Ventricular escape beat

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Animation illustrating the normal activation of the electrical conduction system of the heart: starting from the sinoatrial node, an electrical impulse spreads across the atria, then passes through the atrioventricular node (AV node) and conducts on via the bundle branches towards the ventricles. ECG Principle fast.gif
Animation illustrating the normal activation of the electrical conduction system of the heart: starting from the sinoatrial node, an electrical impulse spreads across the atria, then passes through the atrioventricular node (AV node) and conducts on via the bundle branches towards the ventricles.

In cardiology, a ventricular escape beat is a self-generated electrical discharge initiated by, and causing contraction of the ventricles of the heart; normally the heart rhythm is begun in the atria of the heart and is subsequently transmitted to the ventricles. The ventricular escape beat follows a long pause in ventricular rhythm and acts to prevent cardiac arrest. It indicates a failure of the electrical conduction system of the heart to stimulate the ventricles (which would lead to the absence of heartbeats, unless ventricular escape beats occur).

Contents

Causes

Ventricular escape beats occur when the rate of electrical discharge reaching the ventricles (normally initiated by the heart's sinoatrial node (SA node), transmitted to the atrioventricular node (AV node), and then further transmitted to the ventricles) falls below the base rate determined by the rate of Phase 4 spontaneous depolarisation of ventricular pacemaker cells. [1] An escape beat usually occurs 2–3 seconds after an electrical impulse has failed to reach the ventricles. [2]

This phenomenon can be caused by the sinoatrial node (SA node) failing to initiate a beat, by a failure of the conductivity from the SA node to the atrioventricular node (AV node), or by atrioventricular block (especially third degree AV block). Normally, the pacemaker cells of the sinoatrial node discharge at the highest frequency and are thus dominant over other cells with pacemaker activity. The AV node normally has the second fastest discharge rate. When the sinus rate falls below the discharge rate of the AV node, this becomes the dominant pacemaker, and the result is called a junctional escape beat. If the rate from both the SA and AV node fall below the discharge rate of ventricular pacemaker cells, a ventricular escape beat ensues.[ citation needed ]

An escape beat is a form of cardiac arrhythmia, in this case known as an ectopic beat. It can be considered a form of ectopic pacemaker activity that is unveiled by lack of other pacemakers to stimulate the ventricles. Ventricular pacemaker cells discharge at a slower rate than the SA or AV node. While the SA node typically initiates a rate of 70 beats per minute (BPM), the atrioventricular node (AV node) is usually only capable of generating a rhythm at 40-60 BPM or less. Ventricular contraction rate is thus reduced by 15-40 beats per minute. [3]

If there are only one or two ectopic beats, they are considered escape beats. If this causes a semi-normal rhythm to arise it is considered an idioventricular rhythm.[ citation needed ]

The escape arrhythmia is a compensatory mechanism that indicates a serious underlying problem with the SA node or conduction system (commonly due to heart attack or medication side effect), and because of its low rate, it can cause a drop in blood pressure and syncope.[ citation needed ]

Diagnosis

An electrocardiogram can be used to identify a ventricular escape beat. The QRS portion of the electrocardiogram represents the ventricular depolarisation; in normal circumstances the QRS complex forms a sharp sudden peak. For a patient with a ventricular escape beat, the shape of the QRS complex is broader as the impulse can not travel quickly via the normal electrical conduction system. [4]

The first 2.5 seconds show a normal cardiac cycle. This is followed by a period of delayed sinus activity which initiates a takeover response by the ventricular pacemaker cells resulting in a ventricular escape beat. Two escape beats are shown between 5-8 seconds. Ventricular escape beat cardiogram diagram.jpg
The first 2.5 seconds show a normal cardiac cycle. This is followed by a period of delayed sinus activity which initiates a takeover response by the ventricular pacemaker cells resulting in a ventricular escape beat. Two escape beats are shown between 5-8 seconds.

Ventricular escape beats differ from ventricular extrasystoles (or premature ventricular contractions), which are spontaneous electrical discharges of the ventricles. These are not preceded by a pause; on the contrary they are often followed by a compensatory pause.[ citation needed ]

Management

Cilostazol

Third degree AV block can be treated with Cilostazol which acts to increase Ventricular escape rate [5]

Ouabain

Ouabain infusion decreases ventricular escape time and increases ventricular escape rhythm. However, a high dose of ouabain can lead to ventricular tachycardia. [2]

Related Research Articles

Cardiac pacemaker Network of cells that facilitate rhythmic heart contraction

The contraction of cardiac muscle in all animals is initiated by electrical impulses known as action potentials. The rate at which these impulses fire, controls the rate of cardiac contraction, that is, the heart rate. The cells that create these rhythmic impulses, setting the pace for blood pumping, are called pacemaker cells, and they directly control the heart rate. They make up the cardiac pacemaker, that is, the natural pacemaker of the heart. In most humans, the concentration of pacemaker cells in the sinoatrial (SA) node is the natural pacemaker, and the resultant rhythm is a sinus rhythm.

Systole

The systole is the part of the cardiac cycle during which some chambers of the heart muscle contract after refilling with blood. The term originates, via New Latin, from Ancient Greek συστολή (sustolē), from συστέλλειν, and is similar to the use of the English term to squeeze.

Third-degree atrioventricular block Medical condition

Third-degree atrioventricular block is a medical condition in which the nerve impulse generated in the sinoatrial node in the atrium of the heart can not propagate to the ventricles.

Electrical conduction system of the heart Transmits signals generated usually by the sinoatrial node to cause contraction of the heart muscle

The electrical conduction system of the heart transmits signals generated usually by the sinoatrial node to cause contraction of the heart muscle. The pacemaking signal generated in the sinoatrial node travels through the right atrium to the atrioventricular node, along the Bundle of His and through bundle branches to cause contraction of the heart muscle. This signal stimulates contraction first of the right and left atrium, and then the right and left ventricles. This process allows blood to be pumped throughout the body.

Supraventricular tachycardia Abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart. There are four main types: atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff–Parkinson–White syndrome. Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.

Right bundle branch block Medical condition

A right bundle branch block (RBBB) is a heart block in the right bundle branch of the electrical conduction system.

A junctional escape beat is a delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the atrioventricular junction. It occurs when the rate of depolarization of the sinoatrial node falls below the rate of the atrioventricular node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. It is a protective mechanism for the heart, to compensate for the SA node no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so.

Atrioventricular block is a type of heart block that occurs when the electrical signal traveling from the atria, or the upper chambers of the heart, to ventricles, or the lower chambers of the heart, is impaired. Normally, the sinoatrial node produces an electrical signal to control the heart rate. The signal travels from the SA node to the ventricles through the atrioventricular node. In an AV block, this electrical signal is either delayed or completely blocked. When the signal is completely blocked, the ventricles produce their own electrical signal to control the heart rate. The heart rate produced by the ventricles is much slower than that produced by the SA node.

Cardiac cycle

The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, dubbed systole. After emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. A normally performing heart must be fully expanded before it can efficiently pump again. Assuming a healthy heart and a typical rate of 70 to 75 beats per minute, each cardiac cycle, or heartbeat, takes about 0.8 seconds to complete the cycle. There are two atrial and two ventricle chambers of the heart; they are paired as the left heart and the right heart—that is, the left atrium with the left ventricle, the right atrium with the right ventricle—and they work in concert to repeat the cardiac cycle continuously,. At the start of the cycle, during ventricular diastole–early, the heart relaxes and expands while receiving blood into both ventricles through both atria; then, near the end of ventricular diastole–late, the two atria begin to contract, and each atrium pumps blood into the ventricle below it. During ventricular systole the ventricles are contracting and vigorously pulsing two separated blood supplies from the heart—one to the lungs and one to all other body organs and systems—while the two atria are relaxed. This precise coordination ensures that blood is efficiently collected and circulated throughout the body.

Premature atrial contractions (PACs), also known as atrial premature complexes (APC) or atrial premature beats (APB), are a common cardiac dysrhythmia characterized by premature heartbeats originating in the atria. While the sinoatrial node typically regulates the heartbeat during normal sinus rhythm, PACs occur when another region of the atria depolarizes before the sinoatrial node and thus triggers a premature heartbeat. The exact cause of PACs is unclear; while several predisposing conditions exist, PACs commonly occur in healthy young and elderly people. Elderly people that get PACs usually don't need any further attention besides follow ups due to unclear evidence. PACs are often completely asymptomatic and may be noted only with Holter monitoring, but occasionally they can be perceived as a skipped beat or a jolt in the chest. In most cases, no treatment other than reassurance is needed for PACs, although medications such as beta blockers can reduce the frequency of symptomatic PACs.

Parasystole is a kind of arrhythmia caused by the presence and function of a secondary pacemaker in the heart, which works in parallel with the SA node. Parasystolic pacemakers are protected from depolarization by the SA node by some kind of entrance block. This block can be complete or incomplete.

Multifocal atrial tachycardia Medical condition

Multifocal atrial tachycardia (MAT) is an abnormal heart rhythm, specifically a type of supraventricular tachycardia, that is particularly common in older people and is associated with exacerbations of chronic obstructive pulmonary disease (COPD). Normally, the heart rate is controlled by a cluster of cells called the sinoatrial node. When a number of different clusters of cells outside the SA node take over control of the heart rate, and the rate exceeds 100 beats per minute, this is called multifocal atrial tachycardia.

Sinoatrial arrest is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes. Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart, such as the atrio-ventricular junction or the ventricles, begins pacing and restores the heart action. This condition can be detected on an electrocardiogram (ECG) as a brief period of irregular length with no electrical activity before either the sinoatrial node resumes normal pacing, or another pacemaker begins pacing. If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm. If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest. This condition is sometimes confused with sinoatrial block, a condition in which the pacing impulse is generated, but fails to conduct through the myocardium. Differential diagnosis of the two conditions is possible by examining the exact length of the interruption of cardiac activity. If the next available pacemaker takes over, it is in the following order:

Accelerated idioventricular rhythm Medical condition

Accelerated idioventricular rhythm is a ventricular rhythm with a rate of between 40 and 120 beats per minute. Idioventricular means “relating to or affecting the cardiac ventricle alone” and refers to any ectopic ventricular arrhythmia. Accelerated idioventricular arrhythmias are distinguished from ventricular rhythms with rates less than 40 and those faster than 120. Though some other references limit to between 60 and 100 beats per minute. It is also referred to as AIVR and "slow ventricular tachycardia."

Junctional rhythm describes an abnormal heart rhythm resulting from impulses coming from a locus of tissue in the area of the atrioventricular node, the "junction" between atria and ventricles.

Sinoatrial block Medical condition

A sinoatrial block is a disorder in the normal rhythm of the heart, known as a heart block, that is initiated in the sinoatrial node. The initial action impulse in a heart is usually formed in the sinoatrial node and carried through the atria, down the internodal atrial pathways to the atrioventricular node (AV) node. In normal conduction, the impulse would travel across the bundle of His, down the bundle branches, and into the Purkinje fibers. This would depolarize the ventricles and cause them to contract.

An ectopic pacemaker is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart. It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat. Acute occurrence is usually non-life-threatening, but chronic occurrence can progress into tachycardia, bradycardia or ventricular fibrillation. In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node. However, in the instance of either a malfunctioning SA node or an ectopic focus bearing an intrinsic rate superior to SA node rate, ectopic pacemaker activity may take over the natural heart rhythm. This phenomenon is called an escape rhythm, the lower rhythm having escaped from the dominance of the upper rhythm. As a rule, premature ectopic beats indicate increased myocyte or conducting tissue excitability, whereas late ectopic beats indicate proximal pacemaker or conduction failure with an escape 'ectopic' beat.

Junctional ectopic tachycardia Medical condition

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node. In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia or congenital JET.

Arrhythmia Group of conditions in which the heartbeat is irregular, too fast, or too slow

Arrhythmia, also known as cardiac arrhythmia or heart arrhythmia, is a group of conditions in which the heartbeat is irregular, too fast, or too slow. The heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath or chest pain. While most types of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

References

  1. C. Andreasen, et al. (2006) Mosby Elsevier, Mosby's Dictionary of Medicine, Nursing & Health Professions 7th edition, p1951
  2. 1 2 Banka VS, Scherlag BJ, Helfant RH (January 1975). "Contractile and electrophysiological responses to progressive digitalis toxicity". Cardiovasc. Res. 9 (1): 65–72. doi:10.1093/cvr/9.1.65. PMID   1122512.
  3. D.D. Costa, W.J. Brady, J. Edhouse (March 2002), BMJ Publishing Group Ltd., ABC of clinical electrocardiography, British Medical Journal: 324:535-538.
  4. Adams MG, Pelter MM (September 2003). "Ventricular escape rhythms". Am. J. Crit. Care. 12 (5): 477–8. doi:10.4037/ajcc2003.12.5.477. PMID   14503433.
  5. Kodama-Takahashi K, Kurata A, Ohshima K, et al. (April 2003). "Effect of cilostazol on the ventricular escape rate and neurohumoral factors in patients with third-degree atrioventricular block". Chest. 123 (4): 1161–9. doi:10.1378/chest.123.4.1161. PMID   12684307.