I. Choice of route of drug administration.
Peripheral venous, central venous access
tracheal intubation (sodium bicarbonate is prohibited)
Intracardiac injection (caution, sodium bicarbonate is prohibited)
Second, commonly used drugs
Purpose: ① improve the effect of cardiac compressions, stimulate the heart to resuscitate, enhance muscle contraction; Jieyang City People’s Hospital, Department of Emergency Medicine, Huang Guoliang
②Increase peripheral vascular resistance, increase myocardial blood flow (MBF) and cerebral blood flow (CBF);
③Lower the defibrillation threshold to facilitate defibrillation and/prevent recurrence of VF;
(iv) Correction of acidemia or electrolyte imbalance.
(i) Catecholamines
1. Epinephrine
Epinephrine remains the most frequently used and effective drug during cardiac resuscitation.
Aortic diastolic pressure should be at least 4.0-5.5 kPa (30-40 mmHg) to achieve the coronary perfusion pressure (difference between aortic diastolic pressure and right atrial diastolic pressure) required for cardiac resuscitation. During chest compressions alone, the average aortic diastolic pressure is 1.4-2.0 kPa (10.0 19.6 mmHg).
The α-receptor excitatory effect (increased peripheral vascular resistance) and appropriate β-receptor excitatory effect (increased myocardial contractility and dilated coronary arteries) possessed by epinephrine increase the perfusion pressure generated by compression of the heart. It also stimulates cardiac resumption and enhances cardiac contractility, changing the low-amplitude fine fibrillation waves to high-amplitude coarse fibrillation waves during cardiac fibrillation, which facilitates defibrillation by electric shock.
Recent studies have found that the peak epinephrine pressor response is 2-3 min after the drug is administered, and disappears after 5 min. The original standard dosage (epinephrine 0.5-1.0mg sedation, repeated at 5min) showed little increase in aortic diastolic pressure, so the original standard amount was small and the interval was long. In contrast, epinephrine 0.2mg/kg can increase the aortic diastolic pressure to 5.7kPa (40mmHg), which greatly improves the recovery rate of autonomic circulation. Early use of high-dose epinephrine is now commonly advocated. Early application of high-dose epinephrine improves survival, while late use only improves the rate of recovery of autonomic circulation and does not improve survival. The first dose of epinephrine 1mg (adult amount) diluted in 1ml or 10ml was administered by sedation and repeated after 5min. Some authors have reported epinephrine doses of up to 55 mg throughout CPR.
However, other authors have suggested that high-dose epinephrine only increases the rate of recovery of autonomic circulation and is not related to survival. In addition, epinephrine increases intrapulmonary shunts, decreases end-expiratory partial pressure of carbon dioxide, decreases arterial partial pressure of oxygen and increases partial pressure of carbon dioxide, and epinephrine can exacerbate the imbalance of myocardial oxygen supply and demand, leading to myocardial systolic band necrosis.
It is believed that simple excitation of a receptor methotrexate is superior to epinephrine.
2.Cardiovascular drugs
Norepinephrine: The incidence of arrhythmias after defibrillation is high and should not be routinely used in CPR, but can be used as intravenous drip to increase peripheral vascular resistance and increase arterial pressure (MAP).
Isoprenaline: It does not have beneficial effects such as increasing MBF, and can be reserved for use after cardioversion.
The old “old triad” (epinephrine, norepinephrine, isoprenaline) has long been abandoned. The “new triad” (epinephrine, lidocaine, atropine) is advocated.
Atropine has the ability to reduce myocardial vagal tone, accelerate the speed of sinus node excitation impulses and improve atrioventricular conduction. It is effective in sinus bradycardia, especially for those with severe sinus bradycardia combined with hypotension, low tissue perfusion or combined with frequent premature ventricular contractions.
Lidocaine can inhibit the ectopic excitation of the ventricle, especially the ventricular arrhythmia caused by reflex excitation during myocardial ischemia, and also can improve the threshold of ventricular fibrillation; the application of lidocaine can not only reduce the occurrence of ventricular fibrillation, but also create favorable conditions for electric shock defibrillation, which itself also has defibrillation effect.
(ii) Calcium.
Calcium should be used with caution: high plasma Ca2+ concentration and excessive intracellular Ca2+ load can put the myocardium and vascular smooth muscle in a spastic state, increasing the chance of forming a “stone heart” and possibly aggravating reperfusion injury in the brain.
The indications are limited to hyperkalemia, low (free) calcium state (after massive application of ACD anticoagulation) or calcium channel blocking erythrotoxicity, and other conditions causing pacing weakness.
(iii) Alkaline drugs.
After ischemia and hypoxia, lactic acid, a product of anaerobic alcoholysis, is increased and “washout acidosis” (washout acidosis) is produced after the microcirculation is restored to perfusion. The lactic acid formed in excess can be buffered to form lactate (L-) and H2CO3, the former does not affect pH, and the latter dissociates quickly into H2O and CO2 (physically dissolved). Since HCO3- is consumed by buffering lactate, NaHCO3 should be used to increase plasma [HCO3-].
According to the principle of “acid-base balance”, alkaline supplementation should be done carefully to avoid medical alkalemia, which is more harmful to the organism. Alkalemia does not improve the success rate of defibrillation and ultimate survival rate; alkalemia shifts the oxygen dissociation curve of hemoglobin to the left and inhibits oxygen release from hemoglobin; HCO3- dissociated from NaCO3 can combine with H+ to produce large amount of CO2, which can freely pass the blood-brain barrier and cell membrane and enter brain and cardiac muscle cells to form “paradoxical” intracellular acidosis; alkalemia shifts K+ from extracellular to intracellular and causes hypokalemia. This can lead to hypokalemia, which can endanger the heart in severe cases.
III. Defibrillation by electric shock
1.Electrical shock defibrillation mechanism
Electrical defibrillation is to shock the heart with a certain amount of electric current, so that all the myocardium is depolarized at the same time in the instant and is in the non-phase, which inhibits the ectopic excitation foci and creates conditions for the normal pacing point to retransmit the impulse and restore the normal rhythm and effective heartbeat, thus aborting ventricular fibrillation.
Early defibrillation with alternating current. Alternating current excites the sympathetic nervous system and predisposes to tachyarrhythmias after defibrillation. Nowadays, DC defibrillators are mostly used, which have the advantages of strong electrical energy release, short discharge time, small total electrical energy consumption, lighter muscle contraction, less body heat production, and easy portability. However, it has the effect of excitation of parasympathetic nerve, after defibrillation may have a transient chronic arrhythmia or atrioventricular block.
2.Timing of defibrillation
The current view is that early defibrillation is desirable. As long as the defibrillation conditions are available, blind defibrillation can be performed if necessary. If defibrillation can be performed within 3 min of the onset of ventricular fibrillation, 70% to 80% of patients will recover adequate perfusion heart rate.
Timing: ①Ventricular fibrillation or cardiac arrest can be defibrillated immediately within 2 min of detection;
If cardiac arrest is not detected in time, defibrillation is performed within 2 min of basic life support ABC.
Ventricular fibrillation is divided into coarse fibrillation and fine fibrillation. In the former, the ECG shows higher voltage ventricular fibrillation waves with wider amplitude and coarse peristalsis of the myocardium visible to the naked eye when the chest is opened; in the latter, the ECG waveform is more subtle and the myocardium peristalsis is weak. In any case, if the fine fibrillation cannot be changed into coarse fibrillation, defibrillation is ineffective.
Drugs (lidocaine, bromobenzyme, quinidine and β-blockers) can prevent VF or VT, but once it occurs, it is impossible to terminate it with drugs alone, and too much of them may turn the heart into an uncontrollable nonpulsatile state. Therefore, lidocaine, for example, should only be used in moderation to alter the ventricular fibrillation threshold and as an adjunct to defibrillation. In any case, electrical defibrillation is the most effective method for the treatment of coarse fibrillation.
IV. Cardiac pacing
A pacemaker is an instrument that excites myocardial contraction with artificial electrical stimulation. Epicardial or endocardial stimulation pacing can be used. In cases of bradycardia (including sinus bradycardia and third-degree AV block) combined with hypotension, a pacemaker is recommended if a fast heart rate can be maintained with atropine and isoprenaline.
V. Monitoring of CPR
Effective monitoring during CPCR can identify problems and deal with them in time to improve the success rate of CPCR.
1.Direct arterial pressure monitoring
2.Exhaled unexpired CO2 concentration (ETCO2) monitoring
3.Pulse oxygen saturation (SpO2) or transdermal partial pressure of oxygen (tcPO2)
4.Invasive or non-invasive hemodynamics
5.Non-invasive cerebral oxygen saturation