Ventricular fibrillation (VF) is the most commonly identified arrhythmia in cardiac arrest patients. This arrhythmia is a severe derangement of the heartbeat that usually ends in death within minutes unless corrective measures are promptly taken. The number of survivors after out-of-hospital cardiac arrest has increased with expansion of community-based emergency rescue systems, widespread use of automatic external defibrillators (AEDs), and increasing numbers of lay persons trained in bystander cardiopulmonary resuscitation (CPR).
NextPathophysiologyVF occurs in a variety of clinical situations but is most often associated with coronary artery disease (CAD) and as a terminal event. VF may be due to acute myocardial infarction or ischemia, or it may occur in the setting of chronic infarct scar. Intracellular calcium accumulation, the action of free radicals, metabolic alterations, and autonomic modulation are some important influences on the development of VF during ischemia. Thrombolytic agents reduce the incidence of ventricular arrhythmias and inducible ventricular tachycardia (VT) after myocardial infarction (MI).
Cardiovascular events, including sudden cardiac death (SCD) from VF (but not asystole), most frequently occur in the morning and may be related to increased platelet aggregability. (Aspirin reduces the frequency of this form of mortality.) A spike in the number of SCDs appears to occur during the winter months.
VF can occur during any of the following conditions or situations: Antiarrhythmic drug administrationHypoxiaIschemiaAtrial fibrillationVery rapid ventricular rates in the preexcitation syndromeElectrical shock administered during cardioversionElectrical shock caused by accidental contact with improperly grounded equipmentCompetitive ventricular pacing to terminate VTMost prehospitalized patients with cardiac arrest (65-85%) have VF identified as the initial rhythm by emergency rescue personnel. Approximately 20-30% of patients from all documented sudden death events have bradyarrhythmia or asystole at the time of initial contact, indicating a terminal event from massive myocyte necrosis, pump failure, or VF progression to asystole. Only 7-10% have sustained VT as the initial rhythm on contact, and VT is associated with the best overall prognosis. When documentation is available, it often shows that rapid VT precedes VF. In patients with ischemic heart disease, the most common form of VT is monomorphic, which arises from a reentrant focus. In patients who survive an MI, it has been demonstrated that those with frequent premature ventricular contractions (PVCs), particularly complex forms such as multiform PVCs, short coupling intervals (R-on-T phenomenon), or VT (salvos of 3 or more ectopic beats), are at increased risk of sudden death. Even though many patients have anatomic and functional cardiac substrates that predispose them to develop ventricular arrhythmias, only a small percentage develop VF. The interplay among the regional ischemia, left ventricular (LV) dysfunction, and transient inciting events (eg, worsened ischemia, acidosis, hypoxemia, wall tension, drugs, metabolic disturbances) has been proposed to be the precipitator of VF. PreviousNextEpidemiologyFrequencyUnited StatesSCD accounts for approximately 300,000 deaths per year in the United States, of which 75-80% are due to VF. More deaths are attributable to VF than to lung cancer, breast cancer, or AIDS. This represents an incidence of 0.08-0.16% per year in the adult population. VF is commonly the first expression of CAD and is responsible for approximately 50% of deaths from CAD, often within the first hour after the onset of an acute MI or coronary syndrome.
In several population-based studies, the incidence of out-of-hospital cardiac arrest has been noted as declining in the past 2 decades, but the proportion of sudden CAD deaths in the United States due to VF has not changed. A high incidence of VF occurs among certain population subgroups (eg, patients with congestive heart failure [CHF] with ejection fraction
The time dependence of risk for VF has been noted in several studies, with an increased number of events in the first 6-24 months after surviving a major cardiovascular event. Recurrence of VF in survivors of cardiac arrest can be up to 30% in the first year.
InternationalThe frequency of VF in industrialized Western nations is similar to that in the United States. The incidence of VF in other countries varies as a reflection of CAD prevalence in those populations. The trend toward increasing frequency of VF events in developing nations is thought to reflect a change in dietary and lifestyle habits.
Mortality/MorbidityA witness is not present in up to 40% of the approximately 225,000 deaths attributed to VF in the United States each year. For most people who experience VF, survival depends on the presence of individuals who are competent in performing basic life support, rapid availability or arrival of personnel and apparatus for defibrillation and advanced life support, and transfer to a hospital.
Even under ideal circumstances, only an estimated 20% of patients who have out-of-hospital cardiac arrest survive to hospital discharge. In a study of out-of-hospital cardiac arrest survival in New York City, only 1.4% of patients survived to hospital discharge.[1] Other studies in suburban and rural areas have indicated survival rates up to 35%.[2] Placement of AEDs throughout communities and training people to use them has the potential to markedly improve outcomes from SCD. One study suggests routine coronary angiography with potentially associated percutaneous coronary intervention may favorably alter the prognosis of resuscitated patients with stable hemodynamics who are submitted to mild therapeutic hypothermia after out-of-hospital cardiac arrest.[3]
Upon presentation to an emergency department (ED), the most important determinants of survival include (1) an unsupported systolic blood pressure (SBP) greater than 90 mm Hg, (2) a time from loss of consciousness to return of spontaneous circulation (ROSC) of less than 25 minutes, and (3) some degree of neurological responsiveness.
A major adverse outcome from a VF event is anoxic encephalopathy, which occurs in 30-80% of patients.
A study conducted in Minnesota on all adult patients who experienced out-of-hospital cardiac arrest (OHCA) VF from 1990-2008 found that long-term survivors of OHCA VF have long-term memory deficits compared with the normal population at the same age and education level. These findings provide a baseline for cognitive outcomes studies as new techniques are developed to improve survival.[4]
RaceMost data are inconclusive regarding racial differences and the incidence of VF. Some studies suggest that a greater proportion of coronary deaths were sudden in blacks compared with whites. In a report by Gillum on SCD from 1980-1985, the percentage of CAD deaths occurring out of the hospital and in EDs was found to be higher in blacks than in whites.[5]
SexMen have a higher incidence of VF than women (3:1). This ratio generally reflects the higher incidence of CAD in men. Recent evidence suggests that a major sex difference may exist in the mechanism of MI. Basic and observational data point to the fact that men tend to have coronary plaque rupture, whereas women tend to have plaque erosion. Whether this biologic difference accounts for the male predominance of VF is unclear.
AgeThe incidence of VF parallels the incidence of CAD, with the peak of VF occurring in people aged 45-75 years. The incidence of VF increases with age in men and women of all races because the prevalence of CAD increases with age. However, the proportion of sudden deaths from CAD decreases with age. In the Framingham Heart Study, the proportion of sudden CAD deaths was 62% in men aged 45-54 years, but this percentage fell to 58% in men aged 55-64 years and to 42% in men aged 65-74 years.[6] According to Kuller, 31% of deaths are sudden in people aged 20-29 years.[7]
PreviousProceed to Clinical Presentation , Ventricular Fibrillation
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