Cardiac arrest analysis

Date: 2019-02-25
Times of browsing: 10


Cardiac arrest refers to the sudden termination of cardiac ejection function, the aortic pulsation and heart sound disappear, and important organs (such as the brain) are severely ischemia and hypoxia, leading to the termination of life. This unexpected sudden death is medically known as sudden death. The most common cause of cardiac arrest is ventricular fibrillation. If the patient is called without a response, the pressure is on the squat and the underarm is unresponsive, and the patient is determined to be in a coma. Then pay attention to observe the patient's chest and abdomen with or without undulating breathing. If there is no pulsation of the carotid artery and femoral artery, the heart can not hear the heartbeat, it can be determined that the patient has a cardiac arrest.




The common causes of cardiac arrest in the 2005 American Heart Association Cardiopulmonary Resuscitation and Cardiovascular Emergency Guidelines are summarized as follows:

1. O2 deficiency.

2. 2 hypokalemia / hyperkalemia and other electrolyte abnormalities.

3. low temperature / body temperature is too high.

4. low blood volume.

5. hypoglycemia / high blood sugar.

6. drugs.

7. heart pack stuffing.

8. pulmonary embolism.

9. coronary vascular embolization.

10. pneumothorax, asthma.


Clinical manifestations

The clinical course of cardiac arrest or sudden cardiac death can be divided into four periods: prodromal phase, onset phase, cardiac arrest and death.


1. Precursor period

Many patients have prodromal symptoms such as angina, shortness of breath or palpitations, prone to fatigue and other non-specific complaints before or after a cardiac arrest. These prodromal symptoms are not unique to sudden cardiac death, but are common before any heart attack. There is data showing that 50% of cardiac deaths have been consulted within one month before sudden death, but their complaints are often not necessarily related to the heart. Among survivors of cardiac arrest outside the hospital, 28% had angina or anxious exacerbations before cardiac arrest. However, prodromal symptoms only suggest a risk of developing cardiovascular disease, but not a subgroup of sudden cardiac death.


2. Incidence period

That is, the period of acute cardiovascular changes before cardiac arrest, usually no more than 1 hour. Typical manifestations include: prolonged angina or chest pain in acute myocardial infarction, acute dyspnea, sudden palpitations, persistent tachycardia, dizziness, etc. If a sudden cardiac arrest occurs without warning signs beforehand, 95% are cardiogenic and have coronary artery disease. From the continuous electrocardiogram records obtained from the sudden death of the heart, it can be seen that there are often changes in ECG activity within hours or minutes before sudden death, with the increase in heart rate and the progression of ventricular premature beats being the most common. Sudden death in ventricular fibrillation, often preceded by a continuous or non-sustained ventricular tachycardia. These patients with arrhythmia are mostly awake before the onset and are short in the onset of the disease (from onset to cardiac arrest). Most of the abnormalities of the electrocardiogram are ventricular fibrillation. Some patients have developed circulatory failure, have been inactive before cardiac arrest, and have even been comatose, with a long onset period. There are often non-cardiac diseases before dying cardiovascular changes. Electrocardiographic abnormalities are more common in ventricular arrest than ventricular fibrillation.


3.Cardiac arrest


The complete loss of consciousness is characteristic of this period. If you do not immediately rescue, you usually enter the death period within a few minutes. Rarely spontaneous reversal.

Cardiac arrest is a sign of clinical death. The symptoms and signs are as follows: 1 heart sound disappears; 2 pulse can not be touched, blood pressure can not be measured; 3 sudden loss of consciousness or accompanied by brief convulsions, convulsions are often systemic, mostly occur in the heart Within 10 seconds after the stroke, sometimes the eyeball is skewed; 4 breaths intermittently, sighing, and then stop. Most occur within 20 to 30 seconds after cardiac arrest; 5 coma, mostly occurs after 30 seconds of cardiac arrest; 6 pupil dilated, more than 30 to 60 seconds after cardiac arrest. However, this period has not yet reached biological death. If timely and appropriate rescue, there is a possibility of recovery.

The success rate of recovery depends on: 1 sooner or later the recovery begins; 2 where the cardiac arrest occurs; 3 the type of cardiac electrical activity disorder (ventricular fibrillation, ventricular tachycardia, electrocardiographic separation, ventricular arrest); 4 cardiac arrest The clinical situation of the patient before the stop. If cardiac arrest occurs in a place where cardiopulmonary resuscitation can be performed immediately, the success rate of recovery is higher.

Under the condition that the hospital or the intensive care unit can be immediately rescued, the success rate of the resuscitation depends mainly on the clinical condition of the patient before the cardiac arrest: if it is an acute cardiac condition or a temporary metabolic disorder, the prognosis is better; if it is chronic In advanced heart disease or severe non-cardiac conditions (such as kidney failure, pneumonia, sepsis, diabetes, or cancer), the success rate of recovery is no higher than the rate of recovery from cardiac arrest outside the hospital. The success rate of the latter depends mainly on the type of ECG activity during cardiac arrest, with the best prognosis for ventricular tachycardia (67% success rate), followed by ventricular fibrillation (25%), ventricular arrest and electromechanical The prognosis of the separation is poor. Old age is also an important factor affecting the success of recovery.



4. Biological death period

The evolution of cardiac arrest to biological death depends mainly on the type of cardiac arrest and the timeliness of cardiac resuscitation. Ventricular fibrillation or ventricular arrest, if no cardiopulmonary resuscitation within 4 to 6 minutes, the prognosis is poor. If there is no cardiopulmonary resuscitation within 8 minutes, there will be no survival unless it is in special circumstances such as low temperature. From the statistics, witnesses who immediately performed cardiopulmonary resuscitation and early defibrillation are the key to avoiding biological death. The most common cause of death during hospitalization after cardiac resuscitation is damage to the central nervous system. Hypoxic brain damage and infection secondary to long-term use of respirators accounted for 60% of the cause of death, low cardiac output accounted for 30% of the cause of death, and only 10% of deaths due to recurrence of arrhythmia. The prognosis of cardiac arrest associated with acute myocardial infarction depends on whether it is primary or secondary: hemodynamics is not unstable when the former cardiac arrest occurs; the latter is secondary to unstable hemodynamic conditions. Therefore, if the primary cardiac arrest can be immediately recovered, the success rate can reach 100%; while the prognosis of secondary cardiac arrest is poor, the success rate of recovery is only about 30%.




ECG performance

1. Ventricular fibrillation or flutter, accounting for about 91%;

2. Electrocardiographic separation, wide and deformed, low amplitude QRS, frequency 20 ~ 30 beats / min, does not produce myocardial mechanical contraction;

3. The ventricle is still, showing a straight line without electric waves, or only seeing the atrial wave. Ventricular fibrillation remained unresolved for more than 4 minutes, almost all of which turned to ventricular quiescence.



1. Loss of consciousness.

2. The carotid artery and femoral artery beat and the heart sound disappeared.

3. Sighing breath, if you can not restore blood circulation urgently, stop breathing soon.

4. The pupils are scattered and the light reflection is weakened and disappeared.




1. Initial and second phase recovery


(1) Restoring effective blood circulation

① Immediate chest compressions. The main point is: the patient is supine, the back is placed on the ground or the hard board is placed on the back. The surgeon's palms are overlapped, and the elbows are straight. The shoulders are pressed vertically to press the middle and lower 1/3 of the sternum of the patient, and the lower part of the sternum is subsided by about 4 cm. The frequency is 70 to 80 beats / min.

② ECG monitoring, if it is ventricular fibrillation, it is DC asynchronous defibrillation.

③ Adrenaline: First intravenous injection, if you do not have time to establish a venous access, you can inject intracardiac or tracheal injection.

④ If it is difficult to defibrillate for a while, or defibrillation once, do not repeat the law, you can choose amiodarone, lidocaine, bromide or procainamide intravenously, drug defibrillation and electric defibrillation at the same time, Can improve the success rate of recovery.

⑤ If the ventricle is still at the time of ECG monitoring, isoproterenol can be added intravenously, and it can be repeated after 3 minutes.

⑥ If the ventricular still medication is ineffective, the chest external pacing is performed as soon as possible, or the temporary pacing is performed through the vein.

⑦ Resuscitation is still ineffective for 20 minutes, can open the chest and press the heart, and continue to use the drug until hopeless.


(2) Immediately evacuate the airway and artificial respiration when the breathing stops.

① Put the patient's head back, raise the lower jaw, and remove the foreign body in the mouth.

② Tight interface to the mouth artificial respiration, to pinch the patient's nostrils when blowing, such as the patient's teeth closed tightly, deliciously blowing the nose, so that the patient's chest is raised effectively, blowing 12 to 16 times per minute, artificial respiration and chest Cardiac compression is performed alternately at 1:5 or 2:10. 3 oxygen. If the spontaneous breathing is not resumed in 415 minutes, mechanical ventilation should be used for tracheal intubation as soon as possible, instead of using respiratory stimulants, so as not to increase the oxygen consumption of the brain or cause convulsions.

(3) Correction of acidosis

Because the main cause of acidosis during cardiac arrest is hypoperfusion and CO 2 accumulation, a large amount of intravenous sodium bicarbonate can increase tissue CO 2 , blood over-alkali, Hb oxygenation curve shifts left, oxygen release is inhibited, and tissue loss is aggravated Oxygen inhibits myocardial and brain cell function, causes high sodium and hyperosmotic state, and reduces the success rate of resuscitation. Therefore, it is best not to use it before establishing stable blood circulation and effective ventilation.

If a patient with cardiac arrest occurs outside the hospital, a freehand resuscitation operation should be performed on the spot, and as soon as possible, try to escort to a nearby medical unit for a second-stage resuscitation.

2. Recovery recovery

Cardiac arrest first aid

(1) Maintain blood circulation Cardiac resuscitation often has hypotension or shock. Blood volume should be appropriately supplemented and vasoactive drugs should be used to maintain blood pressure at normal levels.

(2) Maintain effective ventilation function Continue to inhale oxygen. If the spontaneous breathing has not recovered, you can continue to use the artificial ventilator; if the spontaneous breathing is restored but not stable and stable, you can use respiratory stimulants, such as nikethamide, sylvestre or sulphate or intravenous drip; Actively prevent respiratory infections.

(3) ECG monitoring found that arrhythmia is handled as appropriate.

(4) Active brain resuscitation If the cardiopulmonary resuscitation takes a long time, the brain function will be damaged to varying degrees, manifested as disturbance of consciousness, leaving mental and activity abilities, and even forming vegetative, so brain resuscitation is the focus of the later period. 1 If the disturbance of consciousness is accompanied by fever, the head ice cap should be cooled; if the blood pressure is stable, artificial hibernation can be performed, and chlorpromazine and promethazine are usually administered intravenously or intramuscularly. 2 prevention and treatment of cerebral edema: dehydration agent, adrenal glucocorticoid or albumin. 3 improve brain cell metabolism drugs: such as ATP, coenzyme A, cerebrolysin, citicoline and so on. 4 oxygen radical scavenger. 5 hyperbaric oxygen chamber treatment.

(5) Protecting kidney function Closely observe urine volume and serum creatinine to prevent acute renal failure.

3. First aid measures

Rescue of cardiac arrest must be race against time. Never wait for an ambulance to arrive at the hospital for treatment. Take the following first-aid measures to take the cardiopulmonary resuscitation.

(1) chest compression, one hand holds the patient's neck and then lifts up, while the other hand presses the patient's forehead and pushes it backwards, so that the lower jaw is upturned and the head is reclined, which is good for ventilation. Do chest compressions. Have the patient back a hard board and do mouth-to-mouth resuscitation. Observe the patient's pupil. If the pupil is narrowed down (the most sensitive and meaningful sign of life), the face and lips will turn red, indicating that the rescue is effective.

(2) Acupuncture at the point of the middle of the person or the palm of the hand, the Laogong point and the foot heart Yongquan point, play a rescue role.

(3) Quickly remove the pharyngeal vomit, so as not to block the respiratory tract or pour into the lungs, causing asphyxia and aspiration pneumonia.

(4) The head packs the ice pack to cool down.

(5) rushed to the hospital for treatment.


In patients with successful cardiac arrest and resuscitation, it is important to assess the function of the left ventricle in a timely manner. Compared with patients with normal left ventricular function, patients with left ventricular dysfunction are more likely to have recurrent cardiac arrest, have a poorer response to arrhythmia drugs, and have a higher mortality rate.

Primary ventricular fibrillation in the early stage of acute myocardial infarction is caused by non-hemodynamic abnormalities, and it is easy to obtain cardioversion after timely defibrillation. Prognosis is good in patients with acute inferior myocardial infarction complicated by slow arrhythmia or cardiac arrest caused by ventricular arrest. In contrast, acute extensive anterior wall myocardial infarction with cardiac arrest caused by atrioventricular or internal blockade often has a poor prognosis.

Cardiac arrest secondary to acute large-area myocardial infarction and hemodynamic abnormalities, the immediate mortality rate is 59% to 89%, and cardiac resuscitation is often not successful. Even if the recovery is successful, it is difficult to maintain a stable hemodynamic state.


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