Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia encountered in clinical practice. It is estimated that AF affects over 3 million adults in the United States, with prevalence increasing with age.1 Overall AF prevalence is around 1-2% in adults under 60 years old but rises to nearly 10% in those over 80 years. AF is characterized by rapid and disorganized electrical activation of the atria, leading to ineffective atrial contraction. This results in an irregularly irregular ventricular response as impulses conduct variably through the AV node. Hemodynamic consequences include loss of atrial kick, irregular ventricular filling, and potential for tachycardia-mediated cardiomyopathy. AF may be classified as first detected, paroxysmal, persistent, or permanent based on duration of arrhythmogenic episodes.
Supraventricular tachycardia (SVT) is a generic term that refers to any abnormally rapid heart rhythm that originates above the bundle of His in the conduction system. It is characterized by a sudden onset and termination of a regular, narrow QRS complex tachycardia. The heart rate during SVT is typically between 150-250 beats per minute. SVT is caused by either abnormal automaticity, triggered activity, or reentry. The most common mechanisms of SVT are atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) involving an accessory pathway. Other less common forms include atrial tachycardia, sinus node reentrant tachycardia, and intra-atrial reentrant tachycardia.Both utilize a reentrant circuit that allows rapid activation of the atria and ventricles. AVNRT involves reentry within the AV node, while AVRT involves an accessory pathway that connects the atria and ventricles outside of the AV node. This chapter will focus specifically on AV nodal reentrant tachycardia.
Monomorphic ventricular tachycardia (MVT) and polymorphic ventricular tachycardia (VT) are abnormal heart rhythms that demand attention. MVT is characterized by fast, regular ventricular contractions originating from one ventricular focus, and it poses significant risks such as hemodynamic instability, syncope, sudden cardiac death, or progression to ventricular fibrillation. It affects approximately 100,000 people annually in the U.S. and often signals underlying heart conditions like myocardial infarction, cardiomyopathy, arrhythmogenic right ventricular dysplasia, or long QT syndrome. Clinical pharmacists play a crucial role in identifying MVT on ECG, aiding in antiarrhythmic medication selection, monitoring for efficacy and side effects, and educating patients for improved outcomes. In contrast, polymorphic VT, although less common than MVT, is a highly unstable and life-threatening heart rhythm disorder characterized by irregular, rapid ventricular beats, commonly associated with sudden cardiac death, particularly exemplified by torsades de pointes. Polymorphic VT arises in the presence of underlying heart diseases, electrolyte imbalances, drug toxicity, or channelopathies affecting myocardial repolarization. Clinical pharmacists are instrumental in recognizing polymorphic VT on ECG, comprehending its mechanisms, and facilitating appropriate pharmacological interventions to prevent progression to ventricular fibrillation and cardiac arrest. Prompt recognition and intervention are pivotal in both MVT and polymorphic VT cases to ensure better patient outcomes.