Tachycardia

Tachycardia
Rhythm strip showing a run of ventricular tachycardia (VT)
ICD-10	R00.0
ICD-9	785.0
MeSH	D013610

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 On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Tachycardia All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Tachycardia
CDC on Tachycardia
Tachycardia in the news
Blogs on Tachycardia
Directions to Hospitals Treating Tachycardia
Risk calculators and risk factors for Tachycardia

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

Overview

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.

Classification

The 12 lead ECG can help distinguish between the various types of tachycardias, generally distinguished by their site of pacemaker origin:

• Sinus tachycardia, which originates from the Sino-atrial (SA) node, near the base of the superior vena cava
• Ventricular tachycardia, any tachycardia which originates in the ventricles.
• Supraventricular tachycardia (SVT), which is a tachycardia paced from the Atria or the AV node. SVT rhythms include:
  • Atrial fibrillation
  • AVNRT or AV nodal reentrant tachycardia
  • AVRT or AV reentrant tachycardia
  • Junctional 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.

Pathophysiology

Haemodynamic responses

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.

Sinus tachycardia

The most common type of tachycardia is sinus tachycardia, which is the body's normal reaction to stress, including fever, dehydration, or blood loss (shock). It is a technical narrow complex tachycardia. In the absence of heart disease, it tends to have a narrow QRS complex on the ECG. Treatment is generally directed at identifying the underlying cause.

Ventricular tachycardia

Main article: 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 to the more serious ventricular fibrillation. Ventricular tachycardia is a common, and often lethal, complication of a myocardial infarction (heart attack).

Exercise-induced ventricular tachycardia is a phenomenon related to sudden deaths, especially in patients with severe heart disease (ischaemia, acquired valvular heart and congenital heart disease) accompanied with left ventricular dysfunction. A case of a death from exercise-induced VT was the death on a basketball court of Hank Gathers, the Loyola Marymount basketball]] star, in March 1990.

Both of these rhythms normally last for only a few seconds to minutes (paroxysmal tachycardia), but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.

SVT Rhythms

Main article: Supraventricular tachycardia

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.

Causes

Common Causes

The most common cause of the latter is orthostatic hypotension (also called postural hypotension), a sudden drop of blood pressure that occurs with a change in body position (e.g., going from lying down to standing up). When tachycardia occurs for this reason, it is called postural orthostatic tachycardia syndrome (POTS).

Fever, hyperventilation and infection leading to sepsis are also common causes of tachycardia, primarily due to increase in metabolic demands and compensatory increase in heart rate.

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.

Endocrine disorders such as pheochromocytoma can cause epinephrine release and tachycardia independent of the nervous system. Hyperthyroidism is also known to cause tachycardia.

Causes by Organ System

Cardiovascular	Arrhythmogenic right ventricular dysplasia, AV Nodal Reentrant Tachycardia, AV-dissociation, Bradycardia-tachycardia syndrome, Cardiac amyloidosis, Cardiac arrhythmia, Cardiac tamponade, Cardiogenic shock, Congestive Heart Failure, Ebstein's Anomaly of the Tricuspid Valve, Inappropriate Sinus Tachycardia, Inferior vena cava syndrome, Multifocal atrial tachycardia, Nonparoxysmal Junctional Tachycardia, Paroxysmal supraventricular tachycardia, Polymorphic ventricular tachycardia, Premature ventricular contractions, Pulseless ventricular tachycardia, Torsade de pointes, Wolff-Parkinson-White syndrome,
Chemical / poisoning	3-Quinuclidinyl benzilate, Arsenic Poisoning, Bothrops, Caffeine, Carbon monoxide poisoning, Cardiac effects of insect bites, Hydroxyethyl starch, Mercury poisoning, Methadone withdrawl, Scombroid,
Dermatologic	No underlying causes
Drug Side Effect	Amlodipine, Amphetamine, Anticholinergic, Antipsychotic, Atropine, Abciximab (patient information), Benzatropine, Biperiden, Bupropion, Caspofungin, Clofarabine, Clomipramine, Clonidine, Daptomycin, Desflurane, Desoxyn, Diethylcathinone, Diflunisal, Digoxin, Diltiazem, Dimenhydrinate, Diphenhydramine, Doxapram, Doxepin, Ephedrine, Epinephrine, Ethcathinone, Iloprost, Imipramine, Isoproterenol, Isosorbide mononitrate, Levomepromazine, Levomethamphetamine, Levosimendan, Lomotil, Maprotiline, Methcathinone, Methylphenidate, Metoclopramide, Milnacipran, Minoxidil, Modafinil, Motofen, Nalbuphine, Nalmefene, Nialamide, Neuromuscular-blocking drugs, Olanzapine, Opioid, Paliperidone, Papaverine, Phentermine, Pipradrol, Procainamide (patient information), Procyclidine hydrochloride, Propantheline, Pseudoephedrine, Sumatriptan, Terbutaline, Tizanidine, Trazodone, Tuaminoheptane, Vardenafil, Zopiclone withdrawl,
Ear Nose Throat	No underlying causes
Endocrine	Graves' Disease, Toxic multinodular goitre,
Environmental	No underlying causes
Gastroenterologic	Accessory pancreas, Gastroenteritis, Megacolon, Peritonitis, Retroperitoneal hematoma, Ulcerative colitis,
Genetic	Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia, Costello syndrome,
Hematologic	Ruptured spleen, Sickle-cell disease,
Iatrogenic	Blood transfusion,
Infectious Disease	Clostridium Difficile, Cotton fever, Ebola, Lassa fever, Malaria, Scarlet fever, Tuberculosis,
Musculoskeletal / Ortho	No underlying causes
Neurologic	Autonomic neuropathy, Dysautonomia,
Nutritional / Metabolic	Adams Nance syndrome, Acute Porphyria, Beriberi Heart Disease, Betel nut, Foods containing tyramine, Hypoglycemia, Hypomagnesemia, Metabolic acidosis,
Obstetric/Gynecologic	Aortocaval compression syndrome, Fetal distress, Omphalitis,
Oncologic	Insulinoma,
Opthalmologic	No underlying causes
Overdose / Toxicity	Aconitum, Benzylpiperazine, Bupropion, Cocaine, Diflunisal, Imipramine, Lomotil, Long-term effects of alcohol, Procainamide, Procyclidine hydrochloride, Xanthine,
Psychiatric	No underlying causes
Pulmonary	Acute Chest Syndrome, Asthma, Community-acquired pneumonia, Hemothorax,
Renal / Electrolyte	No underlying causes
Rheum / Immune / Allergy	Kawasaki disease,
Sexual	No underlying causes
Trauma	Commotio cordis,
Urologic	No underlying causes
Miscellaneous	Chronic fatigue syndrome, Dipping tobacco, Hyperthermia, Malignant hyperthermia, Pheochromocytoma, Postural orthostatic tachycardia syndrome,

Causes in Alphabetical Order

3-Quinuclidinyl benzilate Abciximab (patient information) Accessory pancreas Aconitum Acute Chest Syndrome Acute Porphyria Adams Nance syndrome Alcohol Withdrawal Amanita phalloides Amlodipine Amphetamine Anticholinergic Antipsychotic Aortocaval compression syndrome Arrhythmogenic right ventricular dysplasia Arsenic Poisoning Ashman phenomenon Asthma Atropine Autonomic neuropathy AV Nodal Reentrant Tachycardia AV-dissociation AVNRT Benzatropine Benzylpiperazine Beriberi Heart Disease Betel nut Biperiden Blood transfusion Bothrops Bradycardia-tachycardia syndrome Brugada syndrome Bupropion Caffeine Carbon monoxide poisoning Cardiac amyloidosis Cardiac arrhythmia Cardiac effects of insect bites Cardiac tamponade Cardiogenic shock Cardiovascular Effects of Cocaine Caspofungin Catecholaminergic polymorphic ventricular tachycardia Chlorprothixene Chronic fatigue syndrome Clofarabine Clomipramine Clonidine Clostridium Difficile Commotio cordis Community-acquired pneumonia Congestive Heart Failure Costello syndrome Cotton fever Daptomycin Desflurane Desoxyn Diethylcathinone Diflunisal Digoxin Diltiazem Dimenhydrinate Diphenhydramine Dipping tobacco Dosulepin hydrochloride Doxapram Doxepin Dysautonomia Ebola Ebstein's Anomaly of the Tricuspid Valve Ephedrine Epinephrine Ethcathinone Fetal distress Foods containing tyramine Gastroenteritis Graves' Disease Hemothorax Hydroxyethyl starch Hyperthermia Hyperthyroidism

Hypoglycemia Hypomagnesemia Iloprost Imipramine Inappropriate Sinus Tachycardia Inferior vena cava syndrome Insulinoma Isoproterenol Isosorbide mononitrate Kawasaki disease Lassa fever Levomepromazine Levomethamphetamine Levosimendan Lomotil Long-term effects of alcohol Malaria Malignant hyperthermia Maprotiline Megacolon Mercury poisoning Metabolic acidosis Methadone withdrawl Methcathinone Methylphenidate Metoclopramide Milnacipran Minoxidil Modafinil Motofen Multifocal atrial tachycardia Nalbuphine Nalmefene Neuromuscular-blocking drugs Nialamide Nonparoxysmal Junctional Tachycardia Olanzapine Omphalitis Opioid Paliperidone Palytoxin Papaverine Paroxysmal supraventricular tachycardia Peritonitis Phentermine Pheochromocytoma Pipradrol Polymorphic ventricular tachycardia Porphyria Postural orthostatic tachycardia syndrome Premature ventricular contractions Procainamide (patient information) Procyclidine hydrochloride Propantheline Pseudoephedrine Pulseless ventricular tachycardia Retroperitoneal hematoma Ruptured spleen Scarlet fever Scombroid Scopolamine Sepsis Serotonin syndrome Sick sinus syndrome Sickle-cell disease Sumatriptan Supraventricular Tachycardias Terbutaline Tizanidine Torsade de pointes Toxic multinodular goitre Toxidrome Trazodone Tuaminoheptane Tuberculosis Ulcerative colitis Vardenafil White coat hypertension Wide Complex Tachycardias Wolff-Parkinson-White syndrome Xanthine Zopiclone withdrawl

Treatments

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. If the tachycardia originates from the sinus node (sinus tachycardia), treatment of the underlying cause of sinus tachycardia is usually sufficient. On the other hand, if the tachycardia is of a potentially lethal origin (ie: ventricular tachycardia) treatment with anti arrhythmic agents or with electrical cardioversion may be required. Below is a brief discussion of some of the main tachyarrhythmias and their treatments.

The electrocardiac management of atrial fibrillation and atrial flutter is either through medications or electrical cardioversion. Pharmacologic management of these arrhythmias typically involves diltiazem or verapamil as well as beta-blocking agents such as atenolol. The decision to use electrical cardioversion depends heavily on the hemodynamic stability of the presenting patient; in general those patients who are unable to sustain their systemic functions are electrically converted although conversion to a normal sinus rhythm can be performed with amiodarone. An interesting type of atrial fibrillation which must be carefully managed is when it appears in combination with Wolff-parkinson White. In this case, calcium channel blockers, beta-blockers and digoxin must be avoided to prevent precipitation of ventricular tachycardia. Here, procainamide or quinidine are often used. Of note: patients who have been in atrial fibrillation for more than 48 hours should not be converted to normal sinus rhythm unless they have been anti-coagulated to an INR of 2-3 for at least 4 weeks.

In the case of narrow complex tachycardias (juntional, atrial or paroxysmal), the treatment in general is to first give the patient adenosine (to slow conduction through the AV node) and then perform vagal maneuvers to slow the rhythm. If this does not convert the patient, amiodarone, calcium channel blockers or beta-blockers are commonly employed to stabilize the patient. Again as in atrial fibrillation, if a patient is unstable, the decision to electrially cardiovert him/her should be made.

With wide complex tachyarrhythmias or ventricular tachyarrhythmias, in general most are highly unstable and cause the patient significant distress and would be electrically converted. However one notable exception is monomorphic ventricular tachycardia which patients may tolerate but can be treated pharmacologically with amiodarone or lidocaine.

Above all, the treatment modality is tailored to the individual, and varies based on the mechanism of the tachycardia (where it is originating from within the heart), on the duration of the tachycardia, how well the individual is tolerating the fast heart rate, the likelihood of recurrence once the rhythm is terminated, and any co-morbid conditions the individual is suffering from.

ACC / AHA Guidelines- Recommendations for Permanent Pacemakers That Automatically Detect and Pace to Terminate Tachycardias (DO NOT EDIT)

“

Class IIa 1. Permanent pacing is reasonable for symptomatic recurrent SVT that is reproducibly terminated by pacing when catheter ablation and/or drugs fail to control the arrhythmia or produce intolerable side effects. (Level of Evidence: C) Class III 1. Permanent pacing is not indicated in the presence of an accessory pathway that has the capacity for rapid anterograde conduction. (Level of Evidence: C)

”

ACC / AHA Guidelines- Recommendations for Permanent Pacemakers That Automatically Detect and Pace to Terminate Tachycardias (DO NOT EDIT)

“

Class I 1. Permanent pacing is indicated for sustained pause-dependent VT, with or without QT prolongation. (Level of Evidence: C) Class IIa 1. Permanent pacing is reasonable for high-risk patients with congenital long-QT syndrome. (Level of Evidence: C) Class IIb 1. Permanent pacing may be considered for prevention of symptomatic, drug-refractory, recurrent AF in patients with coexisting SND. (Level of Evidence: B) Class III 1. Permanent pacing is not indicated for frequent or complex ventricular ectopic activity without sustained VT in the absence of the long-QT syndrome. (Level of Evidence: C) 2. Permanent pacing is not indicated for torsade de pointes VT due to reversible causes. (Level of Evidence: A)

”

Sources

• The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities