Ventricular fibrillation is caused by many intersecting waves of folded electrical activity, and the ECG shows a chaotic recording curve. At the cellular level, electrical activity may still be present, but there is no mechanical contraction in terms of overall cardiac effect and therefore no effective cardiac output. What is ventricular fibrillation Within seconds ventricular fibrillation can lead to unconsciousness and, if not treated aggressively, usually to convulsions and irreversible damage to the brain (due to prolonged cerebral ischemia) after about 5 minutes. The patient then dies quickly. What are the symptoms Acute myocardial infarction combined with VF in the first few hours, in the absence of shock or heart failure, is called primary VF. These cases are often associated with severe coronary artery disease and are prone to recurrence after survival. These patients require further investigations, including exercise testing, coronary angiography, and invasive electrophysiology. As the nursing resuscitation community increases and more patients are saved from sudden out-of-hospital death, implantable defibrillators (ICDs) should be considered for those at risk of recurrence. Acute myocardial infarction with shock, with or without heart failure, is secondary to VF, and these patients have severe ventricular disease. VF can also be complicated by myocardial reperfusion after thrombolytic therapy for acute myocardial infarction (mostly in ventricular autonomic rhythm). This suggests that early reperfusion has occurred. It is commonly associated with coronary artery disease, especially acute myocardial infarction or severe myocardial ischemia; third-degree AV block with extremely slow ventricular rate; severe hypokalemia or hyperkalemia; acute viral myocarditis; toxic effects of digitalis, quinidine, antimony, chloroquine, etc.; electrocution, drowning; cardiac surgery and hypothermic anesthesia. Circulatory respiratory arrest, loss of consciousness, followed by generalized convulsions in the form of A-S (Adams-Stokes) syndrome. What are the treatment efforts Artificial respiratory cardiopulmonary resuscitation: the method of estimating the presence or absence of voluntary breathing is for the operator to place the ear close to the patient’s mouth and nose and listen to the sound of air escaping or feel the air flow, while observing the chest rise and fall. If the thorax does not rise and fall and there is no airflow, the patient is not breathing and artificial ventilation must be started immediately. The observation time is usually within 3-5 seconds. Endotracheal intubation is the best way to establish artificial ventilation. When the time or conditions do not allow, mouth-to-mouth breathing is an effective and easy method of artificial ventilation. After keeping the airway open, the operator pinches the patient’s nostrils with the hand placed on the patient’s forehead and the thumb and forefinger, takes a deep breath and then presses his or her lips against the patient’s lips for deep and fast forceful blowing until the patient’s chest is raised, and then allows the patient to exhale naturally. When two people perform CPR, the lungs should be expanded once every 5 seconds; when a single person performs mouth-to-mouth breathing and chest compressions simultaneously, the lungs should be expanded twice every 15 seconds. Oxygen can also be supplied by mask. The above-mentioned mouth-to-mouth breathing is only a temporary emergency measure, and should be immediately and correctly endotracheal intubation, with artificial airbag extrusion or artificial ventilator for assisted breathing and fluid infusion to correct hypoxemia. If necessary, arterial partial pressure monitoring should be performed. Chest compression: chest compression is to make the whole thoracic cavity internal pressure change and produce suctioning effect, improve systemic blood flow, and help maintain the suctioning effect of important organs, improve systemic blood flow, and help maintain the blood perfusion of important organs. Thoracic compression takes the saber process as the positioning mark, and places the index and middle fingers across the top of the acromion, with the median part of the sternum above the fingers as the compression zone. The operator places the root of the palm of one hand on the compression zone, parallel to the direction of the patient’s long axis of the sternum, and the palm of the other hand overlaps on the back of the previous hand and remains parallel, with the fingers of both hands interlocked or extended, but should not touch the chest wall. When pressing, the elbow should be straight, relying on the shoulder and back strength, press vertically downward with force to depress the sternum about 3-5 cm, followed by sudden relaxation. The rate should be about 80-100 times/minute. The compression should be smooth, even and regular. The compression and relaxation time should be approximately equal. The main symptoms of chest compressions are rib or sternal fracture, pericardial blood accumulation or filling, hemothorax, pneumothorax, pulmonary contusion, liver and spleen laceration, and fat embolism. The correct method of operation should be followed to avoid complications as much as possible. It should be noted that chest compressions are not the same as performing compressions, and effective chest compressions only bring the cardiac index close to 40% of the low limit of normal, which is much less than the cardiac index of most patients after restoration of voluntary contraction. Therefore, it is important to try to restore an effective autonomic rhythm rapidly while chest compressions are being performed. The next stage of CPR is to give the patient intensive life support measures. At the same time, the above basic life support treatment is not stopped immediately, but is gradually transitioned to the second phase. Defibrillation and resuscitation: cardiac autonomic conduction system Defibrillation and resuscitation to rapidly restore an effective cardiac rhythm is a crucial step for successful resuscitation. Once ventricular fibrillation or sustained rapid ventricular tachycardia is identified on ECG monitoring, immediate DC defibrillation with 200 J energy should be performed. If ineffective, switch to 300 J or 360 J energy. Failure of one or two initial electrical defibrillations suggests a poor prognosis, but resuscitation efforts should not be abandoned. At this point, efforts should be made to improve ventilation and correct blood biochemical abnormalities, including improving the management of oxygen cooperative acidosis. In addition to ensuring adequate blood oxygenation, intravenous sodium bicarbonate is sometimes necessary, especially in patients who are difficult to resuscitate with electrical defibrillation. The dose of sodium bicarbonate is 1 mmol/kg. Half a dose can be repeated every 10-15 minutes during cardiopulmonary resuscitation. However, bicarbonate overdose may cause alkalosis, hypernatremia and hyperosmolar state. Arterial blood pH, partial pressure of oxygen and partial pressure of carbon dioxide should be monitored during the inter-resuscitation period whenever possible. Medication: Intravenous lidocaine is beneficial in maintaining electrical stability of the heart during the intercuspitation period. Intravenous push lidocaine 1 mg/kg should be given. This dose may be repeated after two minutes if resuscitation is unsuccessful or if partial electrode stability continues to exist. This is followed by a continuous intravenous drip. If ventricular fibrillation is maintained after initial treatment, intravenous epinephrine should be given and electrical defibrillation should be repeated. Throughout resuscitation, the above dose may be repeated every 5 minutes if necessary, and intracardiac epinephrine may be used in the absence or minimal establishment of intravenous or endotracheal routes of administration. If these treatments fail, other antiarrhythmic drugs may be used instead. The most commonly used are procainamide and bromobendazole. For refractory ventricular tachycardia and ventricular fibrillation, amiodarone is recommended. In cases of refractory ventricular fibrillation due to acute hyperkalemia, hypocalcemia or poisoning with calcium channel blocker application, 5-10 ml of 10% calcium gluconate can be given intravenously (at a rate of 2-4 ml/min). Calcium should not be used routinely during the intercardiorespiratory period. Bradyarrhythmias or cardiac arrests with pulseless electrical activity of straining are different from ventricular fibrillation. Every effort should be made to restore a stable autonomic rhythm or to try to pace the heart while giving the patient basic life support. Commonly used drugs are epinephrine and atropine given intravenously. Isoprenaline (1 mg, diluted to 10 ml of 1:10,000 solution) can also be used. The main risk of intracardiac injection is coronary and myocardial tears. If available, temporary artificial cardiac pacing, such as extracorporeal pacing and bedside intracardiac pacing via the left subclavian vein, should be performed. Mechanistic analysis: After cardiopulmonary resuscitation to restore cardiac rhythm, the focus should then be on maintaining a stable new point and hemodynamic state. Continuous intravenous infusion of lidocaine or common lucaine amine helps to maintain cardiac stability. Catecholamines are better at stabilizing the electrical activity of the heart (e.g., bringing the ventricular fibrillation wave from fine to coarse and accelerating the autonomic rhythm of slow arrhythmias). When the time-varying effects of epinephrine are not required, dopamine or dobutamine, which have a stronger positive inotropic effect, may be considered. Isoprenaline can be used to treat bradycardia in primary or post-electrical defibrillation to increase heart rate and increase cardiac output. In the absence of pulsatile electrical activity, catecholamines are still ineffective and calcium chloride, 2-4 mg/kg, can sometimes be tried, but its efficacy is uncertain. What I can do When ventricular fibrillation occurs, defibrillate blindly if the condition is unmonitored, adjust the joules if there is cardiac monitoring, cardiac compressions, and balloon-assisted breathing. If ventricular fibrillation occurs and the person has started to convulse and is unconscious, electric defibrillation should be applied urgently at this time, if once does not work, 2 more times, and if there is no defibrillator at the time of the attack, emergency manual cardiopulmonary resuscitation should be performed first. What can happen The electrical characteristics of ventricular fibrillation are similar to those of atrial fibrillation, but its prognosis is quite poor. In ventricular fibrillation, the ventricular muscle fibers simply fibrillate without forming a coordinated and effective contraction. Since no blood is pumped out of the heart at this time, the patient dies quickly unless immediate treatment is given.