Ventricular arrhythmias
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Causes of Ventricular Arrhythmias
Cardiac causes
Acute and chronic ischemic heart disease
Cardiomyopathy
Valvular heart disease
Mitral valve prolapse
Noncardiac causes
Stimulants: caffeine, cocaine, alcohol
Metabolic abnormalities: acidosis, hypoxemia, hyperkalemia, hypokalemia, hypomagnesemia
Drugs: digoxin (Lanoxin), theophylline, antipsychotics, tricyclic antidepressants, antiarrhythmics with proarrhythmic potential [e.g., flecainide (Tambocor), dofetilide (Tikosyn), sotalol (Betapace) and quinidine)
| example | regularity | atrial frequency | ventricular frequency | origin (SVT/VT) | p-wave | effect of adenosine | |
|---|---|---|---|---|---|---|---|
| Wide complex (QRS>0.12) | |||||||
| Ventricular Tachycardia | 
| regular (mostly) | 60-100 bpm | 110-250 bpm | ventricle (VT) | AV-dissociation | no rate reduction (sometimes accelerates) |
| Ventricular Fibrillation | 
| irregular | 60-100 bpm | 400-600 bpm | ventricle (VT) | AV-dissociation | none |
| Ventricular Flutter | 
| regular | 60-100 bpm | 150-300 bpm | ventricle (VT) | AV-dissociation | none |
| Accelerated Idioventricular Rhythm | 
| regular (mostly) | 60-100 bpm | 50-110 bpm | ventricle (VT) | AV-dissociation | no rate reduction (sometimes accelerates) |
| Torsade de Pointes | 
| regular | 150-300 bpm | ventricle (VT) | AV-dissociation | no rate reduction (sometimes accelerates) | |
| Bundle-branch re-entrant tachycardia* | 
| regular | 60-100 bpm | 150-300 bpm | ventricles (VT) | AV-dissociation | no rate reduction |
| (*) Bundle-branch re-entrant tachycardia is extremely rare | |||||||
Premature Ventricular Complexes (PVCs)
A premature ventricular complex is characterized by the premature occurrence of a QRS complex that is bizarre in shape and lasts longer than 120 msec. The T wave is large and usually of opposite polarity to the QRS complex.
A premature ventricular complex is usually followed by a full compensatory pause. The term “ventricular bigeminy” refers to alternating normal sinus and premature ventricular complexes. Three or more successive premature ventricular complexes are arbitrarily defined as ventricular tachycardia. Premature ventricular complexes become more prevalent with increasing age and occur in association with a variety of stimuli.
It is important to determine whether underlying structural heart disease is present and left ventricular function is impaired.Other common causes include electrolyte abnormalities, stimulants, and some medications.
Management
Patients Without Heart Disease
In the absence of heart disease, PVCs are associated with little or no increased risk of developing a dangerous arrhythmia. In this situation, the risk-to-benefit ratio of antiarrhythmic drug therapy does not support routine treatment.[1] It is important to review medications, determine if stimulants are being used, and correct electrolyte abnormalities. If no underlying cause is found, the optimal approach is patient reassurance. Patients should be made aware of the potential dangers of antiarrhythmic drug therapy as determined in the Cardiac Arrhythmia Suppression Trials (CAST and CAST II).[1] [1]
CAST showed that the risk of dying increased, rather than decreased, with successful long-term suppression of premature ventricular complexes after myocardial infarction in older patients. At best, CAST II showed no impact on long-term survival from drug treatment that successfully suppressed premature ventricular complexes. If patients with multiple premature ventricular complexes have severe, disabling symptoms, beta blockers are the safest initial choice.Referral to a cardiologist is indicated if beta-blocker therapy is not effective. In this situation, the next agents to be tried would be class I antiarrhythmic drugs, such as flecainide (Tambocor) and amiodarone (Cordarone), although radiofrequency ablation of an ectopic focus may also be an appropriate treatment.
Patients with Structural Heart Disease
The occurrence of premature ventricular complexes in patients with structural heart disease has been shown to significantly increase the risk of subsequent morbidity and mortality. Coronary heart disease, cardiomyopathy, and congestive heart failure are the major cardiac diseases associated with unfavorable outcomes in patients with premature ventricular complexes.
Ventricular Tachycardia
Ventricular tachycardia refers to a rhythm originating from a ventricular ectopic focus at a rate >100 bpm. The electrocardiogram shows a wide complex tachycardia with no associated P waves.
In patients with bundle branch block,Wolff-Parkinson-White syndrome, or aberrant conduction, supraventricular tachycardia can resemble ventricular tachycardia. Because of the morbidity and mortality associated with untreated ventricular tachycardia, any wide-complex tachycardia should be assumed to be ventricular tachycardia until proved otherwise. Physicians should keep in mind that patients with ventricular tachycardia can have minimal symptoms.
Management of Ventricular Tachycardia
The mortality rate within two years is reported to be higher than 30% in patients with non sustained ventricular tachycardia on Holter monitoring and impaired left ventricular function.[1] Two large multicenter trials [1] [1] showed a clear advantage for automatic cardioverter defibrillator implantation over drug therapy in patients who had a malignant ventricular arrhythmia or who had been resuscitated from sudden cardiac death. The selection of high-risk patients for defibrillator implantation should be based on left ventricular function and the findings of electrophysiologic studies.
Implantable defibrillators appear to be most beneficial in patients with a low ejection fraction who are noted to have frequent premature ventricular complexes, non sustained ventricular tachycardia on Holter monitoring, and a history of syncope or nearsyncope. It is critical to rule out coronary heart disease and to optimize the treatment of congestive heart failure in these patients. When ventricular tachycardia is diagnosed in relatively asymptomatic patients, medical treatment should be attempted. New recommendations from the American Heart Association [1] emphasize the initial use of 300 mg of iv. administered amiodarone, followed by repeated 150 mg iv. doses every 8-10 minutes, in patients with pulseless VT.
Patients with stable ventricular tachycardia should be given 150 mg of amiodarone intravenously over 10 minutes, followed by an infusion at 1 mg/minute for 6 hours and then at 0.5 mg/minute until the VT converts to sinus rhythm or another less dangerous rhythm. The alternative treatment is intravenously administered lidocaine (Xylocaine), given first in a 100 mg bolus (or 1 mg/kg) and then in an infusion at 1-4 mg/minute.
In hemodynamically unstable patients, electrical cardioversion should be attempted in accordance with the recently revised advanced cardiac life support (ACLS) protocols.
Automatic implantable cardioverter defibrillators (ICD) are considered the most effective treatment for patients with life-threatening VT or VF. According to expert recommendations, implantation of an automatic cardioverter defibrillator should be considered in these situations[1]:
1. Cardiac arrest resulting from ventricular fibrillation or tachycardia not caused by a transient or reversible cause
2. Spontaneous, sustained ventricular tachycardia
3. Syncope of undetermined origin and sustained VT or ventricular fibrillation (VF) induced during electrophysiologic studies
4. Non sustained VT with coronary artery disease and LV dysfunction if VT or VF is induced during electrophysiologic studies.
Source
1. Zipes DP, Camm AJ, Borggrefe M, et al., ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)Circulation 2006;114;e385-e484
2. Kesh Hebbar A, Hueston WJ, Management of Common Arrhythmias: Part II.Ventricular Arrhythmias and Arrhythmias in Special Populations Am Fam Physician 2002;65:2491-6.
References
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
