Recent Changes in the Cardiac Life Support Guidelines

With the millennium came a new, more evidence-based and globalized version of the rescue guidelines periodically released by the American Heart Association. In this article, the author highlights the 2000 edition's revised cardiac emergency procedures and updated public health recommendations.

By Barbara K. Richardson, MD

Dr. Richardson is vice chairman of the department of emergency medicine, associate clinical professor of emergency medicine, and director of the emergency department of the Mount Sinai Hospital in New York City. The author thanks Dr. Sheldon Jacobson for his thoughtful review of this manuscript.

The International Guidelines 2000 Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care generated a substantive revision of the advanced cardiac life support (ACLS) guidelines published in 1992 by the American Heart Association (AHA). The 2000 guidelines were developed from a new evaluation template designed to steer the process toward a more fully evidence-based and internationally applicable set of resuscitation recommendations.

After the panel had identified a range of topics at a previous conference, they gathered the scientific evidence and assessed its strength and relevance against an eight-point scale that categorized the least reliable data as rational conjecture or common sense and the most reliable as evidence derived from large randomized, controlled trials. A panel of experts assembled from the 1999 American Heart Association Evaluation Conference, in collaboration with the 2000 International Liaison Committee on Resuscitation, then outlined their recommendations in three classes, as they had done in previous editions, according to the strength of the evidence supporting those recommendations. To these new guidelines, the panel members added an "Indeterminate" category to address available data that were not sufficiently reliable, complete, or accurate to support or reject a particular resuscitation recommendation (see table below). Although the panel believed in the validity of an evidence-based approach, they acknowledged that available research is often insufficient to allow firm conclusions to be drawn in some instances.

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Basic Life Support Guidelines for Lay Rescuers

Simplification is the overarching theme of the 2000 basic life support (BLS) recommendations for the lay-that is, nonmedical or professional-rescuer. According to Cummins and colleagues, only 15% of lay rescuers can assess a pulse within 10 seconds, and 45% report no pulse when a pulse is present (Annals of Emergency Medicine, vol. 43, p. 780, 1999). In revising the guideline for lay rescuers, the International Guidelines 2000 Conference recommended that rescuers should not depend on the unreliable pulse assessment as an indication of perfusion but instead on signs of life, such as breathing, movement, and coughing.

For lay rescuers who do not have pocket masks and are attempting to restore spontaneous circulation, or for those who are unable or unwilling to provide mouth-to-mouth ventilation, the guidelines confirm that chest compression alone (a class IIa recommendation) is preferable to not performing CPR. For adults, 100 compressions per minute remains the standard. The compression-to-ventilation ratio, regardless of the number of rescuers attending to the victim, remains at 15:2.

The rationale for grouping two ventilations to cause less frequent interruption of chest compression is derived from the results of real-time echocardiography, which demonstrate that better cardiac blood flow is generated when chest compression is performed with less frequent interruption for ventilation; hence, the 15:2 ratio is recommended until a professional rescuer establishes a patent airway via endotracheal intubation. At that point, an asynchronous 5:1 compression-to-ventilation ratio would be optimal.

For resuscitating an unconscious victim, the BLS guidelines for lay rescuers no longer recommend the application of abdominal thrusts to relieve an obstructed airway. The lay person is directed instead to focus on maintaining CPR and limit his or her effort in clearing the airway to oral inspection and removal of any visible foreign body. In contrast, for professional health-care providers, who are expected to maintain their skills through practice and retraining, the guidelines still recommend both pulse assessment and abdominal or chest compression for relieving foreign body obstruction.

The most critical impediment to successful resuscitation, and the most difficult variable to control outside the hospital, is the time that is wasted before cardiac symptoms are recognized and advanced care systems activated or reached. To ensure the greatest chance of recovery, a person who suffers cardiac arrest should undergo defibrillation within five minutes of the event, but research has shown that outside the hospital, that goal cannot be achieved by EMS systems alone.

One proposed solution suggests that certain citizens should be trained to recognize cardiac arrest, call EMS immediately, use an automatic external defibrillator (AED), and provide CPR. In fact, nonmedical professionals, such as firemen, security guards, and airline personnel, whose occupations define them as "first responders," are ideal candidates for such training, particularly in the use of AEDs, which should be prominently displayed in public places.

These recommendations were inspired by the dramatic success AEDs had demonstrated after they were installed throughout a major Chicago airport in 1999. Since the defibrillators were installed, many passengers who suffered cardiac arrest in the terminals there have been saved by the devices. A recently enacted federal regulation will require all major air carriers to install AEDs by 2003. Many public institutions have purchased or installed these devices or are in the process of implementing training programs for their use. In view of this trend, the ongoing, massive NIH-sponsored Public Access Defibrillation trial has been gathering data to assess the acceptance and outcome of AED programs nationwide. In addition to the first responders described, other candidates for AED and resuscitation training include assigned employees at work sites and family and friends of patients at high risk for cardiac sudden death.

Citizens must be trained to recognize not only cardiac arrest but stroke and acute myocardial infarction (MI) and to call 911 or an EMS immediately to ensure that the stricken person can be brought to a hospital in time to receive reperfusion therapy, if he or she is eligible. Studies have shown that the damage-limiting benefit conferred by reperfusion via fibrinolysis (a class I recommendation) can be gained only when the fibrinolytic drug is administered within 3 hours after onset of symptoms of stroke or within 12 hours of the onset of symptoms of acute ST-segment elevation MI. At high-volume medical centers, the preferred reperfusion method to treat ST-segment elevation MI (STEMI) is percutaneous angioplasty, if it is available within 90 minutes of a patient's arrival at the ED.

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Implications for EMS Personnel

The new guidelines emphasize that stroke should be accorded the same high priority as that for acute MI, because the time to intervention in acute MI and stroke is crucial to the reversal of ischemia. The Cincinnati Prehospital Stroke Scale and Los Angeles Pre-hospital Stroke Screen (LAPSS) provide efficient, validated tools that emergency medical personnel can use to screen for acute neurologic deficits.

The Cincinnati Scale, described in a 1997 addendum to the guidelines, states that any evidence of acute facial asymmetry, upper extremity drift, or slurred speech is a sign of possible stroke that warrants notification to the hospital and emergency transportation personnel. The LAPSS is a similar tool to detect neurologic asymmetry, but it also addresses a victim's age, the duration of symptoms, and the possibility of other disorders that can mimic stroke, such as diabetic hypoglycemia or a postictal state. A brief medical and functional history is also part of the screening process, because a patient's underlying health problems may affect his or her eligibility for fibrinolysis.

In addition to emphasizing advance notice and rapid delivery of victims of stroke to the hospital, the guidelines stress that victims should be transported to hospitals that are equipped with rapid computed tomography (CT) and have expertise in the administration of fibrinolysis and management of stroke victims.

For victims of cardiac arrest who have ventricular fibrillation (VF) or tachycardia (VT), rapid defibrillation is paramount. All health care providers should be familiar with the application and use of AEDs. Such devices are able to interpret and identify "shockable" rhythms in an unresponsive patient. During the machine's analysis phase, rescuers must avoid any contact with the patient that could create movement artifacts. They must also be wary of any inappropriate recommendation to perform defibrillation. The audible prompts that are featured on commercially available units greatly enhance proper use of the equipment. Once applied to any unresponsive victim, the AED will provide within a period of a minute three shocks if ventricular fibrillation or tachycardia is detected and if the rhythm does not change. Biphasic wave form defibrillation, a feature available on many AEDs, provides similar results with lower defibrillating energies and is considered to be at least as effective as traditional monophasic defibrillation.

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Airway Management Guidelines for Heatlh Care Providers

Only medical staff who are skilled in advanced airway management procedures should provide such treatment. Esophageal-tracheal or laryngeal mask airways are acceptable alternate devices for maintaining difficult airways, if rescuers are trained in their use. To maintain their skills, medical professionals should, ideally, perform endotracheal intubation at least 6 to 12 times a year.

To confirm tracheal placement of a ventilation tube, some form of capnometer, such as an end tidal CO2 device or monitor, or esophageal detector must be used, and the confirmation should be documented on the patient record. In addition, the proper placement of the tube must be verified by the more traditional methods and signs, including direct visualization of the tube through the vocal cords, the presence of equal breath sounds and rising chest, the absence of stomach gurgling, evidence of improved oxygen saturation as determined by pulse oximetry, and a corroborative chest film. This version of the guidelines emphasizes that particular attention be paid to securing the tube with a device built for the purpose or with tape, because tube dislodgement is relatively common and can cause significant problems if it is not detected immediately.

Patients who have undergone intubation and are no longer in cardiac arrest should be administered a tidal volume lower than what was previously recommended, 6 to 7 ml/kg delivered over 1.5 to 2.0 seconds. The guidelines consider continued hyperventilation to be potentially harmful and therefore do not recommend the procedure, except to reduce increased intracranial pressure. A normal respiratory rate of 12 to 15 breaths is the standard rate except when a prolonged expiratory phase, as occurs in status asthmaticus, is evident. In that case, a reduced tidal volume and ventilatory rate and sedation therapy creates permissive hypercapnia and less risk of lung rupture and ensures a safer, more gradual return of normal lung function as inflammation and bronchospasm subside.

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Drug Therapy in ACLS

In cardiac arrest, drug therapy remains secondary to the primary goals of early CPR, defibrillation, and definitive airway management. In the current ACLS guidelines, the protocols for recognizing and treating asystole, pulseless electrical activity (PEA), and bradycardia remain unchanged from the previous edition. The guidelines specify that after intravenous access for fluids is established-and, in the case of PEA, adequate oxygenation is restored-a 1-mg bolus of epinephrine should be administered as the potentially reversible causes of the asystole or PEA are explored (see table below).

The approach to treating symptomatic bradycardia is to first assess the adequacy of oxygenation and then administer, in order, atropine, transcutaneous pacing, dopamine, epinephrine, and, finally, an isoproterenol infusion at the lowest doses. Because patients who have high-grade heart block or a transplanted heart do not respond to atropine, the resuscitation sequence should start with transcutaneous pacing.

The treatment of asystole, which includes administering boluses of epinephrine and atropine every three minutes, ventilation, and CPR, frequently fails to achieve return of spontaneous circulation. Some patients may have established do-not-attempt-resuscitation (DNR) orders or living wills prohibiting the taking of heroic measures at the end of their life. When such a request is made known to rescuers, they should respect the patient's wishes and withhold resuscitation and provide comfort instead.

The guidelines panel has downgraded the status of high-dose epinephrine as a treatment for VF and VT. Even though the drug was slightly better than low-dose preparations in inducing the return of spontaneous circulation, it was not associated with a significant increase in the rate of survival to the time of hospital discharge.

On the basis of limited but promising data by Lindner and colleagues, vasopressin, or antidiuretic hormone-given in a single 40-U intravenous, supraphysiologic dose-is now recommended (class IIb) as an equivalent substitute for epinephrine in the initial treatment of VF or VT refractory to defibrillation shocks or in prolonged resuscitation procedures (Lancet, vol. 349, p. 535, 1997). The adverse effects attributed to epinephrine that occur during the postresuscitation period of increased myocardial oxygen demand do not occur when nonadrenergic vasopressin is administered. The evidence supporting the use of vasopressin in treating asystole or PEA is insufficient at this time.

Vasopressin can be administered via the intraosseous route. Should the single vasopressin dose fail, the guidelines suggest that sequential epinephrine be given 10 minutes after the administration of vasopressin. A large European randomized controlled trial is currently underway comparing the effects of each drug in subjects who had suffered out-of-hospital cardiac arrest.

Previously recommended as the first drug to be given after epinephrine in treating VF of VT, lidocaine has been downgraded in the ACLS guidelines to indeterminate status, because the data regarding that drug's effectiveness are conflicting. Lidocaine may still be given (a class IIb recommendation)-in doses of 1.5 mg/kg up to a maximum of 3 mg/kg-if defibrillation or epinephrine therapy has first successfully converted a patient's VF or VT. However, for treating stable or recurrent VT, lidocaine has been superseded by procainamide and amiodarone.

When hypomagnesemia is suspected (serum magnesium level less than 2.0 mEq/L), the guidelines suggest that magnesium, given in intravenous doses of 1 to 2 grams, be limited to the treatment of torsade de pointes or VF or VT. The guidelines have removed bretylium as an option, owing to its limited supply, variable efficacy data, and significant adverse effects.

Amiodarone (a class IIb recommendation) is now preferred over lidocaine or procainamide in the treatment of VF or pulseless VT that does not respond to three defibrillation shocks and a first dose of either epinephrine or vasopressin. Versatile amiodarone (class IIa) can also be used to enhance conversion of stable monomorphic or polymorphic VT and to control ventricular rate or induce conversion of rapid atrial fibrillation. It is a class IIb choice for treating preexcited atrial tachycardia that occurs in Wolff-Parkinson-White syndrome. The ACLS guidelines panel included amiodarone in their recommendations on the basis of the results of the Amiodarone for Resuscitation of Out-of-Hospital Cardiac Arrest (ARREST) trial, which enrolled 504 patients from Kings County, Washington, who suffered out-of-hospital cardiac arrest. In that study, subjects were randomly assigned to receive amiodarone or placebo in a 300-mg dose diluted in 20 to 30 ml of dextrose or saline given by rapid infusion; the agents were given before any other antiarrhythmic drug was administered.

According to Kudenchuk and colleagues, who reported the study results in 1999, the rate of survival to the time of hospital admission was 29% higher among those patients who received amiodarone (New England Journal of Medicine, vol. 341, p. 871, 1999). The drug had long been considered the antiarrhythmic agent of choice for pulseless or unstable patients known to have depressed left ventricular function and VF or VT, but in this trial the survival rate among all patients in the amiodarone group was higher.

When amiodarone is used to convert atrial or ventricular rhythms in the presence of a pulse, the 150-mg dose should be given via slow push over 10 minutes. The pediatric dose for treating VF or VT arrest is 5 mg/kg when a pulse is absent, 2 mg/kg when it is present. In adults, once the rhythm has converted or the rate is controlled-as is done in treating atrial fibrillation-a continuous infusion of 1.0 mg/minute should be administered over 6 hours, then 0.5 mg/minute over 18 hours, or to a maximum daily dose of 2 gm. Guidelines for administering infusions to young children have not been devised. Because the solution can crystallize, a glass IV bottle and a 22-micron inline filter must be used during the infusion. Central line access is recommended when prolonged administration is necessary.

Amiodarone can cause symptomatic bradycardia, QT-interval prolongation and hypotension, which may be related to the rate of infusion. Fluids, pressor agents, chronotropic agents, and pacing for symptomatic bradycardia can be employed if reducing the infusion rate fails to counteract the adverse effects.

Data from the ARREST trial did not evaluate amiodarone in treating in-hospital cardiac arrest, nor did they indicate an associated increase in the rate of survival to the time of hospital discharge. Currently, investigators in the ALIVE trial are examining those issues while comparing the efficacy of amiodarone with that of lidocaine.

Until those study results are available, the ACLS guidelines recommend that defibrillation therapy be administered rapidly and that a single antiarrhythmic agent be given to most patients who do not respond to shock-induced defibrillation. They also suggest that some patients, particularly those who have known severe cardiomyopathy, may benefit from early administration of amiodarone. As always, the recommended shock-drug-shock sequence of administration should be followed.

To produce useful drug selection guidelines, investigators in future studies must gather accurate data regarding their patients' time to first defibrillation, survival to the time of hospital discharge, and neurologic status.

The ACLS guidelines explain that postresuscitation care should focus on minimizing the risks of multiple-organ system dysfunction and sepsis. In addition, they recommend that mildly hypothermic patients, who may gain protective benefit from a lowered body temperature, should not undergo active rewarming procedures. The recommendations concerning pressor and inotropic agents remain similar to those of previous guidelines. For patients who have systolic heart failure and tachycardia unresponsive to dopamine and dobutamine, the guidelines suggest that milrinone, a phosphodiesterase III inhibitor, can be given alone or in combination with dobutamine (see sidebar at the end of the article).

The guideline text discusses in detail three parenteral antiarrhythmic agents-also available in oral preparations-currently used in Europe that have not received FDA approval. Flecainide, a sodium channel blocker, is used to treat supraventricular tachycardia (SVT), atrial fibrillation or flutter, and SVT accompanied by Wolff-Parkinson-White syndrome. Propafenone, a nonselective beta-blocker, is given for the same indications. Sotalol, another nonselective beta-blocker, is used to treat SVT and VT. Ibutilide, used in the conversion of atrial fibrillation and flutter, and esmolol, a fast-acting beta-blocker, are the parenteral options in the U.S. and have similar risk and benefit profiles. Both flecainide and propafenone have been reported to be associated with a higher mortality among patients who have ischemic heart disease.

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ACLS Overview of Acute Coronary Syndromes

The current guidelines amplify the necessity of letting the pathophysiology of STEMI and non-STEMI guide the approach to therapy. All patients who have acute MI should receive aspirin, beta-blockers, nitrates, oxygen, heparin, and morphine, if no contraindications exist. In STEMI, plaque rupture creates an occlusive thrombosis involving a fibrin mesh, a condition that justifies the administration of a fibrinolytic agent such as reteplase. In non-STEMI, the platelets predominate and produce incomplete occlusion, creating unstable angina, a disorder that responds to glycoprotein IIb/IIIa inhibitors, particularly as a bridge to percutaneous transluminal coronary angioplasty (PTCA).

All patients presenting with unexplained chest pain or an anginal equivalent should undergo immediate electrocardiography. This type of chest pain can be either STEMI or non-STEMI. Sometimes, the electrocardiogram (ECG) is nondiagnostic, but when a patient has continued chest pain that is unresponsive to therapy, a second ECG can improve the accuracy of the diagnosis. Other causes, such as aortic dissection or pericarditis, must be considered.

In the treatment of STEMI, emergent angioplasty, if available, is preferred when fibrinolysis is contraindicated or when a patient is in shock or had previously undergone stent placement. All victims of MI should also receive aspirin; heparin; oxygen; nitrates, if the cardiac pain does not abate; and beta-blockers, if they are not contraindicated by overt congestive heart failure, active asthma, hypotension, bradycardia, or cocaine use.

As a bridge to rapid revascularization in patients in cardiogenic shock, immediate cardiac consultation and a circulatory assistance device may be helpful. Angioplasty has been improved significantly by the introduction of new types of balloons, stents, and antiplatelet therapy. Coronary artery bypass grafting is generally reserved for left main heart disease or triple-vessel disease accompanied by reduced LV function. In the absence of hypotension, early angiotensin-converting enzyme (ACE) inhibitor therapy is indicated for all patients who have acute MI (STEMI or non-STEMI) and evidence of LV dysfunction (ejection fraction of less than 35%). Patients who are hemodynamically stable should receive ACE inhibitors within six hours of their arrival to the ED.

Another subset of patients with chest pain will have non-STEMI or ST-segment depression greater than 1 mm, dynamic ST changes, or deep T-wave inversions suggestive of ischemia, any of which increases a patient's risk for an adverse cardiac event, such as recurrent ischemia, depressed LV function, or death. These patients also benefit from antiplatelet therapy, if not otherwise contraindicated, consisting of aspirin, antithrombin therapy with reduced-dose unfractionated heparin (UFH), and glycoprotein IIb/IIIa platelet adhesion/aggregation inhibition to reduce clot propagation.

Heparin therapy, downgraded in this version of the guidelines, should begin with an initial bolus of 60 U/kg and continue with a maintenance dose of 12 U/kg/hour, adjusted to maintain an activated partial thromboplastin (PTT) time of 50 to 70 seconds. The PTT should be monitored at six hours after the start of therapy. For patients who weigh over 70 kg, the maximum bolus dose of heparin is 4000 units; the maximum maintenance dose, 1000 U/hour. This dose reduction in the guideline provides a greater margin of safety for patients receiving multiple agents, which can cause hemorrhage.

Beta-blockers and nitrates should also be administered, as to patients who have non-STEMI, and urgent catheterization should be considered. The glycoprotein IIb/IIIa inhibitors, which include abciximab, eptifibatide, and tirofiban, share the same contraindication profile with heparin and have shown the greatest benefit in reducing the risk of MI, revascularization, and death at six months after an early percutaneous catheter procedure is performed.

Careful monitoring of anticoagulation is essential during heparin therapy to prevent intracranial hemorrhage or other bleeding disorders. All nursing stations in which patients are undergoing heparin therapy should have the AHA/ACC Heparin Dosing Nomogram available for reference. Low-molecular-weight heparin (LMWH) is an acceptable alternative to UFH (an Indeterminate class recommendation).

A practical approach to antithrombin therapy would be to give unfractionated, short-acting heparin to patients who are likely to undergo immediate angioplasty or when revascularization is expected. However, LMWH, if available, may reduce risk further in all other patients who have unstable angina that is associated with an intermediate to high risk of an adverse cardiac event and in whom cardiac catheterization is not an immediate priority.

The LMWH preparations offer several distinct advantages: they are easier to administer (in subcutaneous preparations), they don't necessitate PTT monitoring, and they are associated with fewer hemorrhagic complications and a lower incidence of recurrent angina, MI, and death at 14 days after administration. Protamine, in particular, has a shorter half-life and the ability to reverse adverse effects, which is the reason why UFH is still favored by some catheterization laboratories for patients who require emergent angioplasty.

The third and largest subset of patients who have chest pain and nondiagnostic ECGs have ST- or T-wave changes of less than 1 mm or a normal ECG, yielding a low to intermediate risk for an adverse cardiac event. Treatment typically consists of aspirin combined with other agents, such as nitrates to treat pain. Beta-blocker therapy may be necessary as well.

These patients, who are often admitted to chest pain observation units, typically undergo serial electrocardiography and cardiac marker testing over a 6- to 12-hour observation period. It is during that time that the nature of a patient's chest pain often becomes clear. The usual causes include noncardiac disorders, acute MI, and probable angina that warrants further investigation. Patients with a very elevated or rising troponin level are at greater risk for an adverse cardiac event within months of its initial detection and may benefit from a more aggressive (in-hospital) evaluation. Patients who have nondiagnostic findings will require further risk assessment, which may include functional or imaging studies such as stress echocardiography, pharmacologic or exercise stress testing, PET scanning, cardiac catheterization, or, in the near future, MRI angiography.

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Special Resuscitation Situations

Previous editions of the ACLS guidelines have addressed the treatment of cardiac arrest that occurs during trauma, hypothermia, pregnancy, near drowning, and electrical shock. The toxicology section has been expanded in the new edition to include a caution against the administration of beta-blockers in favor of benzodiazepines and nitrates to patients who have chest pain accompanied by cocaine poisoning. The toxicology section also recommends, among many other antidotes, alkalinization therapy as the primary treatment for tricyclic antidepressant-induced tachycardia; high-dose atropine for treating organophosphate poisoning; glucagon, and possibly isoproterenol, for countering the toxic effects of beta-blockers; and calcium for treating calcium channel blocker poisoning. In the treatment of suspected opiate overdose accompanied by severe respiratory depression, the guidelines stress that normal ventilation must be restored via bag valve mask before naloxone can be administered safely.

The ACLS guidelines also review the causes, symptoms, characteristic ECG findings, and treatment of various electrolyte disorders, including those relating to magnesium, calcium, and sodium imbalance. Hyperkalemia is the most frequent of those disorders and most likely to lead to sudden deterioration if untreated.

The appropriate treatment of hyperkalemia depends on a patient's symptoms and serum potassium level. A mild elevation (5 to 6 mEq/L) may resolve after the cause is eliminated and sodium polystyrene sulfonate or furosemide is administered. Higher elevations of potassium accompanied by symptoms such as weakness, altered mental status, and ECG evidence of peaked T waves or prolonged PR or widened QRS intervals are a signal for more aggressive cardiac protection via calcium therapy. Intravascular potassium stores can be temporarily reduced by administering D50W/insulin, bicarbonate, and nebulized albuterol. Life-threatening hyperkalemia usually necessitates emergent dialysis. A second ECG should be carefully examined after calcium therapy is administered to confirm the resolution of the potassium-related changes. If those changes persist, the drugs should be administered again along with more emergent dialysis.

Suggested Reading Braunwald E, et al.: The ACC/AHA Guidelines for Unstable Angina. J Am Coll Cardiol. 36:1055, 2000. Cummins RO, et al.: Cardiopulmonary resuscitation techniques and instruction: When does evidence justify revision? Ann Emerg Med 43:780, 1999. Cummins RO, et al.: Low-energy biphasic wave form defibrillation: Evidence-based review applied to emergency cardiovascular care guidelines. Circulation 97:1654, 1998. Fuster V, et al.: The unstable atherosclerotic plaque: Clinical significance and therapeutic intervention. Thromb Haemost 78:247, 1997. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. An International Consensus on Science. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102(suppl I):I-1-252, 2000. Kong DF, et al.: Clinical outcomes of therapeutic agents that block the platelet glycoprotein IIa/IIIb integrin in ischemic heart disease. Circulation 98:2829, 1998. Kudenchuk PJ, et al.: Amiodarone for out-of-hospital resuscitation after cardiac arrest from ventricular fibrillation. New Engl J Med 341:871, 1999. Lindner KH, et al.: Randomized comparison of epinephrine and vasopressin in patients with out of hospital ventricular fibrillation. Lancet 349:535, 1997. O'Rourke MF, et al.: An airline cardiac arrest program. Circulation 96:2849, 1997.

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