AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

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).

Pathophysiology

VF 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 administration
  • Hypoxia
  • Ischemia
  • Atrial fibrillation
  • Very rapid ventricular rates in the preexcitation syndrome
  • Electrical shock administered during cardioversion
  • Electrical shock caused by accidental contact with improperly grounded equipment
  • Competitive ventricular pacing to terminate VT
• Most 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.

Frequency

United States

SCD 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 <30%, patients in the convalescent phase after MI, patients who survived cardiac arrest); unfortunately, only a small percentage of total VF events occur in these patients.

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.

International

The 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/Morbidity

A 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 (Lombardi, 1994). Other studies in suburban and rural areas have indicated survival rates up to 35% (Waalewijn, 1998). Placement of AEDs throughout communities and training people to use them has the potential to markedly improve outcomes from SCD.

• 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.

Race

Most 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.

Sex

Men 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.

Age

The 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 (Gordon, 1971). According to Kuller, 31% of deaths are sudden in people aged 20-29 years.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Obtaining a thorough history from the patient, family members, or other witnesses is necessary to obtain insight into the events surrounding the episode of VF. Patients at risk for VF may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints. Up to 45% of persons who have VF have been noted to visit their physician in the 4 weeks before death, although up to 75% of these patients' complaints were not related to the cardiovascular system. A history of LV impairment (LV ejection fraction [LVEF] <30-35%) is the single greatest risk factor for sudden death from VF. Risk factors that relate to CAD and to subsequent MI and ischemic cardiomyopathy are also important and include a family history of premature CAD, smoking, dyslipidemia, hypertension, diabetes, obesity, and sedentary lifestyle. Specific considerations include the following:

• Coronary artery disease
• • Previous cardiac arrest
  • Syncope
  • Prior MI, especially within 6 months
  • LVEF less than 30-35%
  • History of frequent ventricular ectopy (>10 PVCs/h or nonsustained VT)
  • Drop in SBP or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia
• Dilated cardiomyopathy (DCM) from any cause (but most commonly due to ischemic or idiopathic etiology)
• • Previous cardiac arrest
  • Syncope or near-syncope
  • LVEF less than 30-35%
  • Use of inotropic medications, particularly in patients with decompensated CHF or acute myocardial ischemia
• Hypertrophic cardiomyopathy (HCM), obstructive or nonobstructive
• • Previous cardiac arrest
  • Syncope or near-syncope
  • Family history of SCD
  • Symptoms of decompensated heart failure
  • Drop in SBP or ventricular ectopy upon stress testing
  • Palpitations
  • Usually asymptomatic
• Valvular heart disease
• • Severe uncorrected aortic or mitral stenosis
  • Severe mitral or aortic regurgitation
  • Valve replacement within 6 months
  • Syncope
  • History of frequent ventricular ectopy
• Myocarditis
• • LVEF less than 30-35%
  • Symptoms of decompensated heart failure
  • Previous cardiac arrest
  • Syncope or near-syncope
• Congenital heart disease
• • Functional causes
  • Autonomic nervous system
  • Metabolic toxic electrolyte imbalance
• Long QT syndrome
• • Family history of long QT syndrome and SCD
  • Medications that prolong the QT interval (acquired long QT syndrome)
• Wolff-Parkinson-White (WPW) syndrome (with atrial fibrillation or atrial flutter with extremely rapid ventricular rates): With extremely rapid conduction over an accessory pathway, degeneration to VF can occur.
• Brugada syndrome, arrhythmogenic right ventricular (RV) cardiomyopathy/dysplasia, others

Physical

Risk stratification and prognosis determination is absolutely crucial in the ED evaluation and treatment of patients with VF. Initial evaluation studies show that patients who survive to ED presentation can be stratified by a cardiac arrest score, which has excellent diagnostic value. The cardiac arrest score, developed by Thompson and McCullough, can be used for patients with witnessed out-of-hospital cardiac arrest and is defined by the following criteria:

• Clinical characteristic points
• • ED SBP greater than 90 mm Hg = 1 point
  • ED SBP less than 90 mm Hg = 0 points
  • Time to ROSC less than 25 minutes = 1 point
• Time to ROSC more than 25 minutes = 0 points
• Neurologically responsive = 1 point
• Comatose = 0 point
• Maximum score = 3 points
• Patients with a score of 3 points can be expected to have an 89% chance of neurologic recovery and an 82% chance of survival to discharge (see Image 1).
• Recent work from McCullough and colleagues indicates that even in the setting of ST elevation and early invasive management with primary angioplasty and intraaortic balloon pump insertion, patients with low cardiac scores are unlikely to survive (McCullough, 2002).
• Severe anoxic encephalopathy in patients with scores of 0, 1, or 2 suggests the use of conservative management with empiric supportive and medical therapy. Given the very poor actuarial survival rates for these patients, invasive management with catheterization and electrophysiology studies (EPS) is rarely justified.

Causes

• Ischemic heart disease: Cardiac arrest attributable to ventricular arrhythmias may be due to chronic scar or to acute MI/ischemia. A chronic infarct scar can serve as the focus for reentrant ventricular tachyarrhythmias. This can occur shortly after the infarct or years later. Many studies support the relationship of symptomatic and asymptomatic ischemia as markers of myocardium at risk for arrhythmias. Patients resuscitated from out-of-hospital cardiac arrest have an increased recurrence of cardiac arrest and express an increased incidence of silent ST-segment depression. Experiments inducing myocardial ischemia in animal models have a strong relationship with the development of VF.
• • In postmortem studies of people who have died from VF, extensive atherosclerosis is the most common pathologic finding. In survivors of cardiac arrest, coronary heart disease with vessels showing greater than 75% stenosis is observed in 40-86% of patients, depending on the age and sex of the population studied. Autopsy studies show similar results; in one study of 169 hearts, approximately 61% of patients died of VF, and more than 75% stenosis in 3 or 4 vessels and similar severe lesions were present in at least 2 vessels in another 15% of cases. No single coronary artery lesion is associated with an increased risk for VF.

    Despite these findings, only approximately 20% of VF-related autopsies have shown evidence of a recent MI. A greater proportion of autopsies (40-70%) show evidence of a healed MI. Many of these hearts also reveal evidence of plaque fissuring, hemorrhage, and thrombosis.

  • The Coronary Artery Surgery Study (CASS) showed that improving or restoring blood flow to an ischemic myocardium decreased the risk of VF, especially in patients with 3-vessel disease and heart failure, compared with medical treatment over a 5-year period (Holmes, 1989). This finding suggests that transient acute ischemia is one of the major triggering events for sudden arrhythmic death.
  • The efficacy of beta-blocking agents, such as propranolol, in decreasing sudden death mortality rates, especially when administered to patients who had MI with VF, VT, and high-frequency PVCs, is thought to be partially caused by the ability of beta-blockers to decrease ischemia. Beta-blockers also increase the VF threshold in ischemic animals and decrease the rate of ventricular ectopy in patients who had MI.
  • Reperfusion of ischemic myocardium with thrombolysis or direct angioplasty can induce transient electrical instability by several different mechanisms. Coronary artery spasm is a condition that exposes the myocardium to both ischemia and reperfusion insults. The exact mechanism of coronary artery spasm is not known.
  • Roles of the autonomic nervous system, especially the alpha-adrenergic activity, vagal activity, vessel susceptibility, and humoral factors, particularly associated with platelet activation and aggregation, are being investigated as possible mechanisms of coronary vasospasm.
  • Nonatherosclerotic coronary artery abnormalities, including congenital lesions, coronary artery embolism, coronary arteritis, and mechanical abnormalities of the coronary artery, are associated with an increased incidence of sudden death.
• Nonischemic cardiomyopathies: Patients with nonischemic cardiomyopathies are the second largest group of patients who experience VF. Nonischemic myopathies, for the purposes of this article, can be divided into dilated and hypertrophic categories.
• • Dilated cardiomyopathy
    • Nonischemic DCM is becoming increasingly more common, with an incidence of approximately 7.5 cases per 100,000 persons each year. Of cases of VF, 10% are estimated to be attributable to DCM. The prognosis is very poor for these patients, with a 1-year mortality rate of 10-50%, depending on the New York Heart Association functional class; approximately 30-50% of these deaths are caused by VF.
    • The causes of DCM are uncertain, but viral, autoimmune, genetic, and environmental (alcohol) origins are implicated. The predominant mechanism of death appears to be ventricular tachyarrhythmia, although bradyarrhythmia and electromechanical dissociation have also been observed, especially in patients with advanced LV dysfunction. Extensive fibrosis of the subendocardium, leading to dilated ventricles and subsequent generation of reentrant tachyarrhythmias, is a proposed mechanism for VF.

      Multiple factors contribute to increased risk for VF in this population. The most important hemodynamic predictor is an increase in end-diastolic pressure and subsequent wall tension. Other important factors are increased sympathetic tone, neurohumoral activation, and electrolyte abnormalities.

    • Many drugs used in the treatment of heart failure, such as antiarrhythmics, inotropic agents, and diuretics, have proarrhythmic properties, which may provoke arrhythmias in some patients.
    • Unlike ischemic cardiomyopathy, increased asymptomatic ventricular ectopy and nonsustained VT are not predictive of VF in DCM. Approximately 80% of persons with DCM have these findings on Holter monitoring, hence the lessened value of this diagnostic tool. Given the possibility of sustained VT being the underlying cause, aggressively pursue a history of syncope.
  • Hypertrophic cardiomyopathy
  • • HCM is usually an autosomal dominant, incompletely penetrant genetic disorder resulting from a mutation in one of the many (>45) genes encoding proteins of the cardiac muscle sarcomere. Among the described genetic abnormalities, mutations occur in the genes coding for the beta-myosin heavy chains, cardiac troponin T, and myosin-binding protein C. The incidence of VF in this population is 2-4% per year in adults and 4-6% per year in children and adolescents. HCM is the most common cause of VF in people younger than 30 years.
    • The vast majority of young people who die of HCM are previously asymptomatic. Most experience VT/VF while at rest or with mild exertional activity; however, in a significant portion of these patients, the VF event occurs after vigorous exertion. HCM is the single greatest cause of VF in athletes and is therefore the major entity for which to screen during the physical examination of an athlete.
    • The mechanism of VF in HCM is not entirely understood. The postexertional drop in blood pressure and shunting of blood to extracardiac tissues is postulated to worsen the outflow tract gradient and may therefore induce cardiac ischemia and malignant arrhythmias. This downward cycle does not revert spontaneously, and it responds poorly to resuscitative efforts.
• Arrhythmogenic RV cardiomyopathy/dysplasia
• • Arrhythmogenic RV cardiomyopathy/dysplasia is characterized by replacement of the RV wall with fibrofatty tissue. Involvement of the interventricular septum and left ventricle is associated with poorer outcomes.
  • Genetic defects in chromosomes 1 and 14 (bands q23-q24)have recently been discovered to correspond to some phenotypic expressions of this disease. Autosomal dominant inheritance can occur, and approximately 30% of cases occur as a familial disorder.
  • Arrhythmogenic RV dysplasia affects men more often than women. The annual incidence rate of VF in this population is approximately 2%. Patients may present with signs and symptoms of RV hypertrophy and dilation, often with sustained monomorphic or polymorphic VT of the left bundle-branch block morphology with an axis usually between negative 90-100°.
  • Atrial arrhythmias may be present in up to 25% of patients. Syncope and sudden death are often associated with exercise. In many patients, sudden death is the first manifestation of the disease. Clinicians should be alerted to the epsilon wave finding on ECG studies (see Image 2). The epsilon wave can be present in up to 23% of patients after the first VT attack. The percentage of patients with the epsilon wave finding on ECG increases to 27% and 34% at 5 and 10 years, respectively, after the first VT event.
  • Uhl anomaly is a condition in which the RV wall is extremely thin secondary to apposition of endocardial and epicardial layers. Uhl anomaly usually manifests in the pediatric age group, while arrhythmogenic RV cardiomyopathy usually manifests in adults.
• Valvular diseases: These include aortic stenosis and other valvular lesions.
• • Aortic stenosis
  • • SCD was fairly common in patients with progressive aortic stenosis before the advent of surgical therapy for valvular heart disease.
    • Most deaths caused by aortic stenosis were sudden. In a 1980 study by Chizner et al of 42 patients who had isolated aortic stenosis and did not undergo valve replacement, up to 56% of deaths were sudden at 5-year follow-up. Of these 42 patients, 32 were symptomatic, and 10 were asymptomatic.
    • The mechanism of sudden death is unclear, and both malignant ventricular arrhythmia and bradyarrhythmia have been documented.
    • VF accounts for up to 20% of deaths after aortic valve replacement and remains the second most common cause of postoperative death in this population. The incidence of VF after aortic valve surgery is highest in the first 3 weeks after the procedure and then plateaus at 6-month follow-up.
  • Other valvular lesions
  • • Patients with aortic insufficiency usually present with signs of heart failure and progressive LV dilatation. As part of this process, reentrant or automatic ventricular foci may develop and ultimately lead to symptomatic ventricular arrhythmia. After valve replacement, LV wall tension can be expected to lessen and risk of arrhythmia can be expected to decrease.
    • Mitral stenosis is becoming increasingly uncommon in the United States because of widespread use of antibiotics in primary streptococcal infections. SCD due to mitral stenosis is very rare.
    • The incidence of VF is low in patients with mitral valve prolapse (MVP). MVP has a 5-7% incidence in the general population. In clinically significant MVP, the risk of VF seems to rise along with the total mortality rate. Kligfield et al estimated that the incidence of sudden death varies with the presence of symptoms and the severity of mitral regurgitation.
    • Ventricular tachyarrhythmias are the most frequent arrhythmia in patients with VF. Risk factors for VF to consider in these patients include a family history of VF, echocardiographic evidence of a redundant mitral valve, repolarization abnormalities, and lengthening of the corrected QT interval (>420 milliseconds [ms] in women and >450 ms in men).
• Congenital heart disease: In the pediatric and adolescent age groups, VF occurs with an annual incidence of 1.3-8.5 cases per 100,000 persons, accounting for approximately 5% of all deaths in this group. The causes of SCD are much more diverse in children than adults. In reviewing 13 studies involving 61 children and adolescents with VF, Driscoll and Edwards found 50% of cases were due to HCM; 25%, to anomalous origin of the left coronary artery; and the remaining, to aortic stenosis, cystic medial necrosis, and sinus node artery obstruction. The following is a classification of VF in the pediatric population:
• • Congenital causes of VF in patients with known, previously recognized (including repaired) heart disease include the following:
  • • Tetralogy of Fallot
    • Transposition of the great arteries
    • Fontan operation
    • Aortic stenosis
    • Marfan syndrome
    • Eisenmenger syndrome
    • Congenital heart block
    • Ebstein anomaly
  • Acquired causes of VF in patients with known, previously recognized (including repaired) heart disease include the following:
  • • Kawasaki syndrome
    • DCM or myocarditis
  • Causes of VF in patients with previously unrecognized heart disease who have structural heart disease include the following:
  • • HCM
    • Congenital coronary artery abnormalities
    • Arrhythmogenic RV dysplasia
  • Causes of VF in patients with previously unrecognized heart disease who do not have structural heart disease include the following:
  • • Long QT syndrome
    • WPW syndrome
    • Primary VT and VF
    • Primary pulmonary hypertension
    • Commotio cordis (traumatic blow to the chest wall causing VT/VF)
  • The predominant mechanism is ventricular arrhythmia. In patients with tetralogy of Fallot after postoperative correction of the anomaly, up to 10% have VT, and the incidence of sudden death is 2-3%. In the Fontan procedure to correct a physiologic single ventricle, even atrial arrhythmias can cause severe hemodynamic compromise and arrhythmic death. Patients who develop secondary pulmonary hypertension (Eisenmenger syndrome) despite attempted correction of the anatomic defects have a very poor prognosis. The terminal event may be bradycardia or VT progressing to VF.
• Primary electrophysiologic abnormalities: These generally comprise a group of abnormalities in which patients have no apparent structural heart disease but have a primary electrophysiologic abnormality that predisposes them to VT or VF. Some imaging techniques have detected abnormal sympathetic neural function in these patients. An ECG study can provide clues to the diagnosis; consider a familial component to these conditions.
• • Long QT syndrome
  • • Idiopathic long QT syndrome, in which patients have a prolonged QT interval with a propensity to develop malignant ventricular arrhythmias, is a rare familial disorder.
    • Two forms of congenital long QT syndrome have been described. The Jervell and Lange-Nielsen syndrome associated with deafness has an autosomal recessive pattern of inheritance. The Romano-Ward syndrome is not associated with deafness and has an autosomal dominant pattern of inheritance with variable penetration. This syndrome accounts for 90% of long QT syndrome cases. The Romano-Ward syndrome has been associated with gene mutations of SCN5A on chromosome 3, the HERG gene on chromosome 7, and the KVLTQT1 gene on chromosome 11.
    • The genetic alteration in a myocellular channel protein that regulates the potassium flux during electrical repolarization is thought to be the primary electrophysiologic abnormality. A relationship with sympathetic nervous system imbalance also appears to exist. The prolongation that occurs makes these patients susceptible for development of a specific form of VT called torsade de pointes.
    • The clinical course of patients with long QT syndrome is quite variable, with some patients remaining asymptomatic and others developing torsade de pointes with syncope and sudden death. Thirty percent of patients are identified while being evaluated for syncope or aborted sudden death. Patients at high risk for VF include those with deafness and first-degree relatives of patients with VF. VF in these patients is associated with emotional extremes, auditory auras or stimulation, and vigorous physical activity. Symptoms usually begin in childhood or adolescence.
    • Diagnosis of congenital long QT syndrome requires the presence of 2 major criteria or 1 major criterion and 2 minor criteria. Major criteria include (1) long QT interval (QTc >420 ms in females and >450 ms in males), (2) stress-induced syncope, and (3) a family history of long QT syndrome. Minor criteria include (1) congenital deafness, (2) T-wave alternans, and (3) bradycardia (in children).
    • Treatment for long QT syndrome includes beta-blockers, high thoracic left sympathectomy, and implanted cardioverter/defibrillators (ICDs).
  • Acquired long QT syndrome
  • • A number of antiarrhythmics (especially class I-A and class III) and other medications, electrolyte abnormalities, cerebrovascular diseases, and altered nutritional states cause QT prolongation and put patients at risk for torsade de pointes. This usually occurs when QT prolongation is associated with a slow heart rate and hypokalemia.
    • The QT interval is prolonged in up 32% of patients with intracranial hemorrhage (especially in subarachnoid hemorrhages). Lesions in the hypothalamus are thought to lead to this phenomenon.
    • Sudden death due to ventricular arrhythmia has been reported in patients with hypocalcemia, hypothyroidism, and nutritional deficiencies associated with modified starvation diets and in patients who are obese and on severe weight-loss programs.
    • Class I-A antiarrhythmic drugs that cause acquired long QT syndrome include quinidine, disopyramide, and procainamide. Class III antiarrhythmic drugs that cause acquired long QT syndrome include sotalol, N-acetyl procainamide, bretylium, amiodarone, dofetilide, and ibutilide.
    • Other drugs that cause acquired long QT syndrome include bepridil, probucol, tricyclic and tetracyclic antidepressants, phenothiazines, haloperidol, antihistamines (eg, terfenadine, astemizole), antibiotics (eg, intravenous erythromycin, sulfamethoxazole/trimethoprim), chemotherapeutics (eg, pentamidine, anthracycline), serotonin antagonists (eg, ketanserin, zimeldine), and organophosphorous insecticides.
    • Electrolyte abnormalities that cause acquired long QT syndrome include hypokalemia, hypomagnesemia, and hypocalcemia.
    • Altered nutritional states and cerebrovascular disease that cause acquired long QT syndrome include intracranial and subarachnoid hemorrhages, stroke, and intracranial trauma.
    • Hypothyroidism and altered autonomic status (eg, diabetic neuropathy) can cause acquired long QT syndrome.
  • WPW syndrome
  • • WPW syndrome is a rare cause of sudden death.
    • Most patients with WPW syndrome and VF develop atrial fibrillation with a rapid ventricular response over the accessory pathway, which induces VF (see Image 3). In a study by Klein et al of 31 patients with VF and WPW syndrome, a history of atrial fibrillation or reciprocating tachycardia was an important predisposing factor. The presence of multiple accessory pathways, posteroseptal accessory pathways, and a preexcited R-R interval of less than 220 ms during atrial fibrillation are associated with higher risk for VF.
    • In patients at high risk, preventing the occurrence of arrhythmias is possible by interrupting the anomalous pathway with surgery or radiofrequency ablation techniques.
  • Brugada syndrome
  • • In 1992, Brugada and Brugada described a syndrome of a specific ECG pattern of right bundle-branch block and ST-segment elevation in leads V₁ through V₆ without any structural abnormality of the heart that was associated with sudden death.
    • The gene responsible for this syndrome has recently been discovered to be the cardiac sodium channel gene SCN5A on chromosome 3.
    • Patients with this syndrome are at high risk for VF. In a follow-up study of 63 patients with the syndrome in 33 centers worldwide, asymptomatic patients were found to have the same risk for arrhythmia as patients who had an episode of aborted sudden death. Treatment with amiodarone and/or beta-blockers did not confer a lesser risk of death, whereas the patients with ICDs had no deaths due to arrhythmia. Thus, placement of an ICD is considered the treatment of choice for Brugada syndrome.
  • Primary VF
  • • An estimated 3-9% of cases of VT and VF occur in the absence of myocardial ischemia. Up to 1% of patients with out-of-hospital cardiac arrest have idiopathic VF with no structural heart disease. Up to 15% of patients younger than 40 years who experience VF have no underlying structural heart disease. In a 1993 study, Belhassen and Viskin noted that 11 of 54 patients had histologic abnormalities on endomyocardial biopsy.
    • VF usually has no preceding symptoms. The prognosis is unfavorable, and patients have a recurrence rate of as much as 33%. Conversely, idiopathic VT is generally associated with a benign prognosis.
    • The most common form of idiopathic VT originates from the RV outflow tract (RVOT) and has a left bundle-branch block/inferior or right axis morphology. Idiopathic VTs that originate from the LV outflow tract (LVOT), aortic root, or LV septum are less common. Idiopathic VT is often provoked by exercise.
    • Treatment has included beta-blockers or calcium channel blockers; however, at present, radiofrequency ablation of the VT focus is generally very effective for idiopathic VT. Patients with idiopathic VF are typically treated with ICDs.
  • RVOT tachycardia
  • • RVOT tachycardia is the most common form of idiopathic VT, comprising 70-80% of all idiopathic VTs. RVOT tachycardia is a rare cause of VF. It has been referred to as exercise-induced VT, adenosine-sensitive VT, and repetitive monomorphic VT.
    • RVOT tachycardia occurs in patients without structural heart disease and arises from the RV outflow region. Current data suggest that triggered activity is the underlying mechanism of RVOT tachycardia. RVOT tachycardia is believed to be receptor mediated because exogenous and endogenous adenosine can terminate this process. Maneuvers that increase endogenous acetylcholine antagonize this process.
    • Symptoms typical of RVOT tachycardia include palpitations and presyncope or syncope, often occurring during or after exercise or emotional stress. VT can also occur at rest. The ECG during VT displays a left bundle-branch block/inferior axis morphology.
    • Treatment is based on frequency and severity of symptoms. The first line of therapy is a beta-blocker or calcium channel blocker. Patients with symptoms not relieved by medical therapy are best treated with radiofrequency catheter ablation. Successful ablation is reported in 83-100% of cases.
  • Lown-Ganong-Levine syndrome
  • • This syndrome is characterized by tachyarrhythmias, short PR interval, and normal QRS duration.
    • Most of these patients appear to have enhanced atrioventricular (AV) nodal conduction and "typical" supraventricular tachycardia (usually AV nodal reentrant tachycardia or, less commonly, AV nodal tachycardia using a concealed accessory pathway).
    • Some patients may have a rapidly anterograde-conducting accessory AV connection, which theoretically poses a risk of extremely rapid rates and degeneration to VF.
• Pulmonary embolism is a frequent cause of sudden death in people at risk. Risk factors include previous personal or family history of deep venous thromboembolism, malignancy, hypercoagulable states, and recent mechanical trauma such as hip or knee surgery. Patients with pulmonary embolism can develop fatal ventricular arrhythmias (eg, VF) due to hemodynamic collapse and/or severe hypoxia.
• Aortic dissection or aneurysmal rupture is a rather uncommon but significant cause of out-of-hospital cardiac arrest. Predisposing factors for aortic dissection include genetic deficiencies of collagen such as Marfan syndrome, Ehlers-Danlos syndrome, and aortic cystic medial necrosis. VF may be an observed finding at the scene of an aortic aneurysmal rupture.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Arrhythmogenic RV dysplasia
Brugada syndrome

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Cardiac enzymes (eg, creatine kinase, myoglobin, troponin): Elevations in these enzyme levels may indicate ischemia and MI. The extent of myocardial damage can usually be correlated to the extent of elevation in the enzyme levels. Patients are at increased risk for arrhythmia in the peri-infarct period.
• Electrolytes, calcium, and magnesium: Severe metabolic acidosis, hypokalemia, hyperkalemia, hypocalcemia, and hypomagnesemia are some of the conditions that can increase the risk for arrhythmia and sudden death.
• Quantitative drug levels (eg, quinidine, procainamide, tricyclic antidepressants, digoxin): Drug levels higher than those indicated in the therapeutic index may have a proarrhythmic effect. Subtherapeutic levels of these drugs in patients being treated for specific cardiac conditions can also lead to an increased risk for arrhythmia. Most of the antiarrhythmia medications also have a proarrhythmic effect.
• Toxicology screen: Looking for drugs that can lead to vasospasm-induced ischemia (eg, cocaine) is warranted if suspicion exists. Obtaining drug serum levels (eg, antiarrhythmics) may also be warranted.
• 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) may be useful in the diagnosis of decompensated CHF as the provocative etiology of VF. BNP is highly specific and sensitive for the diagnosis of decompensated CHF when elevated 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.

Imaging Studies

• Chest radiography: This may reveal whether a patient is experiencing CHF. Radiographs can also show signs of LV or RV hypertrophy. Signs of pulmonary hypertension may be evident.
• Echocardiography: Two-dimensional echocardiography with Doppler is essential in the evaluation of VF.
• • A number of studies have demonstrated that the use of 2-dimensional echocardiograms to evaluate left wall-motion abnormalities after an acute MI (using the LV wall-motion score index) is useful in predicting outcome and the risk for major cardiac events, including sudden death.
  • A decrease in the ejection fraction and worsening wall-motion abnormalities upon exercise echocardiography in patients who have had an MI has been suggested to 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 presence or absence of pericardial fluid is advantageous.
• Nuclear imaging techniques
• • Resting thallium Tl or technetium Tc 99m scintigraphy is helpful in assessing myocardial damage after MI.
  • A larger defect has been associated with greater risk for future cardiac events.
  • Exercise nuclear scintigraphy is very sensitive when 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.
  • These tests can be very helpful in patients with low functional capacity such as occurs in chronic obstructive pulmonary disease, peripheral vascular disease, or orthopedic problems.
  • The Multicenter Post-Infarction Research Group provided evidence that resting ejection fraction was the most important noninvasive predictor of SCD, most commonly VF, and other cardiac events in patients with MI.

Other Tests

• ECG: This study is indicated in all patients with VF. Seek evidence of MI, prolonged QT interval, epsilon sign, Brugada sign, short PR, WPW pattern, or other conditions.
• Signal-averaged ECG is of limited value.
• Genetic testing: The value of genetic testing in conditions such as congenital long QT and HCM is still being evaluated. Some studies have recommended the testing of siblings and close relatives of people with VF due to these conditions.

Procedures

• Coronary angiography: Perform cardiac catheterization in patients who survive VF to assess the state of ventricular function and the severity and extent of CAD.
• • The number of vessels with severe obstruction and the degree of LV dysfunction are important variables in predicting cardiac events. Ejection fraction is the best predictor of significant cardiac events and survival.
  • Coronary angiography can also help 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 greatest treatment for the underlying substrate of VT/VF, ischemic myocardium.
• EPS: In targeted patients, EPS play diagnostic, prognostic, and therapeutic roles. EPS are usually performed after ischemic and structural heart disease has been diagnosed and addressed. EPS are generally not indicated for the subset of patients whose 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 EPS for diagnostic and therapeutic reasons.
• • These studies have been used to identify patients who have inducible VT/VF versus noninducible sustained monomorphic VT. 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. Significantly lower ventricular function has also been observed in patients with inducible sustained VT or VF.
  • Inducible bundle-branch reentrant VT can be observed in patients with DCM and in the postoperative period after valvular replacement. Up to 20% of patients with HCM have inducible sustained monomorphic VT. Identification of accessory pathways is possible with these studies. EPS are performed the following in mind:
    • Ablation of VT foci, eg, bundle-branch VT, RVOT tachycardia, and some cases of idiopathic LV tachycardia
    • ICD placement (generally recommended in survivors of VF)

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• Advanced cardiac life support (ACLS): In the event of cardiac arrest, the immediate implementation of ACLS guidelines is indicated. Interest in improving rates of public ACLS training—with a special emphasis on use of early defibrillation by public service personnel (eg, police, fire, airline)—is widespread. These measures can help achieve the greatest public health benefits in the fight against sudden death.
• Defibrillation
• • External electrical defibrillation remains the most successful treatment of VF. A shock is delivered to the heart in order to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objectives are to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker.
  • Successful defibrillation largely depends on 2 key factors: duration between onset of VF and defibrillation and the metabolic condition of the myocardium. VF waveform usually begins with a relatively high amplitude and frequency; it then degenerates to smaller and smaller amplitude until asystole after approximately 15 minutes, possibly from depletion of the heart's energy reserves. Consequently, early defibrillation is vital; emergency response teams can perform defibrillation before arrival at the ED.
  • Defibrillation success rates decrease 5-10% for each minute after onset of VF. Success rates of 85% have been reported in strictly monitored settings where defibrillation was most rapid.
  • Factors that increase the energy required for successful defibrillation include the following:
  • • Time before defibrillation begins
    • Paddle size
    • Paddle-to-myocardium distance (eg, obesity, mechanical ventilation)
    • Use of conduction fluid (eg, disposable pads, electrode paste/jelly)
    • Contact pressure
    • Elimination of stray conductive pathways (eg, electrode jelly bridges on skin)
    • Previous shocks, which decrease defibrillation threshold
  • The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy can cause myocardial injury and arrhythmias.
  • Larger paddles result in lower impedance, which allows the use of lower-energy shocks. Approximate optimal sizes are 8-12.5 cm for an adult, 8-10 cm for a child, and 4.5-5 cm for an infant. Position one paddle below the outer half of the right clavicle and one over the apex (V₄-V₅).
  • Artificial pacemakers or ICDs necessitate the use of anteroposterior paddle placement.
  • Before any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion.
  • Patient must be dry and not in contact with metallic objects. Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied.
  • If contraction is reestablished following defibrillation, a period of low cardiac output (ie, postcountershock myocardial depression) may occur. Cardiac output recovery may take minutes to hours.
  • Defibrillation causes serum creatine phosphokinase levels to increase proportionate to the amount of electric energy delivered. If customary voltage is used to defibrillate a patient, the proportion of myocardial fraction (CK-MB) should remain within reference ranges unless an infarction has caused myocardial injury.
  • Although precordial thump is less appropriate for VF than for VT, it really is appropriate in neither. Use it only for witnessed monitored arrests in which no defibrillator is immediately available.
• Algorithm
• • Activate emergency response system.
  • Initiate CPR.
  • Verify that the patient is in VF as soon as possible (ie, AED, quick look with paddles).
  • Defibrillate the patient (adult, 200 J; child, 2 J/kg or equivalent biphasic energy).
  • Defibrillate the patient (adult, 200-300 J; child, 2-3 J/kg or equivalent biphasic energy).
  • Defibrillate the patient (adult, maximum 360 J; child, 4 J/kg child; maximum biphasic energy varies with manufacturer).
  • Check for pulses/rhythm.
  • Perform CPR for 1 minute with attention to the following:
  • • Properly positioning the electrode
    • Attempting tracheal intubation and IV access
    • Administering epinephrine every 3 minutes
  • Correct the following if necessary and/or possible:
  • • Hypoxia
    • Hypovolemia
    • Hyperkalemia/hypokalemia and metabolic disorders
    • Tension pneumothorax
    • Tamponade
    • Toxic/therapeutic substances
    • Thromboembolic/mechanical obstruction
  • Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
  • Administer amiodarone (300 mg IV). If not available, use lidocaine (1-1.5 mg/kg bolus).
  • Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
  • Administer lidocaine (1 mg/kg IV) if amiodarone was used in the first round.
• Other options are as follows: If not used in the first round, administer amiodarone (300 mg IV) now, and repeat lidocaine.
• • Administer amiodarone IV bolus only once.
  • Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
  • If no response, administer epinephrine 1 mg IV push or vasopressin (40 U IV push). Vasopressin can be used only once. Wait 10 minutes after vasopressin administration before giving epinephrine.
  • Administer a procainamide infusion (50 mg/min IV) to a total of 1 g.
  • Following the third shock, intervals between consecutive jolts should not exceed 1 minute.
  • Assess use of the following in conjunction with subsequent defibrillation attempts, and administer a shock 30 seconds after each dose of the indicated drug:
  • • Lidocaine (1-1.5 mg/kg IV; maximum 3 mg/kg total)
    • Amiodarone (0.5 mg/min following bolus dosing above or IV loading protocol below)
    • Epinephrine (0.1-0.2 mg/kg IV): For adults, 1 mg IV every 3 minutes is typically used; alternative dosing regimens are advocated (ie, high, intermediate, escalating).
    • Procainamide (30 mg/min IV; maximum 17 mg/kg total in refractory VF)
    • Magnesium sulfate (1-2 g IV push) in cases of probable hypomagnesemia or refractory VF
    • Sodium bicarbonate (1 mEq/kg IV push) in cases of known preexistent hyperkalemia or known tricyclic antidepressant overdose
  • Three initial defibrillation attempts take precedence over CPR as soon as a defibrillator or AED is available.
  • Lidocaine and epinephrine can be administered through an endotracheal tube if IV attempts fail. Use 2.5 times the IV dose.
• Refractory VF
• • Lack of response to standard defibrillation algorithms is challenging. Addition of magnesium and/or procainamide is often ineffective.
  • If not used earlier, consider the following amiodarone-loading protocol: 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.
  • Such reported alternatives as transesophageal and intracardiac defibrillation or thoracotomy with internal defibrillation are generally impractical because of limited experience and availability of equipment and trained personnel.
• Postresuscitative care
• • Continue successfully used antiarrhythmics. Maintain lidocaine at 1-4 mg/min, bretylium at 1-2 mg/min, and amiodarone at 0.5 mg/min.
  • Control any hemodynamic instability.
  • Administer vasopressors as indicated.
  • • Postdefibrillation arrhythmias (mainly AV blocks) have been reported in up to 24% of patients. The incidence is related to the amount of energy used for defibrillation.
    • Check for complications (eg, aspiration pneumonia, CPR-related injuries).
    • Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).
• Medical stabilization: Careful postresuscitative care is essential to survival because studies have shown a 50% repeat in-hospital arrest rate for people admitted after a VF event. Treatment of myocardial ischemia, heart failure, and electrolyte disturbances are all justified by the results of multiple randomized trials investigating acute MI and CHF. Empiric beta-blockers are reasonable in many circumstances because of favorable properties discussed in Causes. Empiric antiarrhythmics, including amiodarone, should not supersede ICD placement unless control of recurrent VT is needed while the patient is hospitalized.

Surgical Care

Most survivors of VF should be treated with ICDs. Transvenous ICDs can be placed with minimal morbidity and mortality.

• Radiofrequency ablation: Now routinely available, radiofrequency ablation is indicated for patients with AV bypass tracts, bundle-branch block VT, RVOT tachycardia, idiopathic LV tachycardia, and more rare forms of automatic foci VT (which almost never cause VF). Unfortunately, most cases of VF are not amenable to radiofrequency ablation and require ICD placement. VF is an exception because of preexcited tachycardias in patients with WPW syndrome. In these patients, successful catheter ablation of the accessory pathway(s) is the appropriate therapy.
• Several multicenter trials have examined the prophylactic use of ICD therapy in patients at high risk for VF.
• • The annual VF rate in patients with these devices has been reduced from 25% to 1-2%. ICD placement is beneficial in high-risk patients in whom electrophysiologic-guided therapy with antiarrhythmics has failed. In several studies comparing ICD placement with antiarrhythmic therapy in patients with VT/VF and/or prior cardiac arrest, ICD placement has been shown to be associated with significantly decreased mortality rate (Myerburg, 1997; Cappato, 1999; Domanski, 1999).
  • The use of ICDs as primary prevention for VF is still being investigated in ongoing trials. Newer ICDs have pacing capabilities and have addressed bradyarrhythmias either causing or complicating VT or VF.
  • Currently, the transvenous approach to implantation is universally applied and favored over the thoracotomy implants. In the Multicenter Automatic Defibrillation Implantation Trial (MADIT) 1, prophylactic use of ICDs in patients with a history of MI, LVEF of less than 35%, documented episode of nonsustained VT, and inducible nonsuppressible VT had a 54% reduction in mortality during any follow-up interval compared with patients treated with conventional medical therapy. In MADIT 2, the ICD conferred a 31% reduction in mortality in patients with prior MI and LVEF of 30% or less. In MADIT 2, there was no requirement for nonsustained VT or EPS (Moss, 1996; Moss, 2002).
• Cardiac surgery can be a primary treatment for VF via a variety of strategies.
• • Surgical treatment in patients with ventricular arrhythmias and ischemic heart disease includes coronary artery bypass grafting (CABG). The CASS study illustrated that patients with significant CAD and operable vessels who underwent CABG had a decrease in the incidence of VT/VF arrest compared with patients on conventional medical treatment. The reduction was most evident in patients who had 3-vessel disease and CHF (Holmes, 1989). By itself, CABG only prevents recurrent VF if the ejection fraction is normal and ischemia was the cause of the arrest. Even in these patients, ICDs are frequently placed after CABG.
  • Surgical treatment of ventricular arrhythmias in patients with nonischemic heart disease includes excision of VT foci after endocardial mapping and excision of LV aneurysms. This is practiced very infrequently, however, given the efficacy of ICDs.
  • Aortic valve replacement is associated with improved outcome in patients with hemodynamically significant valvular stenosis and well-preserved ventricular function. In patients with MVP associated with significant valvular regurgitation and LV dysfunction, malignant tachyarrhythmias, such as VT and VF, have been reported. These patients are candidates for mitral valve replacement.
  • Orthotopic heart transplantation is indicated in patients with SCD and refractory heart failure, in whom significant improvement in actuarial survival is expected. Given a limited donor service, this form of treatment is expected to be beneficial for very few people who survive VF.
  • Patients with long QT syndrome who do not respond to beta-blockers are candidates for ICD placement or high thoracic left sympathectomy.

Consultations

• A cardiologist should always participate in the care of these patients. Cardiac electrophysiologists should also be involved in the care of these patients, which generally involves ICD placement.
• Other consultants include an interventional cardiologist and cardiac surgeon. Such consultations are made on a case-by-case basis.

Diet

• Patients with CAD are advised to follow a diet low in fat and cholesterol. Patients with severe heart failure should monitor their fluid and sodium intake.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medications (eg, vasopressin, epinephrine, amiodarone) are used after 3 defibrillation attempts are performed to restore normal rhythm.

Amiodarone can also be used on a long-term basis in patients who refuse ICDs or who are not candidates for ICDs.

Drug Category: Antiarrhythmic agents

Can raise fibrillation and defibrillation thresholds, but amiodarone can restore normal cardiac rhythm.

Drug Category: Anticholinergic agents

Improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade.

Drug Category: Vasopressor agents

Augment both coronary and cerebral blood flow present during the low flow state associated with CPR. Use has resulted in short-term resuscitation benefits in the setting of prolonged out-of-hospital CPR for VF in adults.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Resuscitated patients must be admitted to an intensive care unit and monitored because of the high recurrence risk.
• • Patients typically have an underlying etiology that must be investigated and treated.
  • They require stabilization and monitoring for possibility of a coexistent emergency or complication.
  • Intubated patients require mechanical ventilation.
  • Evaluation of ischemic injury to the CNS, myocardium, and other organs is essential.
• Survivors should have thorough diagnostic testing to establish the underlying etiology of the VF episode.
• If available, perform indicated interventions to improve long-term prognosis.
• ICDs are used for patients at high risk for recurrent VF. Studies indicate that patients with VF arrest who receive ICDs have improved long-term survival rates compared with those receiving only medications. ICDs effectively provide early defibrillation (Lessmeier, 1993; Meissner, 1993; Domanski, 1999; Maron, 2000).

Further Outpatient Care

• Provide typical outpatient ICD follow-up in addition to the follow-up care appropriate for associated cardiac and other conditions.

Transfer

• Patients should be cared for at centers where intensive cardiac monitoring and appropriate invasive and noninvasive studies can be performed. In general, a cardiovascular service, including interventional cardiology, electrophysiology, and cardiac surgery, is needed.

Complications

• CNS ischemic injury
• Myocardial injury
• Postdefibrillation arrhythmias
• Aspiration pneumonia
• Defibrillation injury to self or others
• Injuries from CPR and resuscitation
• Skin burns
• Damage to implanted electronics (eg, ICDs, pacemakers)
• Death

Prognosis

• Prognosis for survivors of VF strongly depends on the time elapsed between onset and medical intervention as well as on the particular etiology for VF. VF that occurs within the first 48 hours of the onset of acute MI has no bearing on prognosis, but VF associated with acute MI that occurs outside this time frame is associated with a high rate of recurrence and a poorer prognosis.
• • Early defibrillation often makes the difference between long-term disability and functional recovery. Prognosis of morbidity and mortality for people who have had VF can be made using the cardiac arrest score developed by Thompson and McCullough (see Physical).
  • The detection of the underlying cause of VF and the availability of treatment options play an important role in the natural history and prognosis of VF.
• VF is a frequently encountered problem for emergency physicians, internists, and cardiologists. Ischemic cardiomyopathy in all adult cases and HCM in pediatric and adolescent cases are at the top of the differential diagnosis.
• • Death and disability after successful resuscitation directly correlate with the degree of CNS damage occurring during the event. Prognosis is poor without intervention by 4-6 minutes after onset of VF. Few individuals survive when VF lasts more than 8 minutes without intervention. Once the patient is resuscitated, the clinical course is largely predicted by the ED presentation of hemodynamic stability, early neurologic recovery, and duration of the resuscitation. Reported survival rates after defibrillation vary widely. Some systems report survival rates exceeding 50%, whereas others are as low as 3%.
  • Patients who survive the initial phases require a systematic evaluation of LV performance, myocardial perfusion, and electrophysiologic instability. Survivors of VF have a recurrence rate on the order of 20-25% per year, making ICD placement important in most patients.
  • Modern treatment with ICD placement has saved lives and will likely be an area of continued clinical growth.
  • Preventive measures are essentially measures of CAD prevention. Efforts to inform and train the public about external defibrillator use will probably have the greatest public health impact on improving survival rates of VF.

Patient Education

• For excellent patient education resources, visit eMedicine's Heart Center, Cholesterol Center, and Public Health Center . Also, see eMedicine's patient education articles Atrial Fibrillation, Chest Pain, Heart Rhythm Disorders, Coronary Heart Disease, Heart Attack, CardiopulmonaryResuscitation (CPR), and Tetralogy of Fallot.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to recognize ischemic heart disease and to initiate early treatment: The importance of early recognition and treatment cannot be overestimated because approximately 80% of SCD cases can be attributed to ischemic heart disease.
• Failure to use appropriate medical therapy for ischemic heart disease (eg, beta-blockers): A specialist in cardiovascular disease must be involved in the care of patients who have had a VT/VF cardiac arrest or who have symptoms of ischemic heart disease, valvular disorders, or presentations with complex arrhythmias.
• Failure to educate patients about the consequences of noncompliance with medical therapy
• Failure to consider survivors of VF for ICD placement
• Failure to counsel families regarding the poor likelihood of favorable outcome according to risk stratification level

MULTIMEDIA

Section 10 of 11