Respiratory arrest and cardiac arrest are to be distinguished from each other, but leads one inevitably to another when there is no treatment. (See also respiratory failure Respiratory failure and mechanical ventilation, dyspnea and hypoxia in desaturation.)

Cardiac arrest is the cessation of cardiac mechanical activity that leads to the cessation of blood flow. Cardiac arrest prevents blood from flowing to vital organs and provide them with oxygen. If left untreated, it leads to death. Sudden cardiac arrest is the unexpected completion of the circulation in a short period after symptom onset (sometimes without warning). Sudden cardiac arrest occurs outside the hospital in the United States at about 400,000 people a year, with a mortality of about 90%. Respiratory arrest and cardiac arrest are to be distinguished from each other, but leads one inevitably to another when there is no treatment. (See also respiratory failure Respiratory failure and mechanical ventilation, dyspnea and hypoxia in desaturation.) Etiology In adults, is the sudden cardiac arrest usually the result of a pre-existing cardiac disease. Here should be mentioned especially coronary heart disease. For a large proportion of these patients sudden cardiac arrest is the first manifestation of previously unrecognized cardiac disease. Among the other causes include circulatory shock due nichtkardiogener disorders (pulmonary embolism, gastrointestinal bleeding, trauma), respiratory failure, metabolic dysfunction and overdoses of medications or drugs. In children, cardiac causes of sudden cardiac arrest far less frequently (<15-20%). instead are here trauma, poisoning and various respiratory disorders (eg. as airway obstructions, nicotine inhaler, drowning, infections and sudden infant) of prime importance. Pathophysiology As a result of cardiac arrest, there is a generalized ischemia. At the cellular level it processes take place that affect organ function after resuscitation. The main consequences are the direct cell damage and cellular edema. A particular disadvantage, the formation of cell edema in the CNS affects. Here, there is only a minimal expansion possibility of brain mass, so that a rise in intracranial pressure is often the result. Thus the reduction of cerebral perfusion in the post resuscitation phase is accompanied inevitably. A significant proportion of successfully resuscitated patients have short-term or long-term cerebral dysfunctions (to coma from mild confusion) can be seen in a changed attention, as well as seizures, or a combination of both. The decrease in ATP production results in a loss of membrane integrity at the cellular level. It comes here to potassium efflux, and the influx of sodium and calcium. The significant increase in intracellular sodium leading to cell edema. The excessive increase of calcium is damaged mitochondrial structures (suppression of ATP production). At the same time the accumulation of nitrate oxides increases (thus are increasingly formed damaging free radicals). Under certain circumstances, increased activated proteases occur, which then continues to have a harmful effect on cells. Abnormal ion flux also leads to depolarization of neurons that results in the release of neurotransmitters, some of which are harmful (which is aggravated deterioration of intracellular calcium overload z. B. glutamate activates a specific calcium channel). Inflammatory mediators (z. B. IL-1B, tumor necrosis factor-?) are formed. Some of these mediators cause micro thrombosis and loss of vascular integrity. This results in a further strengthening of edema. Some mediators trigger apoptosis, which leads to accelerated cell death. Symptoms and signs In critically ill or even terminal patients is cardiac arrest usually preceded by a phase of clinical worsening. This leads to shallow breathing, arterial hypotension and a progressive deterioration. When sudden cardiac arrest without any sign of a collapse without warning occurs. Sometimes cardiac arrest is (<5 seconds) accompanied only by a short spasm event. Diagnosis Clinical evaluation ECG monitor and ECG is sometimes possible causes investigated (z. B. by echocardiography, chest x-ray or ultrasound of the breast) The diagnostic results from the clinical signs of apnea, no pulse and loss of consciousness. Arterial blood pressure is not measurable. Pupils dilate and become unresponsive after a few minutes to light. The ECG monitor shows ventricular fibrillation (ventricular fibrillation, VF), ventricular tachycardia (VT) or asystole. Occasionally slowed rhythm images, such as an extreme bradycardia find. Here, too, usually occurs mere electrical activity without detectable pulses (electro-mechanical decoupling) or just an extreme arterial hypotension, in which no peripheral blood pressure is measured. The patient is examined for potentially treatable causes; H: hypoxia, hypovolemia, acidosis (hydrogen ion), hyperkalemia or hypokalemia, hypothermia, hypoglycemia T: helpful in remembering the "H's and T's" are taking tablets or toxins, cardiac tamponade, pneumothorax, thromboembolism (massive pulmonary embolism), trauma Unfortunately, many of these causation remain during resuscitation often unknown. The mere clinical examination of the patient along with an ultrasound and a chest radiograph can secure the tension pneumothorax. An ultrasound of the heart may represent the extent of myocardial contractions; also can by ultrasonography a cardiac tamponade, a massive hypovolemia ( "empty heart"), an overload of the right ventricle with regard to pulmonary embolism, and focally impaired heart wall mobility impairments who have a myocardial infarction suspect are detected. Rapid blood tests at the bedside detect abnormal Kalkum- and glucose levels. A brief history of their family members may possibly indicate an overdose. The forecast survival to hospital discharge, especially in neurological integrity, is a far better result than just the return of spontaneous circulation. Survival rates vary considerably, favorable factors are: early and effective CPR by passers-by or members of local Observed cardiac arrest cardiac arrest in the hospital (especially with a monitoring Monitor) Initial rhythm of VF or VT Early defibrillation (for VT or VF after initial chest compressions) Supply after resuscitation, including induced hypothermia (z. B. targeted cooling to 34 ° C), circulatory support and access to the cardiac catheterization when many factors are low (eg. B. VF is experienced in an intensive care or emergency room) may be about 20% of the to discharge patients from hospital survive. If factors are equally unfavorable (z. B. patients in asystole alone and at home, sudden cardiac arrest outside the hospital), survival is unlikely. Overall, the survival rate after cardiac arrest outside hospital in between 1 and 70%, the very wide bandwidth and reflects differences inclusion criteria again the statistics, and differences in the effectiveness of the system. About 8-30% of survivors have neurological dysfunction, and one third returns to the state back in front of the cardiac arrest. The survival rate for cardiac arrest in the hospital is about 26%. Cardiopulmonary resuscitation treatment If possible, treatment of the underlying cause care after resuscitation decisive importance is attached to the rapid intervention. CPR (Cardiopulmonary resuscitation (CPR) in adults) is a proven response to a cardiac arrest; the rapid introduction of uninterrupted chest compressions ( "hard and fast press") and early defibrillation of patients having a VF or VT (more common in adults) are the key to success. In children, the most have asphyxiale causes of cardiac arrest, the existing rhythm is usually a bradyarrhythmia, followed by asystole. However, about 15-20% of the children come (especially when the sudden cardiac arrest no respiratory symptoms have gone before) with a VT or VF in the treatment and also require rapid defibrillation. The incidence of VF as the first recorded rhythm increases in children> 12 years. Such primary causes must be treated immediately. now find themselves in such a situation no treatable conditions, but still detectable heartbeats or pulses, you have to start from a severe state of shock and immediately (with the intravenous fluid resuscitation for., 1 l 0.9% saline, blood bank, or a combination ) begin. If a response to the i.v. Fluid administration is insufficient, most doctors give one or more vasopressors (eg. As norepinephrine, epinephrine, dopamine, vasopressin), but there is no solid evidence that they improve the chances of survival. In addition to treating the cause, belonging to the treatment after a resuscitation methods to optimize the O2 supply, antiplatelet therapy and therapeutic hypothermia.


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