In-hospital Cardiopulmonary Resuscitation during Asystole: Conclusion
The direct px activity of norepinephrine results in a stimulation of myocardial contractility, which may be further enhanced by the presence of atropine, which would diminish increases in reflex vagal tone. In the case of the profoundly hypotensive patient undergoing CPR, the net result is an increase in systemic blood pressure and cardiac output, and improvement in venous return. As an indirect effect of the hemodynamic action of norepinephrine, coronary blood flow and thus oxygen supply to the myocardium would be improved. Once cardiac activity has been reestablished, norepinephrine then serves to maintain cardiac function and output and to increase tissue perfusion pressure. Unfortunately, catecholamines, such as norepinephrine, may enhance pacemaker activity of ectopic pacemakers as well as decrease overdrive suppression, the net result being an increase in the automaticity of ectopic foci.
Lidocaine is a class 1 antiarrhythmic drug that is thought to act by decreasing the inward flux of sodium during cardiac membrane depolarization. This results in a decrease in the rate of rise of phase 0 depolarization and the “overshoot” of the action potential, and subsequently the speed of impulse conduction is decreased. This latter effect may help to convert a unidirectional block into a bidirectional block, thus interfering with the propagation of reentrant arrhythmias. Furthermore, lidocaine has the ability to suppress abnormal automaticity. This effect would help to offset the deleterious effects of norepinephrine on ectopic foci and would help the sinoatrial node to be the dominant pacemaker, thus exerting overdrive suppression on the other potential abnormal automatic sites. Source
Moreover, unlike some of the other antiarrhythmic agents, at therapeutic concentrations, lidocaine exerts minimal effects on peripheral vascular resistance, arterial pressure, myocardial contractility, and cardiac output. This combination of factors would seem to indicate that lidocaine may be a preferred agent to add to the regimen of a patient receiving CPR if IV infusion of norepinephrine, for maintenance of cardiac function and output, is going to be instituted. This idea is supported by the data analyses which suggest that the combination of norepinephrine and lidocaine was the most effective treatment for asystole.
It appears that the addition of norepinephrine and lidocaine to the treatment regimen recommended by the AHA for in-hospital arrests characterized by asystole (epinephrine and atropine) may result in improved 24-h survival. While the small sample size prohibits statistical analysis, it is noteworthy that 25 percent (three of 12) of those patients who received the entire sequence were discharged. Though not statistically significant, it is noteworthy that patients who arrested in the ICUs had a somewhat higher survival rate, indicating the benefits of intensive monitoring and immediate initiation of CPR. Prospective studies are needed in which experimental variations with these treatment modalities can be compared and validated in large samples and various hospital locations.