CARDIAC ARREST

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CRITICAL RESUSCITATIONS

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CARDIAC ARREST Daniel J. DeBehnke, MD, and Gary L. Swart, MD

Sudden cardiac death is an important problem in our society. A significant number of deaths caused by cardiovascular disease are the result of sudden cardiac death. Despite significant laboratory and clinical research on cardiac arrest, there has been a minimal effect on resuscitation rates. In fact, some large metropolitan EMS systems have reported hospital discharge rates of only 1%to 2% for cardiac arrest patient^.^,^^ The American Heart Association (AHA) has established six events that, when performed quickly, may improve outcome from cardiac 1. Recognition of early warning signs 2. Activation of EMS system 3. Basic cardiopulmonary resuscitation (CPR) 4. Defibrillation 5. Intubation 6. Administration of intravenous medications While striving to accomplish these system events quickly, the emergency physician still is faced with many unresolved issues regarding resuscitation of the cardiac arrest victim. This article identifies many of the controversial issues in the resuscitation of the cardiac arrest victim and presents a synopsis of the literature so the clinician can make informed decisions regarding intervention in the cardiac arrest patient. PREHOSPITAL CARE Factors Affecting Prehospital Survival

Care of the out-of-hospital sudden death victim begins in the field with the initiation of bystander CPR and activation of the available EMS From the Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin

EMERGENCY MEDICINE CLINICS OF NORTH AMERICA

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VOLUME 14 * NUMBER 1 FEBRUARY 15'96

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system. Reported survival-to-hospital discharge rates have varied from 2% to 33% in nontraumatic cardiac arrest.32Factors affecting survival of prehospital cardiac arrest victims include the following: cause of arrest, presenting cardiac rhythm, witnessed arrest, time to initiation of bystander CPR, and time to initiation of advanced cardiac life support (ACLS).41Furthermore, the lack of desire by patient or family for resuscitation, presumably indicative of the patient’s preterminal health status, and a history of severe chronic illness negatively affect survival in attempted resu~citation.~” It is well known that the cause of cardiac arrest determines the dysrhythmia present and that the dysrhythmia bespeaks the actions necessary to improve resuscitability. For instance, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) associated with irritable myocardium secondary to focal ischemia will benefit from early initiation of CPR and ACLS, whereas asystole or pulseless electrical activity (PEA) caused by a global cardiac insult or hypovolemia may not. Common sense suggests that CPR and ACLS initiated early would be most effective. This has been true with improved survival rates in those patients with witnessed arrest and shortened time to initiation of ACLS.” The effect of bystander CPR on survival in cardiac arrest has been controversia1.9*In a review of studies of bystander CPR performed before 1990, Hoekstra41draws the conclusion that bystander CPR improves survival in all arrest rhythms; however, in EMS systems with a short response time, this improvement is not significant.

Automated Defibrillation The use of automated defibrillators by emergency medical technicians (EMTs) specially trained in their use (EMT-D) shortens the time to defibrillation in VF cardiac arrest and shortens the time to other therapeutic interventions performed by paramedic^.^^ Improved survival rates using EMT-Ds have been shown in the rural settingg1where the time to defibrillation dropped from 16.3 to 8.8 minutes. Survival rates, however, were not different in an urban EMS system where the time to defibrillation dropped from 6 to 3.5 minutes.45Judgment on the efficacy of EMTD programs in the urban setting should be held until studies from multiple urban settings can be performed.

Prehospital Termination of Resuscitation When resuscitation with prehospital ACLS is not successful, there is little utility in transporting the victim to the hospital for further resuscitation. Recently reported survival to hospital discharge rates in patients transported and resuscitated in the emergency department are 0% to 2Y0.l~. 37, 44, Io7 When the presenting rhythm is considered, there is a threefoldlo7to fivefold12greater efficacy in continued resuscitative efforts

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in patients with persistent VF despite ineffective prehospital efforts. The numbers of survivors of failed attempts at prehospital resuscitation, all of whom had VF, are as follows: 6 of 952'' and 6 of 216.'07All patients who failed to respond to prehospital resuscitation for asystole and PEA died before hospital discharge.'*,'(I7 It has been suggested that termination of prehospital resuscitative efforts should be reserved for those patients with asystole and PEA, but that those with VF should be transported for emergency department resuscitation. CARE OF THE CARDIAC ARREST VICTIM IN THE EMERGENCY DEPARTMENT History Circumstances of Arrest

Emergency department assessment of the cardiac arrest victim must include obtaining facts pertinent to the cause and prognosis of the arrest. Witnesses, if available, should be queried as to the time of collapse and the interval of collapse to first CPR. Witnesses may also be able to provide the patient's symptoms before arrest, the presence of trauma or toxins, medical history, medications, and allergies. EMS personnel should be questioned as to the time of first defibrillation and the course of the resuscitation including medications and route given, number of defibrillation attempts, other interventions undertaken, such as intubation and vascular access, and the rhythms encountered. Utstein Time Intervals

To improve the reproducibility of reporting cardiac arrest results, delegates to the Utstein Consensus Conference in 1990 have recommended the Utstein style for uniform reporting of data from out-ofhospital cardiac arrest.= The core time intervals of the Utstein style include the following: time of collapse/time of recognition, time of call receipt, time vehicle stops at scene, time of first CPR attempt, time of first defibrillatory shock, time of return of spontaneous circulation, and time of CPR abandoned/death. Although the details of the Utstein reporting system were conceived to standardize reporting of cardiac arrest in the literature and are beyond the scope of this article, the core time intervals suggested are those pertinent to the cause and prognosis of the arrest. Physical Assessment A BCs

Regardless of interventions in the field, the physical assessment of the cardiac arrest victim in the emergency department should begin

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with a reassessment of airway, breathing, and circulation (ABCs). It must be ensured that there is a patent airway. If the patient has had an airway intervention in the field, the adequacy of that intervention must be assessed. Endotracheal intubation should be performed if there is any question of airway patency or security. Although it is possible that high tissue oxygen levels following a period of hypoperfusion may result in the formation of toxic oxygen radicals, currently it is recommended that arrest victims be ventilated with 100% oxygen to maximize tissue oxygenation. Increasing the respiratory rate after return of spontaneous circulation may help to reverse the acidosis associated with tissue hypoperfusion. The patient’s circulatory status must also be considered. This is generally determined by palpation of pulses at the carotid or femoral arteries. Absence of pulses with a monitored rhythm of VF or asystole helps to confirm the rhythm; however, perpendicular leads should be checked to assure that fine amplitude VF is not mistaken for asystole. Pulseless VT should be treated as VF. Finally, the presence of PEA during an attempted resuscitation must stimulate a consideration of reversible causes including hypovolemia, hypoxia, acidosis, pulmonary embolism, tension pneumothorax, and pericardial tamponade (Fig. 1). SPECIFIC INTERVENTIONS Airway Interventions

lnvasive Airway Techniques Although endotracheal intubation is the airway management procedure of choice in cardiac arrest, familiarity with alternative methods is necessary as they may be encountered in the Emergency Department following prehospital use. The common airway management techniques include the bag-valve mask (BVM), the esophageal obturator airway (EOA), the esophageal gastric tube airway (EGTA), the pharyngeotracheal lumen airway (PTL), and the esophageal-tracheal combitube (ETC). The EOA and EGTA consist of a blindly placed esophageal tube with a distal balloon used to occlude the esophagus and a BVM to provide ventilation. The PTL consists of a double (distal/proximal) lumen tube, a large proximal pharyngeal balloon, and a smaller distal balloon. The tube may be placed in the trachea or esophagus, and the patient is ventilated with the appropriate lumen to provide ventilation. The ETC is similar to the PTL with several refinements, most importantly a selfpositioning posterior pharyngeal balloon. In a recent review of invasive airway techniques, Pepe and associates” state that there appears to be no physiologic advantage of the EOA/EGTA over BVM or endotracheal intubation. Although the EOA/ EGTA can be as effective as endotracheal intubation, it is often considerably less effective and has a high reported complication rate. Further-

CARDIAC ARREST PEA includes

Electromechanical dissociation (EMD) Pseudo-EMD Idioventricular rhythms * Ventricular escape rhythms * Bradyasystolic rhythms * Postdefibrillation idioventricular rhythms

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* Continue CPR L

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Intubate at once

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* Obtain IV access

Assess blood flow using- Doppler .. ultrasound

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Consider possible causes (Parentheses=possible therapies and treatments) Hypovolemia (volume infusion) Hypoxia (ventilation) Cardiac tamponade (pericardiocentesis) Tension pneumothorax (needle decompression) Hypothermia (rewarming) Massive pulmonary embolism (surgery, thrombolytlcs) Drug overdoses such as tricyclics, digitalis. B-blockers, calcium channel blockers Hyperkalemia' Acidosis7 * Massive acute myocardial infarction

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Epinephriue I mg I V push.

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repeat every 3-5 minutes

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If absolute bradycardia (c beatdmin) or relative bradycardia. give atropine I mg 1V Repeat every 3-5 min up to a total of 0.04 me/ka§

Class I: definitely helpful Class IIa: acceptable, probably helpful Class Ilb: acceptable. possibly helpful Class 111: not indicated. may be harmful 'Sodium bicarbonate I mEqkg is Class I if patient has known pre-existing byperkalemia. S o d i u m bicarbonate I mEq/kg: Class IIa * if known pre-existing bicarbonate-responsive acidosis if overdose with tricyclic antidepressants to alkalinize the urine in drug overdoses Class Ilb if intubated and long arrest interval upon return of spontaneous circulation after long arrest interval class nr * hypoxic lactic acidosis t The recommended dose of epinephrine is 1 mg I V push every 3-5 min. If this approach fails. several Class IIb dosing regimens can be considered. * Intermediate: epinephrine 2-5 mg I V push, every 3-5 min Escalating: epinephrine 1 mg-3 mg-5 mg I V push (3 min apart) High epinephrine 0.1 m g k g IV push. every 3-5 min 5 Shorter atropine dosing intervals are possibly helpful in cardiac arrest (Class IIb).

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Figure 1. Algorithm for pulseless electrical activity (PEA) (electromechanical dissociation [EMD]). (From Emergency Cardiac Care Committee and Subcommittees, American Heart Association: Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 268:2199-2240, Copyright 1992, American Medical Association; with permission.)

more, they suggest that PTL and ETC may have benefits over BVM and EOA/EGTA; however, the data are not yet conclusive. Confirming Endotracheal Tube Placement The classical instruction in confirmation of endotracheal intubation, visualization of the vocal cords, and passage of the tube through them

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followed by auscultation of bilateral axillary breath sounds may be applicable in the best circumstances, where visualization of the vocal cords is not obscured by blood, vomit, or the need to maintain cervical immobilization. In these difficult circumstances, further confirmation of tube placement can be obtained through qualitative, semiquantitative, or quantitative measurement of expired CO,. The persistent detection of COz following intubation confirms tube placement in the trachea, as any appreciable level of COz is cleared from the esophagus quickly.% Conversely, lack of CO, detection may indicate esophageal intubation or the extremely low CO, levels associated with prolonged cardiac arrest.

Breathing Interventions Need for Ventilation

The need for ventilation during CPR recently has been questioned from a physiologic standpoint. The fear of body-fluid exposure during mouth-to-mouth resuscitation and the complexity that ventilation adds to the performance of CPR also begs the question from a pragmatic standpoint. In a comparison of chest compression with and without ventilation and no intervention in a swine VF model, survival and neurologic outcome were the same with and without ventilation, but dismal with no intervention.'O This study was confounded by the use of 100% F10, in the pre-arrest phase. In active compression decompression (ACD) CPR (described later) performed in dogs, minute ventilation was doubled in ACD-versus standard-CPR with the dogs intubated but not actively ventilated.', Furthermore, arterial blood gases in both CPR types showed CO, levels consistent with adequate ventilation. Finally, minute ventilation measurements reached 6.6 -t 0.9 L/min (physiologic -6 L/min) in four adult humans undergoing ACD-CPR.'O Although these data are intriguing, it is not possible to recommend withholding artificial ventilation in the cardiac arrest victim without further study. lnspiratory Pressure and Ventilatory Timing Variation

Mouth-to-mouth, BVM, and invasive airway ventilation are performed using intermittent positive pressure ventilation (IPPV).Variation in inspiratory pressure and timing have been used in CPR to affect hemodynamics as well as to seek alternative ventilatory techniques. Resuscitation rates using continuous tracheal oxygen insufflation without IPPV have been found to be equivalent to standard IPPV and CPR in VF arrest in dogs.67The prebreathing of oxygen by rescuers during mouth-to-mouth resuscitation has been suggested as a way to improve patient oxygenation during CPR.w A theoretic advantage to improved oxygenation during CPR is that it might allow for a higher compression to ventilation ratio, thus increasing the flow of highly oxygenated blood

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to the tissues.R4No comparison of resuscitation rates using oxygen versus room air ventilation in CPR has been performed to test this theory. Circulatory Assessment Interventions lnvasive Hemodynamic Monitoring

Hemodynamic assessment of the circulatory efficacy of CPR focuses on the coronary perfusion pressure (CPP). CPP is equal to the aortic relaxation (or diastolic) pressure (AoRP) minus the right atrial relaxation (or diastolic) pressure (RARP) and represents the gradient for blood flow through the coronary arteries. The theory is that a certain minimum coronary blood flow is required to maintain a resuscitable metabolic milieu within the cardiac myocytes. Research conducted by Neimann and coworkersfi in dogs showed a 100% positive predictive value of peak CPP for return of spontaneous circulation (ROSC). Paradis and colleagues7ostudied 100 humans in cardiac arrest and found a CPP 215 had a positive predictive value of 57% for ROSC. One might question the feasibility of collecting simultaneous AoRP and RARP pressure tracings in the cardiac arrest victim. An alternative, although less significant in its correlation to ROSC, is to measure the AoRP alone.65,7n AoRP measurements can be obtained from peripheral arterial sites based on work by Rivers and a ~ s o c i a t e sFollowing .~~ epinephrine use in cardiac resuscitation, femoral or radial arterial pressures correlate with aortic pressures. End-Tidal C02Monitoring

A less invasive indicator of CPR efficacy is the measurement of endexpiratory (or end-tidal) carbon dioxide (ETCO,). ETCO, correlates well with cardiac output, CPP, and ROSC rates in animal ~ t u d i e s , 8 ~ and ,~,~~~ with ROSC rates in human studies of cardiac arrest.9n Caution must be exercised in the interpretation of ETCO, following the use of epinephrine. Following epinephrine adminjstra tion, the CPP will increase, cardiac output will decrease, and a concomitant decrease in ETCO, is e ~ p e c t e d . ’Although ~,~~ a decrease in ETCO, during resuscitation is a poor prognostic indicator in nonepinephrine-treated this is not true in humans treated with epinephrine during cardiac arrest.I7 Venous Oxygen Saturation Monitoring

The oxygen saturation of venous blood (SVO,) also can be used to monitor resuscitative efforts in cardiac arrest. Rather than reflecting hemodynamics or blood flow, SVO, reflects the balance of oxygen delivery and consumption during cardiac arrest. High SVOz measurements imply that adequate oxygen is being supplied to meet the metabolic

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demands of the tissue, whereas low SVO, suggests high consumption or inadequate delivery to meet tissue demands. Rivers and colleaguesm report that cardiac arrest patients who achieve ROSC have significantly higher SVO, levels during resuscitation than those who do not. RHYTHM-SPECIFIC THERAPY

Ventricular Fibrillation and Pulseless Ventricular Tachycardia Interventions

Defibrillation. The mainstay for the treatment of VF or VT is electrical defibrillation. Defibrillation works by causing simultaneous depolarization of all fully refractory myocardial cells. Current ACLS guidelines recommend three stacked shocks of 200, 300, and 360 J as first-line therapy for VF and VT.W These shocks should be spaced closely to decrease the transthoracic impedance and improve the chance of defibrillation. Firm pressure on the defibrillation paddles is essential for A conducting jelly or pad also should be proper energy distribution.26,46 used. The currently recommended paddle placement for defibrillation is sternal-apical; however, anteroposterior (precordial-posterior) paddle placement is an option. Improve Coronary and Cerebral Perfusion Pressure. If initial defibrillation is not successful, improvement of the CPP using adrenergic agents is recommended. The CPP is a major determinant of resuscitation success in animal models of CPR.65,89 Human studies also have shown CPP to be a major determinant of survival.70Improved CPP during VF may increase the chances of subsequent defibrillation. Currently, epinephrine (0.02 mg/kg) is the adrenergic agent of choice in VF cardiac arrest.% Epinephrine’s a1 and a2 vasoconstrictor properties cause an increase in CPP. Epinephrine can be administered intravenously or endotracheally. If administered endotracheally, a 2.5 times increase in dosage is recommended.34 Stabilize the Myocardium. Two other agents have been recommended during VF and VT: lidocaine and bretylium. Lidocaine is used during cardiac arrest as an adjunct to defibrillation, especially in cases of refractory VF. The animal studies of lidocaine use actually show an l9 In a clinical increased defibrillation threshold when lidocaine is study comparing lidocaine with epinephrine in persistent VF cardiac arrest, lidocaine was associated with a threefold increased incidence of asystole following defibrillation.10gA prospective clinical trial of lidocaine use in VF cardiac arrest is necessary. Currently, the AHA classifies lidocaine as a class IIa (acceptable, probably helpful) agent (Fig. 2). Bretylium is an anti-arrhythmic agent that can be used in VF or VT. Experimental and clinical evidence supporting bretylium use in cardiac arrest is sparse. In one clinical study, superior resuscitation rates were

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ABCS

:lass 1: definitely helpful :lass IIa: acceptable. probably helpful :lass IIb: acceptable, probably helpful :lass 111: not indicated. may be harmful * Precordial thump is a Class IIb action in witnessed arrest, no pulse. and no defibrillator immediately available The recommeded dose of epinephrine is I mg IV push every 3-5 min. If this approach fails. several Class IIb dosing regimens can be considered: Intermediate: epinephrine 2-5 mg IV push. every 3-5 min. Escalating: epinephrine I mg-3mg5mg IV push (3 min apart) High: epinephrine 0.1 m&g IV push every 3-5 min. 5 Sodium bicarbonate (ImEqnCg) is Class I if patient has known pre-existing hyperkalemia [I Multiple sequenced shocks (200J. 3001. 360J) are acceptable here (Class I). especially when medications are delayed I Lidocaine 1.5 m a g IV push. Repeat i n 3-5 min to total loading dose of 3-5 mg/kg; then use Bretylium 5 mg/kg IV push. Repeat in 5 min at 10 mgikg Magnesium sulfaCe 1-2 g IV in torsades de pointes or suspected h y p o magnesemic state or severe refractory VF Procainamide 30 mg/min in refractory VF (maximum total 17 mg/kg) # Sodium bicarbonate ( I mEqAg IV): Class IIa if known pre-existing bicarbonatcresponsive acidosis i f overdose with tricyclic antidepressants io alkalinize the urine in drug overdoses Class lib if intubated and continued long arrest interval upon return of spontaneous circulation after long arrest interval Class I11 hypoxic lactic acidosis

Perform CPR until defibrillator attached*

VFNT oresent on defibrillation 1

Defibrillate up to 3 times if needed for mrsistent VWVT (200 I. 200-300 J. 360 I)

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Rhythm after the first 3 shocks? I

l o r , resumnt VFNT

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Go to Fig

circulation

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Continue CPR lntubate at once Obtain IV access

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Assesses vital signs

Suppor~airway Support breathing Provide medications appropriate for blood pressure, heart rate. and rhythm

4 Epinephrine I mg I V

push $0 repeat every 3-5 min

Administer medications of probable benefit (Class Ila) in persisienf or recurrent VFNT I#

A medication11

Figure 2. Algorithm for ventricular fibrillation and pulseless ventricular tachycardia (VF/ VT). Cardiac Care Committee and Subcommittees, American Heart - (From . .. Emergency . . .. , , ~ - ~ 2:-----ASSOClallOn: tiuiaellnes lor caralopulmonary resuscirarion anu ernergeritiy tiaruiati tiat e. JAMA 268:2199-2240, Copyright 1992, American Medical Association: with permission.) A

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found when bretylium was used as the initial life-support measureF6 Bretylium also was found to improve resuscitation rates in cases of refractory VF.q5As with lidocaine, randomized clinical trials of bretylium use and bretylium and lidocaine comparison are needed. Currently, the AHA classifies bretylium as a class IIa agent, also (Fig. 2).

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Novel Approaches

Pharmacologic. In animal models of VF cardiac arrest, higher doses of epinephrine have been studied and have improved CPP, myocardial and cerebral blood flow, and defibrillation success compared with standard doses of epinephrine. Recently, two clinical studies have failed to show any benefit in survival or neurologic recovery in patients treated with high-dose e~inephrine.'~, 97 Current A H A guidelines are 1 mg of epinephrine intravenously every 3 to 5 minutes with escalation to 5 mg after failure of the 1 mg dose (class IIb, acceptable, possibly helpful) (see Fig. 2).' Other adrenergic agents may prove useful in resuscitation from VF cardiac arrest. One of the proposed detrimental effects of epinephrine is concurrent PI and p2 receptor stimulation. Methoxamine is a pure CY adrenergic agonist and could possibly be helpful in cardiac arrest. Brown and associates,13however, studied methoxamine in a porcine model of cardiac arrest and found that defibrillation rates and regional myocardial blood flow were improved with high-dose epinephrine (0.2 mg/kg) compared with methoxamine (0.1, 1, or 10 mg/kg). Roberts and associates"' found that methoxamine (20 mg) improved resuscitation rates compared with high-dose epinephrine (0.2 mg/kg) in a canine model. In a clinical study, Olson and coworkersfi6compared epinephrine (0.5 mg) and methoxamine (5 mg), and found no difference in resuscitation rates using methoxamine. Because of these equivocal results, methoxamine cannot be recommended until further supportive evidence is obtained. Phenylephrine is another pure CY agonist that could be used in cardiac arrest. Redding and P e a r ~ o nshowed ~~ no difference in resuscitation or 24-hour survival comparing epinephrine and phenylephrine in a canine VF model. Brown and associatesI6 compared 0.2 mg/kg of epinephrine, and 0.1 mg/kg and 1 mg/kg phenylephrine in a porcine VF model, and found improved defibrillation rates, myocardial blood flow, and oxygen extraction ratios in those animals receiving epinephrine. A clinical study of out-of-hospital cardiac arrest showed no difference in resuscitation rates comparing epinephrine and ~henylephrine.9~ These equivocal results have precluded recommendation of phenylephrine in cardiac arrest. Norepinephrine is an a', C Y ~PI, agonist and could prove useful in cardiac arrest. Brown and colleague^'^ studied various doses of norepinephrine compared to high-dose epinephrine (0.2 mg/kg) and showed no difference between norepinephrine and epinephrine in improving regional cerebral blood flow. Hoeckstra" studied high-dose norepinephrine (0.2 mg/kg) compared with epinephrine (0.2 mg/kg) in a canine model of VF and found improved myocardial blood flow in the norepinephrine group; however, there was a trend toward decreased resuscitation rates with norepinephrine. This may have been due to increased myocardial oxygen consumption because of the PI component of norepi-

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nephrine.j3 Based on these studies, norepinephrine is not recommended for use in resuscitation from cardiac arrest. Other Resuscitation Approaches. One of the laboratory models for producing PEA cardiac arrest is defibrillation following 2 to 3 minutes of no flow VF without epinephrine administration (post-countershock PEA). Clinically, defibrillation of VF frequently results in PEA. Hargarten and associate^^^ found that PEA occurred in 10% to 15% of patients defibrillated from VF. Some authors have recommended delaying defibrillation until adequate CPP has been produced by way of epinephrine administration and CPR. Niemann and colleagues" studied epinephrine and CPR preceding countershock in a canine model of VF arrest and found improved resuscitation rates compared with standard therapy (immediate countershock). Menegazzi and associates6' found similar results in a porcine model of VF cardiac arrest. These studies support the hypothesis that a period of myocardial perfusion before defibrillation may be beneficial. To date, clinical studies with delayed defibrillation have not been performed. One of the determinants of successful initial defibrillation is the duration of VF. As noted earlier, a period of myocardial perfusion before defibrillation may be useful in prolonged VF. Estimates of the duration of VF, however, are notoriously unreliable. One objective means to estimate the duration of ventricular fibrillation is the fast fourier transform analysis of the ventricular fibrillation waveform. Several authors have found characteristic dominant and median frequency measurements that are associated with the duration of VF.IH,% Perhaps future resuscitation algorithms (initial defibrillation versus drugs, CPR, and subsequent defibrillation) will be based on some VF waveform analysis with an estimate of the cardiac arrest duration. Pulseless Electrical Activity Assessment

PEA is a state of cardiac electrical activity without detectable peripheral pulses. This may not, necessarily mean however, lack of myocardial contraction or aortic blood flow. Paradis and defined the term pseudo-EMD or pseudo-PEA in a study of human cardiac arrest in which patients without pulses had detectable aortic pressures when invasive monitoring was instituted. The patients with pseudo-PEA were more likely to have return of spontaneous circulation with standard doses of epinephrine compared with patients in true PEA.69 In the same study, 14 of 18 patients with pseudo-PEA who received high-dose epinephrine had return of spontaneous c i r c ~ l a t i o n . ~ ~ It appears that determination of the contractile state of the heart may guide therapy in PEA arrest. Successfully resuscitated PEA patients have QRS widths less than nonresuscitated patients (0.09 ? 0.03 second versus 0.12 ? 0.06 ~ e c o n d )Also, . ~ no patients in pseudo-PEA have been

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found to have initial QR deflections > 0.2 Although these EKG changes may correlate with the presence of pseudo-PEA, there is significant overlap. Echocardiography in the emergency department can be helpful in determining cardiac activity and aortic valve opening with aortic blood flow. If available, immediate echocardiography should be performed to differentiate pseudo-PEA from true PEA. If possible, placement of a peripheral or central arterial line can be useful in detecting subclinical cardiac contractions. If pseudo-PEA is present, aggressive resuscitation with adrenergic agents should be performed. Intervention

Pharmacologic therapy has been the mainstay of treatment for PEA arrest. Epinephrine should be used to improve the CPP. Because most PEA arrests are bradycardiac, atropine may be a useful pharmacologic agent. Current AHA recommendations are epinephrine 1 mg intravenously and atropine (up to 0.04 mg/kg) for bradycardia less than 60 beats per minute (see Fig. 1). Novel Approaches

Pharmacologic Agents. Other pharmacologic agents have been studied in PEA cardiac arrest. Again, the dosing issue for epinephrine has been investigated. Ralston and found that the median effective dose of epinephrine intravenously was 14 pg/kg in a postcountershock PEA model. LindneP compared epinephrine and norepinephrine in an asphyxia1 PEA model and found 100% resuscitation rates in both groups. In that same study, epinephrine resulted in resuscitation earlier than norepinephrine; however, there were no hemodynamic differences between drugs. DeBehnke and associatesx compared standarddose epinephrine and high-dose epinephrine and found no difference in return of spontaneous circulation rates in a post-countershock model of PEA. Current AHA guidelines recommend epinephrine dose escalation to 5 mg intravenously after failure of the 1 mg dose.%If pseudo-PEA is detected or suspected, early escalation to higher doses of epinephrine should be considered. Methoxamine has been studied in PEA cardiac arrest. Redding and colleagues" found a 100% resuscitation rate using 20 mg of methoxamine in an asphyxial model of PEA. In a clinical study of PEA, 10 mg of methoxamine and 1 mg of epinephrine were compared in 80 cases of prehospital and inhospital PEA arrest. Fifty-five percent of patients were resuscitated in each group with only one patient being discharged from the hospital (epinephrine group).lohClinical studies using higher doses of methoxamine (20 mg or more) have not been performed. p, stimulation with agents such as isoproterenol produces improved chronotropy and inotropy. However, p stimulation also causes vasodilation, which decreases cerebral and myocardial blood flow. This negative physiologic effect of p stimulation precludes recommendation of p ago-

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nist use in PEA arrest. Aminophylline is a competitive antagonist of adenosine and has been used to treat bradyarrhythmias in patients not in cardiac arrest. Viskin and coworkerslogadministered 250 mg of aminophylline to patients in bradyasystolic (PEA) cardiac arrest that were refractory to epinephrine and atropine and achieved a return of spontaneous circulation rate of 73%. One patient was discharged from the hospital alive.'" Although this brief report does show promise for the use of aminophylline in PEA arrest, further animal and clinical studies need to be performed before recommending its use. Pacing. There is some theoretic merit to attempting pacemaker capture of patients in PEA cardiac arrest. The literature, however, does not seem to support this assumption. Several studies of transcutaneous pacing in PEA cardiac arrest have found the technique easy to use but 33, In a prospective no patient has survived to hospital discharge.27* randomized study, Barthell and coworkers8studied transcutaneous pacing in prehospital cardiac arrest and found no difference in resuscitation or survival rates in patients paced versus those not paced. Based on these studies, transcutaneous pacing of PEA cardiac arrest does not appear warranted. Asystole Assessment

Asystole represents a state of severe myocardial dysfunction and resuscitation rates from this rhythm have been poor (2% to YO).^ Asys-. tole most commonly is a rhythm that represents death and is generally not a rhythm to be treated. It is important for the emergency physician to determine whether the rhythm is asystole versus fine VF, which may be amenable to countershock. This can be accomplished by checking the rhythm in another lead or changing the placement of "quick look" paddles by 90 degrees. The emergency physician should assure that leads are properly applied and that the monitoring equipment is functioning properly before determining that a rhythm is truly asystole. Interventions

As with PEA arrest, the mainstay of therapy for asystolic cardiac arrest is improving CPP using epinephrine (1 mg every 3 to 5 minutes) and CPR and increasing the chronotropic activity of the heart using atropine (0.04 mg/kg total dose) (Fig. 3).% Novel Approaches

Pharmacologic Agents. Other agents to improve CPP and the inotropic and chronotropic activity of the heart are theoretically useful in asystole but have not been supported by the literature. Therapy with

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* Continue CPR

lntubate at once * Obtain IV access

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Confirm asystole in more than one lead

Consider possible causes Hypoxia Hyperkalemia Hypokalemia F're-existing acidosis Drug overdose * Hypothermia

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Consider immediate wanscutaneous pacing I~, TCPP 3

*Epinephrine 1 mg IV push. t S repeat every 3-5 min

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Atropine I mg IV,repeat every 3-5 min up to a total of 0.04 mgkgtll

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Consider Termination of effons ' I

Class I: definitely helpful Class IIa: acceptable. probably helpful Class IIb: acceptable, possibly helpful Class Ill not indicated, may be harmful 'TCP is a Class n b intervention. Lack of success may be due to delays in pacing. To be effective Tcp must be performed early. simultaneously with drugs. Evidence does not support routine use of TCP for asystole tThe recommended dose of epinephrine is I mg IV push every 3-5 min. If this approach fails, several Class IIb dosine reeimens can be considered: Intermediate: eDinephrine 2-5 mp.I V oush - . every 3-5 rnin Escalating: epinephrine I mg-3mg-Smg IV push (3 min apan) High: epinephrine 0.1 mgkg IV push, every 3-5 min $Sodium bicarbonate I +/kg is Class I if patient has known pre-existing hyperkalemia 6 Shorter atropine dosing intervals are Class IIb in asystolic arrest II Sodium bicarbonate 1 mEq/kg: Class Ila if known pre-existing bicarbonate-responsive acidosis if overdose with tricyclic antidepressants to alkalinize the urine in drug overdoses Class IIb if intubated and continued long arrest interval upon return of spontaneous circulation after long arrest interval Class m hypoxic lactic acidosis q If patient remains in asystole or other agonal rhythms after successful intubation and initial medications and no reversible causes are identified. consider termination of resuscitative efforts by a Dhvsician. Consider interval since amst.

-

I

I

- .

-

Figure 3. Asystole treatment algorithm. (From Emergency Cardiac Care Committee and Subcommittees, American Heart Association: Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 268:2199-2240, Copyright 1992, American Medical Association; with permission.)

agents, such as high-dose epinephrine, methoxamine, norepinephrine, and isoproterenol, have not been shown to be of benefit in asystolic cardiac arrest. Defibrillation. Because fine VF can masquerade as asystolic cardiac arrest, some authors have advocated defibrillation of asystole in the event that the rhythm is VF. This practice should be discouraged. Martin and associate^^^ studied patients in asystole who received initial countershock compared with those without countershock. Although no statistical differences were found in resuscitation and hospital discharge rates,

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outcome in the asystolic patient tended to be better when initial countershock was not used.s9 Pacing. As with PEA arrest, transcutaneous pacing is easy to perform in asystolic arrest but does not seem to impact survival. In a prospective controlled study, Cummins and compared transcutaneous pacing with no pacing in 371 asystolic patients and found no benefit from transcutaneous pacing even when initiated early in cardiac arrest. Although the AHA classifies transcutaneous pacing as a class 1% intervention (see Fig. 3), the literature does not support its use in asystolic cardiac arrest.% CIRCULATORY ADJUNCTS Open-Chest CPR

Until the 1960s, cardiac compression during cardiac arrest was performed by open cardiac massage. There is evidence that improved blood flow results from open chest massage.29There are many reports of animal models of open chest CPR and numerous human case reports in the literature. It appears from the literature that if open chest CPR is initiated after 20 minutes of cardiac arrest, successful outcome is unlikely?’, a Early recognition of cardiac arrest, basic life support, and early defibrillation are the backbone of resuscitation from cardiac arrest. Open chest CPR is easy to perform and requires minimal skill and equipment; however, the true indications for open chest CPR have not yet been determined. No large randomized study of open chest CPR versus standard ACLS has been performed. Until such studies are performed, the decision to initiate open chest CPR should be based on the physician’s clinical judgment and institutional policy. High-Impulse CPR

Chest compression is a complex interaction of four performance variables: rate, duration, force, and depth. Early studies suggested that prolonged compression duration combined with a lower rate was most efficacious in CPR.”, ln2 These studies used carotid flow index and aortic systolic pressure as outcome measures, however, now understood not to correlate with resuscitation. In 1984, Maier and associatess7described a manual CPR technique in which compressions were performed at rates between 60 and 150 cpm using ”brief compressions of moderate force.” They referred to this CPR technique as high-impulse CPR. Further studies to refine this technique have focused on high rates of compression and have been plagued by the irreproducibility of compression duration, force, and depth in manual CPR.IWIt seems, however, that shorter compression durations either in combination with or independent of increased rate improve hemodynamics”, lol* and ROSC.36

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Interposed Abdominal Compression

Continuous abdominal compression during CPR had been used to increase peripheral vascular resistance; however, a high rate of liver injury prevented its widespread acceptance.6In 1982, interposed abdominal counterpulsation-CPR (IAC-CPR) was first reported and noted to improve cardiac output and CPP.74When IAC-CPR was carried to clinical trials, Mateer and colleaguesh1found no difference in resuscitation rates in arrest patients receiving standard CPR versus IAC-CPR in the prehospital setting. Interest in IAC-CPR has recently resurfaced with modifications in the technique based on perceived weaknesses of earlier studies? Vest CPR

Two recent human studies have examined the efficacy of a pneumatic device to cycle intrathoracic pressure independent of standard anteroposterior chest compression.38* y4 Both studies showed an improvement in CPP compared with standard-CPR. Smithline and associates% showed adequate ventilation of arrest victims without the use of positive pressure ventilation. Halperin et a1'P technique (vest-CPR) uses a circumferential pneumatic vest which cycles between positive and zero pressure. Although not a new technique, vest-CPR is a novel method of generating blood flow in cardiac arrest. Smithline's technique consists of a breastplate that cycles between positive and negative pressure, and most closely resembles active compression-decompression CPR (ACDCPR) in mechani~rn.~~ Active Compression-Decompression CPR

The stimulus for the development of active compression-decompression CPR (ACD-CPR)is the report of a case of successful cardiac resuscitation using a toilet plunger.56ACD-CPR is performed using a chest compression device fitted with a suction cup to allow active decompression of the chest following compression. This technique has been evaluated in animal models and humans and has been shown to improve minute ventilation, CPP,", lo5 and cerebral and myocardial blood In three human trials of inhospital cardiac arrest, ROSC and 24-hour survival were improved; however, survival to hospital discharge was not.21,92. In4 Circulatory Assist Devices Cardiopulmonary Bypass

Cardiopulmonary bypass provides excellent reperfusion pressures and has been shown to be superior to standard ACLS in animal models

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of cardiac arrest.”Z7’ There are clinical reports and case series of patients in cardiac arrest resuscitated using cardiopulmonary bypass.“, 63, 78 It is clear that emergency cardiopulmonary bypass is a powerful resuscitation tool if implemented early. The problem with implementing cardiopulmonary bypass in cardiac arrest has been obtaining vascular access early enough in cardiac arrest. Vascular access for cardiopulmonary bypass can take up to 10 to 15 minutes, which is precious time during cardiac arrest. Newer bypass units that use femoral vessel access appear to allow for decreased bypass cannulation times. Currently, cardiopulmonary bypass appears to be a reperfusion tool that may be applicable in appropriately staffed, dedicated resuscitation institutions. Direct Mechanical Ventricular Actuation

Direct mechanical ventricular actuation (DMVA) is a suction-cup device that can be applied to the heart to improve perfusion pressures during cardiac arrest. The suction cup is applied to the myocardium and is actuated by positive and negative pneumatic forces to cause systole and diastole. The device requires an open chest for application. The DMVA has been used in animal models of cardiac arrest and has been shown to improve blood flow and resuscitation rates.3 A clinical feasibility trial was performed with this device showing ease of placement (less than 2 minutes from skin incision) and immediate improvement in hemodynarnic~.~ Further clinical trials of this device need to be performed before its use can be recommended in clinical cardiac arrest. SPECIAL SITUATIONS Pediatric Arrest

Pediatric cardiac arrest can be contrasted with that of the adult, primarily based on cause. Although the adult cardiac arrest is most often caused by atherosclerotic heart disease and ischemia resulting in irritable myocardium and VF, the pediatric cardiac arrest is most often secondary to sudden infant death, drowning, and respiratory arrest.31 Consequently, the most common cardiac rhythm disturbances in children are asystole and PEA.31 Management of the pediatric cardiac arrest victim is similar to the management of cardiac arrest in adults when controlled for similar causes. Age differences in pediatric arrest therapy are related to differences in equipment size and drug dosing based on patient size and weight. Numerous tables and graphs exist to aid in the determination of drug doses and equipment sizes in the pediatric cardiac arrest. Perhaps the most complete and easiest to use is the Breslow tape, which bases these measurements on the length of the supine patient. The tape contains the drug and equipment guidelines for patient size in the segment of the tape corresponding to the length of the patient.

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Traumatic Arrest The cause of adult traumatic cardiac arrest is usually due to absolute hypovolemia related to hemorrhage or relative hypovolemia related to the mechanical impediment of venous return, such as tension pneumothorax or pericardial tamponade. Thus, the rhythm disturbance in traumatic cardiac arrest is more often asystole or PEA than VF. The resuscitation of traumatic cardiac arrest is notoriously difficult despite extremely aggressive and costly attempts.s5,83 Thoracotomy is performed on many traumatic arrest victims; however, its reported efficacy and indications have been intensely debated. Although there is much controversy in the literature, two studies have been most specific in presenting indications for resuscitative thoracotomy in the traumatic cardiac arrest victim."5,55 The reported indications are based on the following observations: (1) a presenting rhythm of asystole or the lack of vital signs at the time of prehospital intervention is dismal except in cases of VF; (2) the best resuscitation rates are in patients with penetrating injuries isolated to the thorax; and (3) poor but not dismal resuscitation rates are obtained in patients with blunt trauma. Given this, the indications for resuscitative thoracotomy are (1) signs of life present at the time of prehospital intervention, which are lost en route to, or in, the emergency department; and (2) penetrating injuries to the thorax or abdomen. Blunt injury is considered a relative contraindication to thoracotomy.", 55 POSTRESUSCITATION ISSUES

Treat Underlying Cause of Arrest Following return of spontaneous circulation, attention should be directed toward continued treatment of the underlying cause of arrest and assurance of adequate tissue perfusion and oxygenation. If ventricular arrhythmias were the cause for arrest, appropriate postresuscitation anti-arrhythmic therapy should be instituted. If the cardiac arrest was secondary to acute myocardial infarction, urgent cardiac catheterization and angioplasty should be considered. If these services are not available and the CPR time was less than 10 minutes, thrombolytic therapy can be instituted if no other contraindications exist.lo3The acid base status of the patient should be stabilized with adequate alveolar ventilation for respiratory acidosis and judicious use of bicarbonate for metabolic acidosis. Electrolyte abnormalities should be diagnosed and treated at this time. Inadequate tissue reperfusion and blood pressure should be addressed in these patients. If hypotension is secondary to hypovolemia, fluid therapy should be instituted, usually based on right heart catheterization values. Hypotension secondary to poor pump function should be treated with pressor support. Dobutamine may be useful in these

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cases. Inotropic support should be guided by right heart catheter values (cardiac output/cardiac index). Appropriate Monitoring of Perfusion

Despite normalization of blood pressure and heart rate postresuscitation, some patients may be experiencing continued myocardial dysfunction and poor tissue oxygenation and perfusion. The use of hemodynamic monitoring (including central venous oximetry) may be helpful in diagnosing poor tissue perfusion/oxygenation. Lactate levels may also be useful in determining the adequacy of tissue perfusion."2dCalculation of the shock index (heart rate/systolic blood pressure; normal = 0.5 to 0.7) also can be used as a noninvasive measure of left ventricular stroke work, but is less sensitive in the assessment of oxygen tran~port.'~ Brain Resuscitation In the search for improved methods of resuscitation from cardiac arrest, the emphasis has been on myocardial resuscitation with less emphasis on cerebral resuscitation. Investigators and clinicians know that many patients' hearts can be resuscitated while their brains are irreparably damaged. There have been laboratory and clinical studies of different drugs and therapies to improve neurologic outcome following cardiac arrest. To date, however, none has gained popular acceptance. Calcium channel blockers have been believed to improve neurologic outcome following arrest but two clinical studies of calcium channel blockers (nimodipine and lidoflazine) have failed to show improvement in neurologic function following cardiac arrest.', In animal models, such therapies as high postresuscitation perfusion pressures, hypertensive hemodilution, mild hypothermia, and detoxification with hemo9h Continued reabsorption have been studied with variable results.R5, search in the area of cardiopulmonary-cerebral resuscitation is necessary to determine which therapy or group of therapies will be most useful in these patients. Current cardiopulmonary-cerebral resuscitation clinical care should address the following issues: 1. Defibrillate VF cardiac arrest early. This is the ultimate therapeutic modality for improving neurologic outcome following cardiac arrest. By decreasing the ischemic time to the brain, neurologic injury will be avoided. 2. Establish and increase cerebral perfusion pressures. This can be established through good bystander CPR and improvement in perfusion pressures through pharmacologic therapy (mainly epinephrine). Novel pharmacotherapy and CPR techniques may improve neurologic outcome.

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3. Control of blood glucose postresuscitation. It appears from animal data that hyperglycemia during cerebral ischemia drives anaerobic glycolysis and causes increased brain lactate and acidosis.* Human studies have shown that increased blood sugar in cardiac arrest patients is associated with impaired neurologic recovery.% 4. Decrease reperfusion injury. This goal remains in the research phase. Decreasing reperfusion injury could be accomplished through the use of free radical scavengers, 21-amino steroids, novel calcium entry blockers or via hypothermia, hemodilution, or increased postresuscitation perfusion pressures.

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18. Carlisle EJF, Kernohan WG, Anderson J, et al: Fourier analysis of ventricular fibrillation of varied aetiology. Eur Heart J 11:173-181, 1990 19. Chow MS, Kluger J, Lawrence R, et al: The effect of lidocaine and bretylium on the defibrillation threshold during cardiac arrest and cardiopulmonary resuscitation. Proceedings of the Society for Experimental Biology and Medicine 18263-67, 1986 20. Cohen TJ, Tucker KJ, Lurie KG, et al: Active compression-decompression: A new method of cardiopulmonary resuscitation. JAMA 2672916-2923, 1992 21. Cohen TJ, Goldner BG, Maccaro PC, et al: A comparison of active compressiondecompression cardiopulmonary resuscitation with standard cardiopulmonary resuscitation for cardiac arrests occurring in the hospital. N Engl J Med 329:19181921, 1993 22. Cohen TJ, Tucker KJ, Redberg RF, et al: Active compression-decompression resuscitation: A novel method of cardiopulmonary resuscitation. Am Heart J 124:11451150, 1992 23. Cummins RO, Chamberlain DA, Abramson NS, et al: Recommended guidelines for uniform reporting of data from out-of-hospital cardiac arrest: The Utstein style. Ann Emerg Med 20:861-874, 1991 24. Cummins RO, Omato JP, Thies WH, et al: Improving survival from sudden cardiac arrest. The "chain of survival" concept: A statement for health professionals from the Advanced Cardiac Life Support Subcommittee and the Emergency Cardiac Care Committee, American Heart Association. Circulation 83183S1847, 1991 25. Cummins RO, Reid Graves J, Larsen MI', et al: Out-of-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac arrest. N Engl J Med 328:1377-1382,1993 26. Dahl C, Ewy G, Thomas E: Transthoracic impedance to direct current discharge: Effect of repeated countershocks. Med Instrum 10151-154, 1976 27. Dalsey WC, Syverud SA, Hedges JR: Emergency department use of transcutaneous pacing for cardiac arrests. Crit Care Med 13:399401, 1985 28. DeBehnke DJ, Angelos MG, Leasure JE: Use of cardiopulmonary bypass, high-dose epinephrine, and standard-dose epinephrine in resuscitation from post-countershock electromechanical dissociation. Ann Emerg Med 21:1051-1057, 1992 29. Del Guercio LRM, Feins NR, Cohn JD, et al: Comparison of blood flow during external and internal cardiac massage in man. Cardiovasc Surg 171 (Suppl 1):11711180, 1965 30. Dull SM, Graves JR, Larsen MI', et al: Expected death and unwanted resuscitation in the prehospital setting. Ann Emerg Med 23:997-1002, 1994 31. Eisenberg M, Bergner L, Hallstrom A: Epidemiology of cardiac arrest and resuscitation in children. AM Emerg Med 12:672474, 1983 32. Eisenberg MS, Horwood BT, Cummins RO, et al: Cardiac arrest and resuscitation: A tale of 29 cities. AM Emerg Med 19:179-186, 1990 33. Eitel DR, Guzzardi LJ, Stein SE, et a 1 Noninvasive transcutaneous cardiac pacing in prehospital cardiac arrest. Ann Emerg Med 16531-534, 1987 34. Emergency Cardiac Care Committee and Subcommittees, American Heart Association: Guidelines for cardiopulmonary resuscitation and emergency cardiac care, 111: Adult Advanced Cardiac Life Support. JAMA 268:2219, 1992 35. Esposito TJ, Jurkovich GJ, Rice CL, et al: Reappraisal of emergency room thoracotomy in a changing environment. J Trauma 31S81-887, 1991 36. Feneley MP, Maier GW, Kern KB, et al: Influence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs. Circulation 77240-250, 1988 37. Gray WA, Capone RJ, Most A S Unsuccessful emergency medical resuscitation-are continued efforts in the emergency department justified? N Engl J Med 325:13931398, 1991 38. Halperin HR, Tsitlik JE, Gelfand M, et al: A preliminary study of cardiopulmonary resuscitation by circumferential compression of the chest with use of a pneumatic vest. N Engl J Med 329:762-768, 1993 39. Hargarten KM, Stueven HA, Waite EM, et al: Prehospital experience with defibrilla-

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