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Ventricular Fibrillation
Updated: Jul 28, 2008
Introduction
Background
Ventricular fibrillation (VF) begins as a quasiperiodic reentrant pattern of excitation in the ventricles with resulting poorly synchronized and inadequate myocardial contractions. The heart consequently immediately loses its ability to function as a pump. As the initial reentrant pattern of excitation breaks up into multiple smaller wavelets, the level of disorganization increases. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible. VF is the primary cause of sudden cardiac death (SCD).
Pathophysiology
Sudden cardiac death can be viewed as a continuum of electromechanical states of the heart: ventricular tachycardia (VT), VF, pulseless electrical activity (PEA), and asystole. VF is the most common initial state, and, because of insufficient perfusion of vital cardiac tissues, it degenerates to asystole if left untreated.
The etiology of VF remains incompletely understood. It often occurs in the setting of acute cardiac ischemia or infarction, and acute myocardial infarction (MI) is diagnosed in up to half of sudden-death survivors. The incidence of sudden death is also relatively high in the postinfarction period for months after an MI. Abnormal rapid stimulation of the ventricles can lead to fibrillation. This can occur during VT or in conditions, such as Wolff-Parkinson-White syndrome, when atrial fibrillation or flutter waves pass rapidly through a bypass tract to the ventricular musculature. Severe left ventricular dysfunction, a variety of cardiomyopathies, and acquired or idiopathic long QT syndrome also increase the risk of fibrillation.
Multiple events may lead to the initiation of VF. One etiology is mechanical or electrical stimulation of the myocardium during the early phase of repolarization (termed R-on-T phenomenon). When an impulse is delivered to the heart during the time period that corresponds to the upslope of the T wave, the ventricular myocardium is in a variable state of excitability because some of the muscle is still partly or completely refractory. The impulse may propagate electrically through the tissue but at a decreased rate through a tortuous pathway. Slowed abnormal conduction may allow the wave of depolarization to circle around and reexcite areas that have had sufficient time for repolarization.
Sustained VF may be due to a relatively small number of macroreentrant circuits or rotors, which are relatively stationary or drift through the 3-dimensional volume of the ventricular myocardium. These rotors may activate the cardiac muscle fibers at a high frequency, with secondary wavefronts emanating, traveling, and breaking up at variable distances from the source.
All fibrillation is not the same. VF begins as a coarse, irregular deflection on the ECG, then degenerates to a fine, irregular pattern, and eventually becomes asystole. These electrocardiographic changes reflect the electrical changes described above. The probability of successful defibrillation decreases as the VF waveform becomes smoother with time.
Frequency
United States
The incidence of SCD in the United States is approximately 300,000 cases per year. The distribution of rhythms found in patients with cardiac arrest depends largely on the average duration of the arrest state and, thus, the emergency medical system (EMS) response times. In monitored settings, such as casinos, where average response times are less than 5 minutes, the initial rhythm is VF in approximately 70% of patients. A circadian pattern of SCD has also been reported.
International
VF also is prevalent worldwide, with a reported predominance in the northern hemisphere. Among some European populations, the annual incidence of cardiac arrests exceeds 6 cases per 10,000 people.
Mortality/Morbidity
The likelihood of survival of cardiac arrest victims also depends on the duration of arrest prior to treatment. Improved outcomes occur in patients who have a witnessed arrest, receive bystander cardiopulmonary resuscitation (CPR), obtain defibrillation and advanced cardiac life support from EMS personnel within 10 minutes of onset, and present with an initial rhythm of VF.
Cardiac arrests witnessed by bystanders have a better prognosis because the victim is more likely to receive early treatment. The rate of survival from VF in the community varies from 4-33%. The survival rate of all cardiac arrest victims regardless of presenting rhythm has been reported to be as high as 18% and as low as 2% in various EMS systems. Large urban centers tend to have lower rates of survival. These lower rates of survival have been attributed to lower rates of bystander CPR, longer response intervals, and fewer patients presenting with VF.
Race
Black males have the highest incidence of SCD.
Sex
SCD is more common among males than females, although the rates become similar for patients older than 70 years.
Age
Incidence initially peaks during the first 6 months of life, then rapidly declines until a second peak in those aged 45-75 years.
Clinical
History
- VF often occurs without forewarning. The following symptoms, while not necessarily specific for SCD or VF, may develop before any major cardiac event:
- Chest pain and other angina equivalents
- Dyspnea
- Easy fatigue
- Palpitations
- Syncope
- Immediately preceding acute cardiac arrest, possible increase in heart rate, presence of premature ventricular contractions (PVCs), or period of VT
Physical
- No pulse or respiration
- Unconsciousness
- Wide and chaotic QRS complexes on cardiac monitor
Causes
- Cardiac, structural heart disease
- Myocardial ischemia or infarction due to coronary artery disease: Coronary atherosclerosis and its consequences are responsible for approximately 80% of sudden cardiac deaths in the United States.
- Cardiomyopathy: Dilated and hypertrophic cardiomyopathies are the second most important cardiac causes of sudden death. The degree of functional and physiologic left ventricular impairment is correlated with the risk of sudden death.
- Dilated
- Hypertrophic
- Arrhythmogenic right ventricular cardiomyopathy or dysplasia
- Aortic stenosis
- Aortic dissection
- Pericardial tamponade
- Congenital heart disease
- Myocarditis
- Cardiac, no structural heart disease
- Catecholaminergic polymorphic ventricular tachycardia and right ventricular outflow tract tachycardia
- Mechanical (commotio cordis) or electrical accidents
- Preexcitation (including Wolff-Parkinson-White syndrome)
- Heart block
- Drug-induced QT prolongation with torsades de pointes
- Channelopathies
- Long QT syndrome
- Short QT syndrome
- Brugada syndrome
- Noncardiac respiratory
- Bronchospasm
- Aspiration
- Sleep apnea
- Primary pulmonary hypertension
- Pulmonary embolism
- Tension pneumothorax
- Metabolic or toxic
- Electrolyte disturbances and acidosis
- Medications or drug ingestion
- Environmental poisoning
- Sepsis
- Neurologic
- Seizure
- Cerebrovascular accident - Intracranial hemorrhage or ischemic stroke
- Drowning
More on Ventricular Fibrillation |
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| References |
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Further Reading
Keywords
VF, ventricular fibrillation, sudden cardiac death, SCD, tachycardia, ventricular tachycardia, VT, pulseless electrical activity, PEA, asystole, acute cardiac ischemia, acute cardiac infarction, acute myocardial infarction, MI, cardiac arrest
