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Ventricular Tachycardia
Updated: Sep 17, 2009
Introduction
Background
Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute with wide QRS complexes. VT may be monomorphic (originating from a single focus with identical QRS complexes) or polymorphic (may appear as an irregular rhythm, with varying QRS amplitudes and morphology). Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration; longer runs are considered sustained VT.
No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following:
- Rate greater than 120 beats per minute (usually 150-200)
- Wide QRS complexes (>140 ms)
- Presence of atrioventricular (AV) dissociation
- Fusion beats
- Capture beats
Other historical factors suggesting VT are prior ischemic or structural heart disease. It may exist without cardiovascular collapse but when hemodynamic compromise occurs, it may deteriorate rapidly into a more malignant dysrhythmia: ventricular fibrillation (VF). Therefore, this tachydysrhythmia must be addressed swiftly to avoid morbidity or mortality.
Pathophysiology
As mentioned before, ventricular tachycardia (VT) is usually a consequence of structural or ischemic heart disease, with breakdown of normal conduction patterns. Increased automaticity (which tends to favor ectopic foci) or activation of reentrant pathways in the myocardium can exist to generate the dysrhythmia. Electrolyte disturbances, ischemia, and sympathomimetics may increase the likelihood of VT in the susceptible myocardium.
AV dissociation is apparent in approximately half of VT episodes, and, when present, it is a hallmark characteristic of VT.1 This occurs when the sinus node is depolarizing the atria at a rate that is usually slower than the pathologic ventricular rate. P waves can be visualized at times in between or embedded in the QRS complexes, but the two have their own independent rates. Fusion beats and capture beats can occur in the presence of VT depending on the refractory period of the AV node and the timing of ventricular and atrial depolarizations, respectively.
Fusion beats have a mixed morphology, due to normal AV/His bundle conduction occurring simultaneously with abnormal (wide complex QRS) ventricular depolarization. Thus, a normally conducted impulse travels from the AV node through the normal conduction pathway (a narrow QRS), and the competing impulse originates from the abnormal ectopic ventricular focus (a wide QRS). The two converge leading to a mixed (fused) QRS.
A capture beat occurs when an atrial impulse arrives at the AV node at a "fortuitous" time when the AV node has just recovered from its refractory period. The timing has to be just right as the AV node is frequently in its refractory state due to retrograde conduction from the rapid ventricular rhythm. When this occurs, conduction will proceed normally through the AV node/His-Purkinje system, "capturing" the ventricle and leading to a narrow QRS complex.
AV dissociation.
Fusion, capture beats, and AV dissociation.
Retrograde conduction can also exist from the ventricles to the atria via the AV node. This is NOT AV dissociation and reveals itself in an ECG as a 1:1 correlation between the wide QRS complex and an inverted P wave. This is also seen in two different types of wide-QRS complex SUPRAventricular tachycardias, which are often confused with ventricular tachycardia: (1) antidromic AV reentrant tachycardia (AVRT) and (2) AV nodal reentrant tachycardia with aberrant conduction (AVNRT).
Antidromic AVRT may occur depending on the properties of the atrioventricular node and the accessory conduction pathway to develop a reentry mechanism. Forward, or anterograde, conduction through the accessory pathway may occur to depolarize the ventricles abnormally (without use of a normal HIS-Purkinje system). This leads to a widened QRS complex with backward, or retrograde, conduction through the AV node, which thus generates retrograde P waves. AVNRT with aberrant conduction occurs when a reentrant circuit in the AV node propagates impulses both anterograde through an abnormal His-Purkinje system (thus the wide QRS) and also retrograde through the atria creating retrograde P waves. These two rhythms may be indistinguishable from VT with 1:1 ventriculoatrial conduction.
Retrograde P's #1.
The most common cause of monomorphic sustained VT is a prior MI with ventricular myocardial scar formation. The presence of myocardial fibrosis is a substrate for slow conduction pathways and associated reentry mechanisms. Nonsustained VT and ectopy are due to abnormal automaticity mechanisms and more commonly associated with acute myocardial ischemia.
A distinctive variant of VT is torsade de pointes, with its unusual shifting-axis QRS complexes that appear (on ECG) as if the heart is rotating upon an axis. It typically occurs during sinus rhythm and in the presence of drugs or conditions that prolong the QT interval (eg, type 1A antiarrhythmics, hypomagnesemia, droperidol). The dysrhythmia may occur either in the presence or in the absence of myocardial ischemia or infarction.
Torsades de pointes.
A second variant of VT is accelerated idioventricular rhythm. Sometimes termed slow ventricular tachycardia, this dysrhythmia presents with a rate of 60-100 beats per minute. It typically occurs with underlying heart disease (ischemic or structural), is transient, and only rarely is associated with hemodynamic compromise or collapse. Treatment of the dysrhythmia itself usually is not required unless significant hemodynamic impairment develops.
Due to advances in molecular biology, a number of inherited dysrhythmic disorders with a propensity toward VT have been described. Brugada syndrome, congenital long and short QT syndrome, and catecholaminergic-sensitive VT have complex inheritance patterns. Mechanistically, each disorder is characterized by imbalanced ion transport across the cardiac cellular membrane, which leads to abnormalities in cardiac repolarization, and thus increased risk of dysrhythmia. These syndromes have all been linked to sudden cardiac death. Patients with these disorders are being managed with a combination of genetic typing, antidysrhythmic medications, lifestyle modification, and implantable cardioverter-defibrillator (ICD) placement.
Frequency
United States
Nonsustained, short runs of VT are frequently observed dysrhythmias, but sustained monomorphic VT is uncommon in the ED setting due to aggressive treatment of myocardial ischemia.
International
VT and coronary artery disease are common throughout most of the developed world. In developing countries, VT and other heart diseases are relatively less common.
Mortality/Morbidity
- Morbidity and mortality in VT arise principally from spontaneous degeneration into the more malignant ventricular defibrillation.
- Even without such degeneration, VT can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.
Sex
- Currently, most patients presenting with VT are men.
- As coronary artery disease (CAD) becomes more common in women, it seems certain that the incidence of VT in women will increase.
Age
- VT is unusual among pediatric patients, although when present there is associated congenital heart disease, or it occurs in the postoperative cardiac setting. Tachydysrhythmias in this population generally are PSVT.
- VT incidence rates peak in the middle decades of life, following the incidence of structural heart disease.
Clinical
History
Most patients with ventricular tachycardia (VT) present to the ED with symptoms of either ischemia or hemodynamic compromise. These may include the following:
- Chest discomfort
- Dyspnea
- Diaphoresis
- Nausea
- Palpitations
- Anxiety or feeling of "impending doom"
- Syncope and presyncope
Physical
Besides tachycardia, findings generally reflect the degree of hemodynamic instability.
- Signs of congestive heart failure (CHF)
- Hypotension
- Hypoxemia
- Jugular venous distention
- Rales
- Mental status changes
- Anxiety
- Agitation
- Lethargy
- Coma
- Subtle signs of AV dissociation
- Irregular cannon a waves in the jugular pulse
- Variable intensity of the first heart sound
- Beat-to-beat changes in systolic blood pressure
Causes
As noted above, ventricular tachycardia (VT) generally is a consequence of ischemic or structural heart disease or electrolyte deficiencies (eg, hypokalemia, hypocalcemia, hypomagnesia). It can also be triggered by the following:
- Use of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine)
- Drugs that prolong the QT complex (eg, type 1A antidysrhythmics, droperidol and related phenothiazines) - These in particular cause torsade de pointes.
- Rheumatologic disorders that affect the myocardium systemic such as systemic lupus erythematosus and rheumatoid arthritis
- Other structural congenital disorders such as right ventricular dysplasia and tetralogy of Fallot
- Digitalis toxicity - This can lead to biventricular tachycardia.
- Inherited channelopathies as mentioned above
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| References |
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References
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Further Reading
Keywords
ventricular tachycardia, VT, tachydysrhythmia, ventricular ectopic focus, fusion beats, atrioventricular dissociation, AV dissociation, wide QRS complexes, ventricular fibrillation, VF, paroxysmal supraventricular tachycardia, PSVT, torsade de pointes, accelerated idioventricular rhythm, congestive heart failure, pulmonary edema, jugular venous distention,hypotension, CAD, structural heart disease, hypokalemia, hypocalcemia, hypomagnesia, methamphetamine, cocaine, genetic arrhythmia syndrome, cardiac channelopathy
