Heart Failure Heart Function Classification New York Heart Association Heart Function Classification 1. Killip classification is used to assess the functional status of the heart in patients with acute myocardial infarction. Grade I: no pulmonary sternal steal sac woven Ⅱ: lung with large poopum segment Т笥l/2 lung field. Grade III: lung with a large pulmonary segment Т笥l/2 lung fields (pulmonary edema). Grade IV: shock. 2.New York Heart Association (NYHA) grading The instrument applies to the grading of cardiac function in patients with simple left heart failure and systolic heart failure. Class I: The patient has heart disease, but physical activity is not limited. General physical activity does not cause excessive fatigue, palpitations, shortness of breath or angina pectoris. Class II: The patient has heart disease to the extent that physical activity is mildly restricted. No symptoms at rest, but general physical activity causes excessive fatigue, palpitations, shortness of breath or angina pectoris. Class III: The patient has heart disease to the extent that physical activity is significantly limited. No symptoms at rest, but less than general physical activity causes excessive fatigue, palpitations, shortness of breath or angina pectoris. Grade IV: The patient has heart disease and has symptoms of cardiac insufficiency or angina at rest, and any physical activity increases the discomfort. Basic etiology and causative factors (a) Basic etiology of heart failure Coronary heart disease has become the main cause of heart failure in patients under 75 years of age in Europe, similar to the situation in China. A recent survey in Shanghai showed that 65, 8% of heart failure in the region was due to coronary heart disease. Hypertension is also an important causative factor for heart failure in elderly people. According to the pathophysiological abnormalities, the basic etiology of heart failure can be divided into: 1. weakened myocardial contractility myocarditis, cardiomyopathy and coronary artery disease, etc. 2, increased afterload Hypertension, aortic stenosis, pulmonary hypertension and pulmonary stenosis, etc. 3, increased preload mitral stenosis, tricuspid stenosis, mitral regurgitation, aortic regurgitation, atrial septal defect, ventricular septal defect and diseases with increased metabolic demand (hyperthyroidism, arteriovenous fistula, etc.). (B) Causes of heart failure 1. Inappropriate treatment Mainly inappropriate dosage of digitalis (over or under) and combined use of drugs that inhibit myocardial contractility (isoptin, beta blockers) or cause water and sodium retention (high-dose nonsteroidal anti-inflammatory drugs). 2. Infections Respiratory infections and infective endocarditis are more important triggers. 3, arrhythmias Especially atrial fibrillation with fast ventricular rate and other rapid arrhythmias. 4.Pulmonary artery embolism. 5. Excessive physical or mental strain. 6, Combined diseases with increased metabolic demand, such as hyperthyroidism and arteriovenous fistula. Infection, arrhythmias and improper treatment are the most important triggers of heart failure. Types of heart failure 1, left heart failure, right heart failure and total heart failure. 2, Acute heart failure and chronic heart failure. 3, Systolic heart failure and diastolic heart failure. 4, high power circulatory heart failure. Pathophysiology 1. Compensation of heart failure After abnormal heart function leads to heart failure, a series of compensatory reactions occur: (1) Localized heart: dilatation of heart chambers, hypertrophy of heart muscle and increased heart rate. (2) Systemic: several neuroendocrine systems are activated, the more important of which are: the sympathetic nervous system and the renin-angiotensin system, as well as the release of antidiuretic factors. In the process of cardiac function compensation, Fran-Starling mechanism, ventricular remodeling and neurohumoral activation play an important role. 2, ventricular remodeling Primary myocardial damage and cardiac overload increase ventricular wall stress, leading to reactive hypertrophy and dilatation of the ventricle, with changes in both myocardial cells and the composition of the extracellular matrix a collagen network, which is the process of ventricular remodeling. When myocardial hypertrophy is insufficient to overcome wall stress, progressive enlargement of the left ventricle with hypofunction progresses to the end stage of irreversible myocardial damage. Clinical manifestations: 1. manifestations of low cardiac output ① fatigue, weakness, and lethargy; ② decreased work tolerance; ③ increased nocturia and oliguria; ④ anxiety, headache, and insomnia. 2. Left heart insufficiency (1) Symptoms: mainly the clinical manifestations of pulmonary stasis: 1) Dyspnea: manifested as exertional dyspnea, nocturnal paroxysmal dyspnea and telescopic breathing, and acute pulmonary edema may appear in severe cases. Exertional dyspnea can be the first symptom, and with the aggravation of left ventricular insufficiency, the labor intensity that induces shortness of breath proceeds to decline. The mechanism of its occurrence is the increase of cardiac blood volume by exercise, the increase of left atrial pressure, and the aggravation of pulmonary stasis. Sitting breathing refers to a condition in which breathing distress occurs in the prone position and is relieved by elevating the head or sitting. It is a nonspecific symptom and any condition that decreases lung volume can cause the condition. Unlike telescopic breathing, nocturnal paroxysmal dyspnea occurs during nighttime sleep when the patient awakens suddenly with severe anxiety and a sense of suffocation due to wheezing and the need to sit up quickly, usually with a wheezing sound, hence the name cardiogenic pulmonary edema. Acute pulmonary edema is the most serious clinical manifestation of acute left heart failure (see Acute Left Heart Failure). (2) Other: cough and hemoptysis. (2) Signs: both lungs, especially the two lung bases can often be heard as wet sternal pain woven P brain 锟누锟ーツ even amine buck tongue warrants navigation S3 prancing horse rhythm and heart enlargement and other signs of pre-existing heart disease. 3, right heart insufficiency (1) symptoms: due to chronic persistent stasis and edema of the organs, the patient may have loss of appetite, nausea, vomiting, abdominal distension, abdominal pain and urination, increased nocturia, etc. (2) Signs: jugular venous filling or anger; positive hepatic venous reflux sign (this sign helps to distinguish heart failure from other causes of hepatomegaly); hepatomegaly pressure pain; pendulous symmetric edema; pleural and ascites, ascites mostly occurs in the late stage of the disease, mostly related to cardiogenic cirrhosis; right heart gallop rhythm; cyanosis. 4. Total heart failure Clinical manifestations of left and right heart failure coexist, but pulmonary stasis manifestations such as nocturnal paroxysmal dyspnea are conversely less severe than in simple left heart failure. 5. Complications (1) Arrhythmia. (2) Electrolyte disturbance: low potassium is common. (3) Stasis of the liver, in severe cases, cardiogenic cirrhosis may occur. (4) Thromboembolism: it can lead to pulmonary embolism. Diagnosis and differential diagnosis 1. Diagnosis Since there is no reliable defined value for the diagnosis of heart failure in terms of heart/ventricular function or blood flow, pressure, chamber diameter or volume, the diagnosis of heart failure is a clinical judgment based on history, physical examination and certain auxiliary findings. The following conditions must be met for diagnosis: (1) the presence of symptoms of heart failure (during exercise or at rest); (2) evidence of cardiac insufficiency (at rest); and (3) a good clinical response to anti-heart failure treatment. The first and second are necessary for diagnosis; the third is for reference only. Finding objective evidence of cardiac insufficiency is important for the diagnosis of heart failure. Echocardiography is a simple, safe, noninvasive test and should be used routinely. Plasma natriuretic peptide, (e.g. ANP) levels have a very high negative predictive value, and in untreated patients, if their levels are normal, the diagnosis of heart failure can be excluded. Electrocardiogram, chest X-ray, exercise test and invasive hemodynamic tests can provide diagnostic information. 2. Differential diagnosis Dyspnea caused by left heart failure should be differentiated from dyspnea caused by pulmonary diseases. Cardiogenic asthma is sometimes difficult to distinguish from bronchial asthma, but if the patient produces pink frothy sputum, it can be diagnosed as cardiogenic asthma. Edema and ascites caused by right heart failure should be differentiated from renal edema, pericardial diseases such as constrictive pericarditis, liver cirrhosis and endocrine diseases. Treatment (c) Treatment The treatment of heart failure aims at: (1) prevention: to prevent progressive exacerbation of heart failure or to prevent progression from cardiac insufficiency to heart failure; (2) improving or maintaining the patient’s quality of life; (3) prolonging the patient’s life span and improving survival rate. The principle of treatment is to remove the cause of the disease (the causative factor of the underlying cause) and improve the state of heart failure. Specific details are as follows: 1. General treatment (1) Removal of causes: treatment for underlying heart disease, such as controlling hypertension, increasing blood supply to ischemic myocardium, and correcting abnormalities in valve structure; attention should also be paid to eliminating the causative factors of heart failure; infection, rapid arrhythmia and improper treatment are the most common causative factors, which should be identified and treated. (2) Diet: appropriate caloric intake to prevent obesity; control water and sodium intake, 24-hour fluid intake should be less than 1000-1500ml for patients with severe heart failure. (3) Rest: avoid physical overwork and mental stimulation, but should not be bedridden for a long time, and should perform moderate activities. 2, drug treatment (1) diuretic application: diuretic is still the main drug for heart failure treatment, it can relieve the “congestion” symptoms of heart failure, the efficacy is exact and rapid. According to the different diuretic action site, divided into 3 categories: 1) diuretic action in Henle collaterals: these drugs are mainly furosemide (tachyphylaxis), the use of 20 ~ 40mg times, 1 ~ 3 times / d, or 20 ~ 40mg / times intravenous injection, sometimes the dosage can be as high as 1000mg / d. The strongest diuretic effect of these drugs, even in the glomerular filtration rate is low also has a significant diuretic effect. The effect. 2) Diuretics acting on the distal tubule: the representative preparation is hydrochlorothiazide, the usage is 25mg/time, 1~3 times/d; these drugs have a long duration of action, but the diuretic effect is not as good as the tab diuretics, and it depends on the glomerular filtration rate. 3) Diuretics acting on the collecting duct: the main drugs are spironolactone, 20-40mg/dose, 3-4 times/d, and aminoglutethimide, 50-100mg/dose, l-3 times/d. These drugs are relatively weak, but have potassium preservation (inhibition of H+-K+ exchange), or have a direct role against aldosterone, and are often used in combination with other diuretic drugs. Continuous heavy diuresis can lead to severe electrolyte disturbances and acid-base imbalance. Excessive diuresis can also cause hypovolemia, hypotension, circulatory failure and azotemia. Clinically, attention should be paid to the rational application of diuretics: ① intermittent use of potassium excretory diuretics to restore the electrolyte balance of the body; while potassium-protective diuretics have a slower onset and weaker effect, so they should be applied continuously; ② when potassium excretory and potassium-protective diuretics are used, it is generally not necessary to supplement potassium salts; potassium-protective diuretics cannot be combined with potassium salts; ③ choose diuretics according to the severity of the disease; ④ choose tab diuretics when renal insufficiency, and prohibit the use of potassium-protective diuretics. Potassium-protective diuretics are prohibited; ⑤ adjust the dose according to the treatment response; ⑥ pay attention to water and electrolyte disorders, especially hypokalemia, hypomagnesemia and hyponatremia; ⑦ pay attention to drug interactions; ⑧ thiazides have adverse effects on lipid metabolism and glucose metabolism, and can cause hyperuricemia. (2) vasodilators: vasodilators for the treatment of chronic heart failure is a milestone in therapeutics. phentolamine, sodium nitroprusside, and subsequently nitroglycerin, which were used in the 1970s, had a significant effect on improving hemodynamics. In particular, the use of angiotensin-converting enzyme inhibitors (ACEI) for the treatment of chronic heart failure in the mid- to late-1980s was a major therapeutic advancement that contributed positively to reducing the number of hospitalizations, improving quality of life, and prolonging survival in patients with heart failure. 1) Sodium nitroprusside simultaneously dilates arteries and veins and reduces the pre and afterload of the ventricles. It is mainly used in patients with advanced heart failure characterized by reduced cardiac output and increased left ventricular filling pressure and resistance of the body circulation. It is administered intravenously at a starting dose of 0,3ug/(kg?min), and then the dose is increased slowly according to the blood pressure response, with the maximum dose not exceeding 10ug/(kg?min). The most common side effect is hypotension. Large doses, especially when accompanied by renal insufficiency, are prone to thiocyanate or cyanide poisoning. 2) Nitrates: mainly dilate veins and small pulmonary arteries. Oral preparations are nitroglycerin 0, 5mg containing; Isosorbide dinitrate 20mg, 2 times / day; Isosorbide mononitrate 20mg, 2 times / day, this drug has high bioavailability and long duration of action. However, care should be taken to maintain at least a few hours of “nitrate free period” at night, so as to possibly avoid nitrate resistance. Add 10mg of nitroglycerin to 250ml of 5% glucose solution and drip at an initial rate of 10ug/min, gradually increasing by 5-10ug/min, paying attention to reflex tachycardia and hypotension. 3) Angiotensin-converting enzyme inhibitor (ACEI): The main function is to inhibit the production of angiotensin II in the circulation and local tissues, and also has the effect of dilating small arteries and veins. It can relieve and eliminate symptoms, improve hemodynamic changes and left ventricular function, reverse left ventricular hypertrophy, and improve exercise tolerance. More importantly, its effect on reducing morbidity and mortality is better than that of simple vasodilators, so it should be used first, but not in patients with severe renal failure, bilateral renal artery stenosis and hypotension. The main side effect is hypotension, especially the first dose of hypotension, so attention should be paid to monitoring blood pressure, renal function and potassium. It should not be combined with potassium salts or potassium-protective diuretics to avoid hyperkalemia. In addition, cough is the most common side effect of these drugs. Commonly used preparations are captopril, initial dose 6, 25mg, maximum dose 50mg, 3 times/day; Enalapril, initial dose 2, 5mg, maximum dose 10-20mg, 2 times/day; Monola initial dose 5-10mg, maximum dose 40mg, once a day. (3) digitalis drugs digitalis has more than 200 years of history of application, but is still the main drug for the treatment of heart failure. 1) Commonly used digitalis preparations and doses: digoxin tablets 0, 25mg / d, after about 5 half-lives (5-7 days) to reach steady-state therapeutic blood concentrations. Trichosanthin C (Cidilan) injection 0, 2 ~ 0, 4mg / time, according to the condition can be repeated several times, 24 hours total 1, 0 ~ 1, 6mg sedation; toxic trichosanthin K injection 0, 25 ~ 0, 5mg / time, sedation. 2) Indications: Patients with moderate or severe systolic heart failure, particularly effective in patients with atrial fibrillation with rapid ventricular rate. 3) Conditions in which it is not recommended: ① preexcitation syndrome combined with atrial fibrillation; ② second degree or high degree atrioventricular block; ③ pathological sinus node syndrome, especially in the elderly; ④ simple diastolic heart failure such as hypertrophic cardiomyopathy; ⑤ simple severe mitral stenosis with sinus rhythm without right heart failure; ⑥ acute myocardial infarction, especially in the first 24 hours, unless combined with atrial fibrillation or (and) enlarged heart chambers. 4) Factors affecting the dose: the elderly, myocardial ischemia and hypoxia or acute lesions (such as acute myocardial infarction, pulmonary heart disease, acute diffuse myocarditis), severe heart failure, hypokalemia or (and) hypomagnesemia, and renal decompensation, etc., are more sensitive to digitalis drugs and should be applied in reduced doses. 5) Interaction with other drugs: many drugs such as quinidine, propafenone, verapamil, amiodarone, etc. when combined with digoxin, the latter serum concentration can be increased by 70% to 100%, it is appropriate to reduce the dose of digoxin by half. The effect of digoxin can be weakened by the acid control agent for the treatment of ulcer disease, so it should be taken separately. 6) Toxic reactions of digitalis: clinical manifestations include: (1) gastrointestinal reactions such as loss of appetite, nausea, vomiting, etc.; (2) neurological manifestations such as headache, depression, weakness, blurred vision, yellow or green vision, etc.; (3) cardiotoxicity, mainly manifested as various types of arrhythmias, ventricular duplex rhythm, triplex rhythm, junctional escape rhythm and non-paroxysmal junctional tachycardia, accounting for a total of about 2/3, atrioventricular conduction block may also occur. Atrioventricular conduction block may also occur. 7) Treatment measures for digitalis toxicity: including immediate discontinuation of digitalis; phenytoin sodium or lidocaine can be applied in the presence of tachyarrhythmias; in the case of ectopic tachyarrhythmias with hypokalemia, potassium salts can be given intravenously, but it is prohibited in those with AV block. (4) Other positive inotropic drugs: non-gastrointestinal drugs for patients with end-stage heart failure, generally used only for a short period of time during cardiac transplantation or acute deterioration of heart failure. 1) Dobutamine: a derivative of dobutamine with strong selective βl receptor effects, which increases myocardial contractility, is only available in intravenous formulations and can produce significant short-term kinetic effects. The commonly used dose is 2,5-7,5ug/(kg, min), intravenous drip. Each course of treatment usually does not exceed 1 week. The drug can increase ventricular arrhythmias and mortality. 2) Milrinone: phosphodiesterase inhibitor. Use: 50ug/kg intravenous injection, then 0,25-0,5ug/(kg, min) intravenous drip. Because it has the possibility of increasing sudden cardiac death, it should not be used for long-term treatment of heart failure. (3) Calcium sensitizers: such as Levosimendan, which can reduce the rate of death 3 days to 6 months after acute myocardial infarction and has better safety than dobutamine. (5) β-blockers: Although it is not the first-line treatment for heart failure, β-blockers should be used on top of standard therapy (cardiac stimulants, diuretics, and angiotensin-converting enzyme inhibitors) in patients with stable mild, moderate, or severe heart failure, either ischemic or nonischemic. β-blockers do not have class effects, and there is now clear evidence of evidence-based medicine The three main beta-blockers that are considered to be used in the treatment of heart failure are bisoprolol, carvedilol, and metoprolol. Their mechanisms for treating heart failure are mainly: reducing sympathetic tone in the heart, prolonging diastole, and upregulating β-adrenergic receptors. Carvedilol also has vasodilatory and antioxidant properties. Treatment should be started with small doses and slowly increased to reach the target dose as much as possible. The recommended uses by the European Society of Cardiology are listed in Table 7-12-1. The main side effects are myocardial depression, worsening heart failure, induction of asthma and peripheral vasoconstriction. (6) Antiarrhythmic: mainly for combined atrial fibrillation, non-paroxysmal or paroxysmal ventricular tachycardia. Because class I antiarrhythmic drugs (such as cardioplegia) have significant arrhythmogenic effects as well as adverse hemodynamic effects, they should be avoided as much as possible. Class III antiarrhythmic drugs, such as amiodarone, are relatively safe and effective. (7) Anticoagulation therapy: Aspirin and heparin can be used according to the underlying disease and clinical manifestations, but the effect of long-term use of these drugs on heart failure still needs further observation. 3. Device and surgical treatment (1) Revascularization: There is no data from controlled studies to support that hemodynamic reconstruction (interventional therapy or surgery) treatment can improve the symptoms of heart failure patients. (2) Pacemakers and implantable cardioverter-defibrillators (ICDs): Atrial sequential pacing should be given priority when heart failure is combined with bradycardia; ICDs can be implanted in heart failure patients with recurrent ventricular tachycardia/ventricular fibrillation episodes in which drugs are ineffective. (3) Blood ultrafiltration: Short-term treatment for patients with pulmonary edema and/or intractable congestive heart failure to reduce preload or buy time for heart transplantation. . (4) Heart transplantation: Heart transplantation significantly prolongs life expectancy, enhances exercise capacity, and improves quality of life in patients with end-stage heart failure. The current 5-year survival rate of heart transplantation can reach 70% to 80%. 4.Therapeutic methods still under investigation: angiotensin II antagonists, endothelin antagonists, neutral endogenous peptidase inhibitors (ANP/BNP), pressor antagonists, cardiomyoplasty, artificial hearts, ventricular assist devices, metabolic therapy, myocardial stem cell transplantation, and new positive inotropic drugs (such as DPI210-106) have been effective in the treatment of heart failure. The treatment of heart failure has some efficacy, but it is still in the clinical research stage and there is no final conclusion. Definition and countermeasures of intractable heart failure Definition and countermeasures of intractable heart failure Intractable heart failure, also known as refractory heart failure, is a condition in which severe heart failure symptoms do not improve despite treatment with ACEI and/or other vasodilators, as well as diuretics and digitalis systems. The first step in the management of intractable heart failure is to try to find the possible causes of the intractable heart failure and try to correct them. Possible causes of intractable heart failure include rheumatic activity, infective endocarditis, anemia, hyperthyroidism, electrolyte disturbances, digitalis overdose, recurrent pulmonary embolism, co-infection, heavy alcohol consumption, and concomitant receipt of drugs with water and sodium retention (e.g., corticosteroids) and/or negative inotropic effects (e.g., calcium antagonists, certain antiarrhythmics). In addition to the causative treatment, the anti-heart failure treatment should be adjusted and the combination of diuretics, vasodilators and positive inotropic drugs should be enhanced. If necessary, blood ultrafiltration can be used to treat intractable edema. Acute heart failure Start the breakdown exercise Etiology of acute heart failure (a) Etiology of acute heart failure Acute heart failure is a syndrome of inadequate perfusion of tissues and organs and acute bruising due to acute cardiac lesions caused by a rapid decrease in cardiac blood output. The common causes are: 1. acute myocardial ischemia or infarction. 2, acute myocardial infarction combined with acute mitral regurgitation due to papillary muscle rupture, ventricular septal perforation, rupture of the free wall of the heart and cardiac tamponade. 3.Acute valve perforation (mitral valve or aortic valve). 4, Poorly controlled severe hypertension. 5, Myocarditis. 6, Persistent arrhythmia. 7, Acute pulmonary embolism. Clinical manifestations The most common clinical manifestation is acute pulmonary edema, which is characterized by: (1) sudden onset of extreme shortness of breath and anxiety, with a sense of near death; (2) coughing and pink frothy sputum; (3) rapid breathing, profuse sweating, cold, pale, cyanotic skin; (4) dry sunglasses with hyper-P2 and S3 in both lungs. Resuscitation measures for acute left heart failure 1. to reduce venous reflux. 2, high flow oxygen inhalation (10-20ml/min pure oxygen inhalation), and should be put in the wetting bottle of alcohol or silicone defoamer. 3, morphine 3 ~ 5mg, intravenous injection, is still an extremely effective measure for the treatment of acute pulmonary edema; however, it is contraindicated for those with intracranial hemorrhage, mental disorders, chronic pulmonary insufficiency. Reduce the amount for the old and frail. 4.Furosemide (tachyphylaxis) 20～40mg sedation, pushed out within 2min, is also the main treatment method. 5.Application of vasodilator, can use sodium nitroprusside or nitroglycerin IV, sodium nitroprusside initial amount 20-40ug/min, every 5min, increase 5u/min. maintenance amount 300ug/min; nitroglycerin initial amount 5-10ug/min, every 3min increment 5ug/min, maintenance amount 50-100ug/min, until pulmonary edema relief or arterial Systolic blood pressure drops to 100mmHg, if there is hypotension, it is appropriate to combine with dobutamine. 6.Maohuaxin C 0,4mg, intravenous, for atrial fibrillation with rapid ventricular rate or known cardiac enlargement with left ventricular systolic insufficiency, forbidden for severe mitral stenosis with sinus rhythm. 7.Aminophylline 0,25g diluted with glucose water and slowly pushed intravenously is particularly effective in relieving bronchospasm, and also has positive inotropic effect, dilates peripheral blood vessels and diuretic effect. 8.Ligation of extremities in rotation to reduce preload.