Sudden cardiac death

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About epidemiological risk factors for disease etiology and pathogenesis of clinical diagnosis and treatment of pathophysiological Edit this paragraph disease prevention Expand Introduction Sudden cardiac death (sudden cardiac death, SCD) refers to the heart due to various reasons cause of sudden death. That there can occur in patients with or without heart disease, often without any life-threatening early performance, sudden loss of consciousness during the acute onset of symptoms within 1 hour after death, is a non-traumatic natural death, is characterized by unexpected rapid death . More than 91% of SCD is caused by arrhythmias, and some non-cardiac conditions such as heart accidental rupture, pulmonary embolism, etc. can also rapid death within one hour, but its mechanism and prevention of sudden arrhythmic death is different with . With the implantable cardioverter defibrillator (implantable cardioverter defibrillator, ICD) for clinical applications, through its monitoring system to further deepen the understanding of SCD [1]. Edit this paragraph epidemiology in industrialized countries as a major cause of adult deaths due to coronary heart disease SCD, SCD incidence reported in the literature for the year from 0.36 to 1.28/1000, but the sudden death of the hospital is not included in the statistics. Therefore, the actual population of SCD incidence may be higher. At different ages, sex and history of cardiovascular disease in populations, SCD incidence vary widely, from 60 to 69 years old men with a history of heart disease in SCD incidence of up to 8 per year / 1000.80% of hospital death occurred in home, 15% occurred in the road or public place. Fu Wai Hospital, led by a multi-center prospective series of studies (fifteen national public relations issues) for the first time come to China, the incidence of sudden cardiac death 41.84/10 million, the total number of deaths of sudden cardiac death up to 544,000 / year, among the first countries in the world, suggesting that prevention of sudden cardiac death in China arduous task. Edit this paragraph risk factors (a) age, gender epidemiological analysis, increasing age is a risk factor for SCD. In children 1 to 13 years age group, 19% of all sudden cardiac, youth 14 to 21 years age group SCD accounted for 30% of all sudden death. All of sudden death in older SCD accounted for 80% to 90% or more, largely with coronary heart disease incidence increased with age, because more than 80% of SCD patients suffering from coronary heart disease. Male than female SCD incidence (about 4:1), in the Framingham study, men and women between the ages of 55 to 64 difference in the incidence of larger (almost 7:1), because in this age group, the incidence of coronary heart disease than men women significantly increased. (Two) hypertension and left ventricular hypertrophy Hypertension is a risk factor for coronary heart disease, but the cause of hypertension is the main mechanism of SCD left ventricular hypertrophy. Framingham study showed increased left ventricular mass per 50g/m2, SCD increased risk of 45%. (Three) of LDL-C hyperlipidemia and coronary heart disease increased in all clinical types are relevant, including the SCD. Statin drugs can be reduced by 30% to 40% of coronary death (including SCD) and non-fatal myocardial infarction. (Four) have confirmed that eating too many epidemiological data of saturated fatty acids and too little intake of unsaturated fatty acids were increased risk of coronary heart disease, but did not directly observe its effect on the incidence of SCD. American Studies on 20,551 cases from 40 to 84 years without history of myocardial infarction prospective observational men showed at least a week to eat fish once a person is a monthly incidence of SCD who ate fish less than once a half. (Five) exercise the degree of coronary artery disease patients with moderate physical activity can help prevent cardiac arrest and SCD occur, and strenuous exercise are likely to trigger SCD and acute myocardial infarction. Adults from 11% to 17% of the cardiac arrest occurred in strenuous exercise during or immediately after exercise, and ventricular fibrillation related. This is also reflected in the rehabilitation of patients with heart disease research and exercise stress test process, the incidence of cardiac arrest were 1/12000 ~ 1/15000 (Rehabilitation Research) and 1/200 (exercise stress test) is a common heart patients the incidence of cardiac arrest six times. (Six) Drinking excessive alcohol consumption, especially drunkenness increases the risk of SCD occurs in alcoholics often find QT prolongation, which is easy to trigger ventricular tachycardia, ventricular fibrillation. But studies have found moderate alcohol consumption may reduce the incidence of SCD. (Seven) heart rate and heart rate variability study confirmed that heart rate is an independent risk factor for SCD, and its mechanism is not clear, may be associated with reduced vagal tone related. Impaired heart rate variability and 24 hours slowest heart rate> 65 beats / min in SCD risk is about 2 times normal. (Eight) Smoking Smoking is one of the triggering factors for SCD, increased platelet adhesion due to smoking is easy, reducing ventricular fibrillation threshold, increased blood pressure, induced coronary artery spasm, so carboxyhemoglobin accumulation and utilization of myoglobin damage and reduce cycle portability oxygen carrying capacity, leading to nicotine-induced catecholamine release. 20 daily smokers compared with non-smokers each year incidence of SCD were 31/1000 and 13/1000. (Nine) sudden change in lifestyle mental factors, personal and social factors and emotional loneliness and life overburdened with SCD caused by repressed emotions are closely related. (Ten) for some patients with a family history family history is an important risk factor. Known that certain single-gene diseases such as long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, catecholaminergic polymorphic ventricular tachycardia prone to cause SCD. Other risk factors include intraventricular conduction block, abnormal glucose tolerance test and obesity. Left ventricular dysfunction is male Important factors for SCD. In patients with severe heart failure, non-sustained ventricular tachycardia is an increased incidence of SCD independent factors. Edit this paragraph etiology and pathogenesis of SCD by the vast majority of cardiac structural abnormalities. Adult patients with SCD cardiac structural abnormalities including coronary heart disease, hypertrophic cardiomyopathy, valvular heart disease, myocarditis, non-atherosclerotic coronary artery abnormalities, invasive disease and intracardiac anomalies channels. These structural changes are cardiac ventricular tachyarrhythmia occurrence basis, and most of SCD is ventricular tachyarrhythmias due. Some temporary functional factors, such as cardiac electrical instability, platelet aggregation, coronary artery spasm, myocardial ischemia and reperfusion, etc. so that the original stable cardiac structural abnormalities occur instability. Certain factors such as the autonomic nervous system instability, electrolyte imbalance, excessive fatigue, depressed mood and induced ventricular arrhythmias with drugs, can trigger SCD [2]. In the world, especially Western countries, coronary atherosclerotic heart disease is the most common cause of SCD cardiac structural abnormalities. In the United States all the SCD, coronary atherosclerosis and its complications due to SCD by up to 80%, cardiomyopathy (hypertrophic, dilated) accounted for 10% to 15% and the remaining 5% to 10% of SCD by lead to a variety of causes. Edit this paragraph pathophysiological pathophysiological changes are mainly fatal arrhythmias. 75% to 80% of cardiac arrest who first recorded arrhythmia is ventricular fibrillation, ventricular tachycardia and sustained by less than 2%. Arrhythmia common in severe congestive heart failure patients. (A) lethal tachyarrhythmias chronic coronary artery disease often have inadequate regional myocardial blood supply, thus regional myocardial metabolic or electrolyte status changes. Stress myocardial oxygen demand increases, but not a corresponding increase in coronary artery disease blood supply leading to arrhythmia or sudden death. Vasoactive changes (coronary spasm or coronary collateral circulation changes) can face temporary myocardial ischemia and reperfusion in double jeopardy. Coronary artery spasm has not been elucidated, but the local endothelial cell lesions and autonomic nervous system activity play a role. Studies suggest that chronic coronary artery endothelial cell damage and plaque rupture caused by platelet activation and aggregation, not only can lead to blood clots, and can produce a series of biochemical changes, affecting vasomotor regulation, leading to ventricular fibrillation. Rapid polymorphic VT and VF is characteristic of early ischemic arrhythmias, prone to cause SCD, and more from the conduction velocity is not synchronized with the ischemic area and ischemic area exists around absolute refractory period while prone reentry due. Ventricular tachyarrhythmias occurred fairly frequently in the reperfusion period. (Two) slow arrhythmias and cardiac arrest its pathophysiologic changes are mainly sinus and (or) atrioventricular node without normal function, lower self-regulatory organization not replaced due to pacing. Often occurs in severe heart disease, diffuse subendocardial Puken Ye fibrous lesions, hypoxia, acidosis, shock, renal failure, trauma, and other systemic conditions lead to low extracellular K + concentration, Puken Ye cell fraction depolarization phase 4 depolarization slope reduction (self-discipline inhibition), resulting in the loss of self-discipline. This type of arrhythmia is due overall suppression of autonomous cells, the culture is different from acute ischemic lesions. Inhibition of cell function independently when overdrive suppression particularly sensitive, and thus in paroxysmal ventricular tachycardia occurs after the long pause. The latter lead to local hyperkalemia and acidosis, so that self-regulation is further inhibited, eventually occur sustained ventricular asystole or ventricular fibrillation. (Three) the autonomic nervous system and the sympathetic activity likely to cause a fatal arrhythmia arrhythmia, and vagus nerve stimulation on sympathetic with the prevention of lethal arrhythmias and protective effect, because through the inhibition of adenylate cyclase activity , to reduce the release of norepinephrine, produce anti-adrenergic effect. Such as acute myocardial infarction can cause localized cardiac sympathetic and parasympathetic denervation and hypersensitivity to catecholamines, and accompanied by action potential duration and refractory period shortening is not synchronized, easily lead to arrhythmias. Ischemic preconditioning can save early acute coronary occlusion sympathetic and parasympathetic efferent activity, and reduce the incidence of fatal arrhythmias. Regardless of which of the above mechanisms caused by cardiac arrest, marked the clinical death. But biological point of view, this time the body has not really died. Because the body tissue metabolism has not been completely stopped, the body's basic unit of life - cells remained a faint life activities. Such as to be timely and appropriate rescue, there may survive, especially sudden death occurred suddenly and unexpectedly. In cardiac and (or) after the cessation of breathing, blood flow perfusion without interruption, then generates acid-base balance and electrolyte imbalance, acidosis, particularly intracellular and extracellular K concentration increased. The study also found that hypoxia increased production of oxygen free radicals, with the biofilm polyvalent unsaturated fatty acid and combined with high affinity, resulting in cell membrane dysfunction, affecting the membrane permeability and activity of various enzymes, Ca internal flow increased to increase the intracellular Ca, ultimately leading to cell death. Reversible changes at this time to do the show irreversible outcome into biological death. Circulation stops, brain tissue reserves adenosine triphosphate and glycogen is depleted in a few minutes. If the temperature is normal, after cardiac arrest in 8 to 10 minutes, the brain cells can lead to irreversible damage. Liver and kidneys are more sensitive to hypoxia. The important organs in hypoxia and acidosis occurs when the pathophysiological process, which is the heart of the brain lesions, can be further increased hypoxia and acidosis, thus forming a vicious cycle. The longer the blood circulation stops, the lower the success rate of recovery, more complications. If not timely rescue after circulatory arrest hypoxic brain injury often becomes irreversible, is the main cause of death in cardiac arrest; Even successful cardiopulmonary resuscitation temporarily, the end may be due to brain death and deadly; occasionally lives were saved, can still be aftermath of permanent brain damage caused by disability. Therefore, the rescue of cardiac arrest must every minute counts. Edit this paragraph the clinical course of SCD clinical manifestations can be divided into four periods [3]: (a) the prodromal period many patients in the event of cardiac arrest before a few days or weeks or even months of prodromal symptoms, such as angina, shortness of breath or aggravation of heart palpitations, easy fatigue, and other nonspecific complaints. These prodromal symptoms are not unique to SCD, and is common in any prior heart attack. (Two) the incidence of cardiac arrest which led to acute cardiovascular changes prior period, usually not more than one hour. Typical manifestations include: prolonged angina or chest pain, acute myocardial infarction, acute dyspnea, palpitations, sudden, persistent tachycardia or dizziness and so on. If cardiac arrest occur instantaneously, without prior warning,Adidas F50 FG, then 95% of cardiac and coronary artery lesions. Sudden cardiac death were obtained from continuous ECG recordings can be seen in a few hours or minutes before the sudden death often changes the electrical activity of the heart, in which the heart rate and ventricular contraction deterioration upgraded to the most common. Sudden death in ventricular fibrillation who often first sustained burst of sustained ventricular tachycardia or arrhythmia incidence in these patients before the onset of most sober and in their daily activities, the incidence period (from onset of symptoms to cardiac arrest) is short. ECG abnormalities mostly ventricular fibrillation. Another part of the incidence of patients with circulatory failure, cardiac arrest prior to the inactive state, and even unconscious, the incidence of long. Before changes in cardiovascular death often have non-cardiac diseases. ECG abnormalities in cardiac arrest more common than ventricular fibrillation. (Three) cardiac arrest of complete loss of consciousness for the period features. If not immediately rescue, generally within a few minutes into the death phase. Those rare spontaneous reversal. Cardiac arrest followed the signs and symptoms appear as follows: ① heart sounds disappear. ② palpable pulse, blood pressure could not be determined. ③ sudden loss of consciousness or accompanied by paroxysmal convulsions. Often generalized convulsions, cardiac arrest occurred in within 10 seconds after, sometimes accompanied by eye deviation. ④ breathing intermittently, was sighing, after being stopped after cardiac arrest occurred in 20 to 30 seconds. ⑤ coma, cardiac arrest occurred in 30 seconds. ⑥ mydriasis, more than 30 to 60 seconds after cardiac arrest occurs. However, this period has not yet to the biological death. If appropriate timely rescue, the possibility of recovery. Success rate of recovery depends on: ① recovery began sooner or later, ② cardiac arrest occurred in places, ③ abnormal cardiac electrical activity type (ventricular fibrillation, ventricular tachycardia, ventricular cardiac mechanical separation or the pause), ④ former patients in cardiac arrest clinical situations. (Four) biological death from cardiac arrest on the death of the biological evolution of cardiac arrest depends mainly on the type of electrical activity of the heart and cardiac resuscitation timeliness. Ventricular fibrillation or cardiac arrest, as in the first four to six minutes were not cardiopulmonary resuscitation, the prognosis is poor. As in the first 8 minutes, were not cardiopulmonary resuscitation, except in exceptional circumstances such as low temperature, or almost no survival. Edit this section diagnosis of cardiac arrest diagnosis is generally not a problem. But need to quickly determine. Sudden loss of consciousness, carotid or femoral artery pulse disappeared, especially heart sounds disappeared, cardiac arrest is the most important diagnostic criteria. Pale skin color can be large or bruising. Non-medical staff in accordance with loss of consciousness, no breathing movements or just dying respiratory activity, combined with arterial pulse disappeared diagnosis of cardiac arrest. However, respiratory activity can persist after the arrest occurred one minute or longer. On the contrary, such as respiratory movement disappeared or have severe wheezing and pulse but there, suggesting the primary breathing pause, in a very short period of time will lead to cardiac arrest. Edit this paragraph treatment under sudden loss of consciousness, carotid or femoral artery pulse disappeared, especially heart sounds disappeared, no breathing movements or activities just dying breath to diagnose cardiac arrest. Once the diagnosis of cardiac arrest, cardiopulmonary resuscitation should be immediately that (Cardiopulmonary resuscitation, CPR), including basic life support, advanced life support and resuscitation basic post-processing. CPR is aimed at giving clear before treatment, to maintain the central nervous system, heart and other vital organs of vitality [4]. Basic Life Support (BLS) refers to maintaining an open airway and respiratory and circulatory support. SCD also includes the identification and recovery of postural asphyxia management. Identification of SCD first confirm rescuers, victims and bystanders are safe. Check the victim's reaction, jiggle shoulders and shouted: "Are you okay?." If there is no response, then call for help, the victim on his back and then use the tilt head upward, lifting the jaw open airway techniques. To keep the airway open and observe thorax activities, listen to breath sounds, with cheeks feel airflow. If normal breathing, be put into the recovery position, call an ambulance, a continuous check breathing. If breathing is not normal chest compressions. Chest compressions, check your pulse should not exceed 10 seconds. If the patient has no pulse, you should immediately begin chest compressions. In order to push the best, the patient should be lying supine hard surface (such as flat or ground), the rescuer should press the palms on the center of the chest, between the sternum double nipple on the other hand parallel to the overlap pressure on its back, and to ensure that pressure is not transmitted to the ribs. Body perpendicular to the victims chest, arms straight, press the chest 4 ~ 5 cm. After each compression, dropping the pressure but keep your hands and thorax are not isolated, pressing frequencies 100 / min or so. Should minimize interruptions in chest compressions. Artificial respiration again after 30 compressions open the airway. Keeping the mouth and jaw lifting, wrap their lips after normal inspiratory mouth to ensure tightness. Blowing and observe the thorax flattering, blowing one second, which is effective in relief of artificial respiration. Leaving patients with mouth and observe the gas discharge and chest down. Artificial respiration again, then re-chest compressions, there should be no delay during the pressing ventilation ratio 30:2. Otherwise, unless the patient began to breathe normally without re-checking that interrupt recovery. Early defibrillation early defibrillation for cardiac arrest patients save crucial. Rescue personnel if not witnessed cardiac arrest outside the hospital, and tried in the ECG should be performed before defibrillation approximately 5 cycles of CPR. A CPR cycle includes 30 chest compressions and two breaths. If the chest compressions is 100 times / min speed, then 5 cycles of CPR for 2 minutes. Of-hospital ventricular fibrillation cardiac arrest type clinical studies support the defibrillator before the first CPR. Shock defibrillation success was defined as at least 5 seconds after termination of ventricular fibrillation. According to defibrillation waveform different types of modern defibrillator is divided into one-way and two-way type. When using two-way defibrillator can be selected in either of two waveforms in a specific energy range, and each waveform are valid for termination of ventricular fibrillation. First shock when using the straight-line bidirectional waveform defibrillation should choose 120J-200J, and the second and subsequent two-way shock should choose the same or higher energy. Unidirectional wave defibrillator defibrillation energy should be chosen first 200J, 300J and defibrillation is unsuccessful then select 360J; also the first time that as soon as possible in order to select 360J shock cardioversion. In vitro automatic defibrillator (AED) is a reliable computer intelligent device, it can through sound and image prompts to guide non-professional emergency personnel and medical personnel on the type of ventricular fibrillation cardiac arrest for safe defibrillation. Rescue personnel practices will defibrillator paddles on the patient's sternum bare-breasted front outer lateral. Electrode plate on the right side of the right clavicle in patients below the left nipple electrode plate placed flush with the left lateral chest down. The first shock energy of 2 J / Kg, subsequent shock energy of 4 J / Kg. Not recommended for use in patients with cardiac arrest pacing therapy, while patients with symptomatic bradycardia pacing therapy is taken into account. Now generally agreed that chest compressions is very important, there is no exact proof of pacing therapy on the basis of benefit in patients with cardiac arrest is not recommended for patients with cardiac arrest while pacing delays chest compressions. When a pulse is present, can be carried out on patients with symptomatic bradycardia pacing therapy or percutaneous transvenous pacing therapy. Advanced Life Support Advanced Life Support The overall objective is to fully ventilation, hemodynamic cardioversion rhythm into an effective rhythm, maintain and support the recovery cycle. Therefore, in patients with advanced life support is in: the endotracheal tube and oxygen in good; has defibrillation, cardioversion or cardiac pacing has been in; has established intravenous access can input must be drugs. After tracheal intubation, airway management, ventilation purpose is to correct hypoxemia. Thus, the patient's ventilation applications rather than room air oxygen. If possible, it should be monitored arterial oxygen. Hospital usually ventilator support ventilation, hospital patients often rely on balloon - Masks ways to maintain ventilation. Defibrillation - cardioversion ventricular fibrillation is the most common cause of cardiac arrest, a key step in successful resuscitation is rapid cardioversion rhythm. Timely chest compressions and artificial respiration can be maintained, although the heart and brain and other vital organs of vitality, but rarely will fibrillation to normal heart rhythm. Disease treatment drug treatment beneficial effects of epinephrine is mainly because of its α receptor agonism, increase coronary and cerebral perfusion pressure. Indications: is any cause cardiac arrest first medication: every 3 ~ 5 min of CPR used once epinephrine; cause allergic drug of choice; cardiogenic shock, second-line medication. Dose: The initial intravenous dose of 1 mg. When the blood vessels way delay or failure will be 2 ~ 3 mg with sterile water and diluted to 10 mL by intratracheal route. Usage: usually use two dilutions: 1:10 000 (10 mL solution containing 1 mg epinephrine); 1:1 000 (1 mL solution containing 1 mg epinephrine). Atropine can reverse the cholinergic receptor-mediated heart rate, effective disarmament of vagal tone, can be applied to cardiac arrest and pulseless electrical activity, the recommended dose of 1mg intravenously, if asystole persists every 3 - 5 minutes repeated application. Amiodarone. Indications: refractory VF / VT; hemodynamically stable ventricular tachycardia (VT) and other refractory tachycardia. Dose: If the first three shocks after VF / VT persists, with 5% glucose solution was diluted to 300 mg amiodarone to 20 mL, intravenous injection. Lidocaine can suppress premature ventricular fibrillation and acute myocardial infarction. The initial dose was 1-1.5mg/kg, ventricular fibrillation and pulseless ventricular tachycardia persists, increase the interval of 5-10 minutes 0.5-0.75mg/kg IV, the maximum dose of 3mg/kg. Lidocaine is generally only considered when no alternative medicine amiodarone. Magnesium ions can effectively terminate the long QT interval induced torsades de pointes ventricular tachycardia, but on the QT interval of normal ventricular tachycardia is invalid. If the rhythm is torsades de pointes ventricular tachycardia may give 1-2g magnesium diluted 5-20min intravenous / intraosseous infusion. Vasopressin can be used before and after cardiac arrest. Vasopressin has been used to treat vasodilatory shock, such as sepsis syndrome and septic shock. The standard treatment of septic shock include: antibacterial, expansion, vasoconstrictor, cardiac drugs. However, a strong heart and vasoconstrictor drugs boost effect is not obvious, then vasopressin may be effective. Norepinephrine is naturally effective vasoconstriction and inotropic effects of the drug. Norepinephrine is usually reduced renal or mesenteric vascular resistance, but in sepsis can improve renal blood flow and urine output, can be applied to dopamine, benzene kidney or severe hypotension Methoxyamine ineffective and low peripheral vascular resistance patient. Noradrenaline in hypovolemic when applied inappropriately increased myocardial oxygen demand in ischemic cardiomyopathy patients should be used with caution. Add 250ml norepinephrine 4mg of 5% GS or 5% GNS solution, the initial dose of 0.5-1μg / min, with the effects of regulation. Can not be mixed with alkaline solution. Dopamine is catecholamines, dopamine in the recovery used in the treatment of hypotension, especially symptomatic bradycardia or hypotension after resuscitation. In combination with other drugs like dobutamine as hypotension after resuscitation treatment options. The usual dose 2-20μg/kg/min ,10-20μg / kg / min increase system and splanchnic vascular contractility, larger doses and other adrenergic medications reduce visceral organ perfusion. Dobutamine has a positive inotropic effect and can be used to treat severe systolic heart failure. General dose 2-20μg/kg/min, but patients in the emergency large individual differences in response to dobutamine in elderly patients decreased significantly. Dose> 20μg/kg/min, heart rate> 10% can cause or aggravate myocardial ischemia. Milrinone and amrinone are phosphodiesterase (PDE) inhibitor, has a strong heart and a vasodilator. Phosphodiesterase inhibitors combined catecholamines often used to treat severe heart failure, cardiogenic shock, and other applications for individual patients catecholamines invalid. Applications should be OK hemodynamic monitoring. Within 10-15 minutes amrinone be loading dose 0.75mg/kg, and then to 5-15μg / kg / min infusion maintained. Since short half-life of milrinone (1.5-2.0 hours) and less likely to cause thrombocytopenia and often applied, were not required loading dose of 4.5-6 hours to reach stable plasma concentration. Slow bolus loading dose of milrinone (10 minutes 50μg/kg), then 0.375-0.75μg/kg/min intravenous maintain 2-3 days, renal failure dose reduction. Side effects include nausea and vomiting, and hypotension. Recovery after resuscitation and supportive treatment supportive treatment by hemodynamic instability, multiple organ failure and early death due to brain damage caused by the death of the late great significance. Improve the prognosis of patients after resuscitation recovery support advanced life support treatment is an important part. And in patients with ROSC after initial stabilization, there is still a high mortality. At this stage, should strengthen the circulatory, respiratory and nervous systems support; actively seek and treat reversible causes of cardiac arrest causes; monitoring body temperature, aggressive treatment of thermoregulation disorders and metabolic disorders. Restoration of spontaneous circulation after resuscitation support the primary purpose of treatment is to restore effective circulation of tissues and organs. The pre-hospital or hospital for treatment of patients with return of spontaneous circulation, must find the cause and treatment resulted in cardiac arrest, cardiac arrest after the treatment of ischemia-reperfusion injury caused by hypoxia. Active and spontaneous hypothermia induced after resuscitation therapy may play a role. Two randomized controlled clinical trials show that for pre-hospital ventricular fibrillation / cardiac arrest remains comatose after resuscitation, induced hypothermia (ROSC within minutes to hours after the temperature dropped to 33 ℃ or 32-34 ℃ , sustained 12-24h) may improve the prognosis. Hypothermia therapy clinical studies are mostly used in vitro techniques such as ice cooling blankets, ice packs, etc., often require several hours to reach the target temperature. Recent studies have started using in vivo infusion of ice-cooling techniques, such as saline, blood vessels built into the cooling ducts, etc., can make the body temperature quickly dropped to the target temperature. During this period, closely observed changes in body temperature is very important. For the recovery of patients after cardiac arrest, such as hemodynamic stability, spontaneous mild hypothermia (> 33 ℃) without rewarming treatment. On pre-hospital cardiac arrest caused by ventricular fibrillation, still unconscious after resuscitation hemodynamic stability but who should be the temperature dropped to 32-34 ℃, and maintain 12-24h. After resuscitation electrolyte imbalance may worsen the prognosis. Although many studies have found that strict glycemic control may improve prognosis and reduce deaths caused by an infection, because the infection is very common after resuscitation. Conduct a detailed clinical examination and chest X-ray examination is very necessary. At this point, you need to pay special attention to resuscitation cardiopulmonary complications, such as pneumothorax and tracheal intubation depth anomaly or ectopic and so on. Mechanical ventilation in patients with arterial blood gas results in accordance with, respiratory rate and extent of work of breathing to adjust, when spontaneous breathing becomes more active, mechanical ventilation should be gradually reduced until it becomes spontaneous breathing. Studies have shown that persistent hypocapnia (low PCO2) may cause decreased cerebral blood flow, increased cerebral ischemia. Cardiac arrest after the restoration of blood flow can lead to lasting 10 to 30 minutes a transient reactive hyperemia, accompanied by sustained long after the low-flow state. During this low perfusion time, the less flow (low oxygen-carrying) and higher oxygen metabolism conflict will occur. If the patient during this time the treatment with high ventilation, low PCO2 generated additional cerebral vasoconstriction effect will be further reduced cerebral blood flow, and further aggravate cerebral ischemia and injury. By the data obtained from patients with brain injury infer maintain normal levels of ventilation PCO2 is appropriate, while the conventional high ventilation therapy may be harmful. Cardiovascular system defibrillation and cardiac arrest after ischemia - reperfusion injury can lead to a transient myocardial stunning and functional disorders, and continued for some time, the vasoconstrictor make improvements. Or due to cardiac arrest during CPR, coronary blood flow interruption or severely reduced, causing myocardial ischemia, myocardial biochemical markers levels. Elevated levels of cardiac biochemical markers might also prompt cardiac arrest due to acute myocardial infarction. Hemodynamic resuscitation after cardiac arrest is usually unstable, multiple organ failure caused by the early death and persistent low cardiac related, it should be evaluated as soon as the patient's electrocardiogram, chest X-ray and electrolytes, cardiac biochemical markers and so on. Resuscitation of cardiac arrest during the first 24h echocardiography to guide subsequent treatment help. Hemodynamic instability via infusion of vasoactive drugs improvement after treatment. Invasive blood pressure monitoring can accurately measure arterial pressure, right to develop the most rational drug combination therapy, so that tissue perfusion to achieve the best help. If necessary, respond to fluid volume and vasoactive substances (such as norepinephrine, dopamine, milrinone, etc.) accurately quantified in order to maintain blood pressure, cardiac output and tissue perfusion. The patient to restore normal brain function and other organ functions are the basic objectives of cardiopulmonary resuscitation. Stage in the recovery of spontaneous circulation, brain tissue after an initial transient hyperemia, due to microcirculation, decreased cerebral blood flow (no-reflow phenomenon). Unconscious patients should be maintained on a normal or slightly elevated mean arterial pressure, in order to ensure that the desired cerebral perfusion. Because heat and agitation can increase oxygen demand, it is necessary to consider the hypothermia treatment for fever. Once convulsions, must immediately be controlled with anti-seizure drugs. Edit this paragraph prevention of SCD prevention remains by far one of modern medicine has not been resolved. In recent years in the prevention of sudden cardiac arrest is to identify the major advances in cardiac arrest high-risk targets. Coronary heart disease, myocardial infarction, especially in the acute stage of rehabilitation and subsequent chronic process, the risk of cardiac arrest is higher. In acute myocardial infarction within the first 72 hours, the potential risk of cardiac arrest can be as high as 15% to 20%. Myocardial infarction rehabilitation period (from the first three days until the first 8 weeks) with a history of ventricular tachycardia or ventricular fibrillation, cardiac arrest whose greatest risk, such as general measures only to treatment, within 6 to 12 months mortality rate as high as 50% to 80%, of which 50% is sudden death. Only positive intervention to improved prognosis, mortality in 18 months can be reduced to 15% to 20%. 1, regular medical examinations: the elderly themselves are heart disease and a high risk of various diseases,adidas f50, should be regularly to the hospital for medical examination. Young, middle-aged work stress, fast-paced life, work life stress is also likely to suffer from coronary heart disease, hypertension and other diseases. Periodic medical examinations to facilitate the timely detection of disease early detection, early treatment, reducing the risk of sudden death. 2, to avoid fatigue and mental stress: fatigue and mental stress causes the body in stress, high blood pressure, heart burden, so that the original heart disease worse. Even if they had no structural heart disease can also cause ventricular fibrillation. So, everyone should work on their own, life has been arranged to control the pace of work and working time, can not be too fast too long. 3, quit smoking, limit alcohol, balanced diet, weight control, proper exercise, maintaining a healthy lifestyle will reduce the incidence of cardiovascular and cerebrovascular diseases. 4, pay attention to the danger signal and the importance of fatigue onset of precursor symptoms: fatigue can cause long-term changes in the body some. Such as anxiety, irritability, memory loss, difficulty concentrating, insomnia and poor quality of sleep, headache, dizziness, tinnitus, sexual dysfunction, hair loss and obvious. When the body does happen, you should adjust the pace of work, proper rest, allowing the body to restore function. If you can not alleviate should immediately go to hospital for treatment. 5, have been suffering from coronary heart disease, hypertension and other diseases under the guidance of a doctor should adhere to medication treatment. 6, attention to risk assessment of ventricular arrhythmias, including routine ECG, exercise stress test, Holter monitoring, other cardiac electrical technology (surface signal averaged ECG), echocardiography, cardiac electrophysiology examination and other tests to clear type of arrhythmia, SCD risk assessment, treatment decisions. 7, pay attention to strengthening the prevention of SCD after myocardial infarction. After acute myocardial infarction, chronic ventricular contraction and sudden cardiac death risk factors, particularly frequent (24-hour ambulatory electrocardiogram showed ventricular contractions at 10 to 30 times / hour) ventricular contraction and paroxysmal, non-sustained ventricular tachycardia. If accompanied by significantly reduced left ventricular ejection fraction (LVEF ≤ 30%), the annual mortality rate of 20%. LVEF, left ventricular volume, heart rate variability or baroreflex sensitivity after myocardial infarction risk stratification of SCD helpful, followed by frequent ventricular contractions, paroxysmal, non-sustained ventricular tachycardia and resting heart rate . Not recommended for routine after myocardial infarction ventricular late potentials and cardiac electrophysiology examination. After myocardial infarction myocardial ischemia aggressive treatment is the main effective measures to prevent sudden death, myocardial infarction, positive exercise test, coronary angiography showed severe stenosis and actively seek their intervention or coronary artery bypass graft surgery treatment can effectively reduce the incidence of sudden death. SCD after myocardial infarction in high-risk patients prophylactic ICD therapy, compared with conventional drug treatment can significantly reduce mortality. And cardiac arrest can also occur in low-risk populations are considered, the fundamental basis for preventive measures should be committed to heart disease and cardiac arrest prevention of predisposing factors.