eMedicine Specialties > Emergency Medicine > Cardiovascular

Ventricular Fibrillation

Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital
A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon; Mazen K Khalil, MD, Post Doctoral Research Fellow, Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation; Aaron Bright, MD, Staff Physician, Department of Emergency Medicine, University of Southern California Keck School of Medicine

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

Differential Diagnoses

Other Problems to Be Considered

Ventricular flutter
Wide complex tachycardia
Supraventricular tachycardia
Pulseless electrical activity (PEA)
Digitalis toxicity
Electrolyte disturbances
Acute pulmonary disorders
Acute toxidromes (eg, cocaine toxicity)

Workup

Laboratory Studies

• Serum electrolyte levels, including calcium and magnesium
• Cardiac enzymes to identify myocardial injury
• Complete blood count (CBC) to detect contributing anemia
• Arterial blood gases (ABGs) to assess degree of acidosis or hypoxemia
• Toxicologic screens and levels as clinically indicated

Imaging Studies

• Chest radiography may identify aspiration pneumonia, pulmonary edema, cardiomegaly, and injury (eg, secondary to cardiopulmonary resuscitation [CPR]).

Other Tests

• Electrocardiography (ECG) to help identify ischemic or proarrhythmic conditions 

Treatment

Prehospital Care

Because of the critical importance of early defibrillation, prehospital care is vital for arrests due to VF that occur outside the hospital. Interventions that impact survival and outcome of resuscitation include the following:

• Witnessed or early recognition of an arrest
• Early activation of emergency medical services (EMS) system
• Bystander CPR slows the degeneration of VF and improves survival.
  • Traditionally, CPR consists of artificial respirations and chest compressions. Mounting evidence demonstrates that chest compressions are the critical action to provide some cardiac perfusion during CPR, and artificial respirations are less important. Interruption of chest compressions to perform artificial respirations by a single resuscitator causes a loss of cardiac perfusion pressure, and even after restarting compressions, it may take some time before the previously obtained perfusion pressure is restored. Current guidelines recommend both artificial respirations and chest compressions for all patients as described in the algorithm below. Future guidelines may reflect developments in this ongoing area of research.
• Automated external defibrillator (AED) application and defibrillation by trained personnel in the field
  • AEDs have revolutionized prehospital VF management because they decrease the time to defibrillation. This is accomplished by having the units prepositioned in the field where cardiac arrests are likely to occur (eg, airports, casinos, jails, malls, stadiums, industrial parks), eliminating the need for rhythm-recognition training and increasing the number of trained personnel and laypeople that can defibrillate at the scene.
  • AEDs are programmed to recognize 3 shockable rhythms: coarse ventricular fibrillation, fine ventricular fibrillation, and rapid ventricular tachycardia. Modern units have a sensitivity greater than 95% and specificity approaching 100% for the 3 shockable rhythms. The greatest difficulty is in distinguishing fine ventricular fibrillation from asystole.
  • AEDs can also be used for children. A pediatric dose-attenuating system should be used, if available, for children up to the age of 8 years, and a conventional AED can be used for children at or older than 8 years or with a corresponding weight of at least 25 kg (55 lb).
• Early access to trained EMS personnel capable of performing CPR, defibrillation, and advanced cardiac life support (ACLS)

Emergency Department Care

• Defibrillation
  • Electrical external defibrillation remains the most successful treatment of VF. A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objective is 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 the following 2 key factors: duration between onset of VF and defibrillation, and metabolic condition of the myocardium. VF begins with a coarse waveform and decays to a fine tracing and eventual asystole. These electrical changes that occur over minutes are associated with a depletion of the heart's energy reserves. CPR slows the progression of these events, but defibrillation is the primary treatment to interrupt the process and return the heart to a perfusing rhythm.
  • Defibrillation success rates decrease 5-10% for each minute after onset of VF. The likelihood of defibrillation success can also be predicted based on the smoothness of the VF tracing. In strictly monitored settings where defibrillation was most rapid, 85% success rates have been reported.
  • Factors that affect the energy required for successful defibrillation include the following:
    • Paddle size: 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.
    • Paddle-to-myocardium distance (eg, obesity, mechanical ventilation): Position one paddle below the outer half of the right clavicle and one over the apex (V4-V5). Artificial pacemakers or implantable defibrillators mandate use of anterior-posterior paddle placement.
    • 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 may lower the chest wall impedance and decrease the defibrillation threshold.
  • Biphasic defibrillation has a number of advantages over monophasic defibrillation including increased likelihood of defibrillation success for a given shocking energy. While this has not translated into a proven survival benefit thus far, if less shocks are required, there may be less interruption of CPR. Lower energy shocks associated with biphasic defibrillation may lead to less myocardial stunning after repeated defibrillation attempts. Furthermore, smaller and lighter defibrillation units are required to produce a biphasic waveform, and this is an important advantage for portable AED units.
    • The optimal energy for first and subsequent defibrillation attempts with a biphasic pulse remains unproven.
    • Operators are advised to use the energy protocols associated with individual devices or to begin with 200 J.
  • Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied.
    • Prior to any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion.
    • The patient must be dry and not in contact with metallic objects.
  • The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy may cause myocardial injury.
    • Defibrillation causes the serum creatine phosphokinase level 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 normal limits unless an infarction has caused myocardial injury.
  • If contraction is reestablished following defibrillation, a period may occur of low cardiac output, termed postcountershock myocardial depression. Cardiac output recovery may take minutes to hours.
    • CPR is important immediately after shock delivery. Many victims demonstrate asystole or pulseless electrical activity (PEA) for the first several minutes after defibrillation. CPR can convert these rhythms to a perfusing rhythm.
    • Provision of immediate CPR post defibrillation is a change included in the new algorithm below.
  • Patients with VF for 4-5 minutes or more at the time defibrillation becomes available may benefit from a 1- to 3-minute period of CPR prior to initial defibrillation. The theoretical benefit of this intervention is "to prime the pump" by restoring some oxygen and other critical substrates to the myocardium to allow successful contraction post defibrillation. The benefit of this intervention has been demonstrated in a prospective clinical trial, and it has now been included as an optional protocol for Emergency Medical Services (EMS) in the ACLS guidelines.{Ref1}
    • AED units that can analyze the smoothness of the VF waveform are now available.
    • These units essentially estimate the duration of fibrillation and likelihood of defibrillation success and advise immediate CPR or defibrillation depending on the reading.
  • Precordial chest thump has been studied in a number of case series for patients in pulseless VT and VF. It has been found to convert VT and VF to a perfusing rhythm in some cases, but it also has converted VT to VF and VF to asystole in other cases. This intervention is no longer routinely recommended.
• Algorithm
  • Activate emergency response system.
  • Initiate CPR and give oxygen when available.
  • Verify patient is in VF as soon as possible (ie, AED and quick look with paddles).
  • Defibrillate once.
    • Adult - Device specific or 200 J for biphasic waveform and 360 J for monophasic waveform
    • Children - 2 J/kg
  • Resume CPR immediately without pulse check and continue for 5 cycles.
    • One cycle of CPR equals 30 compressions and 2 breaths.
    • Five cycles of CPR should take roughly 2 minutes (compression rate 100 per minute).
    • Do not check for rhythm/pulse until 5 cycles of CPR are completed.
  • During CPR, minimize interruptions while the following are performed:
    • Secure intravenous access.
    • Perform endotracheal intubation.
    • Once intubated, continue CPR at 100 compressions per minute without pauses for respirations, and administer respirations at 8-10 breaths per minute.
  • Check rhythm after 2 minutes of CPR.
  • Repeat a single defibrillation if still VF or pulseless VT with rhythm check. Use the same dose as the initial defibrillation for adults, and use 4 J/kg for this and all subsequent defibrillations for children.
  • Resume CPR for 2 minutes immediately after defibrillation.
  • Continuously repeat the cycle of the following:
    • Rhythm check
    • Defibrillation
    • 2 minutes of CPR
  • Vasopressors
    • Give vasopressor during CPR before or after shock when intravenous or intraosseous access is available.  
    • Administer epinephrine 1 mg every 3–5 minutes.
    • Consider administering vasopressin 40 units once instead of the first or second epinephrine dose.
  • Antidysrhythmics
    • Give antidysrhythmic during CPR before or after shock.
    • Administer amiodarone 300 mg IV/IO once, then consider administering an additional 150 mg once.
    • Instead of or in addition to amiodarone, administer lidocaine 1-1.5 mg/kg first dose, then additional 0.5 mg/kg doses up to a maximum total of 3 mg/kg.
  • If undulating polymorphic ventricular tachycardia suggestive of torsades de pointes (TdP), administer 1-2 g magnesium IV/IO.
  • Administer sodium bicarbonate 1 mEq/kg IV/IO in cases of known or suspected preexistent hyperkalemia or tricyclic antidepressant overdose.
  • Lidocaine and epinephrine can be administered through the endotracheal (ET) tube if IV/IO attempts fail. Use 2.5 times the IV dose.
  • Correct the following if necessary and/or possible:
    • Hypovolemia
    • Hypoxia
    • Hydrogen ion (acidosis) - Consider bicarbonate therapy.
    • Hyperkalemia/hypokalemia and metabolic disorders
    • Hypoglycemia (Check fingerstick or administer glucose.)
    • Hypothermia (Check core rectal temperature.)
    • Toxins
    • Tamponade, cardiac (Check with ultrasonography.)
    • Tension pneumothorax (Consider needle thoracostomy.)
    • Thrombosis, coronary or pulmonary - Consider thrombolytic therapy if suspected.
    • Trauma
• Refractory or recurrent VF
  • Lack of response to standard defibrillation algorithms is challenging.
  • After initial amiodarone bolus, consider continued amiodarone therapy with 1 mg/min IV for 6 hours, then 0.5 mg/min for 18 hours.
  • If ongoing ischemia is the suspected cause of recurrent VF, consider emergent cardiac catheterization and angioplasty, and intra-aortic balloon pump placement.
• Postresuscitative care
  • Antidysrhythmics used successfully should be continued. Maintain amiodarone at 0.5-1 mg/min and lidocaine at 1-4 mg/min.
  • Control any hemodynamic instability by administering vasopressors as indicated.
  • Check for complications (eg, aspiration pneumonia, CPR-related injuries).
  • Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).

Consultations

Consult a cardiologist or intensivist for continued inpatient ICU care.

Medication

Treatment goals are to electrically terminate VF so that an organized electrical rhythm follows and restores cardiac output. Success rates significantly decrease as the duration of ischemia increases. Drug therapy to facilitate defibrillation may consist of vasopressors, antidysrhythmics, electrolytes, and other agents.

The theoretical benefit of vasopressor medicines, such as epinephrine and vasopressin, is that they increase coronary perfusion pressure. Coronary perfusion pressure is the difference between aortic and right atrial pressure during the relaxation phase of CPR, and it determines myocardial blood flow. Higher levels of coronary perfusion pressure are associated with increased survival in animal models of VF arrest.

Vasopressors, such as epinephrine, increase coronary perfusion pressure; however, no vasopressors have been proven to increase survival in humans. Nevertheless, they are recommended due to possible benefit. Epinephrine, 1 mg, is recommended every 3-5 minutes once IV or IO access is established, and vasopressin, 40 units, may be administered once instead of the first or second epinephrine dose. Higher doses of epinephrine, 0.1-0.2 mg/kg, have been studied, but they are not clearly beneficial compared with the standard 1-mg dose. Recent data suggest no synergistic effect of administering vasopressin in addition to epinephrine.

Antidysrhythmic agents are recommended when initial defibrillation and vasopressor medicines fail or after successful defibrillation to prevent recurrence. Potential benefits of antidysrhythmic therapy include lowering the threshold for defibrillation and preventing immediate or delayed VF recurrence. Potential risks of antidysrhythmic therapy include hypotension due to decreased myocardial contractility or vascular tone, bradycardia, or asystole. No antidysrhythmic agent has been proven to improve survival to hospital discharge from VF arrest, but amiodarone may increase the likelihood of at least temporarily regaining a perfusing rhythm.

The mechanism of action of most antidysrhythmic agents is to alter the conductance of ions, such as sodium and potassium, across myocardial cell membrane ion conducting channels. Amiodarone and other Vaughn-Williams class III agents decrease the repolarizing flow of potassium across the cell membrane and cause a prolongation of the depolarized period. The cell is refractory to further excitation during this period and may not be able to conduct the VF waveform, thus breaking the reentrant cycle of excitation. Other class III agents that have been studied in cardiac arrest include bretylium and sotalol, but they have not been consistently shown to provide benefit.

Lidocaine is a Vaughn-Williams class IB agent that alters the depolarizing flow of sodium across the cell membrane and may be particularly effective in an ischemic or acidotic environment. Procainamide is a Vaughn-Williams class IA agent that affects both sodium and potassium flow across the cell membrane and may also rarely be used for refractory or recurrent VF.

Additional alternative medications include magnesium sulfate, propranolol, and sodium bicarbonate. Magnesium may be particularly important in stabilizing the cell membrane and in preventing after-depolarizations that are important in the genesis of torsades de pointes. Propanolol or other beta-adrenergic blocking agents may have a calming effect on the myocardium for patients with recurrent persistent VF often described as VF storm. Bicarbonate is useful to block the effects of tricyclic antidepressant overdose, to treat hyperkalemia that may be causing ventricular dysrhythmias, or to treat acidosis associated with prolonged cardiac arrest.

Vasopressors/sympathomimetics

Augment both coronary and cerebral blood flow present during low-flow state associated with CPR.

Epinephrine (Adrenalin)

Increases coronary perfusion pressure but has not been proven to increase survival in cardiac arrest.

Dosing

Adult

1 mg (10 mL of 1:10,000 solution) IV push (IVP) or intraosseous (IO) q3-5min or 0.1 mg/kg IVP q3-5 min; intermediate doses of 2-5 mg IVP q3-5 min also may be used; dose may be increased, as follows: 1 mg, 3 mg, 5 mg IVP given at 3-min intervals; higher doses do not improve survival or neurologic outcome; ET administration requires 2-2.5 times the IV dose

Pediatric

0.01 mg/kg (0.1 mL/kg 1:10,000 solution) IVP or IO q3-5 min; 0.1 mg/kg (0.1 mL/kg 1:1,000 solution) recommended for ET administration

Interactions

Increases toxicity of beta- and alpha-blocking agents and halogenated inhalational anesthetics

Contraindications

Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; local anesthesia in such areas such fingers or toes because vasoconstriction may produce sloughing of tissue; do not use during labor (may delay second stage of labor)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly patients, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

Vasopressin (Pitressin)

A nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction. Its effects on outcome have not been proven to differ from epinephrine in VF arrest. It may be used instead of the first or second dose of epinephrine during cardiac arrest resuscitation. Since it lasts longer than epinephrine, vasopressin is used only once.

Dosing

Adult

40 U IV once only

Pediatric

Not recommended

Interactions

Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects

Contraindications

Documented hypersensitivity; coronary artery disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia

Antidysrhythmics

These agents alter electrophysiologic mechanisms responsible for dysrhythmia.

Lidocaine (Xylocaine, Dilocaine)

Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.

Dosing

Adult

Bolus of 1-1.5 mg/kg IV; repeat prn using 1.5 mg/kg boluses q3-5 min, not to exceed 3 mg/kg; follow with continuous IV infusion of 2 mg/min after return of perfusion; if continuous IV infusion is not started, administer additional boluses of 0.5 mg/kg q10min to maintain effect
ET: Administer 2-2.5 times IV dose

Pediatric

ET, intraosseous (IO), and IV loading: 1 mg/kg (repeat dose twice at 10- to 15-min intervals prn)
Following loading dose, start continuous IV infusion of 20-50 mcg/kg/min

Interactions

Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Contraindications

Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolff-Parkinson-White syndrome; avoid in severe sinoatrial, AV, or intraventricular block if artificial pacemaker is not in place

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia, shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, asystole, heart block, and AV conduction abnormalities

Amiodarone (Cordarone)

Acute actions after IV bolus are to inhibit AV conduction and prolong the AV refractory period; IV amiodarone usually causes a decrease in systemic vascular resistance with coronary and peripheral vasodilatation and variable depressant effects on cardiac contractility. Eventually amiodarone lengthens the duration of repolarization (QT interval corrected for pulse rate) and refractory period in most cardiac tissue. Amiodarone improves the return of spontaneous circulation from VF arrest by uncertain mechanisms, but it has not been shown to improve survival to hospital discharge. When administered chronically, multiple other effects occur on adrenergic tone, thyroid function, and other systems.

Dosing

Adult

300 mg IV bolus; 150 mg IV infused over 10 min, then 1 mg/min continuous infusion for 6 h; maintenance infusion at 0.5 mg/min

Pediatric

5 mg/kg IV or IO; repeat up to total 15 mg/kg, not to exceed 300 mg

Interactions

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels

Contraindications

Documented hypersensitivity; complete AV block; intraventricular conduction defects; patients taking ritonavir or sparfloxacin

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in thyroid or liver disease; hypotension (most common adverse effect), bradycardia, AV block, and torsades de pointes may occur; elevated serum hepatic enzyme levels are common in VT

Bretylium tosylate

Class III antidysrhythmic agent previously used for VF refractory to defibrillation, epinephrine, and lidocaine. Bretylium may increase the fibrillation threshold and ventricular myocardial refractory period by decreasing potassium conductance. Has catecholamine-releasing properties and adverse effects and is not used as initial treatment. Currently not commercially available in the United States.

Dosing

Adult

Initial dose: 5 mg/kg (undiluted) IV over 1 min; for persistent arrhythmia, 10 mg/kg (undiluted) IV over 1 min; repeat at 15-30 min intervals prn; not to exceed 30-35 mg/kg/24 h
Maintenance dose: 1-2 mg/min IV

Pediatric

Not established; suggested dose is 5 mg/kg IV over 1 min; if arrhythmia persists, 10 mg/kg IV over 1 min q15min prn; not to exceed 30 mg/kg; maintenance dose is 5-10 mg/kg/dose IV q6h

Interactions

Increased toxicity reported when taken with pressor catecholamines and digitalis; may increase risk of cardiotoxicity when taken concurrently with sparfloxacin or ofloxacin

Contraindications

Documented hypersensitivity; systemic lupus erythematosus, digitalis-induced arrhythmias, complete heart block, or second- or third-degree heart block if a pacemaker is not in place; avoid in torsade de pointes

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause hypotension, especially in patients with fixed cardiac output (eg, aortic stenosis); caution in renal insufficiency, severe pulmonary hypertension, and aortic stenosis; half-life increases in elderly patients; with renal clearance of 10-50 mL/min, administer 25-50% of dose; rapid IV injections may result in transient hypertension, nausea, and vomiting; limit injection to 5 mL (undiluted) at each injection site

Procainamide (Procanbid)

Vaughn-Williams class IA antidysrhythmic that blocks both sodium and potassium conducting channels. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity, and it widens the QRS interval. Procainamide also increases the refractory period of atria and ventricles with associated lengthening of the QT interval. Procainamide is used to treat both supraventricular and ventricular dysrhythmias.

Dosing

Adult

25 mg/min IV at continued infusion rates until dysrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered; once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min

Pediatric

Not established; the following doses have been suggested: 15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
3-6 mg/kg/dose IV infused over 5 min
Maintenance: 20-80 mcg/kg/min IV administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d

Interactions

Can expect increased levels of procainamide metabolite, NAPA, in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; procainamide may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity

Contraindications

Documented hypersensitivity; complete heart block or second- or third-degree heart block if pacemaker is not in place; torsade de pointes; systemic lupus erythematosus

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Long-term use of this drug leads to development of positive antinuclear antibody test result in 50% of patients; may result in lupus erythematosus–like syndrome in about 20-30% of patients; fatal blood dyscrasias also have been reported with therapeutic doses; plasma concentration of procainamide and its active metabolite, NAPA, may be increased in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency

Electrolytes

These agents are considered therapeutic alternatives for refractory VF. Patients with persistent or recurrent VF following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia. Among electrolyte abnormalities associated with VF are hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VF secondary to other medications. Magnesium sulfate acts as an antidysrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VF caused by hyperkalemia.

Magnesium sulfate

Deficiency in this electrolyte is associated with SCD and can precipitate refractory VF. Magnesium supplementation is used to treat torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.

Dosing

Adult

1-2 g diluted in 100 mL of D5W administered IV over period of 1-2 min for refractory VF and known or suspected hypomagnesemia (Mg⁺² <1.4 mEq/L); not to exceed 30-40 g/d or 1-2 g/h maintenance rate

Pediatric

Not established; suggested dose is 25-50 mg/kg IV q4-6h for 3-4 doses; maximum single dose of 2 g may be administered and repeated if hypomagnesemia persists

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and other agents causing neuromuscular antagonism; increases toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

Contraindications

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May alter cardiac conduction leading to heart block in digitalized patients; when electrolytes are administered parenterally, monitor respiratory rate, deep tendon reflex, and renal function; may produce significant hypertension or asystole

Sodium bicarbonate (Neut)

Only when the patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant, or phenobarbital overdose. Routine use not recommended.

Dosing

Adult

1 mEq/kg/dose IV initially followed by 0.5 mEq/kg/dose IV q10min or as indicated by ABGs

Pediatric

0.5-1 mEq/kg/dose IV repeated q10min or as indicated by ABGs; rate of infusion not to exceed 10 mEq/min

Interactions

Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Contraindications

Patients with alkalosis, hypernatremia, hypocalcemia, severe pulmonary edema, and unknown abdominal pain

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Only to be used to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium level, hypocalcemia, and hypernatremia; caution in electrolyte imbalances, eg, patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation since can cause tissue necrosis

Calcium chloride

Useful in treatment of hyperkalemia, hypocalcemia, or calcium channel blocker toxicity. Moderates nerve and muscle performance by regulating the action potential excitation threshold.

Dosing

Adult

Known or suspected hyperkalemia (K+ > 6 mEq/L): 2-4 mg/kg (10% solution) IV

Pediatric

0.2 mL/kg of IV (10% solution)

Interactions

Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate

Contraindications

VF not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure

Follow-up

Further Inpatient Care

• Resuscitated patients must be admitted to an intensive care unit and monitored because of high risk of a recurrence.
  • They require stabilization and monitoring for possibility of a coexistent emergency or complication.
  • Evaluation of ischemic injury to the CNS, myocardium, and other organs is essential.
  • Patients typically have an underlying etiology that must be investigated and treated.
• Up to approximately half of cardiac arrest survivors have evidence of an acute MI. Both emergent thrombolytic therapy and percutaneous transluminal coronary angioplasty (PTCA) have been used to treat these patients; however, CPR for greater than 10 minutes is considered a relative contraindication to thrombolysis. Emergent cardiology consultation is warranted for all survivors of cardiac arrest, and efforts at revascularization should be attempted, if indicated.
• Patients who remain comatose post resuscitation benefit from 12-24 hours of controlled hypothermia therapy at 32-34 degrees Centigrade (89.6-93.2 degrees Fahrenheit). This can be accomplished with chemical sedation and paralysis to prevent shivering and an external cooling blanket or ice. Hypothermia therapy improves both neurologic outcome and mortality.
• Automated implantable defibrillators (AICDs) are recommended for patients at risk for recurrent VF because they effectively provide early defibrillation. Patients with VF arrest who receive AICDs have improved survival compared with those receiving only medications. However, patients with AICDs may also require oral antidysrhythmic therapy to minimize recurrent device activation.

Deterrence/Prevention

• In the setting of acute myocardial infarction, beta-adrenergic blocking therapy with agents such as metoprolol decrease the likelihood of ventricular dysrhythmias including ventricular fibrillation, and they lower overall mortality. Administer a beta-adrenergic blocking agent during acute myocardial infarction unless contraindicated by bradycardia, heart block, congestive heart failure, or reactive airway disease.

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, AICD, pacemaker)
• Death

Prognosis

• The prognosis for survivors of VF strongly depends on the time elapsed between onset and medical intervention. Early defibrillation often makes the difference between long-term disability and functional recovery.
• Postresuscitation death and disability after successful resuscitation directly correlate with the amount of CNS damaged during the event. Without intervention, by 4-6 minutes after onset of VF, the prognosis is poor. Few survive when VF lasts more than 8 minutes without intervention.
• The reported rate of survival from VF in the community varies from 4-33%. Survival is worst in dense urban and sparse rural areas, principally due to prolonged EMS response times.
• AICD implantation is the primary treatment of survivors of VF. Antidysrhythmic and beta-adrenergic blocking medicines may also be helpful to prevent VF recurrence. While these interventions lower the risk of sudden dysrhythmic death, the AICD in particular does not prevent or retard the progressive congestive heart failure that is often present in these patients.

Patient Education

• For excellent patient education resources, visit eMedicine's Heart Center and Public Health Center. Also, see eMedicine's patient education article Cardiopulmonary Resuscitation (CPR).
• The National Library of Medicine's Medline Plus Web site is another invaluable resource.

Miscellaneous

Medicolegal Pitfalls

• Failure to address underlying causes of VF or to refer patient to appropriate care provider
• Failure to initiate defibrillation immediately following diagnosis of VF
• Failure to adequately train personnel on use of defibrillation equipment
• Failure to keep equipment properly maintained and fully charged

Special Concerns

• VF is the initial rhythm in 4-9% of pediatric cardiac arrests in multiple series. In addition to witnessed arrest and bystander CPR, near-drowning etiology is associated with a better prognosis.
• Survival from cardiac arrest decreases with advancing age, but resuscitation of very elderly persons is not necessarily futile. Nineteen (3.3%) of 512 community-dwelling patients aged 80 years and older survived to discharge in one report.¹ Survival of elderly persons may also be negatively confounded by the observation that they are more likely to arrest in the home, which carries a worse prognosis.
• Hypothermia and VF
  • Endotracheal intubation is recommended when available regardless of body temperature.
  • For patients with moderate hypothermia, 30-34 degrees Centigrade (86-93.2 degrees Fahrenheit), CPR and defibrillation are administered as per the standard algorithm. Active internal rewarming should be administered simultaneously. Intravenous resuscitation medicines should be administered, spaced at longer intervals than normal due to reduced drug metabolism.
  • For patients with severe hypothermia, less than 30 degrees Centigrade (86 degrees Fahrenheit), and VF, a single defibrillation can be attempted. After this, CPR and active internal rewarming should begin. Further defibrillation and resuscitation medications are withheld until a core temperature of 30 degrees Centigrade is reached.
• Family presence during resuscitation is practiced in some health care facilities. While this does not seem to impair or benefit the resuscitation efforts, it may be beneficial to the patient's family members in reconciling the imminent loss of a loved one.
• Termination of resuscitation efforts
  
  
  • The optimal juncture to cease unsuccessful resuscitation efforts and to declare death is controversial. Decision rules have been formulated, but there will always be patients who defy such algorithms.
  • Patients who are pulseless and not severely hypothermic upon arrival by EMS and do not have a return of spontaneous circulation after 25 minutes of ACLS have a dismal prognosis.
  • The decision to terminate resuscitation efforts must be made on an individual basis by the clinician after assessing any possible extenuating factors. Visualization of the heart and a lack of spontaneous cardiac motion on ultrasonography may also be helpful in confirming the prognosis and outcome.

Multimedia

Media file 1: Ventricular fibrillation. Rapidly recurrent despite electrical biphasic defibrillation. Notice that recurrence begins after completion of the T wave and is not due to an R-on-T phenomenon in this case. This episode of ventricular fibrillation (VF) occurred in the emergency department and was present for less than 30 seconds prior to defibrillation, hence the course morphology. Also an undulating amplitude suggestive of torsades de pointes was present; however, the QT interval during sinus rhythm was normal, and the only known predisposing factors for tachydysrhythmia were newly diagnosed coronary artery disease with acute right coronary artery occlusion and a history of rheumatoid pericarditis.

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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

Contributor Information and Disclosures

Author

Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital
Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Mazen K Khalil, MD, Post Doctoral Research Fellow, Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation
Mazen K Khalil, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Aaron Bright, MD, Staff Physician, Department of Emergency Medicine, University of Southern California Keck School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center
Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians and National Association of EMS Physicians
Disclosure: Intellicare Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Charles V Pollack, Jr, MD, MA, FACEP, Professor, Department of Emergency Medicine, University of Pennsylvania College of Medicine; Chairman, Department of Emergency Medicine, Pennsylvania Hospital
Charles V Pollack, Jr, MD, MA, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: sanofi-aventis Honoraria Consulting; sanofi-aventis Honoraria Speaking and teaching; Schering-Polugh Honoraria Consulting; Schering-Plough Honoraria Speaking and teaching; The Medicines Company Honoraria Consulting; GlaxoSmithKline Grant/research funds Other

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