Ventricular Tachycardia Workup

When the patient presents with symptoms of frank hemodynamic compromise, one should defer laboratory tests until electrical cardioversion or defibrillation is performed and the patient is stabilized. The ACC/AHA/ESC 2006 guidelines recommend use of direct current cardioversion with sedation at any time during treatment in patients thought to have sustained monomorphic VT with hemodynamic compromise.^[16]

Assess electrolyte levels of all patients with ventricular tachycardia (VT), including serum calcium, magnesium, and phosphate levels. Ionized calcium levels are preferred over total serum calcium level. Hypokalemia, hypomagnesemia, and hypocalcemia may predispose patients to either monomorphic VT or torsade de pointes.

Obtain, when appropriate, levels of therapeutic drugs (eg, digoxin). Toxicology screens may be helpful in those cases related to recreational drug use.

Evaluate for myocardial ischemia or infarction with serum cardiac troponin I or T levels or other cardiac markers.

As indicated in the ACC/AHA/ESC 2006 guidelines, it is reasonable to maintain serum potassium levels above 4 mM/L in patients with acute MI.^[16]

Go to Pediatric Ventricular Tachycardia for complete information on this topic.

Ventricular tachycardia at acute presentation

If the patient is unconscious or hemodynamically unstable, the diagnosis is made from the physical findings and ECG rhythm strip. Laboratory studies are impractical, and advanced cardiac life support (ACLS) protocols are quickly followed. If circumstances allow, a full 12-lead electrocardiogram should be obtained prior to urgent cardioversion.

If the patient presents with hemodynamic stability, then a 12-lead ECG and electrolytes may be obtained prior to attempted conversion with medications or sedation and cardioversion. Electrocardiography is the criterion standard for the diagnosis of VT.

The electrocardiographic morphology during VT is predictive of the site of origin, regardless of the underlying substrate. Earliest activation is typically closest to the leads with QS complexes during tachycardia.^[19] (See the image below.)

Ventricular tachycardia postconversion

Repeat the ECG after termination of VT to evaluate for acute or chronic infarction, ischemia, scar, ventricular preexcitation, hypertrophy, conduction disease, QT prolongation, and other precordial repolarization abnormalities (Brugada syndrome, arrhythmogenic right ventricular dysplasia).

Include electrolyte levels in an acute evaluation. Hypokalemia is a common VT trigger and is commonly seen in patients taking diuretics. The ACC/AHA/ESC 2006 guidelines recommend potassium (and magnesium) salts as useful in treating ventricular arrhythmias secondary to hypokalemia (or hypomagnesemia) resulting from diuretic use in patients with structurally normal hearts.^[16]

Toxicology screens for cocaine metabolites and tricyclic antidepressants should be performed in accordance with the patient’s clinical history.

Check cardiac enzyme levels if clinical symptoms or signs of ischemia are present. Persistently elevated cardiac enzyme levels may also be an indication of ongoing myocarditis.

In some patients with spontaneous polymorphic VT, genetic studies may be helpful for family screening or for clarifying a diagnosis. (See the section below.)

Following conversion to sinus rhythm, evaluation should usually include echocardiography and coronary angiography to assess for structural and ischemic heart disease. These considerations are paramount in defining further treatment in any patient with VT. These patients often require aggressive management of underlying ischemic heart disease and congestive heart failure.

Adenosine in diagnosis

Historically, the use of adenosine to distinguish between regular wide-QRS complex SVT and VT has been discouraged due to the theoretical precipitation of ventricular fibrillation. According to the ACC/AHA/ESC 2006 guidelines, wide-QRS tachycardia should be presumed to be VT if the diagnosis is unclear.^[16]

However, a study demonstrated that adenosine may be useful and safe as a diagnostic agent in this differentiation.^[20] Adenosine through transient AV nodal blockade should terminate reentrant SVTs, which involve the AV node as a pathway, but will not terminate VT.

Adenosine should not be used for irregular wide-QRS complex tachycardia, as this dysrhythmia may involve atrial fibrillation in presence of an accessory pathway (as demonstrated in the ECG below). In this particular case, adenosine may allow conduction of rapid atrial fibrillatory impulses exclusively through an amenable accessory tract to cause very rapid, intolerable ventricular rates.

Family screening

When a patient is identified with long QT syndrome, short QT syndrome, hypertrophic cardiomyopathy, or right ventricular dysplasia, family screening should be contemplated. This usually can be accomplished with a history and physical examination, combined with noninvasive testing (ECG, echocardiogram, treadmill testing).

In patients with VT related to genetic abnormalities, family screening is essential. Commercial genotyping studies have been available in the United States since 2004.

Spontaneous polymorphic VT may be related to genetic mutations affecting ion channels, as occurs in long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT.

Finally, some patients are predisposed to drug-induced ventricular arrhythmias by otherwise subclinical genetic ion channel defects.

Electrocardiography is the diagnostic tool of choice for confirming the presence of ventricular tachycardia (VT). The ACC/AHA/ESC 2006 guidelines recommend the use of echocardiography in patients with ventricular arrhythmias (VAs) who are thought to have structural heart disease.^[16]

Signal-averaged electrocardiography (SAECG) is a noninvasive test that often produces abnormal results in patients with VT related to prior infarct or right ventricular dysplasia.

The ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death suggest that SAECG, along with heart rate variability (HRV), baroflex sensitivity, and heart rate turbulence may be useful to refine the diagnosis and risk stratification of patients with VAs or those who are at increased risk of developing life-threatening VAs.^[16]

Simultaneous 3-channel recordings and 12-lead tracings are more helpful than rhythm strips to analyze such dysrhythmias.

T-wave alternans testing has also been proposed as a noninvasive risk stratifier for sudden death risk, but definitive studies are still lacking.

The ACC/AHA/ESC 2006 guidelines recommend the use of echocardiography for the subset of patients at high risk for serious VAs or SCD, such as those with dilated, hypertrophic, or right ventricular (RV) cardiomyopathies, as well as acute MI survivors, or those related to patients with inherited disorders related to SCD.^[16]

The ECG below demonstrates a tachycardia with a 1:1 atrial:ventricular relationship. It is not clear from this tracing whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (ventricular tachycardia).

At first glance, sinus tachycardia in the below ECG might be considered with severe conduction disease manifesting as marked first-degree atrioventricular block with left bundle branch block. Looking more closely, electrocardiographic morphology gives clues to the actual diagnosis of VT. These clues include the absence of RS complexes in the precordial leads, a QS pattern in V₆, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy.

Differentiating VT from SVT

Complexes of atypical morphology often are difficult to interpret. Such tachycardias can be PSVT with aberrant conduction. If the patient is unstable, or differentiation between VT and SVT is uncertain, treat rhythm as VT. Recall that the vast majority of patients with wide-complex regular tachycardias will have VT.

Electrocardiographic criteria that support VT over SVT include AV dissociation, capture beats, fusion beats (sometimes at the initiation of the dysrhythmia), QRS duration over 140 ms. Other, more subtle criteria include R or qR pattern in V₁, frontal QRS axis between 180 and 270 degrees, and positive or negative concordance across the precordial leads.^[21]

Electrocardiographic criteria that support SVT over VT include a right bundle branch block (RBBB) pattern when present in the native sinus rhythm, varying bundle branch block, an rsR’ pattern in V₁, or an ectopic P wave preceding the dysrhythmia.^[21]

In a syncopal patient, the ECG should be screened carefully for myocardial infarction, conduction abnormalities, QT-interval prolongation, precordial T-wave inversions, ventricular preexcitation, and ventricular hypertrophy.

Brugada et al^[22] proposed ECG criteria for VT that focused primarily on the QRS morphologies in the precordial leads (V₁ -V₆). The criteria included the following:

• The absence of RS complexes in the precordial leads
• RS duration greater than 100 milliseconds in any precordial lead
• Ventriculoatrial dissociation in any of 12 leads
• Certain QRS morphologies, such as QR or QS in V₆

Vereckei et al refined a different algorithm, based upon the single lead aVR.^[23] They noted the presence of a negative QRS complex in aVR during right or left bundle branch conduction of SVTs. They found that VT mechanism was predicted by the following:

• Presence of an initial R wave in aVR
• Width of an initial r or q wave >40 ms in aVR
• Notching on the initial downstroke of a predominantly negative QRS complex in aVR
• Ventricular activation-velocity ratio (V_i/V_t) less than or equal to 1

Chest radiography is indicated if symptoms suggest the possibility of congestive heart failure or other cardiopulmonary pathology as a contributing factor.

Cardiac computed tomography (CT) scans and cardiac magnetic resonance imaging (MRI) technologies are evolving quickly but have not yet supplanted echo and nuclear imaging for quantification of ventricular function. Cardiac MRI scans can be especially helpful in the evaluation of uncommon myocardial infiltrative diseases, such as sarcoidosis.

Although cardiac MRI is often used for the evaluation of arrhythmogenic right ventricular dysplasia, the diagnostic yield of this test has yet to be clearly defined. Right ventricular angiography may still be the criterion standard imaging study for arrhythmogenic right ventricular dysplasia (ARVD).

The ACC/AHA/ESC 2006 guidelines state that MRI, cardiac CT, or radionuclide angiography can be useful in patients with VAs when echocardiography fails to provide accurate evaluation of LV or RV function and/or assessment of structural changes.^[16]

Occasionally, patients present with recurrent syncope or palpitations. In this setting, an arrhythmic cause of syncope may be sought. Options include Holter monitoring, which has a low yield, or event recording. The goal is to document the patient's rhythm during symptoms. If this is not practical, a provocative electrophysiologic study (EPS) can be performed. The ACC/AHA/ESC 2006 guidelines recommend EP evaluation in patients with syncope of unknown etiology with impaired LV function or structural heart disease.^[16]

Genetic testing, which was also discussed earlier, is now feasible for a variety of abnormalities associated with long QT syndromes, arrhythmogenic right ventricular dysplasia, or dilated or hypertrophic abnormalities. However, the absence of a defined genomic mutation does not exclude these abnormalities; the current approach is not exhaustive and is focused on established monogenic germline abnormalities.

Occasionally, myocardial biopsy with special histologic processing may be useful in the diagnosis of ARVC or a hypertrophic or infiltrative myopathy.

As noted above, most reentrant ventricular tachycardias (VTs) are related to myocardial scarring from ischemic or dilated cardiomyopathy. Fibrotic replacement of myocytes and interweaving of scar tissue with functional myocytes is common along slow conduction zones of VT circuits.

The presence of a dual chamber pacemaker or implantable cardioverter-defibrillator (ICD) can occasionally simplify diagnosis. Most contemporary devices are capable of recording and logging tachyarrhythmias for subsequent analysis during interrogation of the implanted device.

On the other hand, patients with pacemakers and ICDs may present with wide-complex tachycardia (WCT) secondary to rapid ventricular pacing.

Possibilities include tracking of an atrial tachyarrhythmia in a dual-mode, dual-pacing, dual-sensing (DDD) device or an atrial-triggered, ventricular-inhibited (VDD) device; endless loop tachycardia; inappropriate rate responsive pacing due to sensor problems or incorrect sensor programming; and overt pacemaker failure (runaway pacer).

The most common problem involves the patient whose device is tracking atrial fibrillation or flutter. In the absence of a mode-switching algorithm, a VDD or DDD pacer responds by pacing the ventricle at the programmed upper rate limit of the device. Application of a magnet to the pacer generator may terminate endless loop tachycardia or drop the paced rate enough to allow diagnosis of the underlying atrial tachyarrhythmia.

As stated by the ACC/AHA/ESC 2006 guidelines, an ICD should be implanted in patients with nonischemic DCM and considerable LV dysfunction who have sustained VT or VF, are receiving chronic optimal medical therapy, and are reasonably expected to survive with good functional status for more than 1 year.^[16]

The guidelines also recommend ICD therapy for primary prevention to reduce total mortality by a reduction in SCD in patients with nonischemic DCM, with an LV ejection fraction (LVEF) less than or equal to 30-35%, are NYHA functional class II or III, who are receiving chronic optimal medical treatment, and who have a reasonable expectation of living with a good functional status for more than 1 year.^[16]

ICD implantation is recommended, as per the ACC/AHA/ESC guidelines, for prevention of SCD in patients with ARVC and documented sustained VT or VF who are receiving chronic optimal medical treatment and who are reasonably expected to survive with a good functional status for more than 1 year.^[16]

Diagnostic electrophysiologic study (EPS) requires placement of electrode catheters in the ventricle, followed by programmed ventricular stimulation using progressive pacing protocols. Premature ventricular beats^[12] are induced following conditioning pacing drives, in an attempt to induce reentrant arrhythmia. In patients with symptoms suggestive of ventricular tachycardia (VT), this kind of provocative testing can be used to assess whether the ventricles can sustain a reentrant tachyarrhythmia. Diagnostic yield of EPS is highest in patients with reentrant VT circuits.

EPS is particularly relevant in patients who are felt to be at high risk for sudden death due to significant underlying structural heart disease. EPS may be useful in demonstrating whether the substrate for sustained VT is present in a patient presenting with syncope or ischemic, nonsustained VT. In patients with recurrent symptoms related to VT, programmed electrical stimulation can generally reproduce clinically relevant VT circuits.

If right ventricle dysplasia is being considered, many laboratories perform right ventricular angiography as a part of the EPS. Diagnostic abnormalities include right ventricular dilation, dyskinesis, and aneurysms.

In accordance with the ACC/AHA/ESC 2006 guidelines, electrophysiologic (EP) testing is recommended for diagnostic assessment of patients with remote MI and symptoms related to ventricular tachyarrhythmias, including palpitations, presyncope, and syncope, and in patients with CHD to guide and measure the efficacy of VT ablation.The ACC/AHA/ESC 2006 guidelines state that EP testing is reasonable for diagnostic evaluation in patients with palpitations or suspected outflow tract VT.^[16]