Pulseless ventricular tachycardia (VT) should be treated in the same manner as ventricular fibrillation (VF) and thus defibrillation should be performed immediately. Currently, most defibrillator units feature a biphasic waveform, using lower energies (120-150 Joules depending on the specific waveform employed) as compared to monophasic waveform defibrillation with a series of stacked progressively increasing energy shocks starting at 200 and ending at 360 Joules. Chest compressions should also be immediately initiated if access to a defibrillator is delayed. Airway management including bag mask ventilation followed by endotracheal intubation should occur simultaneously during this time. Airway management and intubation should not be allowed to delay defibrillation therapy, however. If spontaneous circulation does not return after initial defibrillation, followed by chest compressions, a second defibrillation is administered and pharmacologic interventions should begin.
Epinephrine 1 mg is administered intravenously followed by 2 minutes of chest compressions to allow the medication to access the circulation. Epinephrine’s benefits include enhanced cerebral and myocardial blood flow, vasoconstriction, and increased peak aortic and coronary perfusion pressures. Epinephrine can be readministered every 3-5 minutes as long as cardiac arrest continues. If intravenous access is limited or absent, epinephrine can be administered via endotracheal tube in a dose of 2-2.5 times that of the intravenous dose.
Vasopressin has been added to the treatment options for pulseless VT/VF based on its ability to improve perfusion of vital organs during cardiac arrest. Vasopressin acts in direct stimulation of V1 receptors on smooth muscle, thus producing constriction leading to improvements in coronary perfusion pressure. Vasopressin has a longer half-life than epinephrine and as such a one-time dose of 40 units is given during resuscitative efforts.
If pulseless VT or VF persist, antiarrhythmic medications may be considered. These include lidocaine and amiodarone. Amiodarone is preferred as a 300 mg dose and causes prolongation of cardiac action potentials and refractory period. Sodium bicarbonate can be considered if there is metabolic acidosis, an overdose of tricyclic antidepressant medications or hyperkalemia. There is no positive outcome benefit for using sodium bicarbonate and in fact it may worsen acidosis through its role in production of carbon dioxide and increasing plasma osmolality.