This page was last edited on 25 August 2013, at 20:33. Ventricular tachycardia can be classified based on its morphology: Another way to classify ventricular tachycardias is the duration of the episodes: Three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 120 beats per minute constitute a ventricular tachycardia. Ventricular tachycardia starts in the heart’s lower chambers. If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds). [13] This should be synchronized to the heartbeat if the waveform is monomorphic if possible, in order to avoid degeneration of the rhythm to ventricular fibrillation. When something goes wrong and signals are sent too quickly, it can cause tachycardia. Kasper, D. (2012). Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. Blood flows from the top chambers of the heart (atria) into the ventricles, then it moves to the lungs and through the aorta to be circulated throughout the body. A person with pulseless VT is treated the same as ventricular fibrillation with high-energy (360J with a monophasic defibrillator, or 200J with a biphasic defibrillator) unsynchronised cardioversion (defibrillation). High-dose magnesium is often used as an antidote in cardiac arrest protocols. The shock may be delivered to the outside of the chest using the two pads of an external defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been inserted. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. [2][3], Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, or a myocardial infarction.[2][3]. Ventricular tachycardia starts in the heart’s lower chambers. Policy, Get useful, helpful and relevant health + wellness information. [2] Otherwise, immediate cardioversion is recommended. Advertising on our site helps support our mission. Tachycardia is a heart rate higher than 100 beats per minute. Occasionally in ventricular tachycardia, supraventricular impulses are conducted to the ventricles, generating QRS complexes with normal or aberrant supraventricular morphology (ventricular capture). The Tachyarrhythmias. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, in particular in combination with one another. In particular, supraventricular tachycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can be given for torsades de pointes or if a low blood magnesium level is found/suspected. Also electrolyte disturbances and ischemia can cause ventricular tachycardias. In certain cardiac alterations, wide QRS complex tachycardias of another etiology can be observed. Individuals suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm. [2] Ventricular tachycardia may result in ventricular fibrillation and turn into sudden death. In the past, ablation was often not considered until pharmacological options had been exhausted, often after the patient had suffered substantial morbidity from recurrent episodes of VT and ICD shocks. If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia. An ICD may also be set to attempt to overdrive pace the ventricle. [14] Evidence does not show that amiodarone is better than procainamide.[14]. New York: McGraw-Hill, Medical Pub. Antiarrhythmic medications can reduce the frequency of ICD therapies, but have disappointing efficacy and side effects. Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers amiodarone, dronedarone, bretylium, sotalol, ibutilide, and dofetilide. after myocardial infarction. [12], If a person still has a pulse, it is usually possible to terminate the episode using electric cardioversion. [2][3] It is found initially in about 7% of people in cardiac arrest. Most patients with ventricular tachycardia have another heart problem, such as coronary artery disease, high blood pressure, an enlarged heart (cardiomyopathy) or heart valve disease. The most common cause of monomorphic ventricular tachycardia is scarring of the heart muscle from a previous myocardial infarction (heart attack). A normal resting heart rate is 60 to 100 beats per minute. Although a few seconds may not result in problems, longer periods are dangerous. The morphology of the tachycardia depends on its cause and the origin of the re-entry electrical circuit in the heart. Last reviewed by a Cleveland Clinic medical professional on 05/10/2019. If this fails after a short trial, the ICD will usually stop pacing, charge up and deliver a defibrillation grade shock. [5] While waiting for a defibrillator, a precordial thump may be attempted in those on a heart monitor who are seen going into an unstable ventricular tachycardia. In monomorphic ventricular tachycardia, the shape of each heart beat on the ECG looks the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle.


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