Preface
Acute heart failure (heart failure) is clinically the most common form of acute left heart failure, while acute right heart failure is less common. Acute left heart failure refers to the acute onset or aggravation of left heart function abnormalities caused by a significant reduction in myocardial contractility, increased cardiac load, resulting in a sudden drop in cardiac output, a sudden increase in pulmonary circulation pressure, increased peripheral circulatory resistance, resulting in pulmonary congestion and acute pulmonary stasis, pulmonary edema, and may be accompanied by tissue and organ perfusion deficiency and cardiogenic shock clinical syndrome.
Acute right heart failure is a clinical syndrome in which the contractility of the right ventricular myocardium decreases sharply or the anterior and posterior loads of the right ventricle increase suddenly for some reasons, resulting in a rapid decrease in right heart blood output. Acute heart failure can be sudden or acute exacerbation on the basis of chronic heart failure, most of which is systolic heart failure, but also diastolic heart failure; most patients have combined organic cardiovascular disease before the onset. For acute heart failure occurring on the basis of chronic heart failure, the condition is stable after treatment and should no longer be called acute heart failure.
Acute heart failure is often life-threatening and must be rescued and treated urgently. In the last 10 years or so, although basic and clinical research on chronic heart failure has made great progress, the following problems still exist in clinical work on acute heart failure.
(1) Clinical studies, especially large prospective randomized controlled trials, are rare and clinical evidence is scarce, making most of the current recommendations for treatment in national guidelines based on experience or expert opinion and lacking sufficient evidence to support them;
(2) China’s own research is seriously lagging behind, lacking clinical information, and even basic epidemiological material is not complete; the management of acute heart failure around the lack of norms, acute heart failure morbidity and mortality rate has decreased but is still an important cause of cardiogenic death, becoming a weak link in the treatment of cardiovascular emergencies in China. In view of the above reasons, the Chinese Society of Cardiovascular Diseases decided to compile a guideline for the diagnosis and treatment of acute heart failure in China, in order to improve the clinical management of this cardiac emergency.
The Heart Failure Specialty Group of the Cardiovascular Disease Section of the Chinese Medical Association formed a writing group and an expert panel for this work, and established the following basic principles for the preparation of the guidelines.
(1) To fully draw on the new and recent developments in this field. New technologies and methods, and draw on the various guidelines developed and promulgated by major foreign academic organizations in cardiovascular disease in recent years;
(2) To be based on China’s national conditions and the traditional habits of clinical management and proven methods and experience, including the guidelines and expert consensus on heart failure and related diseases prepared by China in recent years, so that they load China’s national conditions;
(3) To provide a guideline document that clinicians in basic units and hospitals at all levels can accept and use readily.
This guideline indicates the recommended categories and levels of evidence for the application of drugs and various therapies in an internationally accepted manner. Recommendation categories: Category I is proven and/or agreed to be beneficial and effective: Category II is where the evidence for efficacy is inconsistent or controversial, with relevant evidence tending to be effective for Category IIa and insufficient for Category IIb; Category III is proven or agreed to be useless and ineffective, or even potentially harmful. Level of evidence grading: evidence from multiple randomized controlled clinical trials or multiple meta-analyses for class A; evidence from single randomized controlled clinical trials or non-randomized studies for class B; evidence from small studies or expert consensus for class C.
Epidemiology of acute heart failure
In the United States, there have been 10 million emergency room visits for acute heart failure in the past 10 years. Approximately 15-20% of patients with acute heart failure have their first diagnosis of heart failure, and most have exacerbation of preexisting heart failure. All diseases that cause chronic heart failure can lead to acute heart failure. Recently, with the gradual increase in the number of patients with chronic heart failure, chronic heart failure and acute heart failure episodes have become the main cause of hospitalization of heart failure patients, and the total incidence of heart failure is 0.23% to 0.27% per year. The prognosis of acute heart failure is very poor, with an inpatient mortality rate of 3%, a 60-d mortality rate of 9.6%, and a 3-year and 5-year mortality rate of 30% and 60%, respectively. Acute heart failure due to acute myocardial infarction has a higher mortality rate. The in-hospital mortality rate of patients with acute pulmonary edema is 12%, and the 1-year mortality rate is 30%.
A retrospective analysis of inpatient medical records from 42 hospitals in 1980, 1990 and 2000 showed that heart failure accounted for 16.3% to 17.9% of hospitalized cardiovascular patients, of whom 56.7% were men, with an average age of 63-67 years and more than 60% were over 60 years old; the average length of stay was 35.1, 31.6 and 21.8 d, respectively. The heart failure diseases were mainly coronary heart disease, rheumatic heart valve disease and hypertensive disease. During this 20-year period, coronary heart disease and hypertension increased from 36.8% and 8.0% to 45.6% and 12.9%, respectively, while rheumatic heart disease decreased from 34.4% to 18.6%; the heart function at the time of admission was mostly class III (42.5%-43.7%). This type of hospitalization is basically an acute exacerbation of chronic heart failure.
Etiology and pathophysiological mechanisms of acute heart failure
I. Common causes of acute left heart failure
1. Acute exacerbation of chronic heart failure.
2. Acute acute cardiac necrosis and/or injury.
(1) Acute coronary syndromes such as acute myocardial infarction or unstable angina, acute myocardial infarction with mechanical complications, and right ventricular infarction;
(2) Acute severe myocarditis;
(3) Perinatal cardiomyopathy;
(4) Drug-induced myocardial injury and necrosis, such as antineoplastic drugs and toxicants.
3, acute hemodynamic disorders.
(1) Acute valve massive regurgitation and/or aggravation of existing valve regurgitation, such as mitral and/or aortic valve perforation due to infective endocarditis, mitral tendon cord and/or papillary muscle rupture, valve tears (e.g., traumatic aortic valve tears), and acute damage to prosthetic valves;
(2) Hypertensive crisis;
(3) Severe aortic or mitral stenosis;
(4) aortic coarctation;
(5) pericardial compression;
(6) Acute diastolic left heart failure, mostly seen in elderly patients with poorly controlled hypertension.
II. Pathophysiological mechanisms of acute left heart failure
1, acute cardiac emergency injury and necrosis: ischemic heart disease combined with acute heart failure are mainly the following three conditions: acute myocardial infarction: mainly in view of large myocardial infarction; sometimes acute myocardial infarction can also first manifest symptoms of acute left heart failure, especially in elderly patients and diabetic patients; acute myocardial ischemia: large ischemic area and severe ischemia can also induce acute heart failure, such conditions can be seen in infarcts that are not large in scope This condition can be seen in elderly patients with small infarct size but large ischemic area; chronic cardiac insufficiency, such as old myocardial infarction or chronic ischemic heart disease patients without infarction history, can develop acute heart failure under ischemic attack or other triggering factors.
Myocardial ischemia and the resulting acute cardiac injury leave part of the myocardium in a state of myocardial stasis and myocardial hibernation, and lead to cardiac insufficiency. When coronary blood flow and oxygenation are restored, hibernating myocardial function improves rapidly, while myocardial insufficiency continues for some time when responding to positive inotropic drugs. Severe and prolonged myocardial ischemia will certainly cause irreversible damage to the myocardium.
Acute myocardial infarction or acute severe myocarditis, etc. can cause acute necrosis of the heart, which reduces the contractile units of the heart. Hypertensive emergencies or severe arrhythmias can increase the load on the heart. These alterations can produce hemodynamic disturbances and also activate the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, promoting exacerbation and worsening of the condition in patients with heart failure. The above pathophysiological process can progress due to the underlying lesion redundancy, or rapidly occur under the excitation of multiple triggers and produce acute heart failure.
2, hemodynamic disorders: The main hemodynamic disorders in acute heart failure are: decreased cardiac output (CO), absolute or relative decrease in blood pressure and insufficient perfusion of peripheral tissues and organs, resulting in organ dysfunction and peripheral circulatory disorders, and cardiogenic shock. Left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (PCWP) are elevated, and hypoxemia, metabolic acidosis, and acute pulmonary edema can occur. Elevated right ventricular filling pressures increase venous pressure in the body circulation, stasis in the body circulation and major organs, water-sodium retention and edema.
3, neuroendocrine activation: sympathetic nervous system and RAAS hyperexcitation is a protective compensatory mechanism of the body in acute heart failure, when long-term hyperexcitation will have adverse effects, so that a variety of endogenous neuroendocrine and cytokine activation, aggravating the acute heart injury, decreased cardiac function and hemodynamic disorders, which in turn stimulates the excitation of the sympathetic nervous system and RAAS, forming a vicious circle.
4, cardio-renal syndrome: heart failure and renal failure often coexist and are mutually causal clinically this state is called cardio-renal syndrome. Cardiorenal syndrome can be divided into five types; type 1 is characterized by rapidly deteriorating cardiac function leading to acute renal impairment; type 2 is characterized by chronic heart failure causing progressive chronic kidney disease; type 3 is a primary, rapid deterioration of renal function leading to acute cardiac insufficiency; type 4 is characterized by chronic kidney disease leading to decreased cardiac function and (or increased risk of adverse cardiovascular events; type 5 is characterized by acute or chronic systemic disease leading to The type 5 is characterized by simultaneous failure of cardiac and renal function due to acute or chronic systemic diseases. Obviously, both type 3 and type 4 cardio-renal syndrome can cause heart failure, where type 3 can cause acute heart failure. type 5 cardio-renal syndrome can also induce heart failure or even acute heart failure.
5, acute decompensation of chronic heart failure: stable chronic heart failure can deteriorate sharply within a short period of time, with cardiac function decompensation, manifesting as acute heart failure. The contributing factors are lack of compliance with drug therapy, severe myocardial ischemia, severe infection, severe hemodynamic arrhythmias, pulmonary embolism and renal impairment.
The etiology and pathophysiological mechanism of acute right heart failure
Acute right heart failure is mostly seen in right ventricular infarction, acute massive pulmonary embolism, and right-sided heart valve disease.
Right ventricular infarction rarely occurs alone and is often combined with inferior left ventricular wall infarction. Patients often have varying degrees of right ventricular dysfunction, and approximately 10% to 15% of them may have significant hemodynamic disturbances. The site of vascular occlusion in these patients is usually at the opening of the right coronary artery or prior to the emanation of the proximal right ventricular side branch. Impaired right ventricular diastolic activity due to right ventricular infarction increases right ventricular filling pressure and right atrial pressure; decreased right ventricular blood displacement leads to decreased left ventricular end-diastolic volume and lower PCWP.
Acute massive pulmonary embolism causes obstruction of pulmonary blood flow and persistent severe pulmonary hypertension, which increases and dilates the right ventricular afterload and leads to right heart failure; reduced right ventricular blood displacement leads to changes in body circulation and cardiac function, with decreased blood pressure, tachycardia, and inadequate coronary perfusion; the effect on the respiratory system is mainly impaired gas exchange; the release of various vasoactive drugs constricts the extensive small pulmonary arteries, increasing The release of various vasoactive drugs constricts the extensive small pulmonary arteries, increasing the degree of hypoxia, and radiologically promotes the increase of pulmonary artery pressure, forming a vicious circle.
Acute right heart failure due to right-sided heart valve disease is uncommon and is mostly chronic, but only acute exacerbations manifest as acute right heart failure.
Clinical Classification and Diagnosis of Acute Heart Failure
I. Clinical classification
There is no unified clinical classification of acute heart failure internationally. The classification based on the etiology, causative factors, hemodynamic and clinical characteristics of acute heart failure is easy to understand and is also conducive to diagnosis and treatment.
1.Acute left heart failure.
(1) acute decompensation in chronic heart failure.
(2) acute coronary syndrome.
(3) acute hypertension.
(4) acute heart valve dysfunction.
(5) acute severe myocarditis and perinatal cardiomyopathy.
(6) severe arrhythmia.
2.Acute right heart failure.
3, Non-cardiogenic acute heart failure.
(1) high cardiac output syndrome.
(2) severe renal disease (cardiorenal syndrome).
(3) severe pulmonary hypertension.
(4) large pulmonary embolism, etc.
II. Clinical manifestations of acute left heart failure
1. History and manifestations of underlying cardiovascular disease: Most patients have a history of various heart diseases and various causes of acute heart failure exist. The main causes in the elderly are coronary heart disease, hypertension and senile degenerative heart valve disease, while in young people it is mostly caused by rheumatic heart valve disease, dilated cardiomyopathy, acute severe myocarditis, etc.
2, predisposing factors: common predisposing factors are.
(1) Lack of compliance with drug therapy for chronic heart failure;
(2) Heart volume overload;
(3) Severe infections, especially pneumonia and sepsis;
(4) Severe cranio-cerebral damage or severe psychological stress and fluctuations;
(5) After major surgery;
(6) Decreased renal function;
(7) Acute arrhythmias such as ventricular tachycardia (ventricular tachycardia), ventricular fibrillation (ventricular fibrillation), atrial fibrillation (atrial fibrillation) or atrial flutter with rapid ventricular rate, supraventricular tachycardia, and severe bradycardia;
(8) Bronchial asthma attack;
(9) Pulmonary embolism.
(10) High cardiac output syndrome such as hyperthyroidism crisis, severe anemia, etc.;
(11) Application of negative inotropic drugs such as verapamil, diltiazem, beta-blockers, etc;
(12) Application of non-steroidal anti-inflammatory drugs;
(13) Myocardial ischemia (patency without symptoms);
(14) Acute diastolic dysfunction in the elderly;
(15) drug addiction;
(16) Alcohol abuse;
(17) pheochromocytoma. These triggers can cause sudden onset of heart failure in patients whose heart function is still compensable, or aggravate the condition of patients with existing heart failure.
Early manifestations: Patients with normal heart function may experience unexplained fatigue or significantly reduced exercise tolerance and an increase in heart rate by 15-20 beats/min, which may be the earliest sign of reduced left heart function. Continued development of exertional dyspnea, nocturnal paroxysmal dyspnea, the need to sleep with pillows to elevate the head, etc.; examination can be found in the left ventricle enlargement, early or mid-diastolic gallop rhythm, P2 hyperactivity, wet rales in both lungs, especially at the base of the lungs, but also dry and wet stern dragging stalls gangrenous display tomb δ苷 Xi
4, acute pulmonary edema: the onset of the disease is rapid, the condition can develop rapidly to critical state. Sudden severe dyspnea, sitting breathing, wheezing, irritability and fear, respiratory rate up to 30-50 times / min; frequent cough and coughing out a lot of pink foamy sputum; rapid heart rate on auscultation, apical rhythm can often be heard; both lungs are full of wet rales and croup.
5, cardiogenic shock: the main manifestations are.
(1) persistent hypotension, systolic blood pressure drops below 90 mmHg, or the original hypertensive patients systolic blood pressure decreases ≥ 60 mmHg, and lasts for more than 30 minutes.
(2) Tissue hypoperfusion state, which may include.
(i) wet, cold, pale and cyanotic skin with purple streaks ;
(2) Tachycardia >110 beats/min;
(3) Significant reduction in urine output (180/120 mmHg), rapid development of heart failure, usually normal CI, PCWP >18 mmHg, and normal or interstitial pulmonary edema on X-ray chest radiograph. This state is a hypertensive emergency and the appropriate rate of blood pressure lowering should be grasped. In chronic hypertensive patients, because of impaired blood pressure auto-regulation, rapid blood pressure lowering can lead to insufficient blood supply to the heart, brain, kidneys and other important organs, and rapid blood pressure lowering can aggravate organ ischemia.
If the condition of acute heart failure is mild, the blood pressure can be gradually lowered within 24-48h; in patients with severe condition and pulmonary edema, the mean arterial pressure should be lowered by ≤25% within 1h compared with that before treatment, to 160/100-110mmHg within 2-6h, and the blood pressure can be gradually lowered to normal within 24-48h. Priority is given to intravenous nitroglycerin, and sodium nitroprusside can also be applied. Loop diuretics such as furosemide given intravenously can play an auxiliary role in lowering blood pressure. Urapidil is suitable for patients with rapid increase in heart rate after the application of nitroglycerin or sodium nitroprusside, which cannot be tolerated.
Acute heart failure due to heart valve disease
No medical treatment or medication is likely to eliminate or relieve heart valve disease and the organic damage it causes. Such damage can promote myocardial remodeling and eventually lead to heart failure. During the progression of the disease, a number of factors, especially atrial fibrillation with rapid ventricular rate, infection, and increased physical load, can trigger the loss of heart failure or the onset of acute heart failure. Therefore, early interventional or surgical correction is the only way to prevent heart failure in these patients, and should also be actively considered in some patients with asymptomatic heart valve disease to fundamentally improve their prognosis.
Patients with acute heart failure should, in principle, actively pursue the various therapeutic initiatives listed in this guideline to stabilize their condition and relieve their symptoms so that corrective heart valve surgery can be performed as soon as possible. In patients who have already had heart failure, corrective heart valve surgery is mandatory and should not be delayed. Repeated episodes of heart failure not only aggravate the condition, but also increase the risk of surgery and affect the degree of improvement in postoperative cardiac function.
Acute pulmonary edema due to rheumatic mitral stenosis is often induced by atrial fibrillation with rapid ventricular rates and remains common in rural areas. Effective control of the ventricular rate in atrial fibrillation is extremely important for the successful treatment of acute heart failure. Trichoside C 0.4-0.6 mg can be applied slowly intravenously and repeated once after 1 to 2 h if necessary, with the dose reduced by half. If the effect is not satisfactory, intravenous beta-blockers can be added, and it is advisable to start with a small dose (half of the normal dose) and increase the dose as appropriate until the ventricular rate is effectively controlled. In addition, intravenous amiodarone may be used. Electrical resuscitation may be considered if the drugs are ineffective. Once acute heart failure is controlled and the condition is in remission, interventional or surgical procedures should be considered as soon as possible to relieve valve stenosis.
IV. Acute heart failure occurring in the perioperative period of non-cardiac surgery
This is a more common type of acute heart failure and is one of the causes of death in perioperative patients.
1. Assess the patient’s risk and make risk stratification: According to the risk of possible acute heart failure, preoperative risk stratification can be made.
(1) High risk: unstable angina, acute myocardial infarction (within 7 d), recent myocardial infarction (7 d to 1 month), decompensated heart failure, severe or high-risk arrhythmia, severe cardiac valve disease, and hypertension class III (>180/110 mmHg).
(2) Intermediate risk: history of ischemic heart disease, history of heart failure or decompensated heart failure, cerebrovascular disease (transient ischemic attack, stroke), diabetes mellitus, and renal insufficiency.
(3) Low risk: age >70 years, ECG abnormalities (left ventricular hypertrophy, complete left bundle branch block, pulmonary-specific ST-T changes), non-sinus heart rate, and uncontrolled hypertension. High-risk patients should delay or cancel the procedure. Adequate preoperative prophylaxis should be done in intermediate and low-risk individuals. The co-existence of multiple low-risk factors increases the risk of surgery.
2. Assess the risk of the type of surgery: Different types of surgery pose different risks to the heart. For procedures with higher risk, adequate precautionary treatment should be done before surgery.
(1) Surgery with cardiac risk > 5%: surgery on the aorta and other major vessels, peripheral vascular surgery;
(2)Surgery with cardiac risk of 1% to 5%: intra-abdominal surgery, intrathoracic surgery, head and neck surgery, carotid endarterectomy, plastic surgery, prostate surgery;
(3) Cardiac risk 190~226 umol/L (>2.5~3.0mg/dl).
(2) Creatinine clearance: more sensitive than Scr. In the early stage of renal decompensation (compensatory phase), creatinine clearance decreases while Scr is normal; Scr only starts to increase rapidly when eGFR drops to more than 50% of normal. Therefore, when Scr is significantly higher than normal, renal function is often severely impaired.
(3) eGFR: At present, this index is recommended at home and abroad to evaluate renal function, and eGFR can be calculated according to Scr; the modified calculation formula suitable for Chinese population is: eGFR [ml/(min/1.73m2)]=175×Scr(mg/dl)-1.154×age -0.203×(0.79 female).
2, timely management of related other diseases, such as hypokalemia or hyperkalemia, hypomagnesemia or hypomagnesemia, hyponatremia, and metabolic acidosis, all of which may induce arrhythmias, should be corrected as soon as possible.
3, moderate to severe renal failure to reduce the response to diuretics, may appear refractory edema; in the application of multiple and high doses of diuretics and add dobutamine to increase renal blood flow is still ineffective, should be hemofiltration.
4, severe renal failure should be hemodialysis, especially for those with hyponatremia, acidosis and refractory edema.
ACEI can aggravate renal failure and hyperkalemia, and should be reduced or discontinued if the baseline level of Scr increases by more than 25%-30% and/or its level is >266umol/L (>3.5mg/dl). ARB and spironolactone can also cause hyperkalemia, and digoxin can accumulate poisoning due to reduced exclusion. .
Pulmonary diseases
The coexistence of various pulmonary diseases can aggravate acute heart failure or make it difficult to treat, and effective antibiotics can be selected according to clinical experience. If COPD with respiratory insufficiency, non-invasive mechanical ventilation is preferred during acute exacerbation, which is safe and effective; it is also effective for acute cardiogenic pulmonary edema.
Cardiac arrhythmia
The common arrhythmias in acute heart failure are new-onset atrial fibrillation with rapid ventricular rate or acute heart rate acceleration in chronic atrial fibrillation, or simple sinus tachycardia; ventricular arrhythmias commonly include frequent premature ventricular beats, sustained and non-sustained ventricular tachycardia; non-paroxysmal tachycardia and atrial tachycardia with AVB can also be seen.
Whether the primary arrhythmia induces acute heart failure or acute heart failure causes tachyarrhythmia, the consequence is to aggravate the hemodynamic disorder and further worsen the arrhythmia, which becomes one of the important causes of death in acute heart failure, so the tachyarrhythmia in acute heart failure should be corrected in time.
In acute heart failure, sinus tachycardia, non-paroxysmal junctional tachycardia and atrial tachycardia with AVB are treated by slowing down the ventricular rate and focusing on the treatment of the underlying disease and heart failure. In new-onset atrial fibrillation in heart failure, the ventricular rate is accelerated, which aggravates the hemodynamic disorder, hypotension, pulmonary edema, and myocardial ischemia, and should be immediately electrically resuscitated (Class I, Level C); if the condition is still acceptable or there is no condition for electrical resuscitation or atrial fibrillation recurs after electrical resuscitation, then amiodarone intravenous resuscitation or maintenance of sinus rhythm (Class IIa, Level C) is selected; at this time, the application of ibrit resuscitation is undesirable, and propafenone cannot be used for resuscitation of heart failure with atrial fibrillation (Class III, Level C). The use of ibrit is not advisable and propafenone cannot be used for resuscitation of heart failure with atrial fibrillation (class III, level A).
The treatment of chronic atrial fibrillation in acute heart failure is based on controlling the ventricular rate, and digoxin or furioside C is preferred for intravenous injection (Class I, Grade B); if digitalis is unsatisfactory for controlling the heart rate, amiodarone 150-300 mg (Class I, Grade B) can also be injected slowly intravenously (10-20 min), the purpose of which is to slow down the heart rate, not to restart the rhythm, and such small doses of amiodarone basically cannot restart the rhythm for chronic atrial fibrillation. Atrial fibrillation in acute heart failure is generally not chosen to slow the heart rate with beta-blockers.
Acute heart failure or acute attack of chronic heart failure patients with frequent or joint premature ventricular contractions is common, should focus on anti-heart failure treatment, such as hypokalemia, should be supplemented with potassium, magnesium, generally do not choose anti-arrhythmic drugs. Acute heart failure complicated by persistent ventricular tachycardia, whether monomorphic or polymorphic, most of the hemodynamic instability, and easy to deteriorate into ventricular fibrillation, so the first choice of electric cardioversion correction, but after electric cardioversion ventricular tachycardia easy to recur, can add amiodarone intravenous load 150mg (10min) after intravenous 1mg/min × 6h, followed by 0.5mg/min × 18h (class I, C). Amiodarone needs to be applied to prevent recurrence after electrical defibrillation in ventricular fibrillation.
The antiarrhythmic drugs used in heart failure are amiodarone and lidocaine. Lidocaine can be used in heart failure (Class IIb, Level C), but the intravenous dose should not be too high, 75~150mg (3~5min) intravenously followed by an intravenous drip of 2~4mg/min, and the maintenance time should not be too long, usually 24~30h. Propafenone (Class III, Level A) should not be used for ventricular tachycardia in heart failure.
Regardless of atrial fibrillation or ventricular tachycardia, restoration and maintenance of sinus rhythm is the basic measure in the treatment of acute heart failure. Whether arrhythmia-induced acute heart failure or acute heart failure-induced arrhythmia is the goal of treatment to restore sinus rhythm; if the patient is already in chronic atrial fibrillation, digitalis or amiodarone should be used to control the ventricular rate. In acute heart failure, the first method to rapidly and effectively re-establish sinus rhythm is electrical resuscitation, and pharmacological treatment is to maintain sinus rhythm, reduce recurrence or slow down the ventricular rate.
Patients with bradyarrhythmias do not require special treatment if their hemodynamic status is not affected. Severe slow arrhythmias that aggravate or worsen hemodynamic disturbances, such as third-degree AVB, second-degree type 2 AVB and ventricular rate of 130/80 mmHg), accelerated or bradycardia (≤55 beats/min), significant changes in cardiac rhythm: from regular to irregular or from irregular to regular, frequent and symptomatic premature beats, etc.