Sudden cardiac death in the elderly
Introduction
Introduction to sudden cardiac death in the elderly Senilesuddencardiacdeath (SCD) is an unexpected, natural death that occurs within 1 hour of the onset of symptoms. In the United States, it is estimated that the incidence of sudden cardiac death is between 200,000 and 400,000 cases per year, accounting for more than 50% of all cardiovascular deaths. After a sudden cardiac death, the success rate of recovery is estimated to be only about 20%. And it is estimated that 80% of patients with sudden cardiac death can not live to discharge, and 50% of surviving patients die within 3 years. It can be seen that sudden cardiac death is one of the main causes of death that endangers people's lives and should cause clinicians and The patient is highly vigilant and has early effective preventive treatment. basic knowledge Sickness ratio: 0.0004% Susceptible people: the elderly Mode of infection: non-infectious Complications: myocardial infarction
Cause
The cause of sudden cardiac death in the elderly
Coronary heart disease (35%):
Coronary heart disease (acute ischemic events, chronic ischemic heart disease) is the most common cause of sudden cardiac death. Autopsy of sudden cardiac death found that approximately 80% of patients have varying degrees of coronary artery disease, approximately 2/3 The above patients were 2 or more lesions, and the incidence of sudden cardiac death was significantly increased in patients with myocardial infarction with decreased left ventricular function or severe ventricular arrhythmia.
Cardiomyopathy (20%):
The rate of sudden cardiac death in dilated cardiomyopathy is 2%, and the rate of sudden cardiac death can be significantly increased in patients with ventricular arrhythmia. Cardiac sudden death is more common in patients with hypertrophic cardiomyopathy. Most scholars report hypertrophic myocardium. The annual mortality rate of the disease is 3% to 4%, most of which are sudden cardiac death. In patients with hypertrophic cardiomyopathy, the following conditions are high risk factors for sudden cardiac death: 1 younger, under 30 years old, 2 There is a history of syncope, 3 has a family history of sudden cardiac death, in addition, cardiomyopathy and arrhythmogenic cardiomyopathy caused by various causes are also prone to sudden cardiac death.
Inflammation of the heart valve (15%):
It has been recognized that mitral valve prolapse syndrome can cause sudden cardiac death, but the incidence is not high. According to Jersaty, patients with mitral valve prolapse are prone to sudden cardiac death in the following cases: female patients around 140 years old 2, there is a history of syncope, 3 ECG on ST segment changes or frequent ventricular premature contraction and other ventricular arrhythmias, 4 have "kappa" sound and late systolic or full systolic murmur.
Arrhythmia (15%):
(1) supraventricular arrhythmia: generally not easy to have sudden cardiac death, but in elderly patients, often with severe coronary stenosis or high blood pressure caused by left ventricular hypertrophic cardiomyopathy, left ventricular outflow tract obstruction, rapidity Sudden cardiac arrhythmia is also prone to sudden cardiac death.
(2) ventricular arrhythmia: Most scholars believe that severe ventricular arrhythmia can cause sudden cardiac death, especially in elderly patients with severe structural heart disease, currently, ventricular premature contraction in sudden cardiac death The significance of this is still controversial. Some scholars have found that premature ventricular contraction does not increase the incidence of sudden cardiac death, especially simple ventricular premature contraction without obvious organic heart disease, but some studies suggest that Ventricular premature contraction itself is a risk factor for sudden cardiac death, especially in patients with severe coronary artery disease or myocardial infarction. Frequent ventricular premature contraction has a certain significance for the occurrence of sudden cardiac death, especially the merger. There are left ventricular hypertrophy, indoor conduction block and ST-T changes, and ventricular tachycardia in the sudden death of the heart is greater than ventricular premature contraction, in the clinical, we often put ventricular tachycardia or pair Multi-source and frequent ventricular premature contractions called complex ventricular arrhythmias, and Morganroth's complex ventricular arrhythmia based on the risk of sudden cardiac death caused by complex ventricular arrhythmias It is divided into benign accounted for 30%, its left heart function and hemodynamics are normal, the risk of sudden cardiac death is minimal; potential malignancy accounts for 65%, mild cardiac structure, cardiac insufficiency and ventricular ectopic agitation, Such as ventricular premature contraction and/or non-sustained ventricular tachycardia, no hemodynamic disorder, but increased risk of sudden cardiac death; malignant ventricular arrhythmia accounted for 5%, almost all have hemodynamic performance and Signs (syncope, cardiac insufficiency, myocardial ischemia or hypotension) have the greatest risk of sudden cardiac death. There are five clinical types: 1 continuous unilateral ventricular tachycardia with ventricular rate 230 bpm, and 2 ventricular rate gradually Accelerated ventricular tachycardia may be converted to room rush and/or ventricular fibrillation, 3 ventricular tachycardia with severe hemodynamic disorders such as syncope, left ventricular dysfunction and hypotension, 4 pleomorphism (including long QT syndrome) Combined apical torsion type ventricular tachycardia, 5-ventricular puff and/or ventricular fibrillation initiation arrhythmia is room ward and/or ventricular fibrillation (such as idiopathic ventricular fibrillation, Brugada syndrome), clinical manifestations are - Syndrome of seizures, and most of the sudden cardiac deaths confirmed by electrocardiogram (65%) 85%) is caused by malignant ventricular arrhythmia such as ventricular fibrillation, but slow arrhythmia may also be a potential cause of sudden cardiac death and may have been converted to ventricular fibrillation before recording arrhythmia .
(3) Pre-excitation syndrome: Pre-excitation syndrome patients with atrioventricular reentry tachycardia, atrial fibrillation and other tachyarrhythmia accounted for 40% to 80%, but the risk of sudden cardiac death is low, there are investigations Below 4%, there have been no reports of increased cardiac death in elderly patients.
Other (10%):
In addition to increasing the incidence of coronary heart disease, diabetes can also damage the myocardium and increase the incidence of sudden cardiac death. In particular, the incidence of sudden cardiac death in female patients is more obvious, which is three times higher than that in patients of the same age group without diabetes.
Pathogenesis
1. Pathogenesis It is known that the mechanism of sudden cardiac death is mainly severe ventricular arrhythmia, including ventricular tachycardia, ventricular fibrillation, etc., and some people have sudden severe hemodynamic disorders, heart rupture, etc. .
(1) Ischemic arrhythmia: It is generally believed that ventricular fibrillation is a persistent, rapid and irregular ventricular activation caused by multiple reentry wavelets. The occurrence of ventricular fibrillation must include the following basic conditions: asynchronous and separated local waves. Pre-excitation, conduction delay and shortening of ventricular refractory period, these changes can occur in ischemic myocardium.
Ischemic ventricular arrhythmias include ventricular arrhythmias caused by acute myocardial ischemia and ventricular arrhythmias associated with old lesions after myocardial infarction. If acute myocardial ischemia occurs in the marginal myocardium after scar healing after myocardial infarction, The incidence of ventricular arrhythmia is higher. In acute myocardial ischemia, local myocardial tissue perfusion is insufficient, resulting in myocardial energy metabolism in the ischemic area is significantly lower than normal myocardial tissue, a large amount of free fatty acid (FFA) is accumulated, and intracellular lactic acid content Increase, intracellular potassium, magnesium ion outflow, the negative value of the resting potential further increases, forming a diastolic potential, while the amplitude of the action potential decreases, the rate of depolarization slows, the rate of excitation conduction slows, then the myocardial self-discipline Sexual enhancement, and easy to form conditions of reentry, ventricular reentry arrhythmia and ventricular fibrillation, while patients with left ventricular dysfunction, the incidence of sudden cardiac death is higher, especially left ventricular ejection fraction is less than 30 % is the strongest predictor of sudden cardiac death.
(2) Reperfusion arrhythmia: Reperfusion arrhythmia is now known to be an important mechanism of sudden cardiac death. Reperfusion ventricular arrhythmia can be seen after coronary artery spasm relief, and can also be seen in acute myocardial infarction thrombolytic therapy. Or mechanically comminuted plaque to re-open the completely occluded blood vessels, often re-perfusion arrhythmia occurs a few seconds after recanalization of the coronary artery. Many studies have shown that reperfusion arrhythmias when the coronary artery is recanalized The incidence rate is as high as 82%. Among the different types of reperfusion arrhythmias, 60%-80% are accelerated ventricular arrhythmia and ventricular premature contraction, and arrhythmias that can cause sudden cardiac death are ventricular tachycardia and Ventricular fibrillation, severe bradyarrhythmia can also cause sudden cardiac death, and the type of reperfusion arrhythmia has a certain relationship with the recanalization of the coronary artery. Accelerated chambers are prone to occur in the left anterior descending and left circumflex reperfusion. Sexual autonomic rhythm, ventricular tachycardia and ventricular fibrillation, sinus bradycardia, atrioventricular block, right atrioventricular blockage, reperfusion, experimental study suggestion The mechanism of reperfusion arrhythmia includes triggering agonism, reentry agonism and ectopic autonomic increase. At present, most scholars believe that triggering stimuli occupy an important position in the occurrence of reperfusion arrhythmia, and the reentry mechanism may be related to reperfusion. After myocardial cell electrophysiological recovery is not uniform, myocardial ischemic injury makes myocardial cells electrophysiological changes are not uniform, reperfusion after recanalization to restore blood flow, but restore blood flow after myocardial cell blood supply and metabolic recovery It is also uneven, resulting in inconsistent recovery of myocardial stress in the ischemic area, which is easy to form reentry and cause ventricular tachycardia and/or ventricular fibrillation. In addition, myocardial ischemia-reperfusion injury can also cause differences. Increased autonomy of the excitatory foci, causing ventricular arrhythmia, Pogwizd and other three-dimensional mapping techniques showed that 75% of reperfusion arrhythmias were caused by triggering agonism, and 25% of reperfusion arrhythmias were caused by Caused by the reentry mechanism.
(3) Primary arrhythmia: the cause is unknown, there is no obvious coronary artery or myocardial disease, and severe ventricular arrhythmia and/or ventricular fibrillation often occur suddenly or under certain incentives, and cardiac disease occurs. Sudden death, studies have shown that the mechanism of primary ventricular arrhythmia is mostly triggering excitatory, and some are reentry mechanisms.
(4) Non-arrhythmia: Raizes and other studies have shown that non-arrhythmia caused by cardiac death only accounted for 0.56%, including heart or aortic rupture, myocardial infarction expansion, sympathetic reflex inhibition, and severe cardiac damage caused by various causes Mechanical obstruction, especially in patients with left ventricular dysfunction, the highest incidence of sudden cardiac death, left ventricular dysfunction and often coronary artery disease and diffuse myocardial lesions, and thus may be associated with acute myocardial ischemia or myocardial scar Tissue-induced malignant arrhythmia, resulting in sudden cardiac death, 36% of patients with coronary heart disease and left ventricular dysfunction caused by sudden cardiac death, severe bradycardia or electro-mechanical separation, not accompanied by cardiac arrest Deterioration of symptoms of heart failure, bradyarrhythmia or electro-mechanical separation may cause sudden increase in intraventricular pressure and volume due to end-stage ventricular wall stress due to left ventricular systolic dysfunction, while peripheral vasoconstriction simultaneously presents obstacles and cannot maintain systemic blood pressure , even collapse and syncope, sudden death is caused by hemodynamic disorders, not ECG instability, another Some patients with left ventricular dysfunction with ventricular tachycardia may be caused by arrhythmia.
2. Physiological changes after sudden cardiac death
(1) Heart changes:
1 Primary changes: cardiac pathological changes in cardiac sudden death are mainly from autopsy, but the autopsy pathological results reported by different scholars are very inconsistent, and most scholars study the sudden death of coronary heart disease, the pathological death from coronary heart disease According to the data, the main pathological findings were severe coronary stenosis, thrombosis in the coronary arteries, and severe myocardial ischemia or infarction. Schwartz et al found that more than one third of patients with sudden coronary heart disease had thrombosis in the coronary arteries. Some data at home and abroad suggest that the incidence of acute myocardial infarction in patients with sudden death from coronary heart disease is about 40%, and there is no obvious acute lesion in the sinoatrial node and conduction system in patients with sudden coronary heart disease, which also confirms the sudden death of coronary heart disease. The mechanism of occurrence is caused by unstable ECG. Cardiac sudden death rarely occurs in patients without structural heart disease. In some patients, after sudden cardiac death, even if the gross examination of the heart has no obvious macroscopic lesions, it may be the core of the heart. There are also obvious anomalies in structure and function, such as ion channels, protein structure anomalies, and the like.
2 secondary changes: the energy required for normal heart work comes first from fat, accounting for 67% of total myocardial oxygen consumption, followed by glucose and lactic acid, accounting for 17.9% and 16.46%, respectively, very few from acetic acid, amino acids, pyruvate At the same time, the heart must rely on ATP to maintain the tension and contraction of the ventricular wall. Studies have shown that myocardial ischemia and hypoxia for 10s can be depleted of metabolic substrate, the heart completely loses systolic function, at room temperature, if myocardial ischemia 3 4min, the myocardial phosphoric acid creatine content decreased by 70% to 75%, ATP decreased by 15%, such as effective cardiopulmonary resuscitation during this period, myocardial blood supply improved, myocardial tension can be fully recovered; ischemia 8 ~ 10min, myocardial Endogenous creatine and ATP will be completely depleted. If effective cardiopulmonary resuscitation is performed during this period, the contraction and diastolic function of the heart can still be restored. After effective cardiopulmonary resuscitation is performed 10 minutes later, the chance of successful recovery is significantly reduced.
(2) Pathological changes of other organs:
1 Brain: The energy metabolism of the brain is mainly from glucose, but the brain tissue itself has little reserve for glucose. It must be supplied by circulating blood, and 85% to 90% of the metabolism of brain tissue is aerobic metabolism, while anaerobic glycolysis It only accounts for 5% to 15% of brain tissue metabolism. Therefore, the maintenance of brain tissue metabolism and physiological functions depends entirely on effective blood supply. The blood supply disorder causes brain cell function changes based on ischemia and hypoxia. The primary and secondary damage of the tissue, the primary damage is brain tissue ischemia and hypoxia, ATP can not be synthesized, the cell sodium pump function is lost, the intracellular sodium ions can not be transported to the outside of the cell, potassium ions can not escape from the cell, The cell membrane potential changes, so it can not produce electrical activity, and the cells also lose the function of generating and transmitting impulses. Studies have shown that in the case of complete hypoxia, the bioelectrical activity of the cerebral cortex completely disappears after 20s, and the cerebellum and medulla after 30 to 90s. The bioelectrical activity completely disappears, and the secondary damage caused by ischemia and hypoxia includes two aspects:
A. Intracellular electrolyte disturbance and accumulation of various metabolites cause swelling of brain tissue and cerebral edema.
B. The local circulatory dysfunction of brain tissue is further aggravated. It has been suggested that when the brain tissue is hypoxic and hypoxic caused by cardiac arrest, the lesion mainly appears in the hippocampus of the brain. If the ischemia is further aggravated, it will spread to the whole brain. Including the brainstem and medulla, and after a sudden cardiac death in a patient, if the cardiopulmonary resuscitation can be performed in a timely and effective manner, the blood flow of the brain tissue may be restored, but the brain tissue is affected by complete ischemia and hypoxia, and brain edema. And microcirculatory disorders will continue to develop, and the length of ischemia and hypoxia in brain tissue directly affects the recovery of brain function and the clinical prognosis of patients.
2 kidney: When the cardiac arrest occurs, the blood supply and filtration function of the kidney completely stops. The first is the renal tubule, which causes the necrosis of the renal tubular cells, and gradually affects the basement membrane and the whole nephron. If the time is short, the basement membrane It can be relatively intact, and the kidney function can be restored. However, the time of ischemia and hypoxia is too long, and the renal tubules and glomeruli produce extensive and severe damage, which is prone to acute renal failure.
3 lung: after sudden cardiac death, the lungs may be congested, edema, the main feature of the microscope is pulmonary interstitial edema, and microthrombus formation, long-term lung ischemia and hypoxia is prone to diffuse intravascular coagulation, not only The lung ischemia and hypoxia can be further aggravated by mechanical occlusion, and platelet aggregation can also be caused, and substances such as 5-HT are released to produce terminal airway sputum, and the blood-gas exchange disorder is further deteriorated.
3. Factors associated with sudden cardiac death
(1) The role of the autonomic nervous system in sudden cardiac death: the autonomic nervous system plays an important role in the occurrence of sudden cardiac death. Clinical observations have found that sudden cardiac death in patients with coronary heart disease often occurs between the early hours of the morning and midday. The circadian rhythm changes of nerve activity are consistent. During this time period, sympathetic activity is higher, blood pressure and heart rate are increased, and platelet aggregation is also increased. Experimental studies have shown that stimulation of the heart's sympathetic nerve can reduce the threshold of ventricular fibrillation and increase the incidence of ventricular fibrillation. The danger of stimulating the vagus nerve can reduce the risk of ventricular fibrillation, so excessive sympathetic excitation can promote the occurrence of malignant ventricular arrhythmia, while the excited vagus nerve has the effect of protecting the heart and resisting ventricular fibrillation, but In patients with acute myocardial ischemia or ischemic reperfusion in the posterior wall, most of the afferent receptors due to the vagus nerve are distributed in the inferior posterior wall of the ventricle, where myocardial ischemia or reperfusion after ischemia can trigger Bezold-Jarish reflex. , causing or aggravating slow arrhythmias, such as severe sinus bradycardia, high atrioventricular block, peripheral blood Expansion and low blood pressure, severe cardiac arrest may occur.
(2) Coronary artery spasm: Many patients with sudden cardiac death occur in sleep. The mechanism is mainly vagus nerve excitement during sleep, coronary artery spasm, hypoxia in the heart conduction system, unstable heart, and ventricular fibrillation. Sudden death, but the morphological basis of coronary artery spasm has not yet been provided.
Prevention
Elderly sudden cardiac death prevention
1. Preventive treatment for the cause and various variable risk factors, such as smoking cessation, alcohol, blood pressure, lipid lowering and other treatments.
2. The mechanism of sudden cardiac death in the clinic is mainly malignant ventricular arrhythmia such as ventricular fibrillation. Therefore, the key to the prevention of sudden cardiac death is the prevention of malignant ventricular arrhythmia, generally primary prevention and secondary prevention. Primary prevention refers to the occurrence of malignant ventricular arrhythmia, but there is no clinical malignant ventricular arrhythmia, and the occurrence of malignant ventricular arrhythmia should be prevented. If there is no contraindication, use -receptor resistance. Hysteresis, for patients with chronic congestive heart failure, the use of angiotensin-converting enzyme inhibitor (ACEI), digitalis and diuretics based on -blockers, secondary prevention refers to clinically The occurrence of malignant ventricular arrhythmia, there is no clear cause (such as early acute myocardial infarction, low potassium, low magnesium, antiarrhythmic drugs, arrhythmogenic effects, etc.) can be corrected to prevent the recurrence of malignant ventricular arrhythmia, secondary Prevention of preferred ICD (buried cardioverter defibrillator), such as unconditional application of ICD, should use amiodarone or a combination of antiarrhythmic drugs.
Complication
Elderly sudden cardiac death complications Complications, myocardial infarction
Sudden death can cause acid-base and water electrolysis disorder and re-infarction of myocardial infarction.
Symptom
Symptoms of sudden cardiac death in the elderly Common symptoms Cardiac arrest Sudden arrhythmia Skin paleness loss Loss of convulsions Chest tightness Abdominal discomfort Myocardial infarction
The course of sudden cardiac death can be divided into four periods, namely, the prodromal phase, the beginning of the terminal event, cardiac arrest and biological death. The performance of different patients also has significant differences, according to the statistics of Beijing Fuwai Cardiovascular Hospital. Thirty-six patients with sudden death from coronary heart disease showed immediate symptoms at sudden death, and 20 patients with sudden loss of consciousness in 36 cases, including 8 with convulsions, 1 in the morning in the bathroom, 1 in the bath, and 6 in the sleep. Suddenly, pain in the anterior region of the heart, wheezing, and abdominal discomfort were immediately lost in 8 cases within 20 minutes. It can be seen that some patients may have precordial discomfort and palpitations before the occurrence of sudden cardiac death. Non-specific performance such as shortness of breath, fatigue, but also no prodromal performance, direct cardiac arrest, and some reported sudden death in patients with dynamic electrocardiogram, when the ECG record was mostly ventricular fibrillation, indicating that cardiac arrest is mostly ventricular fibrillation, Some patients have symptoms of cardiac ischemia or left ventricular dysfunction, cardiac arrest occurs immediately, no discomfort is detected before cardiac arrest, and there is asymptomatic myocardial ischemia. It can be determined that the sudden decrease in cerebral blood flow after cardiac arrest can lead to sudden loss of consciousness. The following signs can help determine whether cardiac arrest occurs: loss of consciousness, disappearance of the neck, femoral artery, intermittent or stopped breathing, pale or obvious skin Bun, if the auscultation of heart sounds disappears, the diagnosis can be established. After the diagnosis is established, effective cardiopulmonary resuscitation should be performed immediately.
Examine
Elderly heart death test
Platelet viscosity is normal.
1. Electrocardiogram: It is known that cardiac hypertrophy is the iconic electrocardiogram of sudden cardiac death. The presence of QR-wave group high voltage and sidewall lead-exposed spacer Q wave may be a risk factor for sudden death. Large-area anterior wall myocardial infarction In patients with electrocardiogram, right bundle branch block occurred, and the risk of sudden death at 6 months was about 30%.
2. Holter: Holter can diagnose 39% to 82% of patients with ventricular arrhythmia, and can understand the frequency, complexity, circadian rhythm and other changes of ventricular arrhythmia, especially myocardial infarction and In patients with severe coronary heart disease, ventricular arrhythmias found by dynamic electrocardiography have a clear predictive value for the occurrence of sudden cardiac death. The risk of sudden cardiac death increases with the complexity and frequency of ventricular arrhythmias.
3. Exercise test: Studies have shown that exercise test has a certain predictive value for sudden cardiac death in patients after myocardial infarction.
4. Ventricular late potential (VLP): Ventricular late potential is a local ventricular delayed fragmentation electrical activity recorded on the body surface, which usually appears in the terminal part of QRS and can be extended into ST, showing high frequency (20~ 80Hz), low amplitude (25V=fragmentation wave) for more than 10s. From the available data, ventricular late potential has certain value in predicting fatal tachyarrhythmia in patients, Brethard et al. Patients with coronary heart disease who were positive for ventricular late potential were 3.3 times more likely to have sudden cardiac death than those with negative ventricular late potential.
Diagnosis
Diagnosis and diagnosis of sudden cardiac death in the elderly
Diagnostic criteria
1. History and physical examination: Some patients with sudden cardiac death may have precordial pain, chest tightness, palpitations, shortness of breath, fatigue, etc., in some minutes or days before onset, and some may show acute myocardial infarction, and some may occur. Frequent ventricular contractions, so patients with coronary heart disease, cardiomyopathy or diffuse myocarditis should be highly alert to prevent sudden cardiac death.
2. Heart rate variability (HRV): In the past 10 years, a large number of studies have shown that there is a positive correlation between heart rate variability and sudden cardiac death. In the heart rate variability index, SDNN<50ms is heart rate variability. Highly suppressed, SDNN <100ms is moderate inhibition of heart rate variability, such as inhibition of heart rate variability, suggesting an increased incidence of sudden cardiac death.
3. QT dispersion (QTd): QT dispersion is the difference between the longest and shortest QT interval (QT) of different lead in ECG. Recent studies have shown that QTd can reflect the inhomogeneity of ventricular repolarization. Sexual and electrical instability, the normal reference value of QTd is <50ms, 50~70ms has reference value, and has diagnostic value of >70ms. Clinical studies show that patients with long QT syndrome have ventricular tachycardia after heart attack, heart Patients with sudden death and drug-induced arrhythmia have increased QT dispersion. Studies have shown that QTd in patients with sudden death is much greater than other patients with heart disease, so QTd has a predictive effect on sudden cardiac death.
Differential diagnosis
Clinically, it must be differentiated from syncope, snoring or epilepsy.
