Congestive heart failure

Introduction to Congestive Heart Failure Congestive heart failure (CHF) refers to a pathological condition in which cardiac output is insufficient to maintain tissue metabolism due to systolic and/or diastolic dysfunction in the presence of moderate venous return. Heart failure is due to ventricular pumping or filling function is low, cardiac output can not meet the needs of the body's metabolism, tissue, organ blood perfusion, and pulmonary circulation or systemic congestion, is the clinical synthesis of various heart disease development to severe stages Symptoms, also known as congestive heart failure (CHF). It is characterized by left ventricular hypertrophy or dilatation, leading to neuroendocrine disorders, abnormal circulation, and typical clinical symptoms: difficulty breathing, fluid retention, and fatigue (especially during exercise). Clinical symptoms may change significantly during disease progression, or may not be consistent with cardiac function. If left untreated or treated, the symptoms of heart failure will continue to worsen. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific people Mode of infection: non-infectious Complications: arrhythmia

Causes of congestive heart failure

(1) Causes of the disease

1. The cause of chronic heart failure:

(1) myocardial systolic dysfunction: this is the most common cause of heart failure, including myocarditis caused by various causes, cardiomyopathy, myocardial infarction, ischemic heart disease, myocardial metabolic disorders (such as hypoxia, ischemia, water , electrolytes and acid-base imbalance, etc., which are mainly diastolic dysfunction, found in hypertension, left ventricular hypertrophy, hypertrophic cardiomyopathy, aortic and / or pulmonary stenosis, restrictive cardiomyopathy.

(2) ventricular preload overload: including various causes of valvular insufficiency, intracardiac or intravascular shunt disease, such as atrioventricular septal defect, patent ductus arteriosus, aortic sinus rupture, arteriovenous fistula Wait.

(3) ventricular post-load overload: including pulmonary hypertension caused by various reasons, systemic hypertension (primary and secondary hypertension), left and right ventricular outflow tract stenosis and main, pulmonary stenosis.

(4) Insufficient ventricular preload: leading to left and/or right atrium, systemic circulation and/or pulmonary circulation congestion. These diseases include secondary and tricuspid stenosis, atrial myxoma, pericarditis, cardiac tamponade and restricted myocardium. Sick and so on.

(5) High power circulation status: including hyperthyroidism, anemia, vitamin B1 deficiency, systemic arteriovenous fistula and so on.

2. Causes of chronic heart failure:

(1) Infection: Especially respiratory infection is the most common cause of heart failure, followed by rheumatic activity, urinary tract infection and digestive system infection. Infective endocarditis is an important cause of rapid deterioration of heart disease.

(2) Excessive physical activity, fatigue, emotional excitement and tension.

(3) Pregnancy and childbirth.

(4) arrhythmia: especially rapid arrhythmia, such as: paroxysmal atrial fibrillation, paroxysmal ventricular or supraventricular tachycardia, severe bradycardia, such as complete atrioventricular block.

(5) Too much blood transfusion or infusion (especially containing sodium liquid) is too fast.

(6) Electrolyte disturbance and acid-base imbalance.

(7) The role of drugs: such as the use of negative inotropic drugs or inhibition of myocardial contractility drugs, sodium retention water and digitalis positive inotropic drugs or improper application.

(two) pathogenesis

1. Factors that determine cardiac output: Cardiac output is an important indicator of circulatory system efficiency (including cardiac pumping function). The factors that determine cardiac output are as follows.

(1) Preload: The preload of the heart, that is, the load encountered before contraction, refers to the amount of returning blood, or the end-diastolic volume of the ventricle, or the length of the periventricular end of the ventricular end-diastolic (the initial length), the preload (also known as the volumetric load, First load, volume load or diastolic load) is mainly affected by venous return blood volume and wall compliance, which is the first important factor affecting and regulating cardiac function. Generally, left ventricular end-diastolic pressure is used as an indicator of preload, Frank -Starling's heart law explains the relationship between preload and cardiac output, that is, within the range allowed by myocardial contractility, the stroke volume is mainly determined by the amount of blood returning, and the stroke volume is proportional to the amount of blood returning to the heart. The more the left ventricular myocardial fiber is more elongated (the volume of left ventricular diastolic volume is increased), so the myocardial contractility is enhanced, the stroke volume is increased, and the stroke volume is decreased. The Frank-Starling heart law further clarifies the cardiac output. The relationship between the amount and left ventricular end-diastolic pressure, with left ventricular end-diastolic pressure as the abscissa, reflecting the preload; with each stroke volume or heart beat work or cardiac index as the ordinate, reflecting the ventricle , The draw left ventricle preload in different cardiac output curve of a change in the relationship, i.e. the curve of left ventricular function, left ventricular function can be quantified.

The left ventricular function curve indicates the relationship between left ventricular systolic function and left ventricular preload in normal people and heart failure. In heart failure, the cardiac function curve shifts to the lower right. When the left ventricular end diastolic pressure is >18 mmHg, the lung appears. Symptoms and signs of congestion; if the cardiac output index <2.2L / (min · m2), symptoms and signs of low cardiac output.

(2) Afterload: The impedance (also known as the spurt impedance) faced by the ventricular ejection after the ventricular ejection, that is, the load that is encountered after the ventricular muscle begins to contract, so it is called the afterload, also called the pressure load or systole. Load, afterload refers to the total force of the unit myocardium when shortened in isotonic contraction state. This total force is also the tension of the ventricular wall during ventricular ejection. The size of the posterior load depends on the compliance of the arterial vessels, and the total peripheral resistance. , blood viscosity and blood volume and other factors, the total peripheral resistance is the main determinant of the afterload, but the clinical can not correctly determine the afterload, generally can only use the arterial blood pressure to roughly estimate the resistance of the small arteries widely distributed in the body. Or tension is the most important factor determining the total peripheral resistance. It is susceptible to vasodilators. In the case of constant myocardial contractility and preload, there is a hyperbolic relationship between afterload and stroke volume, ie, the stroke volume is followed. The load is increased and then increased, and then the load is increased (the arterial blood pressure is increased) and reduced. In short, the afterload is negatively correlated with the stroke volume.

(3) Myocardial contractility: myocardial contractility is expressed by myocardial contractility, the latter refers to the contractile force of the myocardium itself that is not related to ventricular load. The strength of contractility can be shortened by isotonic myocardial fibers under established load. In terms of maximum speed, in other words, the initial length of myocardial fibers is the same, and those with larger contractile force indicate that they have stronger contractility, and weaker contractility is the most common cause of heart failure. From the perspective of molecular biology, myocardial contractility is strong. The weak, that is, the size of myocardial contractility depends on the degree of shortening of myocardial contractile protein gliding, and the degree of shortening of sarcomere is mainly affected by two factors:

1 The speed and number of binding of myosin cross-bridge to actin binding sites;

2 The rate of chemical energy conversion at the site of contraction protein interaction, ie the rate at which the ATPase of the myosin head (cross bridge) hydrolyzes ATP, which ultimately depends on the amount of Ca2 released from the sarcoplasmic reticulum.

(4) Heart rate: changes in heart rate can affect stroke volume (stroke volume or stroke volume) and output per minute (cardiac output). Within a certain limit, heart rate increases to increase cardiac output. Because cardiac output = heart rate × heart rate, but if the heart rate is too fast, the ventricular diastolic period is significantly shortened, so that the ventricular filling is insufficient, although the number of heart beats per minute increases, but the stroke volume is reduced, so the heart is bleeding The amount is reduced. Conversely, if the heart rate is too slow, the cardiac output is also reduced. Because the diastole is too long, the filling of the ventricle is already close to the maximum, and then the diastolic time is increased, and the stroke volume cannot be increased accordingly. Therefore, the heart rate is too high. Fast or too slow affects cardiac output. Correcting arrhythmia at this time is the key to improving cardiac function.

(5) Coordination of ventricular contraction and diastolic: when the ventricle contracts, the coordination of the wall motion is an important guarantee for obtaining the maximum stroke volume. When myocardial ischemia or myocardial infarction, the ventricular wall movement is imbalanced, which reduces the stroke volume. , so that the cardiac output is reduced.

(6) Integrity of the heart structure: abnormal heart structure, such as interventricular septal perforation in acute myocardial infarction, or mitral regurgitation caused by rupture of papillary muscle and chordae, and valvular damage caused by rheumatic heart disease, etc. Reduce cardiac output.

Among the six factors that determine cardiac output, the former three are more important for the regulation of cardiac pump function.

2. The basic mechanism of heart failure: The basic mechanism of heart failure development is myocardial systolic and dysfunction. The main mechanisms are as follows:

(1) Myocardial loss and conformational reconstruction (remodeling): The so-called configuration reconstruction (also known as remodeling) includes, in a broad sense, the alteration of the size, number and distribution of myocardial cells, and the amount of collagen interstitial. The alteration of type and distribution, as well as the proportion of myocardial parenchyma and interstitial remodeling, any form of alteration, can cause cardiac dysfunction and even heart failure.

1 Myocardial loss: Myocardial loss includes both cell death and loss of function.

There are two causes of myocardial cell death. One is passive death due to myocardial ischemia, poisoning and inflammation. Localized or diffuse necrosis, fibrosis, and loss of contractility in a large number of myocardium. Causes heart failure or even cardiogenic shock, another is the active death of single cell self-digestion, called apoptosis (aboptosis), referred to as apoptosis or programmed death. Under normal circumstances, cell proliferation and death are It is in a dynamic equilibrium, but when the cell death accelerates and the cell death rate exceeds the cell proliferation rate, various pathological phenomena or diseases may occur due to the imbalance of the balance. Recent studies suggest that cardiomyocyte apoptosis, such as ischemia, can be induced by various injuries. And ischemia-reperfusion, myocardial infarction, rapid ventricular pacing, mechanical stretch and pressure overload caused by aortic stenosis, etc., eventually leading to heart failure.

Loss of cardiomyocyte function means that the cardiomyocytes are not dead, and they have a function of contraction and reserve, mainly in myocardial stunning and myocardial hibernation.

2 interstitial remodeling (remodeling): a collagen network composed of cardiac fibroblasts and secreted collagen (mainly type I and type III, the ratio of which is 7:1), which not only supports the cardiomyocytes. And a fixed protective effect, and can play a non-negligible role in ensuring the coordination and relaxation function of the myocardium and blood supply. The interstitial alteration is characterized by both destructive and proliferative changes. The destructive alteration is mainly seen in acute myocardial ischemia and Dilated cardiomyopathy, proliferative alteration is more common in cardiac hypertrophy caused by excessive cardiac stress overload and late in the capacity overload. With the hypertrophy of the myocardium, the density of the collagen network is also excessively increased, which increases the stiffness of the myocardium and affects the myocardium. The diastolic function, in short, whether the destruction of the collagen network or proliferative alteration, can cause myocardial relaxation and/or contractile dysfunction through different mechanisms, thereby causing the occurrence and development of heart failure.

3 Reconstruction of myocardial systolic and diminished: Reconstruction of cardiac systolic and/or procedural remodeling can reduce the amount of ejection and even cause heart failure. The most common systolic incompatibility is: A, contraction is weakened B, no contraction; C, contractive bulging; D, myocardial contraction of synchrony, recently found that the heart's relaxation also appears similar to the inconsistency of contraction.

4 The role of free radicals in myocardial remodeling and heart failure: More and more data prove that free radicals play an important role in the development of myocardial remodeling and heart failure. The mechanism of free radicals involved in myocardial remodeling and heart failure is In many aspects, mainly through the lipid peroxidation in the structure of cell membrane (including mitochondria, lysosomal membrane, etc.), impaired structure and function, light cell dysfunction or loss, severe cell death .

(2) Cellular energy "hunger" and information transmission system barriers:

1 Cardiomyocyte energy "starvation": The heart is a highly active, high-energy-consuming organ that requires sufficient energy supply regardless of myocardial relaxation or contraction. When myocardial energy is in short supply, the myocardial energy is "starved", which leads to myocardial Shutdown disorder, resulting in heart failure, in the process of myocardial contraction, whether to promote the operation of Ca2 or on the sliding of thick and thin muscles, there must be sufficient energy supply and utilization, otherwise, even if the contraction protein is normal, it will It leads to the weakening of the contractile performance. When the primary myocardial disease, myocardial ischemia or infarction and excessive cardiac load, the myocardial energy metabolism disorder can occur, which can cause the myocardial contraction to be weakened.

2 myocardial receptor-information transmission system disorder: myocardial receptor-information delivery system, especially -adrenal receptor-G protein-adenosine cyclase system plays an important role in myocardial inotropic and chronotropic regulation, when the system is activated When the level of intracellular cyclic adenosine monophosphate (cAMP) is increased, the latter through the phosphorylation of cAMP-dependent protein kinase, on the one hand, the opening of the cell membrane Ca2 channel promotes the influx of Ca2 and strengthens the contractile function of the myocardium. On the other hand, phosphorylation of phosphate-accepting proteins promotes the uptake of Ca2 by the sarcoplasmic reticulum, and enhances the relaxation of the myocardium; it also accelerates the release of sinus node impulses, speeding up heart rate, etc., so when the regulatory system occurs In the case of an obstacle, the heart's relaxation and contraction function may be weakened or abnormal.

It is now proven that in the case of heart failure, the delivery system can present obstacles in the following aspects: A. receptor down-regulation: myocardial beta receptor has two subtypes 1 and 2, 1 receptor accounts for 80% of the total receptor, 2 is affected About 20% of the body, the 1 receptor is down-regulated in heart failure (from 80% can be reduced to 40%), while the 2 receptor is relatively increased (from 20% to 40%), because the 1 receptor is down-regulated, so the catecholamines Positive variable force, weakening or loss of substance regulation effect, which can lead to myocardial dysfunction; BG protein alteration and coupling disorder: G protein is a coupling factor and regulator of various hormone information transmission, which can be divided into The agonistic G protein (Gs) and the inhibitory G protein (Gi) have been shown to increase Gi and decrease Gs in heart failure. At the same time, due to the down-regulation of 1 receptor, the -adrenergic receptor and Gs coupling disorder are affected. Myocardial systolic and diastolic function; C. decreased intracellular cAMP content; D. sarcoplasmic reticulum (SR) barrier to Ca2 uptake and release.

3 Gene structure and abnormal expression: In recent years, due to the advancement of molecular biology theory and technology, more and more facts have proved that many cardiovascular diseases and their heart failure occur, and their development is closely related to their genetic structure and abnormal expression. Gene structure and abnormal expression caused by cardiac overload and/or endocrine hormones are the molecular basis for heart failure.

3. Compensatory function of the heart: When heart failure and heart discharge are insufficient to maintain the energy required by the body tissue, the heart reserve should be used to compensate for the decrease in stroke volume. The compensatory function of the heart is The speed of its effect can be divided into acute (such as increased heart rate, increased contraction, etc.), subacute (heart expansion, increased blood volume, etc.) and chronic (such as cardiac hypertrophy), the main compensatory mechanism has the following five aspects.

(1) Increase the preload to increase the stroke volume: According to Frank-Starling's law, the longer the ventricular muscle fiber stretches, the shortening of myocardial contraction increases, and the stroke volume also increases. According to electron microscopy, the optimal length of myocardial sarcomere For 2.2 m, within this length, the increase in volume and pressure in the heart chamber does not cause dislocation of the muscle fibers. This compensation can also be called the reserve of diastole.

(2) Adrenergic Cardiac nerves and adrenal medulla increase the release of catecholamines to enhance myocardial contractility, increase heart rate, and also allow venous contractions to increase the amount of blood return. This compensation is mainly based on the systolic reserve of the heart.

(3) activation of the renin-angiotensin system (RAS): increase water, sodium retention, to increase blood volume and preload, RAS mainly includes angiotensinogen, renin and angiotensin converting enzyme In three parts, angiotensinogen acts as angiotensin I (AI) through the action of renin, and then angiotensin II (AII) is produced by the action of angiotensin I converting enzyme, which passes aminopeptidase The role of angiotensin III (AIII), AII and AIII have vasoconstriction, boost and promote the secretion of aldosterone, resulting in physiological effects of sodium retention and expansion, heart failure due to renal perfusion and Decreased perfusion pressure, sympathetic excitation and increased catecholamines in the blood, causing the secretion and release of renin in the cells of the juxtaglomerular cells, RAS activation, resulting in vasoconstriction, sodium retention and increased blood volume, which maintains blood pressure and The blood supply of vital organs plays an important compensatory role. Recently, cardiovascular local RAS has also been involved in the occurrence and development of heart failure through different mechanisms and pathways. For example, RAS in the heart can cause coronary vasoconstriction, induce ischemic injury, promote the release of catecholamines in the cardiac sympathetic nerve endings, increase myocardial contractility, and promote hypertrophy of the heart muscle, while vascular RAS can pass through sympathetic nerve endings. Releases norepinephrine (NE), causing contraction of vascular smooth muscle and promoting the growth and proliferation of vascular smooth muscle cells.

(4) Cardiac hypertrophy to reduce wall tension and improve myocardial contractility: As a result of increased pressure load, the ventricular wall tension is increased, and the parallel replication of myocardial protein and sarcomere is stimulated to form centripetal cardiac hypertrophy, according to Laplace's law. The wall tension is inversely proportional to the thickness of the wall. The appearance of cardiac hypertrophy is sufficient at the beginning to restore the tension of the wall to normal. Although the heart has hypertrophy and does not enlarge, if the pressure load continues to rise for several years, the hypertrophic myocardium cannot be maintained. When the wall tension is applied, the heart function is further deteriorated.

(5) Increasing the ability of the surrounding tissue to extract oxygen to increase the oxygen supply capacity per unit of cardiac output: the result is an increase in the oxygen content in the arteriovenous.

Congestive heart failure prevention

Prevention goals for chronic heart failure:

(1) Prevention of initial myocardial injury: Coronary artery disease and hypertension have gradually increased to the main cause of chronic heart failure, actively controlling blood pressure, blood sugar, lipid-lowering therapy and smoking cessation, etc., can reduce the risk of chronic heart failure, except In addition to actively controlling the above cardiovascular risk factors, it is also an important measure to control group A -hemolytic streptococcus infection, prevent rheumatic fever and valvular heart disease, and abstain from alcohol abuse to prevent alcoholic cardiomyopathy.

(2) Prevention of further myocardial injury: during acute myocardial infarction, thrombolytic therapy or coronary angioplasty, so that effective reperfusion of the myocardial segment can prevent ischemic injury, for the recent recovery from myocardial infarction, the application of neuroendocrine Antagonists (ACE inhibitors or beta blockers) reduce the risk of reinfarction or death, especially in patients with chronic heart failure during myocardial infarction, ACE inhibitors and beta blockers There may be complementary benefits. In patients with acute myocardial infarction without chronic heart failure, the use of aspirin may reduce the risk of reinfarction and help prevent chronic heart failure.

(3) Prevention of deterioration after myocardial injury: Left ventricular dysfunction, with or without symptoms, the use of ACE inhibitors can prevent the risk of developing severe chronic heart failure.

Complications of congestive heart failure Complications, arrhythmia, sudden death

Congestive heart failure often complicated by arrhythmia, pulmonary infection, liver dysfunction, renal insufficiency, water and electrolyte disorders.

1. Arrhythmia: Patients with congestive heart failure often have supraventricular and ventricular arrhythmia, severe arrhythmias such as ventricular fibrillation can lead to death, sudden death accounts for 40% to 50% of the total number of deaths, with the progression of congestive heart failure, The relative proportion is slightly decreased. Among the arrhythmia rates of heart failure caused by various diseases, coronary heart disease and rheumatic heart disease are the highest. It is noted that a considerable number of arrhythmias are not caused by the primary disease. It is necessary to find the arrhythmia. Inducing factors such as ischemia, electrolyte imbalance, certain drugs that interact with pump function and electrical stability, such as calcium channel blockers and some antiarrhythmic drugs, digitalis poisoning and secondary diseases, etc., in many cases Arrhythmia with incomplete function is transient, and once the cause is removed, the arrhythmia is also improved.

2. Pulmonary infection: Patients with congestive heart failure are often accompanied by pulmonary circulatory congestion, which increases the chance of pulmonary infection, and heart failure is an important factor in determining the severity and prognosis of pulmonary infection.

3. Liver dysfunction: patients with cardiac insufficiency, especially right heart dysfunction, have different degrees of congestive liver changes, early manifestations of reversible hepatic congestion, chronic liver congestion can lead to cardiogenic cirrhosis.

4. Renal insufficiency: Under normal circumstances, the blood is mainly distributed in the liver (17% to 24%), the kidney (15% to 19%) and the cerebral circulation (10% to 15%) in the resting state; Up to 70% of blood is transferred to muscle groups, heart failure patients, whether during rest or exercise, due to increased peripheral resistance and decreased cardiac output, renal blood flow can be reduced, glomerular filtration rate is reduced and renal blood flow Redistribution changes.

5. Water and electrolyte disorders: heart failure can occur refractory edema due to neurological fluid regulation disorder and diuretic resistance, etc., while kidney damage also aggravates sodium and water retention, eventually forming a vicious circle between heart and kidney, heart failure often occurs concurrently Various electrolyte disorders, common hyponatremia, hypokalemia, hyperkalemia and hypomagnesemia.

Symptoms of congestive heart failure Common symptoms Nausea pink foam-like silicosis, blood stasis, sitting, breathing, third heart sound, running horses, heart discharge, increased myocardial nutrition, spleen hyperactivity

According to the basic mechanism of heart failure, it can be divided into systolic dysfunction heart failure and diastolic dysfunction heart failure. Clinically, according to the heart and blood stasis of the lesion, it can be divided into left heart, right heart and whole heart failure. Left heart failure begins to be more common, followed by pulmonary hypertension, leading to right heart failure, simple right heart failure is rare, and the performance of systolic dysfunction and diastolic dysfunction is discussed separately.

1. Left heart failure symptoms: symptoms of left heart failure, mainly manifested as pulmonary circulation congestion.

(1) fatigue, fatigue: usually limb weakness, general physical activity is fatigue, is the early symptoms of left heart failure.

(2) Dyspnea: It is the earliest and most common symptom of left heart failure. It is the result of decreased lung capacity due to pulmonary congestion and decreased lung sufficiency. Dyspnea is only caused by heavy physical labor. Relief, called "laboratory dyspnea", as the disease progresses, dyspnea can occur in lighter physical activity, the labor force gradually declines, and some manifest as paroxysmal nocturnal dyspnea, usually no difficulty in falling asleep However, after sleeping at night, suddenly chest tightness, shortness of breath and need to be forced to sit up, lighter can be relieved after a few minutes of sitting, but some with cough, cough foam, if accompanied by asthma, can be called cardiogenic Asthma, severe cases can develop pulmonary edema, the mechanism of paroxysmal dyspnea at night may be related to increased venous return during supine, increased diaphragm, decreased vital capacity and increased vagal tone at night. When left heart failure is severe, the patient is even Lying in rest also feels difficulty breathing, forced to take a semi-recumbent position or sitting position, called sitting breathing, due to gravity during sitting, so that part of the blood transferred to the sagging part of the body, can reduce the lungs Blood, lung capacity can increase and decrease the diaphragm.

(3) Acute pulmonary edema: Acute pulmonary edema refers to the infiltration of plasma into the pulmonary interstitium, followed by infiltration into the alveoli, affecting gas exchange, and causing difficulty in breathing, coughing, foaming, etc., caused by heart disease. Acute pulmonary edema, called "cardiac pulmonary edema", is the most common and most important type of pulmonary edema. All of the common causes of cardiogenic pulmonary edema are acute because of the cardiopulmonary edema discussed here. Left heart failure, due to acute myocardial infarction, papillary muscle rupture, rheumatic valvular heart disease, malignant hypertension, acute myocarditis, hypertrophic cardiomyopathy with left ventricular outflow tract obstruction, congenital subaortic stenosis and severe rapidity Arrhythmia, etc., in general, the left ventricular end-diastolic pressure and left atrial pressure increase and pulmonary capillary pressure increased by more than 30mmHg, acute pulmonary edema can occur, according to the development process and clinical manifestations of pulmonary edema, It is divided into the following five periods:

1 Incidence period: The symptoms are not typical. The patient's shortness of breath is sometimes manifested as anxiety and anxiety. The physical examination shows that the skin is pale and damp, and the heart rate is increased. X-ray examination may have typical shadows near the hilar.

2 interstitial pulmonary edema: there is difficulty breathing, but no foaming, there is a sitting breathing, pale skin, often with cyanosis, some patients can see jugular vein engorgement, the lungs can smell wheezing, sometimes accompanied by fine Wet voice.

3 alveolar pulmonary edema period: frequent cough, extreme breathing difficulties, coughing pink foamy sputum and other symptoms, physical examination found that the lungs are full, the water bubble, with wheezing, and galloping, jugular vein anger Zhang, hairpin and other performances.

4 shock period: severe patients can enter this period, manifested as blood pressure drop, pulse breakdown, pale skin, increased cyanosis, cold sweats, confusion, etc., this stage of lung voice can be reduced, but the prognosis is even worse.

5 dying period: heart rhythm and breathing are severely disordered, dying of death.

According to the difference in cardiac output, acute pulmonary edema is clinically divided into two types:

Type I: high-output pulmonary edema or cardiac dysfunctional pulmonary edema, clinically common, patients with blood pressure often higher than before the onset, and have accelerated circulation, increased cardiac output, pulmonary artery pressure And the pulmonary capillary pressure is significantly increased, and the increase in cardiac output is relative. In fact, it is lower than before the onset, but it is still higher than the normal person's resting state. Hypertensive heart disease, rheumatic heart disease (aortic valve or mitral regurgitation), syphilitic heart disease, excessive transfusion or too fast transfusion, etc., are effective in reducing the pre-cardiac load.

Type II: low-output pulmonary edema or cardiac output-lowering pulmonary edema, the patient's blood pressure is constant or decreased, and the cardiac output is reduced, the pulse is weak, and the pulmonary artery pressure is increased. Wide-range acute myocardial infarction, diffuse myocarditis, rheumatic heart disease, high mitral stenosis or aortic stenosis, etc., can be treated with reduced venous return, which may have a temporary effect, but may cause shock.

(4) cough, cough and hemoptysis: caused by alveolar and bronchial mucosal congestion, cough is one of the main symptoms of left heart failure, more obvious in acute left heart failure, sometimes the main performance before the onset of heart failure, Cough is often aggravated during physical labor or lying at night, and can cough up foaming. When acute pulmonary edema, a large amount of pink foamy sputum can be coughed up, mitral stenosis, acute pulmonary edema and pulmonary infarction can cause hemoptysis. The color is bright red, and the amount is uncertain.

(5) Other symptoms: cyanosis may occur in left heart failure, nocturia may increase, left pulmonary artery dilatation may cause symptoms such as hoarseness caused by left recurrent laryngeal nerve, and severe cerebral hypoxia may be associated with mental symptoms such as lethargy and confusion. Cases can occur in a coma.

(6) Signs: In addition to the signs of the original heart disease, the changes caused by left heart failure mainly include the following aspects.

1 cardiac signs: left heart failure, generally have heart enlargement, mainly left ventricular enlargement, but left heart failure caused by acute myocardial infarction and rheumatic heart disease mitral stenosis caused by left atrial failure, no left ventricle Expanded, the latter only the left atrial enlargement, the apical region and its medial audible and diastolic gallop, the second heart sound in the pulmonary valve area, the second heart sound reverse split, the left ventricular can be significantly expanded when the relative mitral valve can occur Incomplete systolic murmur in the apical region, sinus tachycardia often occurs in left heart failure, and severe ventricular arrhythmias can occur in severe cases. Alternate veins are also one of the early important signs of left heart failure.

2 signs of lung: paroxysmal nocturnal dyspnea, both lungs have more wet voice, and can smell wheezing and dry snoring, inhalation and exhalation have obvious difficulties, acute pulmonary edema, both lungs Full of wet voice, wheezing and voice, in the interstitial pulmonary edema, the lungs have no dry and wet voice, only the lungs breath sounds weakened, about 1/4 of patients with left heart failure develop pleural effusion ( See right heart failure).

2. Right heart failure symptoms:

(1) Gastrointestinal symptoms: long-term gastrointestinal congestion, can cause loss of appetite, nausea, vomiting, abdominal distension, constipation and upper abdominal pain symptoms, individual cases of severe right heart failure, may occur as a protein-induced enteropathy.

(2) Kidney symptoms: renal congestion caused by renal dysfunction, may have nocturia, most patients with urine containing a small amount of protein, a small number of transparent or granular tube type and a small number of red blood cells, plasma urea nitrogen can be increased, after heart failure correction, the above The change can be restored to normal.

(3) Pain in the liver area: After hepatic congestion, the upper right abdomen is full of discomfort, liver area pain, severe cases can cause severe pain and misdiagnosis as acute abdomen and other diseases, chronic heart failure patients with chronic heart failure can cause heart Derived cirrhosis.

(4) Dyspnea: On the basis of left heart failure, after right heart failure can occur, due to the reduction of pulmonary congestion, the difficulty of breathing is less than that of left heart failure, but it is still right heart failure. Different levels of difficulty breathing.

(5) Signs: In addition to the original signs of heart disease, the changes caused by right heart failure mainly include the following aspects.

1 cardiac signs: because right heart failure is caused by left heart failure, so heart enlargement is more obvious than left heart failure in right heart failure, showing a whole heart enlargement, patients with simple right heart failure can generally find right ventricle and (or) right atrial hypertrophy, when the right ventricular hypertrophy is significant, in the lower left sternal border, there is a strong and strong pulsation during systole, and obvious pulsation is often seen under the xiphoid process, which is also a manifestation of right ventricular enlargement. Smear of right ventricular diastolic galloping, the right ventricle is significantly enlarged, can cause relative tricuspid regurgitation, in the tricuspid auscultation area can be heard and systolic hairy murmur, if there is relative tricuspid stenosis, Early diastolic murmurs can be heard in the tricuspid auscultation area.

2 jugular vein filling and pulsation: in the right heart failure, due to the elevation of the superior and inferior vena cava, the superficial veins of the external jugular vein, the dorsal vein of the hand and the sublingual vein are abnormally filled, and the jugular vein can be obviously beaten. Intravenous filling is earlier than liver enlargement or subcutaneous edema, so it is an early sign of right heart failure.

3 liver enlargement and tenderness: liver enlargement and tenderness often occur before subcutaneous edema, and every right heart failure patient has no exception, so it is one of the most important and early signs of right heart failure, hepatic jugular vein reflux sign Positive is one of the important signs of right heart failure, but it can also be seen in exudative or constrictive pericarditis. If right heart failure is rapidly aggravated in a short period of time, the liver will increase sharply and extend to the umbilicus. The pain is obvious. And jaundice, elevated transaminase, long-term chronic right heart failure patients with cardiogenic cirrhosis, liver texture is hard, sharp edges, tenderness is not obvious.

4 drooping edema: drooping subcutaneous edema, occurring after jugular vein filling and liver enlargement, is a typical sign of right heart failure, subcutaneous edema is first seen in the sagging part of the body, getting up, edema in front of the foot, ankle and tibia More obvious, especially in the afternoon, as the disease worsened, it showed an upward development. In bed (supine) patients, the edema of the ankle and thigh was more significant. In patients with severe right heart failure, systemic persistent edema, late In patients with whole heart failure, due to malnutrition or liver function damage, plasma protein is too low, and when there is facial edema, the prognosis is poor.

5 Most pleural effusions occur in patients with total heart failure: mainly related to increased venous pressure and pulmonary venous pressure and increased pleural capillary permeability, more often in the left and right chest, often with right pleural fluid More unilateral pleural effusion is also seen on the right side, a small number of patients with pleural effusion caused by simple left heart failure or right heart failure, pleural effusion can induce or aggravate dyspnea, pleural effusion is limited to the right There are many reasons for more explanations. The more reasonable explanation is: the average venous pressure of the right lung is higher than that of the left side, while the volume of the right lung is larger than that of the left lung, and the surface filtration area of the right lung is larger than that of the left lung. Therefore, heart failure is often seen in the right pleural effusion, or the amount of pleural effusion on the right side is more than the left side.

6 Ascites: Ascites can be seen in patients with advanced right heart failure or total heart failure, such patients often have cardiogenic cirrhosis.

7 hairpin: the heartbeat of patients with right heart failure is significantly worse than left heart failure, but the difficulty of breathing is lighter. In patients with simple right heart failure, the hair is mostly peripheral, appearing in the sagging part of the limb and the surrounding part of the body. In patients with whole heart failure, the hair strands are mixed, that is, the central and peripheral hair strands coexist.

8 pericardial effusion: severe and persistent cases of right heart failure, an abnormal amount of fluid leakage in the pericardial cavity, pericardial effusion.

9 other manifestations: some patients with heart failure may have odd pulse, individual cases of severe right heart failure, may have neurological excitement, anxiety and other symptoms, may have significant malnutrition, weight loss and even cachexia.

3. Heart failure: Heart failure has both left and right heart failure.

Examination of congestive heart failure

1. Water, electrolyte imbalance and acid-base balance disorders; hypokalemia or potassium deficiency; hypomagnesemia, hyponatremia.

2. The plasma concentration of atrial natriuretic peptide (ANF) is increased, but its concentration can be decreased in the late stage of heart failure.

3. Urine routine examination has a small amount of protein, red blood cells, transparent tube type or granular tube type.

4. Serum bilirubin, alanine aminotransferase (Alanine aminotransferase) and aspartate aminotransferase may increase slightly, and those who are significantly increased are more common in acute right heart failure, occasionally in chronic right heart failure.

5. May have mild azotemia, low chloride metabolic alkalosis and metabolic acidosis.

6. X-ray examination: X-ray examination of left heart failure can be found in the left ventricle or left atrial enlargement, pulmonary congestion, interstitial pulmonary edema, alveolar pulmonary edema and other changes in pulmonary venous pressure, chronic left heart failure, It can be seen that the pleural thickening between the lungs, or a small amount of pleural effusion, right heart failure secondary to left heart failure, X-ray examination showed that the heart expanded to the sides, simple right heart failure, visible right atrium and right ventricular enlargement, lung The field is clear, in addition, the superior vena cava shadow is widened, may be accompanied by bilateral or unilateral pleural effusion, right heart failure caused by chronic pulmonary heart disease, emphysema, gross lung texture and signs of bronchial infection.

7. Determination of blood circulation time: The left-heart failure patients have prolonged arm-to-lingual circulation time, mostly in 20-30s (normal value is 9-16s), and patients with right heart failure have prolonged arm-to-pulmonary time, which can reach more than 8s (normal 4~) 8s); At the same time, left heart failure, arm-to-lingual time can be significantly prolonged; and in patients with simple right heart failure, arm-to-lingual circulation time should be in the normal range.

8. Electrocardiogram examination: ECG examination can be found in the atrial, ventricular hypertrophy, arrhythmia, myocardial infarction and other basic heart disease, the V1 lead P wave terminal vector (PTF-V1) on the electrocardiogram is a good indicator of left ventricular dysfunction, study It indicates that PTF-V1 has a certain relationship with pulmonary wedge pressure, which can indirectly reflect the load and functional status of left atrium and left ventricle. If there is no mitral stenosis, if PTF-V1 is less than -0.03mm/s, it indicates early left. The existence of heart failure.

9. Cardiac function tests and hemodynamic monitoring: cardiac function tests and hemodynamic monitoring have been used mainly for pump failure caused by acute myocardial infarction, and recently used for cardiomyopathy and valvular heart disease. The development of aging, especially non-invasive hemodynamic monitoring technology, has been widely used in various heart disease changes, and has important value in the diagnosis and treatment of heart failure.

(1) Clinical significance:

1 Early diagnosis, evaluation of cardiac pump function: clinical bedside observation, electrocardiogram, X-ray examination can provide a lot of diagnostic information, but it is difficult to correctly and timely reflect the heart pump function changes, many hemodynamic changes of cardiac pump function can occur Before the above various examinations, hemodynamic monitoring can be performed in time to obtain various hemodynamic accurate parameters, which provides an objective basis for early diagnosis and early treatment of heart failure.

2 Guide clinical classification, choose a reasonable treatment plan: When heart pump failure, according to hemodynamic changes, can be divided into different types, different types need to adopt different treatment options.

3 evaluation of efficacy: in the clinical treatment of vasodilators, often need to be monitored under hemodynamic monitoring, otherwise the dose is not easy to master, in the process of heart failure treatment, can evaluate the efficacy of various drugs, choose the appropriate drugs and combinations, In recent years, the application of computer intervention in "drug therapy information feedback system" has made hemodynamic monitoring enter a new era.

4 Prognosis: The incidence, severity and mortality of pump failure are closely related to cardiac function. Hemodynamic parameters may indicate prognosis and guidance treatment. Hemodynamic monitoring during right ventricular infarction also has special significance. Right ventricular dysfunction is severe and the prognosis is poor.

(2) Observation indicators: Hemodynamic indicators can be divided into the following categories:

1 pressure indicators: including arterial blood pressure, atrioventricular pressure, pulmonary capillary wedge pressure, central venous pressure.

(3)()()

Diagnostic criteria

1.10mmHg18mmHg16mmHg10

(1)

(2)

(3)

(4)

(5)()

(6)

(7)

(8)

(9)PV1V1P(PTF-V1)()

(10)()Kerley

2.

(1)

Framingham()

A.

a.()

b.

c.()

d.

e.

f.

g.

h.>15cmH2O

i.>25s

jXKerley

k.

B.

a.()

b.

c.

d.

e.

f.1/3

g.(120/min)

54.5kg

C.212

Boston1985Carlson>12mmHgBoston(12)X48;57;4X

Killip()5

0%5%

50%X10%20%

50%35%40%

<90mmHg(<20ml/h)>100/min85%95%

(CFHA)(199310·)2(19955·)

A.

a.;

b.

(2)FraminghamBostonForrester4(2)

X

>50%

Differential diagnosis

1.

(1)

(2)X

(3)X

(4)

(5)()pH

(6)

(7)

2.

(1)ST-TX

(2)

(3)

(4)(pickwickian syndrome)

(5)X

3.()

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