Ventricular Fibrillation Workup

Updated: Apr 29, 2014
  • Author: Sandeep K Goyal, MD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Approach Considerations

The presence of ventricular fibrillation (VF) can be confirmed only with an electrocardiogram (ECG). In addition, an ECG is indicated in all patients who have experienced VF, as it may provide evidence of an underlying condition that led to the episode.

Signal-averaged ECG is of limited value. [64] In patients with dilated cardiomyopathy (unlike those with ischemic cardiomyopathy), increased asymptomatic ventricular ectopy and nonsustained ventricular tachycardia (VT) are not predictive of VF. Approximately 80% of persons with dilated cardiomyopathy have these findings on Holter monitoring, hence the limited diagnostic value.

The evaluation of patients who have experienced VF should also include echocardiography, while nuclear imaging studies can help in the assessment of patients at risk for VF. In targeted patients, electrophysiologic (EP) studies play diagnostic, prognostic, and therapeutic roles.

Appropriate laboratory studies may include the following:

  • Serum electrolyte levels, including calcium and magnesium
  • Cardiac enzymes (eg, creatine kinase, myoglobin, troponin)
  • Complete blood count (CBC) to detect contributing anemia
  • Arterial blood gases (ABGs) to assess degree of acidosis or hypoxemia
  • Quantitative drug levels (eg, quinidine, procainamide, tricyclic antidepressants, digoxin)
  • Toxicologic screens and levels as clinically indicated
  • Thyroid-stimulating hormone: Hyperthyroidism can lead to tachycardia and tachyarrhythmias; over a period of time, it can also lead to heart failure
  • B-type natriuretic peptide (BNP)

Elevations in levels of cardiac enzymes may indicate myocardial ischemia or infarction, with the extent of myocardial damage usually correlating with the degree of elevation in the enzyme levels. Patients with myocardial infarction (MI) are at increased risk for arrhythmia in the peri-infarct period.

Measurement of drug serum levels is indicated in patients taking agents that may have a proarrhythmic effect. With some medications, serum levels exceeding the therapeutic index can promote arrhythmia. Subtherapeutic levels of drugs for specific cardiac conditions can also increase the risk for arrhythmia. Most of the antiarrhythmic drugs also have proarrhythmic effects. A toxicology screen for drugs that can lead to vasospasm-induced ischemia (eg, cocaine) is warranted if suspicion exists.

BNP measurement may be useful in the diagnosis of decompensated heart failure as the cause of VF. BNP is highly specific and sensitive for this diagnosis when elevated left ventricular (LV) end-diastolic pressure is causing increased myocardial oxygen consumption and decreased cardiac output, leading to the abnormal myocardial substrate conditions conducive to the development of VF. For more information, see Natriuretic Peptides in Congestive Heart Failure.

Chest radiography may reveal whether a patient is experiencing congestive heart failure. Radiographs can also show signs of left or right ventricular hypertrophy. Signs of pulmonary hypertension may be evident.

First-degree relatives of patients who are diagnosed with dilated cardiomyopathy, hypertrophic cardiomyopathy, or arrhythmogenic right ventricular (RV) dysplasia should be screened. Screening consists of a history and physical examination, an ECG, and an echocardiogram. The value of genetic testing in conditions such as congenital long QT and hypertrophic cardiomyopathy is still being evaluated. Some studies have recommended the testing of siblings and close relatives of people with VF caused by these conditions.



An ECG can identify conditions that place patients at risk for VF, such as the following [65] :

  • MI
  • Prolonged or short QT interval
  • Epsilon sign (arrhythmogenic right ventricular cardiomyopathy/dysplasia [ARVC/D])
  • Brugada sign
  • Short PR interval
  • Wolff-Parkinson-White (WPW) pattern
  • Digitalis toxicity


Two-dimensional (2-D) echocardiography with Doppler is essential in the evaluation of VF. In patients who have had an MI, 2-D echocardiograms to evaluate left wall ̶ motion abnormalities (using the LV wall ̶ motion score index) can help to predict outcome and the risk for major cardiac events, including sudden death. A decrease in the ejection fraction and worsening wall-motion abnormalities with exercise may confer increased risk for the development of VF.

In the course of resuscitative attempts, VF may deteriorate or be succeeded by electromechanical dissociation or pulseless electrical activity; when this occurs, consideration of possible cardiac tamponade arises and may prompt desperate attempts at pericardiocentesis. In such situations, having echocardiographic information regarding not only LV function but also the presence or absence of pericardial fluid is advantageous.


Nuclear Imaging

Resting thallium-201 (201 Tl) or technetium-99m (99m Tc) scintigraphy is helpful in assessing myocardial damage after an MI. [66] In addition, resting scintigraphy tests can be very helpful in patients with low functional capacity (eg, because of chronic obstructive pulmonary disease, peripheral vascular disease, or orthopedic problems).

A larger myocardial defect on scintigraphy has been associated with greater risk for future cardiac events. However, the Multicenter Post-Infarction Research Group provided evidence that resting ejection fraction was the most important noninvasive predictor of sudden cardiac death (SCD), most commonly from VF, and other cardiac events in patients with MI. [67]

Exercise nuclear scintigraphy is very sensitive for detecting the presence, extent, and location of myocardial ischemia. Gibson et al found that pharmacologic-stress nuclear (dipyridamole or adenosine) scintigraphy was better than submaximal exercise ECG and coronary angiography in predicting cardiac death and other cardiac events. [66]


Coronary Angiography

Perform cardiac catheterization in patients with probable coronary artery disease (CAD) who survive VF, to assess the severity and extent of the CAD. The number of vessels with severe obstruction and the degree of LV dysfunction are important variables in predicting cardiac events, with LV ejection fraction being the best predictor of significant cardiac events and survival. Coronary angiography can also help to identify coronary anomalies and other forms of congenital heart disease.

Angiography is performed with the goal of identifying patients who may benefit from revascularization. Revascularization is the single best treatment for ischemic myocardium, which is the most common underlying substrate of VT and VF.


Electrophysiologic Studies

EP studies are usually performed after ischemic and structural heart disease has been diagnosed and addressed as best as it can be. They are generally not indicated for the subset of patients in whom VF occurred within the first 24-48 hours of an acute MI, unless the patient had previous VF events. In all other patients with VF, however, consider EP studies for diagnostic and therapeutic guidance.

EP studies have been used to distinguish patients with inducible VT/VF from those with no inducible sustained ventricular arrhythmias. The presence of inducible sustained VT or VF, at baseline or when the patient is on antiarrhythmic medications, confers a higher risk for sudden death. [68] . Significantly lower ventricular function has also been observed in patients with inducible sustained VT or VF.

Sustained monomorphic VT induced with up to triple extrastimuli confers increased risk of SCD. However, polymorphic VT or VF induced by use of triple extra-stimuli is less specific and may not represent clinically significant arrhythmia. [69, 70]

EP studies can also risk-stratify patients with borderline severe depression of ejection fraction (< 40% but >30%). These patients are candidates for primary prevention with an implantable cardioverter defibrillator (ICD) if a sustained monomorphic ventricular arrhythmia is induced during an EP study. [71]

Inducible bundle-branch reentrant VT can be observed in patients with dilated cardiomyopathy and in the postoperative period after valvular replacement. Up to 20% of patients with hypertrophic cardiomyopathy have inducible sustained monomorphic VT. Identification of accessory pathways is possible with these studies.