The primary pacemaker of the heart is the sinoatrial (SA) node.1 Electrical impulses generated by the SA node at a normal frequency of 60 to 100 beats per minute spread rapidly through the atria and enter the atrioventricular (AV) node. After a brief delay at the AV node, the impulses continue to propagate over the Bundle of His and converge on the Purkinje system as depolarization progresses over the ventricles in an anatomically synchronous and hemodynamically effective fashion.1 When impulse generation and/or impulse conduction malfunctions, the patient develops cardiac arrhythmias.7
Sinus bradycardia - Impulses originate from the sinoatrial node (SA) at a rate <60 beats per minute under the influence of increased parasympathetic (vagal) tone.1 The rhythm is regular. Sinus bradycardia is common in athletes, in patients with hypothyroidism, in patients with increased intracranial pressure, and during treatment with drugs with negative chronotropic action (e.g., β1-adrenergic receptor antagonists, calcium channel blocking agents, and digoxin). The patient may be asymptomatic or experience weakness, palpitation, chest discomfort, dyspnea, and syncope.
Sinus tachycardia - Impulses originate from the SA node at a rate of 100 to 180 beats per minute under the influence of increased sympathetic tone or vagal blockade.1 The rhythm is regular. Sinus tachycardia is found in patients after exercise or smoking; in patients with hyperthyroidism, anxiety, toxic states, fever, anemia, and acute or chronic heart diseases; and in patients consuming stimulants such as tea, coffee, and medications with positive chronotropic effects (e.g., epinephrine). The patient may be asymptomatic or experience weakness, palpitation, chest discomfort, dyspnea, and syncope.
Atrial flutter - Impulses originate from a single abnormal atrial focus at a rate of 250 to 300 beats per minute.1 The rhythm is regular. Because the pace of atrial firing is rapid, some of the impulses reach the AV node during its refractory period. These impulses are not transmitted to the ventricles, and the ventricular rate is slower than the atrial rate. The ratio of atrial to ventricular firing rate is typically 2:1, i.e., the ventricular rate is between 125-150 beats per minute. The patient may be asymptomatic or experience weakness, palpitation, chest discomfort, dyspnea, and syncope.
Atrial fibrillation - Impulses originate from multiple abnormal atrial foci at a rate of 350 to 450 beats per minute.1 Impulses in the atria travel in a random manner and the rhythm is irregular. The AV node is unable to transmit all of the impulses and the ventricular rate is between 120 to 180 beats per minute. Turbulence and/or stasis of blood in the fibrillating atrium can lead to clot formation. Systemic embolization may lead to stroke or stroke-like illness characterized by sudden confusion: acute, painful, pulseless limbs: and an acute abdomen.
Premature ventricular contractions (PVCs) are characterized by a pronounced pause in an otherwise normal rhythm.1 Impulses originate from an ectopic ventricular focus. PVCs may be an occasional finding in otherwise healthy adults and the incidence increases with age, fatigue, emotional stress, and the use of coffee and tobacco. PVCs are considered benign if fewer than six such pauses are noted per minute. PVCs are significant in a patient with a history of cardiovascular diseases, i.e., ischemic heart disease, valvular disease, hypertension, and congestive heart failure.
Ventricular tachycardia (VT) usually evolves from an ectopic focus in a ventricle, which generates ventricular extrasystoles at a rate of 120 to 220 beats per minute.1 VT occurs in patients with organic heart disease and may be precipitated by drugs such as digoxin and tricyclic antidepressants. A patient with sustained VT is almost always symptomatic experiencing fatigue, palpitation, light-headedness, and syncope. VT is a serious arrhythmia, if left untreated, it may lead to ventricular fibrillation manifested as loss of consciousness and sudden cardiac death.
Ventricular fibrillation (VF) - The heart rate is 350-450 beats per minute and the rhythm is irregular.1 The myocardium depolarizes in a chaotic manner. Coordinated ventricular activity ceases. The heart ceases to pump, the blood pressure falls, and unconsciousness occurs. If left untreated, death will follow in about three to five minutes. CAD-associated ischemia-induced electrical instability of the myocardium is the most common cause of VF and it is the main cause of sudden cardiac death, which occurs most frequently in the first few hours after a MI.
Atrioventricular (AV) blocks are characterized by a delay or failure in impulse conduction from the atria to the ventricles.1 It occurs at three levels: first degree, with a delay in impulse conduction; second degree, with an intermittent failure in conduction; and third degree, with permanent failure in conduction. First degree AV block is usually asymptomatic. Second degree AV block may be asymptomatic or manifest as light-headedness and syncope. Third degree or high-grade AV block is characterized by fatigue, light-headedness, syncope and, if left untreated, leads to HF.
Generally, to restore synchronous myocardial contraction, Class I and Class III antiarrhythmic agents are used to treat both supraventricular tachycardias (SVTs) and ventricular tachycardias (VTs), Class II and Class IV antiarrhythmic agents are used to treat SVTs, and cardiac glycosides such as digoxin are used to treat atrial flutter and atrial fibrillation.7 In addition, antiplatelet drugs and/or anticoagulants are prescribed to prevent thromboembolic complications.9 If pharmacological strategies fail, a patient with cardiac arrhythmias requires a pacemaker or an implanted cardiac defibrillator.