History
Ventricular tachycardia (VT) can be symptomatic. Symptoms of VT are often a function of the associated heart rate, or the causal process, such as an acute myocardial infarction (MI). Symptomatic patients typically present with palpitation, lightheadedness, and syncope from diminished cerebral perfusion. Chest pain may result from ischemia or from the rhythm itself. Understandably, patients often experience anxiety. Syncope is more common when VT occurs in the setting of structural heart disease.
Some patients describe a sensation of neck fullness, which may be related to increased central venous pressure and occasional cannon A waves. Dyspnea may be related to increased pulmonary venous pressures and occasional left atrial contraction against a closed mitral valve.
VT may also be asymptomatic, or the symptoms may be those of the associated triggered therapy (eg, an implantable cardioverter-defibrillator [ICD] shock).
Eliciting a history of risk factors for VT is important. These include prior MI, other known structural heart disease, or a family history of premature sudden death. VT must be strongly considered in any syncopal patient with such a history. For athletes, determination of the risk for VT should be part of the preparticipation history and physical examination.
Any patient with a strong family history of premature (ie, before age 40 years) sudden death should be evaluated for inherited arrhythmia syndromes, including the following:
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Arrhythmogenic right ventricular dysplasia
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Catecholaminergic polymorphic VT
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Hypertrophic cardiomyopathy
Physical Examination
Aside from tachycardia, findings in patients with ventricular tachycardia (VT) generally reflect the degree of hemodynamic instability. Episodes of VT are often associated with hypotension and tachypnea. Signs of diminished perfusion may be present, including a diminished level of consciousness, pallor, and diaphoresis. Jugular venous pressure may be high, and cannon A waves may be observed if the atria are in sinus rhythm. The first heart sound (S1) may vary in intensity as a result of loss of atrioventricular (AV) synchrony.
In patients who have converted to sinus rhythm (whether spontaneously or after cardioversion), relevant physical findings would be related to any underlying structural heart disease. These may include displacement of the point of maximal impulse (PMI), murmurs related to valvular heart disease or hypertrophic cardiomyopathy, and an S3 gallop. Rales may be present during sinus rhythm if uncompensated heart failure is present. Sinus rhythm is often interrupted by ventricular extrasystole.
The following changes may be seen in the patient’s mental status:
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Anxiety
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Agitation
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Lethargy
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Coma
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This electrocardiogram (ECG) shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. The tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic study. A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
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This electrocardiogram shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). The patient presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, which is most obvious in leads V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
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At first glance, this tracing suggests rapid polymorphic ventricular tachycardia. It is actually sinus rhythm with premature atrial complex and a superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backward from the final two QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
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Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
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Preexcited atrial fibrillation. The patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over an accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia.
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Curative ablation of ventricular tachycardia (VT). The patient had VT in the setting of ischemic cardiomyopathy. VT was induced in an electrophysiology laboratory, and an ablation catheter was placed at the critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy was applied to tissue through the catheter tip, and VT was terminated when the critical conducting tissue was destroyed.
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Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If a smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have a left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to the rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis. Sometimes “pacing spike detection” must be programmed “ON” in the electrocardiographic system to make the spike apparent.
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Supraventricular tachycardia with aberrancy. This tracing is from a patient with a structurally normal heart who has a normal resting electrocardiogram. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note the relatively narrow RS intervals in the precordial leads.
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Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator.
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Posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red, and late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
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This tracing depicts monomorphic ventricular tachycardia.
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This image demonstrates polymorphic ventricular tachycardia.
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This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.
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This electrocardiogram is from a 48-year-old man with wide-complex tachycardia during a treadmill stress test. Any wide-complex tachycardia tracing should raise the possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of a supraventricular rhythm. By Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from R-wave onset to the deepest part of the S wave is shorter than 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon lead aVR, which shows no R wave, an initial q wave width shorter than 40 ms, and no initial notching in the q wave. The last Vereckei criterion examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in lead aVR. In this case, the initial downward deflection in lead aVR is steeper than the terminal upward deflection, yielding Vi/Vt ratio above 1. All of these criteria are consistent with an aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with a sinus tachycardia mechanism.
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The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.
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A wide QRS complex tachycardia is evident on this electrocardiogram from a 64-year-old man with history of previous myocardial infarction (MI) and syncope. In patients with a prior MI, the most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
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This tracing depicts atrioventricular dissociation.
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Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.
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Note the retrograde P waves in this electrocardiogram.
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Retrograde P waves are also observed in this electrocardiogram.
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This electrocardiogram reveals torsade de pointes.
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Hematoxylin and eosin stain; intermediate power of a healed myocardial infarct. Note the areas of fibrosis (pale pink) dissecting between the myocytes (red).
Tables
| Recommendation | Class |
|---|---|
| Resting 12-lead electrocardiography (ECG) in all patients | Class I |
12-lead ambulatory ECG to evaluate QT-interval changes or ST changes |
Class I |
| Cardiac event recorders when symptoms are sporadic to rule out transient arrhythmias | Class I |
Implantable loop recorders when symptoms are sporadic and suspected to be related to arrhythmias and when a symptom–rhythm correlation cannot be established by conventional diagnostic techniques |
Class I |
Exercise stress testing in adult patients who have an intermediate or greater probability of having coronary artery disease (CAD) to provoke ischemic changes or ventricular arrhythmia (VA) |
Class I |
| Exercise stress testing in patients with known or suspected exercise-induced VA | Class I |
| Echocardiography in all patients | Class I |
Pharmacologic stress testing plus imaging modality study to detect silent ischemia in patients with VAs who have an intermediate probability of having CAD and are physically unable to perform a symptom-limited exercise test |
Class I |
Cardiac magnetic resonance imaging (cMRI) or computed tomography (CT) scanning in patients with VAs when echocardiography does not provide accurate assessment of left- and right-ventricular function and/or evaluation of structural changes |
Class IIa |
Electrophysiologic study in patients with CAD with remote myocardial infarction with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. |
Class I |
Coronary angiography to establish or exclude significant obstructive CAD in patients with life-threatening VAs or in survivors of sudden cardiac death, who have an intermediate or greater probability of having CAD by age and symptoms |
Class IIa |
