Tachycardia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: M.Umer Tariq [2]

Tachycardia is a form of cardiac arrhythmia which refers to a rapid beating of the heart. By convention the term refers to heart rates greater than 100 beats per minute in the adult patient. Tachycardia may be a perfectly normal physiological response to stress. However, depending on the mechanism of the tachycardia and the health status of the patient, tachycardia may be harmful, and require medical treatment. In extreme cases, tachycardia can be life threatening.

Tachycardia can be harmful in three ways. Firstly, if the heart is pumping too fast for an extended period of time it will change the balance of oxygen and carbon dioxide in the hemoglobin in the blood; this is normal during exercise but when resting this is quite dangerous. Second, when the heart beats too rapidly, it may pump blood less efficiently. Thirdly, the faster the heart beats, the more oxygen and nutrients the heart requires. This may leave patients feeling out of breath or cause angina. This can be especially problematic for patients suffering from ischemic heart disease.

Tachycardias can be classified in a variety of ways. One form of classification is whether it is a wide-complex tachycardia, or whether it is a narrow-complex tachycardia. Another way of classifying tachycardia is whether the rhythm is regular or whether it is irregular. Tachycardia can also be distinguished by type; whether is is a sinus tachycardia, a ventricular tachycardia, a supraventricular tachycardia, or atrial fibrillation.

The body contains several feedback mechanisms to maintain adequate blood flow and blood pressure. If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia. This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The pathophysiology of abnormal tachycardias vary with the type of tachycardia.

Tachycardia can be caused by a wide variety of factors. The most common cause is orthostatic hypotension. Other common causes of tachycardia include endocrine disorders, disorders involving the heart, and situations which cause an excess of catecholamines in the body such as fever and exercise. Various medications and illicit drugs can also cause tachycardia.

Tachycardia is defined as heart rate more than 100 beats per minute and it can be sinus tachycardia, ventricular tachycardia or supraventricular tachycardia. Ventricular tachycardia can be distinguished by broad QRS complexes on an ECG.

Treatment of tachycardia is usually directed at chemical conversion (with antiarrythmics), electrical conversion (giving external shocks to convert the heart to a normal rhythm) or use of drugs to simply control heart rate (for example as in atrial fibrillation). The treatment modality used depends on the type of tachycardia and the hemodynamic stability of the patient.

Surgical methods of treatment for tachycardias include device-based treatment such as the implantation of a permanent pacemaker. There are guidelines on the indications for surgical therapy, depending on the type and severity of the tachycardia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: M.Umer Tariq [2]

Tachycardias can be classified in a variety of ways. One form of classification is whether it is a wide-complex tachycardia, or whether it is a narrow-complex tachycardia. Another way of classifying tachycardia is whether the rhythm is regular or whether it is irregular. Tachycardia can also be distinguished by type; whether is is a sinus tachycardia, a ventricular tachycardia, a supraventricular tachycardia, or atrial fibrillation.

• Atrial fibrillation (Afib)
• Atrial flutter
• Multifocal atrial tachycardia
• Premature atrial contractions (PACs)
• Sick sinus syndrome
• Sinus tachycardia
• Supraventricular tachycardia (SVT)
• Wandering atrial pacemaker

• AV nodal reentrant tachycardia
• AV reentrant tachycardia
  • Wolff-Parkinson-White syndrome
  • Lown-Ganong-Levine syndrome

• Junctional rhythm
• Junctional tachycardia
• Premature junctional complex

• Accelerated idioventricular rhythm
• Premature ventricular contractions (PVC)
• Ventricular tachycardia
• Ventricular fibrillation
  • Polymorphic ventricular tachycardia

It is sometimes useful to classify tachycardias as either narrow complex tachycardias (often referred to as supraventricular tachycardias) or wide complex tachycardias. Narrow and wide refer to the width of the QRS complex on the ECG. Narrow complex tachycardias tend to originate in the atria, while wide complex tachycardias tend to originate in the ventricles.

Tachycardias can be further classified as either regular or irregular.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: M.Umer Tariq [2]

The body contains several feedback mechanisms to maintain adequate blood flow and blood pressure. If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia. This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The pathophysiology of abnormal tachycardias vary with the type of tachycardia.

When an electrical impulse begins in any part of the heart, it will spread throughout the myocardium and cause a contraction; see Electrical conduction system of the heart. Abnormal impulses can begin by one of two mechanisms: automaticity or reentry.

Automaticity refers to a cardiac muscle cell firing off an impulse on its own. Every cardiac cell has this potential: if it does not receive any impulses from elsewhere, its internal “pacemaker” will fire off an impulse after a certain amount of time. A single specialized location in the atrium, the sinoatrial node, has a higher automaticity (a faster pacemaker) than the rest of the heart, and therefore is usually the one to start the heartbeat.

Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus, and is by definition a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart’s pumping efficiency, because the signal reaches the various parts of the heart muscle with slightly different timing than usual and causes a poorly coordinated contraction.

Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm depends on where the first signal begins: if it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus, many types of dysrhythmia can result.

Re-entry dysrhythmias occur when an electrical impulse travels in a circle within the heart, rather than moving outward and then stopping. Every cardiac cell is able to transmit impulses in every direction, but will only do so once within a short period of time. Normally the impulse spreads through the heart quickly enough that each cell will only respond once, but if conduction is abnormally slow in some areas, part of the impulse will arrive late and will be treated as a new impulse, which can then spread backward. Depending on the timing, this can produce a sustained abnormal rhythm, such as atrial flutter, a self-limiting burst of supraventricular tachycardia, or the dangerous ventricular tachycardia.

The image shown below displays the mechanism of arrhythmias. After an extra-systole (second image) the fast pathway is still refractory and conduction is by the slow pathway, resulting in a prolongation of the PR interval. The signal that reaches the His by the slow pathway may find the fast pathway conducting and return to the atria (third image), resulting in an echo beat. This may set in motion a re-entry pathway through the AV node resulting in AV nodal tachycardia (fourth image).

Copyleft images obtained courtesy of ECGpedia, http://en.ecgpedia.org/index.php?title=Special:NewFiles&offset=&limit=500

The most common type of tachycardia is sinus tachycardia, which is the body’s normal reaction to stress, which includes scenarios involving fever, dehydration, or blood loss (shock). An increase in sympathetic nervous system stimulation causes the heart rate to increase, both by the direct action of sympathetic nerve fibers on the heart and by causing the endocrine system to release hormones such as epinephrine (adrenaline), which have a similar effect. Increased sympathetic stimulation is usually due to physical or psychological stress (the so-called fight or flight response), but can also be induced by stimulants such as amphetamines.It is a narrow complex tachycardia. In the absence of heart disease, sinus tachycardia tends to have a narrow QRS complex on ECG. Treatment is generally directed at identifying the underlying cause.

Ventricular tachycardia (VT or V-tach) is a potentially life-threatening cardiac arrhythmia that originates in the ventricles. It is usually a regular, wide complex tachycardia with a rate between 120 and 250 beats per minute. Ventricular tachycardia has the potential of degrading into the more serious ventricular fibrillation. Ventricular tachycardia is a common, and often lethal, complication of a myocardial infarction (heart attack).

Exercise-Induced Ventricular Tachycardia a phenomenon related to sudden death, seen in patients with severe heart disease (ischemia, acquired valvular heart and congenital heart disease) accompanied by left ventricular dysfunction.^[1] A case of a death from exercise-induced VT occurred in Loyola Marymount basketball player Hank Gathers,in March of 1990^[2]. Both of these rhythms usually last for only a few seconds to minutes (paroxysmal tachycardia), but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.

A supraventricular tachycardia (SVT) is a tachycardia or rapid rhythm of the heart in which the origin of the electrical signal is either the atria or the AV node. These rhythms, by definition, are either initiated or maintained by the atria or the AV node. This is in contrast to ventricular tachycardias, which are rapid rhythms that originate from the ventricles of the heart, below the atria or AV node. The term SVT encompasses a large number of arrhythmias arising from the atria and AV node, and the term SVT is often incorrectly applied only to the subgroup of AV nodal re-entrant tachycardias.

Atrial fibrillation is one of the most common cardiac arrhythmias. It is generally an irregular, narrow complex rhythm. However, it may show wide QRS complexes on the ECG if a bundle branch block is present. At high rates, the QRS complex may also become wide due to the Ashman phenomenon. It may be difficult to determine the rhythm’s regularity when the rate exceeds 150 beats per minute. Depending on the patient’s health and other variables such as medications taken for rate control, atrial fibrillation may cause heart rates that span from 50 to 250 beats per minute (or even higher if an accessory pathway is present). However, new onset atrial fibrillation tends to present with rates between 100 and 150 beats per minute.

AV nodal reentrant tachycardia is the most common reentrant tachycardia. It is a regular narrow complex tachycardia that usually responds well to vagal maneuvers or the drug adenosine. However, unstable patients sometimes require synchronized cardioversion. Definitive care may include catheter ablation.

AV reentrant tachycardia (AVRT) requires an accessory pathway for its maintenance. AVRT may involve orthodromic conduction (where the impulse travels down the AV node to the ventricles and back up to the atria through the accessory pathway) or antidromic conduction (which the impulse travels down the accessory pathway and back up to the atria through the AV node). Orthodromic conduction usually results in a narrow complex tachycardia, and antidromic conduction usually results in a wide complex tachycardia that often mimics ventricular tachycardia. Most antiarrhythmics are contraindicated in the emergency treatment of AVRT, because they may paradoxically increase conduction across the accessory pathway.

Junctional tachycardia is an automatic tachycardia originating in the AV junction. It tends to be a regular, narrow complex tachycardia and may be a sign of digitalis toxicity.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: M.Umer Tariq [2] Kiran Singh, M.D. [3]

Life threatening causes of tachycardia include cardiac tamponade, cardiogenic shock, pulseless ventricular tachycardia, and stroke. Other common causes of tachycardia are anemia, exercise, fever, and hyperthyroidism.

• Cardiac tamponade
• Cardiogenic shock
• Cyanide poisoning
• Myocardial infarction
• Pulmonary embolism
• Pulseless ventricular tachycardia
• Stroke

• Anemia
• Electrolyte imbalance
• Exercise
• Fever
• Hyperthyroidism
• Hypertension
• Pain

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In an adult, a heart rate faster than 100 beats/minute is considered tachycardia. This number varies with age, as the heartbeat of a younger person is naturally faster than that of an older person’s. During exercise the sinus node increases its rate of electrical activity to accelerate the heart rate. Such normal fast rate that develops is called sinus tachycardia. In contrast, arrhythmias that are due to fast, abnormal electrical activity can cause tachycardias that are dangerous. If the ventricles of the heart experience one of these tachycardias for a long period of time, there can be deleterious effects. Individuals may sense a tachycardia as a pounding sensation of the heart, known as palpitations. If a tachycardia lowers blood pressure it may cause lightheadedness or dizziness, or even fainting (syncope). If the tachycardia is too fast, the pump function of the heart is impeded, and rarely may lead to sudden death.

SADS, or sudden arrhythmia death syndrome, is a term used to describe sudden death due to cardiac arrest brought on by an arrhythmia. The most common cause of sudden death in the US is coronary artery disease. Approximately 300,000 people die suddenly of this cause every year in the US.

Sudden arrhythmia death syndrome (SADS) can also occur from other causes. Also, there are many inherited conditions and heart diseases that can affect young people that can cause sudden death. Many of these victims have no symptoms before dying suddenly.

Causes of SADS in young people are long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular dysplasia (“arrythmia”-causing, “right ventricle”-involving, pre-cancerous malformation).

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