Ventricular Fibrillation Clinical Presentation

Updated: Jun 06, 2018
  • Author: Sandeep K Goyal, MD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Obtaining a thorough history from the patient, family members, or other witnesses is necessary to obtain insight into the events surrounding the episode of ventricular fibrillation (VF). Patients at risk for VF may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic. Up to 45% of persons who have VF have been noted to visit their physician in the 4 weeks before death, although in up to 75% of these patients, the complaints were not related to the cardiovascular system.

A history of left ventricular (LV) dysfunction (LV ejection fraction [LVEF] < 30%-35%) is the single greatest risk factor for sudden death from VF. Risk factors that relate to coronary artery disease (CAD) and to subsequent myocardial infarction (MI) and ischemic cardiomyopathy are also important and include a family history of premature CAD, smoking, dyslipidemia, hypertension, diabetes, obesity, and a sedentary lifestyle. Specific considerations include the following:

  • CAD

  • Previous cardiac arrest

  • Syncope or near-syncope

  • Prior MI, especially within 6 months

  • LVEF less than 30%-35%

  • History of frequent ventricular ectopy (>10 premature ventricular contractions [PVCs] per hour or nonsustained ventricular tachycardia [VT])

  • Drop in systolic blood pressure or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia

  • Dilated cardiomyopathy (DCM) from any cause (but most commonly ischemic or idiopathic)

  • Hypertrophic cardiomyopathy (HCM), obstructive or nonobstructive

  • Use of inotropic medications, particularly in patients with decompensated heart failure or acute myocardial ischemia

  • Valvular heart disease (severe uncorrected aortic or mitral stenosis or regurgitation; valve replacement within 6 months)

  • Myocarditis

Given the possibility of sustained or prolonged VT being the underlying cause, aggressively pursue a history of syncope.

Some forms of congenital heart disease increase the risk for VF. Long QT syndrome (LQTS) can result in VF, particularly in patients with a family history of sudden cardiac death (SCD) (the risk is also increased in acquired LQTS caused by medications that prolong the QT interval). In patients with Wolff-Parkinson-White (WPW) syndrome with extremely rapid conduction over an accessory pathway, degeneration to VF can occur. Other congenital heart diseases that increase VF risk include Brugada syndrome and arrhythmogenic right ventricular (RV) cardiomyopathy/dysplasia (ARVC/D).


VF can occur during any of the following conditions or situations [1] :

  • Antiarrhythmic drug administration

  • Hypoxia

  • Ischemia

  • Atrial fibrillation with very rapid ventricular rates in the presence of preexcitation

  • Electric shock administered during cardioversion

  • Electric shock caused by accidental contact with improperly grounded equipment

  • Competitive ventricular pacing to terminate VT (including that delivered by an implantable device)


Physical Examination

Risk stratification and prognosis determination are crucial in the emergency department (ED) evaluation and treatment of patients with ventricular fibrillation (VF). Patients who survive to ED presentation can be stratified by their cardiac arrest score, which has excellent prognostic value.

The cardiac arrest score, developed by McCullough and Thompson, can be used for patients with witnessed out-of-hospital cardiac arrest. [64] The score uses three criteria: ED systolic blood pressure (SBP), time to return of spontaneous circulation (ROSC) after loss of consciousness, and neurologic responsiveness. The score is calculated as follows [71] :

  • ED SBP: Above 90 mm Hg = 1 point; below 90 mm Hg = 0 points

  • Time to ROSC: Less than 25 minutes = 1 point; longer than 25 minutes = 0 points

  • Neurologically responsive = 1 point; comatose = 0 points

In-hospital mortality rates and neurologic recovery (defined as being discharged home and able to care for oneself), stratified by the initial cardiac arrest score, are shown in Table 2, below.

Table 2: Outcome according to initial cardiac arrest score (Open Table in a new window)

Cardiac Arrest Score

In-Hospital Mortality Rate (%)

Neurologic Recovery (%)













McCullough et al found that even in the setting of ST elevation and early invasive management with primary angioplasty and intraaortic balloon pump insertion, patients with low cardiac arrest scores are unlikely to survive. [72] Consequently, invasive management is rarely justified in patients with scores of 0, 1, or 2; instead, conservative management with empiric supportive and medical therapy may be more appropriate.