The correct answer is B, false. Lidocaine is actually a pure sodium channel blocker and is indicated for the treatment of acute ischemic ventricular arrhythmias.

The correct answer is B, false. All classes of antiarrhythmic drugs are pro-arrhythmic as well as being anti-arrhythmic. For example, reports of torsades de pointes, bradycardia and A-V block are not uncommon. Use of these drugs should be cautious, and decisions made based on the understanding pathology.

The correct answer is A, true. Several studies have indicated that the delivery of less energy causes less myocardial injury and post-resuscitation myocardial dysfunction. Biphasic defibrillators deliver 200 or less joules (instead of the 360 joules delivered by older monophasic defibrillators) because biphasic energy is delivered in two directions instead of the one.

The correct answer is B, false. Adenosine has an ultra rapid alpha-half life. Although it works directly on the sinus and A-V nodes, its effect is typically measured in seconds. Thus, it is not an agent that can provide sustained clinical effects. Further, sinus tachycardia is not an “arrhythmia” per se. Rather, it is almost always caused by underlying issues such as fever, intense pain or hypovolemia. Hence, slowing sinus tachycardia is associated with treatment of the causes with fever reduction, analgesia or volume repletion. If the etiology of a narrow QRS tachycardia is unclear, adenosine is useful in making the differentiation. If after rapid I.V. administration of adenosine, the narrow QRS tachycardia converts back to sinus, a practitioner would be wise to believe sinus tachycardia has been ruled out.

The correct answer is B, false. Although amiodarone has become widely used in the U.S., there are some problems associated with it. First, the onset of action when administering an I.V. can take many hours. Second, the biological half-life is 58 days (range = 15-142 days) creating certain issues if serious complications develop. Further, although the AHA and other groups suggest using amiodarone in refractory ventricular fibrillation, research data shows that its use has no effect on outcome or survival. Another way to state this is: it doesn’t work in refractory VF. Use of this drug should be determined by experienced clinicians with specific training and experience in treating complex arrhythmias.

The correct answer is A, true. Each of the above is true. However, when considering the gravity of each, it is no wonder that survival from a PEA arrest is unlikely. The exception to this statement is of course tension pneumothorax. Any patient receiving positive airway pressure when developing PEA must be ruled out for tension pneumothorax. Treatment is simple: immediate chest decompression. Treating a ruptured aorta or left ventricle is not simple, and is rarely successful.

The correct answer is A, true. Prior to implementation of “early defibrillation” and widespread use of automated external defibrillators, survival from cardiac arrest numbers were disappointing. However, patients shocked out of ventricular fibrillation arrest rapidly have the best statistical outcomes. Although CPR “buys time”, the goal should be rapid defibrillation. When a defibrillator is not indicated in arrest, the survival rates plummet.

The best answer is B, false. CPR does not provide adequate fetal blood flow. Thus, if the arrest was caused by VF (most common mechanism), immediate defibrillation is warranted and proper. If the cause of the arrest is not terminated rapidly, fetal as well as maternal mortality is assured. CPR should be initiated while preparing to defibrillate.

The best answer is A, true. Extensive clinical studies clearly indicate that early administration of aspirin may prevent, or limit infarction size via aspirin’s dramatic anti-platelet actions. In patients without plaque rupture and hemorrhage, there seems to be questionable benefit.