I. Origin of the Heartbeat
II. Palpitations, Premature Beats, and Irregular Beats
III. Tachycardia
IV. Antiarrhythmic Agents
V. Automatic Implantable Cardioverter Defibrillator VI. Conclusion

GLOSSARY
action potential voltage changes generated across the membrane of a nerve or muscle cells when the cell is activated through a variety of stimuli (electrical, chemical, or mechanical).
automaticity the ability to generate a spontaneous action potential.
cardiomyopathy heart muscle disease.
myocardial infarction death of an area of heart muscle due to blockage of a coronary artery by blood clot and atheroma; medical term for a heart attack or coronary thrombosis.
myocardium the heart muscle.
Purkinje fibers the terminal branches of the cardiac conducting system that run along the subendocardium.
ventricular fibrillation the heart muscle does not contract but quivers, therefore there is no heartbeat (cardiac arrest); no blood is pumped out of the heart and death occurs within minutes if the abnormal heart rhythm is not corrected.

• I. ORIGIN OF THE HEARTBEAT
  Arrhythmia is the term used for an irregularity or rapidity of the heartbeat or an abnormal heart rhythm. The patient experiences the sensation as stronger, more forceful, or rapid heartbeats, or skipping of beats; this sensation is commonly called palpitations. The sinus node, a very small group of specialized cells, is located in the upper right corner of the heart (see Fig. 1). The node is about 30 x 3 mm thick. Through its genetic code and the influx
• II. PALPITATIONS, PREMATURE BEATS, AND IRREGULAR BEATS
  A. Definition
• III. TACHYCARDIA
  This is the term used by the medical profession to describe a fast heart rate of greater than 100 per minute. Tachy¬cardias include:
• IV. ANTIARRHYTHMIC AGENTS
  Figure 11 illustrates how myocardial cells generate an action potential in phase zero through a fast influx of sodium ions into cells. This increases the resting potential and voltage of the cell (depolarization). During phase three the cell returns to its resting potential with an efflux of potassium ions. Some antiarrhythmic agents produce their effects by decreasing the rate at which sodium enters the myocardial cell during phase zero. Thus, generation of the action potential of an abnormal impulse is dampened and does not reach sufficient magnitude to produce abnormal beats. Quinidine, disopyramide, procainamide, flecainide, and propafenone decrease the rate at which sodium enters myocardial cells. Beta-adrenergic blocking agents, lido-caine, and several antiarrhythmic agents decrease the rate of automaticity of abnormal rhythms by depressing phase four of the action potential (as indicated by the arrow in Fig. 3). Amiodarone and a unique beta-blocker, sotalol, cause prolongation of the action potential (phase two) and retard the generation of an abnormal impulse. Most important, an increase in the absolute refractory period(phases one and two), protects the heart from dangerous impulse stimuli. During a 20–30 ms vulner¬able period in phase three a strong electrical stimulus or ventricular ectopic beat can readily trigger ventricular tachycardia and ventricular fibrillation.
• V. AUTOMATIC IMPLANTABLE CARDIOVERTER DEFIBRILLATOR
  When life is severely threatened by the recurrence of abnormal heart rhythms that have caused cardiac arrest or recurrent sustained ventricular tachycardia, the auto¬matic implantable cardioverter defibrillator can play a role in the health of selected patients. Recent advances in this area allow a ray of hope. Dr. Saksena in New Jersey has introduced a nonsurgical technique for implanting the automatic cardioverter defibrillator. Clinical trials have shown this to be highly successful.
• VI. CONCLUSION
  We have a long way to go in the management of simple premature beats, more complex extra beats, ventricular tachycardia, and the prevention of ventricular fibrillation, which is the cause of death in many heart patients. Questions still to be answered include the following:
• BIBLIOGRAPHY
  ACC AHA/ESC Guidelines for the management of patients with supraventricular arrhythmias — Executive summary. J. Am. Coll. Cardiol., 42:1494–1529, 2003

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