Ventricular Fibrillation in Emergency Medicine Medication
- Author: Keith A Marill, MD; Chief Editor: Erik D Schraga, MD more...
Treatment goals are to electrically terminate ventricular fibrillation (VF) so that an organized electrical rhythm follows and restores cardiac output. Success rates significantly decrease as the duration of ischemia increases. Drug therapy to facilitate defibrillation may consist of vasopressors, antidysrhythmics, electrolytes, and other agents.
The theoretical benefit of vasopressor medicines, such as epinephrine and vasopressin, is that they increase coronary perfusion pressure. Coronary perfusion pressure is the difference between aortic and right atrial pressure during the relaxation phase of CPR, and it determines myocardial blood flow. Higher levels of coronary perfusion pressure are associated with increased survival in animal models of VF arrest.
Vasopressors, such as epinephrine, increase coronary perfusion pressure; however, no vasopressors have been proven to increase survival in humans. Nevertheless, they are recommended due to possible benefit. Epinephrine, 1 mg, is recommended every 3-5 minutes once IV or IO access is established, and vasopressin, 40 units, may be administered once instead of the first or second epinephrine dose. Higher doses of epinephrine, 0.1-0.2 mg/kg, have been studied, but they are not clearly beneficial compared with the standard 1-mg dose. Recent data suggest no synergistic effect of administering vasopressin in addition to epinephrine.[34, 35]
Antidysrhythmic agents are recommended when initial defibrillation and vasopressor medicines fail or after successful defibrillation to prevent recurrence. Potential benefits of antidysrhythmic therapy include lowering the threshold for defibrillation and preventing immediate or delayed VF recurrence. Potential risks of antidysrhythmic therapy include hypotension due to decreased myocardial contractility or vascular tone, bradycardia, or asystole. No antidysrhythmic agent has been proven to improve survival to hospital discharge from VF arrest, but amiodarone may increase the likelihood of at least temporarily regaining a perfusing rhythm.[36, 37]
The mechanism of action of most antidysrhythmic agents is to alter the conductance of ions, such as sodium and potassium, across myocardial cell membrane ion conducting channels. Amiodarone and other Vaughn-Williams class III agents decrease the repolarizing flow of potassium across the cell membrane and cause a prolongation of the depolarized period. The cell is refractory to further excitation during this period and may not be able to conduct the VF waveform, thus breaking the reentrant cycle of excitation. Other class III agents that have been studied in cardiac arrest include bretylium and sotalol, but they have not been consistently shown to provide benefit.[38, 39]
Lidocaine is a Vaughn-Williams class IB agent that alters the depolarizing flow of sodium across the cell membrane and may be particularly effective in an ischemic or acidotic environment. Procainamide is a Vaughn-Williams class IA agent that affects both sodium and potassium flow across the cell membrane and may also rarely be used for refractory or recurrent VF.
Additional alternative medications include magnesium sulfate, propranolol, and sodium bicarbonate. Magnesium may be particularly important in stabilizing the cell membrane and in preventing after-depolarizations that are important in the genesis of torsades de pointes. Propranolol or other beta-adrenergic blocking agents may have a calming effect on the myocardium for patients with recurrent persistent VF often described as VF storm. Bicarbonate is useful to block the effects of tricyclic antidepressant overdose, to treat hyperkalemia that may be causing ventricular dysrhythmias, or to treat acidosis associated with prolonged cardiac arrest.
Augment both coronary and cerebral blood flow present during low-flow state associated with CPR.
Increases coronary perfusion pressure but has not been proven to increase survival in cardiac arrest.
A nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction. Its effects on outcome have not been proven to differ from epinephrine in VF arrest. It may be used instead of the first or second dose of epinephrine during cardiac arrest resuscitation. Since it lasts longer than epinephrine, vasopressin is used only once.
These agents alter electrophysiologic mechanisms responsible for dysrhythmia.
Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.
Acute actions after IV bolus are to inhibit AV conduction and prolong the AV refractory period; IV amiodarone usually causes a decrease in systemic vascular resistance with coronary and peripheral vasodilatation and variable depressant effects on cardiac contractility. Eventually amiodarone lengthens the duration of repolarization (QT interval corrected for pulse rate) and refractory period in most cardiac tissue. Amiodarone improves the return of spontaneous circulation from VF arrest by uncertain mechanisms, but it has not been shown to improve survival to hospital discharge. When administered chronically, multiple other effects occur on adrenergic tone, thyroid function, and other systems.
Class III antidysrhythmic agent previously used for VF refractory to defibrillation, epinephrine, and lidocaine. Bretylium may increase the fibrillation threshold and ventricular myocardial refractory period by decreasing potassium conductance. Has catecholamine-releasing properties and adverse effects and is not used as initial treatment. Currently not commercially available in the United States.
Vaughn-Williams class IA antidysrhythmic that blocks both sodium and potassium conducting channels. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity, and it widens the QRS interval. Procainamide also increases the refractory period of atria and ventricles with associated lengthening of the QT interval. Procainamide is used to treat both supraventricular and ventricular dysrhythmias.
These agents are considered therapeutic alternatives for refractory VF. Patients with persistent or recurrent VF following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia. Among electrolyte abnormalities associated with VF are hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VF secondary to other medications. Magnesium sulfate acts as an antidysrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VF caused by hyperkalemia.
Deficiency in this electrolyte is associated with SCD and can precipitate refractory VF. Magnesium supplementation is used to treat torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.
Only when the patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant, or phenobarbital overdose. Routine use not recommended.
Useful in treatment of hyperkalemia, hypocalcemia, or calcium channel blocker toxicity. Moderates nerve and muscle performance by regulating the action potential excitation threshold.
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