. The lung capacity can be increased by 10% to 20% when sitting.

C. Effect of diaphragm position: When the patient has hepatomegaly, ascites or flatulence, the supine position can increase the position of the diaphragm muscle more obviously, hinder the diaphragm muscle movement, reduce the effective volume of the abdominal cavity, thereby increasing the difficulty of breathing, and the sitting position can reduce the lungs. Congestion, which reduces the patient's breathing difficulties because:

a. When sitting, part of the blood is transferred to the lower half of the body due to gravity, so that the pulmonary congestion is alleviated.

b. When the seat is sitting, the position of the diaphragm is relatively moved downward, the volume of the thoracic cavity is increased, and the vital capacity is increased; especially when the heart failure is accompanied by ascites and hepatosplenomegaly, the sitting position makes the compressed chest cavity relieve and the ventilation is improved.

c. When the supine body is in the lower part of the body, the edema fluid absorbs more blood, while the sitting position reduces the absorption of the edema fluid, and the pulmonary congestion is relieved.

(3) cough, cough and hoarseness: pulmonary congestion in heart failure, congestion and edema of trachea and bronchial mucosa, increased secretion of respiratory tract, can cause reflex cough, increased cough, sometimes become the main symptom before the onset of heart failure Cough is often aggravated when tired or at night, with cough or foaming. Frequent cough can increase pulmonary circulation pressure and affect venous return, induce paroxysmal dyspnea and aggravate shortness of breath, and also increase right ventricular load, acute lung When edema, a large amount of pink foam sputum can be coughed up, especially in the supine position. When the mitral stenosis is enlarged, the left atrium is enlarged or the common pulmonary artery is dilated. The aortic aneurysm can compress the trachea or bronchi, causing cough. Cough and hoarseness, pulmonary infarction, pulmonary congestion, bronchitis or bronchial pneumonia can cause cough and cough.

(4) hemoptysis: In heart failure, when the pulmonary vein pressure rises, it can be transmitted to the bronchial submucosal vein to dilate it. When the submucosal dilated vein ruptures, it can cause hemoptysis. When the pulmonary capillaries of the blood stasis rupture, it can also cause hemoptysis. The amount of hemoptysis is indefinite, showing a bright red color. The mitral stenosis may have massive hemoptysis (bronchial venular rupture or pulmonary vein hemorrhage). Pulmonary edema or pulmonary infarction may have hemoptysis or coughing pink foamy sputum.

(5) Cyanosis: The face of the patient with severe heart failure such as the lips, the earlobe and the extremities may have dark black hair, that is, the cyanosis, the cyanosis caused by the mitral stenosis, the crotch is more obvious on both sides, forming the mitral valve face, acute lung Significant peripheral cyanosis can occur during edema. The main cause of cyanosis is pulmonary congestion. Pulmonary interstitial and/or alveolar edema affects ventilation and gas exchange in the lungs, resulting in insufficient hemoglobin oxygenation and increased hemoglobin in the blood.

(6) Nocturia increased: nocturia is a common and early symptom of heart failure. The ratio of nocturia to white urine in normal people is 1:3. The amount of urine in the daytime is higher than that in the night, and the nocturia in patients with heart failure increases. The ratio of nocturia to white urine is inverted from 2 to 3:1, and its mechanism may be related to the following aspects:

1 At the time of supine rest, the heart function was improved, the cardiac output was increased, and the subcutaneous edema fluid was partially absorbed, which increased the renal perfusion blood flow.

2 sympathetic excitability decreased during sleep, renal vascular resistance decreased, renal filtration rate increased, normal renal vascular resistance was regulated by sympathetic and renin angiotensin system activity, and renal vascular resistance increased in the upright position and exercise. The sodium-sodium filtration rate is reduced, and the decrease in renal vascular resistance in the supine position increases the sodium-sodium filtration rate. This change in orthostatic regulation is not apparent in normal people, but in patients with heart failure due to circulating norepinephrine The concentration and plasma renin activity increased and became particularly noticeable.

(7) Chest pain: Some patients can produce angina-like chest pain. In patients with primary dilated cardiomyopathy, chest pain can occur in about half of the patients, which may be related to dilated and hypertrophic heart subendocardial ischemia.

(8) Central nervous system symptoms: manifestations of insomnia, anxiety, nightmares, severe hallucinations, paralysis, the latter with time, place, orientation disorder of the character, further development into unresponsive, coma, if caused by heart failure alone , often reminds the end of the disease.

(9) Arterial embolism symptoms: 4% of patients with primary dilated cardiomyopathy have a history of systemic embolism. Follow-up observations show that 18% of patients with heart failure without anticoagulation will have systemic circulation. Embolism, clinical manifestations of cardiogenic systemic embolism, 85% of the embolization site is in the brain or retina.

2, right heart failure: right heart failure is mainly manifested by increased systemic pressure and congestion, resulting in dysfunction and abnormalities of various organs, obvious signs, relatively few symptoms.

(1) Symptoms: The symptoms of right heart failure are mainly caused by congestion caused by the gastrointestinal tract, kidneys, and liver.

1 Gastrointestinal symptoms: Gastrointestinal congestion can lead to loss of appetite, oiliness, nausea, vomiting, bloating, constipation and upper abdominal pain, etc. The pain is often dull or painful, and can be palpated by the upper abdomen or liver. And exacerbation, usually chronic congestion does not cause pain, and when the acute congestion of acute congestion, the patient can produce obvious upper abdominal pain, nausea, vomiting, anaesthesia, and attention to heart medication such as digitalis, quinidine, amiodarone, etc. Identification of side effects, when heart failure worsens, oily can lead to cardiogenic cachexia, a sign of poor prognosis, usually indicating the end of the disease.

2 liver pain: hepatic congestion and swelling of the liver capsule stimulate the splanchnic nerve to cause pain. In the early stage, the main upper right abdomen is full of discomfort or heavy feeling. As the chronic congestion increases, the liver area is painful and uncomfortable. When swelling or chronic congestion is acute, the pain in the liver area is obvious, sometimes it can be severely misdiagnosed as acute abdomen, such as acute hepatitis, cholecystitis, etc., deep inhalation, fatigue, tight band and liver palpation can be aggravated pain.

3 nocturia increased: chronic renal congestion can cause renal dysfunction, renal blood flow in the supine position and absorption of subcutaneous edema fluid, so that nocturia increased with an increase in urine specific gravity (more than 1.025 ~ 1.030), can contain a small amount Protein, transparent or granular tube type, a small number of red blood cells, plasma urea nitrogen can be slightly increased, after treatment with effective anti-heart failure, the above symptoms and laboratory indicators can reduce or return to normal.

4 dyspnea: If right heart failure is secondary to left heart failure, after right heart failure, there is a decrease in ventricular discharge, and pulmonary congestion is reduced, which can reduce the difficulty of breathing in left heart failure, but if there is ventricular failure When the cardiac output is significantly reduced and worsened (can be regarded as the end-stage performance of heart failure or secondary pulmonary hypertension), dyspnea will become very serious, and patients with isolated right heart failure may have different degrees of breathing. Difficulties. The mechanism of its occurrence may be related to the following factors:

A. Increased right atrial and superior vena cava pressure, can stimulate baroreceptors, reflective excitatory respiratory center.

B. The blood oxygen content is reduced, and the acidic metabolite produced by the relative increase of anaerobic metabolism can stimulate the respiratory center to excite.

C. Pleural effusion, ascites and enlarged liver can affect respiratory movements.

5 other: a small number of patients with severe right ventricular failure, due to cerebral circulation congestion, hypoxia or diuretic application induced water and electrolyte imbalance, etc., can also occur central nervous system symptoms, such as headache, dizziness, fatigue, irritability, lethargy , , etc., if the right ventricular outflow tract is severely obstructed (such as severe pulmonary hypertension, pulmonary stenosis), right ventricular stroke volume can not increase with demand, can cause dizziness when active, and may even be similar to left ventricular outflow obstruction Symptoms of syncope, patients with right heart failure due to increased heat production, and slow blood flow slows down heat dissipation, can occur low fever, body temperature is generally <38.5 ° C, heart failure will be antipyretic when compensated, high fever suggests infection or pulmonary infarction.

(2) Signs: There are few signs of heart failure in the elderly, no specificity, common signs are pulmonary wet sputum, slight depression of sacral edema, tachycardia, etc., the elderly often have chronic bronchitis, senile or obstructive Emphysema, auscultation of the lungs has a wet voice, long-term bed rest or debilitated elderly patients with heart failure, edema is more common in the ankle than the lower limbs, normal elderly can be tachycardia with a little fatigue, and not necessarily exist Heart failure, typical signs include alternating veins, third or fourth heart sounds, jugular vein engorgement, heart murmur, enlarged heart, liver, ascites, etc. The typical signs of left and right heart failure are now described as follows:

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

A. Heart enlargement: Generally, left heart failure, especially in the chronic process, has a heart enlargement, with left ventricular enlargement, apical beat to the left, and heart enlargement with tension-like enlargement and myogenic expansion, early heart failure. Within a certain range, with the elongation of myocardial fibers, the contraction force and stroke volume of the myocardium increase correspondingly. At this time, the enlargement of the heart belongs to the expansion of the tension source, and it is an effective compensation method that can immediately exert its function. However, in the late stage of heart failure, the myocardial fiber is further elongated beyond a certain limit, and the effective power of contraction is decreased, thus losing the meaning of compensation. At this time, the heart enlargement is called myogenic expansion, and the heart enlargement is not before the occurrence of heart failure. It must be that in some chronic constrictive pericarditis, restrictive cardiomyopathy, acute myocardial infarction, sudden aggravation of rapid or slow arrhythmia, and rupture of the valve or chordae, heart failure can occur before the heart enlarges.

B. Diastolic galloping: not necessarily left heart failure, but the appearance of this sign is an important evidence for the diagnosis of left heart failure, especially in recent episodes, combined with clinical symptoms, greater significance in judging left heart failure Therefore, some people call it "heart call for help", which can be divided into the following according to the time and mechanism of its occurrence:

a. Early diastolic galloping: also known as the third heart sound galloping horse, is essentially an enhanced pathological third heart sound, occurring in the early stage of ventricular filling, located 0.13 ~ 0.16s after the second heart sound, low pitch, at the apex The area or its inner side, especially the left side of the patient is located at the end of deep exhalation, the most easy to hear, when the heart rate increases faster than 100 times / min, the pathological third heart sound together with the first, second heart sound, composed of three sounds Rhythm, like the hooves of running, due to the early diastolic, called diastolic (early) galloping, suggesting that the ventricular diastolic overload is an important sign of common myocardial failure or acute left ventricular enlargement, physiological third Heart sounds can be heard in healthy adolescents, but rarely occur in adults after the age of 40, but can occur in patients with heart failure at any age, so it is necessary to combine clinical judgments.

b. Diastolic late galloping: also known as the fourth heart sound galloping horse, is a three-tone rhythm composed of pathological fourth heart sound and first and second heart sounds, which occurs in the late diastolic, before the first heart sound Low frequency, low amplitude, low tone, easy to hear in the apical area or inside with a bell stethoscope, the loudest in the left lateral position and exhalation, it has the characteristics of frequent changes, when the function changes, it is normal, normal Atrial contraction can be traced on the heart sound map, but auscultation is generally not easy to hear, only when the left ventricular compliance declines, but when accompanied by atrial fibrillation, mitral stenosis, etc., left atrial contraction weakness or blood inflow When the left ventricle is restricted, it disappears more.

c. Four-tone rhythm and overlapping galloping: Four-tone rhythm, also known as locomotive galloping, means that the pathological third heart sound and the fourth heart sound appear simultaneously, that is, there are two extra heart sounds during diastole, and first, The second heart sounds together form a four-tone rhythm. If the heart rate is easy to hear at 100-110 times/min, the rhythm is like the sound of the wheels colliding with the rails when the train is running, so it is also called the locomotive galloping, if the heart rate is further increased to 120. ~130 times / min, diastolic phase shortened, pathological third, fourth heart sounds nearly overlapping, especially combined with atrioventricular block (prolonged PR interval), atrial contraction in the rapid filling period of the ventricle, accelerated The rapid filling of the ventricle makes the fourth heart sound and the third heart sound overlap and change. In the middle of the diastole, a very loud single sound appears, which is called overlapping galloping. If the carotid sinus is pressed to slow the heart rate, the overlapping horses are again Will separate, restore the four-tone rhythm.

C. Pulmonary valve area Second heart sound hyperthyroidism Patients with pulmonary heart failure The second heart sound hyperplasia often indicates an increase in pulmonary circulation resistance, pulmonary hypertension, in the left heart failure, pulmonary vein and pulmonary capillary pressure rise and expand congestion, pulmonary arterioles Protective contractions and spasms often occur to reduce pulmonary congestion and prevent pulmonary edema, but on the other hand, pulmonary arteriolar contractions and spasm further increase pulmonary hypertension, and long-term spasm can harden the pulmonary arteriolar wall and lumen. Narrowing, resulting in more obvious pulmonary hypertension, the second heart sounds in the pulmonary valve area, when the left heart failure is further aggravated and the contractility is significantly weakened, the left ventricular emptying time is prolonged, and the closure of the aortic valve may lag behind the pulmonary artery. The flap (normally the second heart sound of the pulmonary valve closure component is later closed to the aortic valve), the result is a second heart sound reverse split, more pronounced during exhalation, can be reduced or not obvious when inhaling.

D. systolic murmur in the anterior region: In some patients with heart failure, the left ventricular dilatation causes the atrioventricular annulus to expand or the papillary muscles to shift, resulting in mitral regurgitation, causing systolic reflux murmurs. Full systolic hairy murmur, loudness above two levels, located in the anterior region of the heart or the apex of the apex, to the left and lower arm.

E. Alternate pulse: Some patients with heart failure may have alternating veins. Palpation of peripheral arteries may feel normal pulse rhythm but alternating strength and weakness. Some can only be found when measuring blood pressure. When gradual deflation in pressure measurement, contraction When the pressure is 0.66~4.0kPa (5~30mmHg), only half of the arterial pulse sound or the arterial pulse strength may appear alternately. When the patient takes the seat and lifts the wrist to the shoulder level, it is easy to find alternating veins. Frequently suggesting severe myocardial lesions, such as primary cardiomyopathy, left ventricular outflow obstruction, coronary heart disease and severe hypertension, most patients with third heart sounds and tachycardia, mostly persistent, can also be array After the correction of heart failure, alternating pulse may disappear, the mechanism of alternating pulse may be related to the degree of ventricular diastolic filling. When the ventricular diastolic filling is more, the cardiac output is more, and the pulse is strong and powerful; When the ventricular diastolic filling is insufficient, the pulse can be strong-weak alternately.

Alternate veins need to be differentiated from frequent premature beats. The weaker beats of alternating pulses do not appear early, but may be slightly delayed. Pulse transitions caused by premature beats often appear earlier.

F. Pulmonary bottom wet voice: Patients with left heart failure often have typical signs of wet bottom snoring of the lungs. Usually, when inhaling, a stethoscope can be used to hear the wet sounds on both sides of the lungs. If the wet voice only occurs on one side. Patients, often more common on the right side, but the majority of heart failure patients with wet voices occur on both sides, that is, symmetrical characteristics, if heart failure is limited to the left side of the voice, it is necessary to rule out the occurrence of left lung infarction Possible.

The occurrence of wet voice on the left or right side may also be related to the habit of the patient preferring the left or right side. When the duration of left heart failure is prolonged or aggravated, the wet voice can also develop upward from the lung bottom. When the patient is concerned, paying attention to the extent and extent of recording the wet voice has certain reference value for observing the progress of the disease and judging the curative effect.

G. Pleural effusion: About one-fourth of patients with left heart failure may 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, characterized by a periodic change in the patient's breathing that gradually increases and gradually diminishes. Gradually weakened to a gradual increase and then deepened. After reaching the peak, it gradually slowed down and became shallower until it stopped again. It lasted for 30-60 seconds and re-opened the next cycle. The mechanism was due to the prolongation of blood circulation time during severe heart failure. Pulmonary congestion and hypoxemia lead to cerebral hypoxia, cerebral edema, and can also cause periodic breathing caused by brain dysfunction. When the carbon dioxide retention time is prolonged, the ventilatory response to stimulate the respiratory center is enhanced, causing excessive ventilation, but accompanied by The forebrain (the cerebral cortex and the thalamic nerve cell cluster) has reduced sensitivity to ventilation stimulation and apnea after hyperventilation. During apnea, carbon dioxide retention increases the arterial blood carbon dioxide partial pressure until it exceeds the respiratory center. Stimulus threshold, then over-breathing begins again.

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

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

A. Heart enlargement: When right heart failure is simple, the right ventricle and/or right atrium expand, but right heart failure is often secondary to left heart failure, so the heart is mostly enlarged and the right ventricle is enlarged with hypertrophy. There is obvious pulsation under the xiphoid process. The palpation of the anterior region has a lifting pulsation. If there is obvious pulmonary hypertension and right ventricular activity, it can touch the oscillation of the pulmonary artery in the 2nd and 3rd ribs of the left sternal border, and can be in the sternum. The lower left margin and the xiphoid or anterior region (when the right ventricle is enlarged), the right ventricular diastolic galloping, the inspiratory enhancement, if the right ventricle is enlarged, can cause relative tricuspid regurgitation, in the third The apical auscultation area can be audible and systolic hair-like murmur, enhanced when inhaling, Lang has, the tip area is transmitted, but does not exceed the left anterior line, the murmur is weakened after heart failure control, in addition, when the tricuspid regurgitation is obvious, a large number The blood flow back to the right atrium during the systolic phase, aggravating the systemic congestion, causing the jugular vein and superior vena cava pulsation and hepatic dilatation pulsation in the late stage of contraction, and reflexive sinus tachycardia due to decreased cardiac output.

B. Venous filling, anger and pulsation: abnormal superficial venous filling or engorgement of the external jugular vein is an important sign of right heart failure. In severe cases, it may be accompanied by pulsation. The mechanism is caused by systemic congestion and right heart failure. The cardiac output is reduced, the right ventricular end-diastolic pressure is increased, and the right atrial pressure is also increased. There is no valve between the vena cava and the right atrium, so the right atrial pressure is increased and reversible into the vena cava system. Increased inferior vena cava pressure leads to superficial vein filling or engorgement of the external jugular vein, dorsal vein and sublingual vein. In patients with severe right heart failure, the jugular vein and the superficial vein of the extremity may be pulsating, but in the supine position Because the jugular vein is extremely full and expands, the pulsation is not obvious. Generally, the patient should be observed in a 45° semi-recumbent position. The filling degree of the jugular vein can reflect the level of right atrial pressure, and the severity and prognosis of right heart failure. Have a certain value.

C. Liver, tenderness, positive for jugular jugular venous return: hepatomegaly and tenderness are one of the earliest and most important signs of patients with right heart failure. Patients with right heart failure can have hepatomegaly and tenderness, and the rate of hepatomegaly The faster the tenderness, the more obvious the tenderness is. The liver is more obvious under the xiphoid process. Sometimes the palpation of the right margin is unsatisfactory or unreachable. The palpation of the liver should be combined with the percussion of the liver. Because the liver is drooping, the lower pole of the liver can extend to the right. The distance between the midline of the clavicle and the lower boundary of the clavicle is still between 9 and 11 cm. The liver texture is related to the time of hepatic congestion. Long-term chronic right heart failure can cause cardiogenic cirrhosis. The liver is hard and the edges are sharp, and when the acute right heart failure causes acute hematoma enlargement in the liver, the liver is soft and the edges are blunt.

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

Pressing the liver with the palm of your hand for half a minute can increase the blood flow to the inferior vena cava and the right atrium. However, due to right heart failure, it can not compensate for the increase in blood volume, so that the venous pressure is further increased, and the jugular vein filling is more Obviously, it is called positive for jugular jugular vein regurgitation, which 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 venous reflux identifies the neck. The pulsation of the arteries or veins is useful, but it is not necessarily reliable for potential heart failure, because it is only qualitative and not quantifiable relative to normal; in addition, the jugular venous pressure can vary with changes in intrathoracic pressure.

D. Low drooping edema: Low drooping edema is a typical sign of right heart failure. After jugular vein filling and hepatic enlargement, most cases occur in secondary right heart failure, while isolated right heart failure, Subcutaneous edema can be the first sign. Before heart failure causes peripheral edema, it must first accumulate a large amount of extracellular fluid. It is generally believed that before edema, the body weight has increased by about 10%, that is, when the body fluid retention exceeds 5kg. Edema, the water in the normal adult tissue gap is about 7kg, and the heart water can increase to 15-20kg in heart failure. In heart failure, the water mainly stays in the extracellular space, extravascular and interstitial, and the circulating blood volume and intracellular The water only increased slightly.

The edema fluid tends to accumulate in the area where the hydrostatic pressure is the largest, that is, the lower part of the body. In the upright position, the edema often occurs first in the foot, the ankle and the tibia. It is obvious in the afternoon and recovers at night. As the condition worsens, the cells are made. The external fluid expands and the edema gradually develops. In bedridden patients, the edema of the appendix and the inner thigh is more obvious. In patients who have no breathing, because of the supine, edema can occur in the upper arm and hand, but rarely affects the face. Unless infants and young children, systemic edema can occur in the advanced stage of untreated chronic heart failure, edema can affect the genitals, chest, limbs and head, but very few patients with fluid retention more than 45kg, chronic edema can lead to Low-grade skin, especially erythema in the anterior temporal bone, induration, hyperpigmentation, these patients are also prone to subcutaneous cellulitis.

E. Pleural effusion: pleural effusion can occur in any cause of heart failure, most of which occur in patients with heart failure, and pleural effusion is often bilateral, unilateral pleural effusion is more common on the right side, bilateral pleural effusion often right(2%)(0.2%0.5%)

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