Heart Rhythm Disorders

The primary function of the heart is to supply blood and nutrients to the body. The regular beating, or contraction, of the heart moves the blood throughout the body. Each heartbeat is controlled by electrical impulses traveling through the heart. In the normal heart these electrical impulses occur in regular intervals. When something goes wrong with the heart’s electrical system, the heart does not beat regularly. The irregular beating results in a rhythm disorder, or arrhythmia.
The electrical system regulating heartbeat consists of 2 main areas of control and a series of conducting pathways, similar to the electrical wiring in a house (See Multimedia File 1).
The sinoatrial, or SA, node is located in the right atrium. It provides the main control and is the source of each beat. The SA node also keeps up with the body's overall need for blood and increases the heart rate when necessary, such as during exercise, emotional excitement, or illness such as fever. The SA node is sometimes called the "natural pacemaker" of the heart.
Electrical impulses leave the SA node and travel through special conducting pathways in the heart to the other controller, the atrioventricular, or AV, node. The purpose of the AV node is to provide a pathway for impulses from the atria to the ventricles. It also creates a delay in conduction from the atria to the ventricle. This causes the atria to contract first and allow the ventricles to fill with blood before they contract themselves.
The delay ensures proper timing so that the lower chambers have time to fill completely before they contract.
Normally, the heart beats 60-100 times a minute. This state is called "normal sinus rhythm" or "normal rhythm." Depending upon the needs of the body, it may beat faster (sinus tachycardia) due to stress or slower (sinus bradycardia) such as during sleep.
Arrhythmias
Arrhythmias are abnormalities of the heartbeat. There are many types of arrhythmias, and they are classified by where they begin, (the atria, AV node, or the ventricles). Generally speaking, those that do not originate from the ventricles are called supraventricular arrhythmias while those that come from the ventricles are called ventricular arrhythmias.
The following are some of the more commonly encountered arrhythmias, starting with the supraventricular arrhythmias.
Premature atrial contractions, sometimes called PAC or APC, or premature supraventricular contractions: Another part of the atria sends an electrical impulse soon after the previous beat, causing the heart to contract earlier than expected. This is a very common occurrence in all ages and usually is not serious.
Supraventricular tachycardia, or paroxysmal SVT: Occurs when any structure above the ventricle (usually the atria or the AV node) produces a regular, rapid discharge.
Sick sinus syndrome: Irregular firing by the SA node causes a slower-than-normal heart rate (sometimes alternating with rapid heart rates).
Atrial fibrillation: A common condition caused by electrical impulses discharged at a rapid rate from many different areas of the atria. It usually causes a fast and irregular heartbeat.
Atrial flutter: A condition caused by a rapid discharge from a single place in the right atrium. Typically, the right atrium fires at a rate of 300 beats per minute, but only every other beat is conducted through the AV node, meaning that the ventricular rate is classically 150 beats per minute.
Arrhythmias arising in the ventricle are more likely to be found in people with more serious heart disease but may also be found in healthy individuals.
Premature ventricular complex, or PVC: This electrical impulse starts in the ventricle causing the heart to beat earlier than expected. Usually, the heart returns to its normal rhythm right away.
Ventricular tachycardia: Fast and usually regular impulses come from the ventricles and cause a very rapid heart rate. This is usually a life-threatening tachycardia and needs immediate medical attention, possibly electrical shock or defibrillation.
Ventricular fibrillation: Electrical impulses arise from the ventricles in a fast and disordered sequence. The resulting uncoordinated contractions cause the heart to quiver (appearing like a bag of worms) and lose the ability to beat and pump blood, leading to immediate cardiac arrest.
Arrhythmias can be frightening, but in many cases, especially in younger patients with normal underlying hearts, they are not life threatening and can be effectively treated with medications.
Supraventricular arrhythmias are very common in middle-aged and elderly adults. The older you get, the more likely you are to experience an arrhythmia, especially atrial fibrillation.
Many supraventricular arrhythmias are temporary and not serious, especially if no underlying heart disease is present. These arrhythmias are a response to normal activities or emotions.
Even if an arrhythmia has a serious underlying cause, the arrhythmia itself may not be dangerous. The underlying problem can often be treated effectively.

Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm (AIVR) is a form of ectopic or automatic ventricular arrhythmia usually noted in the acute care setting during cardiac rhythm monitoring. This condition is characterized by a ventricular rate that is slower than traditionally defined ventricular tachycardia (VT). Generally, the heart rate is less than 100 beats per minute (bpm), but some authors have used heart rate less than 120 bpm. It is often, but not always, slightly faster than the underlying sinus rhythm; therefore, the ventricular rate takes over as the predominant rhythm.
AIVR may also be defined as an ectopic rhythm with 3 or more consecutive premature ventricular beats and a rate faster than the normal ventricular intrinsic escape rate of 30-40 bpm but slower than VT.
AIVR is an electrocardiographic diagnosis and does not generally produce any particular symptoms. Making a correct diagnosis remains one of the most important concerns because the usual treatments for patients with the more common form of ventricular arrhythmia, such as VT, may not apply.
Pathophysiology
Enhanced automaticity appears to be the likely electrophysiologic mechanism behind the genesis of AIVR. Enhanced automaticity generally is ascribed to phase-4 depolarization of the action potential of the myocardial cell. AIVR can occur in the His-Purkinje fibers or myocardium under certain abnormal metabolic conditions.
AIVR arises from subordinate or second-order pacemakers and manifests itself when the patient's prevailing sinus rate becomes lower than the accelerated rate (AIVR) of the otherwise suppressed focus. Sinus bradycardia combined with enhanced automaticity of the subordinate site is the common pathophysiology.
Several conditions, including myocardial ischemia (especially inferior wall ischemia or infarction), digoxin toxicity, electrolyte imbalance (eg, hypokalemia), and hypoxemia may accentuate the phase-4 depolarization in the subordinate pacemaker tissues of the atrioventricular (AV) junction or His-Purkinje system, thus increasing the rate of impulse generation. Frequently, when inferior wall ischemia is present, the subordinate pacemaker acceleration coexists with sinus node depression. The latter permits escape and domination of the pacemaker function, which may occur with AV junctional or ventricular rates of only 60-70 bpm. The ectopic mechanism also can begin after a premature ventricular complex or, as described above, when the ectopic ventricular focus simply can accelerate sufficiently enough to overtake the intrinsic rhythm.
The onset of AIVR is gradual (nonparoxysmal). The ventricular rhythm can be regular or irregular and, occasionally, can show sudden doubling, suggesting the presence of exit block. The ventricular rate, commonly 60-110 bpm, usually stays within 10-15 beats of the sinus rate; therefore, the control of the cardiac rhythm occasionally passes back and forth between these 2 competing pacemaker sites.
Fusion beats often develop at the onset and termination of arrhythmia, which occurs when the pacemakers are competing for control of ventricular depolarization. Because of the slow rate, capture beats also are common. Due to the slow rate and nonparoxysmal onset, precipitation of more rapid ventricular arrhythmias rarely is observed. Rhythm termination generally occurs gradually, while the underlying sinus rhythm accelerates or the AIVR slows down.
Accelerated idioventricular rhythm in the reperfusion era
Ever since the beginning of the thrombolytic era, the occurrence of AIVR in patients with acute MI has been considered a specific marker of successful reperfusion following the infusion of the lytic agents.
Whether such association exists with reperfusion through direct percutaneous coronary intervention was investigated in a recent study of 125 consecutive patients undergoing direct percutaneous coronary intervention for a first acute MI. 24-hour Holter monitoring revealed that AIVR appeared in 15.2% of the patients. The incidence of AIVR was not different between patients with TIMI grade 2 flow and those with TIMI grade 3 flow (13% vs 16%). No differences were reported in the incidence of major cardiac events within 12-month follow-up in patients with and without AIVR. However, AIVR was associated with higher vagal tone and lower sympathetic activity, the occurrence of AIVR had no prognostic impact on the clinical course and was not able to discriminate between complete and incomplete reperfusion following percutaneous coronary intervention.