Tachycardia pathophysiology

Tachycardia Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
Echocardiography
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Tachycardia pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Tachycardia pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Tachycardia pathophysiology
CDC on Tachycardia pathophysiology
Tachycardia pathophysiology in the news
Blogs on Tachycardia pathophysiology
Directions to Hospitals Treating Tachycardia
Risk calculators and risk factors for Tachycardia pathophysiology

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

Overview

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.

Pathophysiology

Origin of Impulse

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

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

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

Sinus Tachycardia

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

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

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. A case of a death from exercise-induced VT occurred in Loyola Marymount basketball player Hank Gathers,in March of 1990. 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.

Supraventricular Tachycardia

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

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 (AVNRT)

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

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

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.