Ventricular Tachycardia Clinical Presentation

  • Author: Steven J Compton, MD, FACC, FACP; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Nov 9, 2011
 

History

The main symptoms of VT are palpitation, lightheadedness, and syncope from diminished cerebral perfusion. Chest pain may be due to ischemia or to the rhythm itself. Understandably, anxiety is often present. Syncope is more common 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 cannon a waves. Cannon a waves are related to right atrial contraction against a closed tricuspid valve.

Dyspnea may be related to increased pulmonary venous pressures and occasional left atrial contraction against a closed mitral valve.

Risk factors for VT include prior myocardial infarction, 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, the ACC/AHA/ESC 2006 guidelines for ventricular arrhythmias recommend a preparticipation history and physical examination. The history should include family history of premature or SCD and specific evidence of CVDs such as cardiomyopathies and ion channel disorders.[16] Athletes presenting with syncope should be assessed to uncover underlying CVD or rhythm disorder.[16]

Any patient with a strong family history of premature (< 40 y) sudden death should be evaluated for genetic arrhythmia syndromes, including long QT syndrome, short QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia, catecholaminergic polymorphic VT, and hypertrophic cardiomyopathy.

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Physical Examination

Besides tachycardia, findings of ventricular tachycardia generally reflect the degree of hemodynamic instability.

During ventricular tachycardia (VT)

Tachycardia is 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 may vary in intensity due to loss of AV synchrony.

During sinus rhythm following conversion

Physical findings during normal rhythm are 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 congestive heart failure is present.

Sinus rhythm is often interrupted by ventricular extrasystoles.

Mental status changes

The following changes may be seen in the patient’s mental status:

  • Anxiety
  • Agitation
  • Lethargy
  • Coma

Sudden death

Patients with sudden death may present with syncope first.

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Contributor Information and Disclosures
Author

Steven J Compton, MD, FACC, FACP  Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Coauthor(s)

Steven A Conrad, MD, PhD  Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Gary Setnik, MD  Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Ian S deSouza, MD  Assistant Professor, Department of Emergency Medicine, Kings County Hospital/SUNY Downstate Medical Centers

Ian S deSouza, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Che' Damon Ward, MD  Staff Physician, Department of Emergency Medicine, State University of New York Health Science Center at Brooklyn

Che' Damon Ward, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Justin D Pearlman, MD, ME, PhD, FACC, MA  Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Brian Olshansky, MD  Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

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This is a rapid monomorphic ventricular tachycardia (VT), 280 beats per minute, associated with hemodynamic collapse. This tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic (EP) study. The rhythm later converted to sinus with a single external shock. This patient had an atrial rate of 72 beats per minute (measured with intracardiac electrodes, not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, the surface ECG findings (dissociated P waves, fusion or capture beats) are only present approximately 20% of the time. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT with cycle lengths from 200-240 ms is often termed ventricular flutter.
This is a slow monomorphic ventricular tachycardia (VT), 121 beats per minute, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular function (ejection fraction [EF] 55%). He presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, most obvious in V2 and V3. Slower VT rates and preserved left ventricular (LV) function are associated with a better long-term prognosis.
Repetitive monomorphic ventricular tachycardia (VT) from an asymptomatic 45-year-old female wind surfer with a structurally normal heart. This ECG pattern is typical for idiopathic VT arising from the right ventricular outflow tract. This rhythm is often exertional and, unlike ischemic VT, suppressed by beta blockade or verapamil. The prognosis is good, with the following exceptions: (1) sudden death may be seen if right ventricular dysplasia or exceptionally rapid VT is encountered, and (2) occasionally, patients with incessant VT develop congestive heart failure due to tachycardia-induced cardiomyopathy or frequent ectopy. The cardiomyopathy resolves when the tachycardia is treated.
At first glance, this tracing suggests rapid, polymorphic ventricular tachycardia (VT). This is actually sinus rhythm with a premature atrial complex and superimposed lead motion artifact. The hidden sinus beats can be observed by using calipers to march backwards from the final 2 QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
Torsade de pointes. This is a polymorphic ventricular tachycardia (VT) associated with resting QT-interval prolongation. In this case, it was caused by the potassium channel blocker, sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels.
Preexcited atrial fibrillation. This patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over the accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia (VT).
Curative ablation of ventricular tachycardia (VT). This patient has VT in the setting of an ischemic cardiomyopathy. His VT was induced in the electrophysiology laboratory, and an ablation catheter was placed at a critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy is applied to the tissue through the catheter tip, and VT terminates when the critical conducting tissue is destroyed.
Ventricular pacing at 120 beats per minute Newer pacemakers use bipolar pacing. If the smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia (VT) may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have left bundle branch block (LBBB) morphology with an inferior axis. Causes of rapid pacing include (1) tracking of an atrial tachycardia in DDD mode, (2) rapid pacing due to rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis.
Supraventricular tachycardia (SVT) with aberrancy This is a patient with a structurally normal heart who has a normal resting ECG. This rhythm is an orthodromic reciprocating tachycardia with a rate-related left bundle branch block. Note the relatively narrow RS intervals in the precordial leads.
Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has a reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator (ICD).
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a prior septal myocardial infarction. Earliest activation is recorded in red; late activation shows 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.
Monomorphic ventricular tachycardia.
Polymorphic ventricular tachycardia.
This ECG is from a 32-year-old female with recent-onset congestive heart failure and syncope.
This ECG is from a 48-year-old male with wide complex tachycardia during treadmill stress test. Any wide complex tachycardia tracing should raise the possibility of VT, but closer scrutiny confirms left bundle branch block conduction of a supraventricular rhythm. Starting with the Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from the R wave onset to the deepest part of the S wave is < 100 msec in each of these leads. Ventriculoatrial dissociation is not seen. See Brugada et al (1991) for details of additional morphologic criteria. The Vereckei criteria (2008) are based solely upon aVR, which shows no R wave, an initial q wave width < 40 ms, and no initial notching in the q wave. The last criterion by Vereckei et al examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in aVR. In this case, the initial downward deflection in aVR is steeper than the terminal upward deflection, giving a vi/vt ratio >1. All of these criteria are consistent with aberrantly conducted SVT. The gradual rate changes during this patient's treadmill study (not shown here) were consistent with sinus tachycardia mechanism.
This ECG shows another form of idiopathic ventricular tachycardia, 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 a supraventricular tachycardia with bifascicular conduction block (RBBB/LAFB). Closer examination of lead V1 shows narrowing of the fourth QRS complex, consistent with fusion between the wide QRS complex and a conducted atrial beat, confirming AV dissociation and VT mechanism.
This patient is a 64-year-old man with a history of prior myocardial infarction and syncope. In patients with prior myocardial infarction, the most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
AV dissociation.
Fusion beats, capture beats, and AV dissociation.
Retrograde P's #1
Retrograde P's #2.
Torsades de pointes.
 
 
 
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