The role of pharmacologic therapy during ACLS
The immediate goals of pharmacologic therapy are to improve myocardial blood flow, increase ventricular inotropy, and terminate life-threatening arrhythmias, thereby restoring and/or maintaining spontaneous circulation.
Combined a/b-adrenergic agonists, such as epinephrine, and smooth-muscle V1 agonists, such as vasopressin, augment the mean aortic-to-ventricular end-diastolic pressure gradient (coronary perfusion pressure) by increasing arterial vascular tone.
Phenylephrine and norepinephrine also increase arterial pressure and myocardial blood flow, but neither has been shown to be superior to epinephrine.
Of note, recent data have shown that vasopressin plus epinephrine may be advantageous over epinephrine alone when comparing patients’ survival rates to hospital discharge and residual neurologic deficits.
None of the studies reached statistical significance.
In addition to improving or maintaining myocardial blood flow, pharmacologic therapy during ACLS is also aimed at terminating or preventing arrhythmias, which can further damage an already severely ischemic heart.
VT and VF markedly increase myocardial oxygen consumption at a time when oxygen supply is tenuous because of poor delivery.
Intracellular acidosis only causes the myocardium to be more dysfunctional and irritable, which makes the heart more vulnerable to arrhythmias.
Amiodarone, a class III antiarrhythmic agent, has become the drug of
choice for the treatment of the majority of life-threatening arrhythmias.