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Study Objective: Survival from traumatic cardiac arrest is poor, and some consider resuscitation of this patient group futile. This study identified survival rates and characteristics of the survivors in a physician-led out-of-hospital trauma service. The results are discussed in relation to recent resuscitation guidelines., Methods: A 10-year retrospective database review was conducted to identify trauma patients receiving out-of-hospital cardiopulmonary resuscitation. The primary outcome measure was survival to hospital discharge., Results: Nine hundred nine patients had out-of-hospital cardiopulmonary resuscitation. Sixty-eight (7.5% [95% confidence interval 5.8% to 9.2%]) patients survived to hospital discharge. Six patients had isolated head injuries and 6 had cervical spine trauma. Eight underwent on-scene thoracotomy for penetrating chest trauma. Six patients recovered after decompression of tension pneumothorax. Thirty patients sustained asphyxial or hypoxic insults. Eleven patients appeared to have had "medical" cardiac arrests that occurred before and was usually the cause of their trauma. One patient survived hypovolemic cardiac arrest. Thirteen survivors breached recently published guidelines., Conclusion: The survival rates described are poor but comparable with (or better than) published survival rates for out-of-hospital cardiac arrest of any cause. Patients who arrest after hypoxic insults and those who undergo out-of-hospital thoracotomy after penetrating trauma have a higher chance of survival. Patients with hypovolemia as the primary cause of arrest rarely survive. Adherence to recently published guidelines may result in withholding resuscitation in a small number of patients who have a chance of survival.

Study Objective: Many centers optimize their emergency medical services (EMS) systems to achieve a target defibrillation response interval of "call received by dispatch" to "arrival at scene by responder with defibrillator" in 8 minutes or less for at least 90% of cardiac arrest cases. The objective of this study was to analyze survival as a function of time to test the evidence for this standard., Methods: This prospective cohort study included all adult, cardiac etiology, out-of-hospital cardiac arrest cases from phases I and II of the Ontario Prehospital Advanced Life Support (OPALS) study. Patients in the 21 Ontario study communities received a basic life support level of care with defibrillation by ambulance and firefighters but no advanced life support. Survival was plotted as a function of the defibrillation response interval. The equation of the curve, generated by means of logistic regression, was used to estimate survival at various defibrillation response interval cutoff points., Results: From January 1, 1991, to December 31, 1997, there were 392 (4.2%) survivors overall among the 9,273 patients treated. The defibrillation response interval mean was 6.2 minutes, and the 90th percentile was 9.3 minutes. There was a steep decrease in the first 5 minutes of the survival curve, beyond which the slope gradually leveled off. Controlling for known covariates, the decrement in the odds of survival with increasing response interval was 0.77 per minute (95% confidence interval 0.74 to 0.83). The survival function predicts, for successive 90th percentile cutoff points, both survival rates and additional lives saved per year in the OPALS communities compared with the 8-minute standard: 9 minutes (4.6%; -18 lives), 8 minutes (5.9%; 0 lives), 7 minutes (7.5%; 23 lives), 6 minutes (9.5%; 51 lives), and 5 minutes (12.0%; 86 lives)., Conclusion: The 8-minute target established in many communities is not supported by our data as the optimal EMS defibrillation response interval for cardiac arrest. EMS system leaders should consider the effect of decreasing the 90th percentile defibrillation response interval to less than 8 minutes.

Study Objective: Controversy surrounds the use of buffers during cardiac arrest to correct acidosis. The objective of this study was to determine whether attenuation or neutralization of cerebral acidosis by Carbicarb alters hippocampal glutamate levels, neuronal cell death, and neurologic deficits after reperfusion from asphyxial cardiac arrest in rats., Methods: Rats were prospectively randomized to either a control (n=45), low-dose Carbicarb (LDC; 3 mL/kg, n=45), or high-dose Carbicarb (HDC; 6 mL/kg, n=45) group in a blinded fashion during resuscitation after 8 minutes of asphyxial cardiac arrest. Microdialysis was used to assess brain pH and glutamate. A neurologic deficit score and neuronal cell death in the hippocampus were determined at day 7., Results: Resuscitation was greatest in LDC rats (42/45) and least in HDC rats (28/45) versus that in control rats (34/45). Brain pH was higher in the LDC and HDC rats 10 minutes after resuscitation and remained higher than that of control rats for 120 minutes after resuscitation. Glutamate levels at 10 to 120 minutes after reperfusion were lowest in the LDC rats. LDC rats had the lowest neurologic deficit score (1+/-2) versus that of control rats (13+/-8) and HDC rats (19+/-6). Hippocampal neuronal cell death was lowest in LDC rats (30+/-20) versus that in control rats (86+/-47) and HDC rats (233+/-85)., Conclusion: LDC administered during resuscitation from asphyxial cardiac arrest attenuated acidosis, improved resuscitation, and reduced neurologic deficits and the number of dead hippocampal neurons. Neutralization of cerebral acidosis with HDC increased the number of dead hippocampal neurons and neurologic deficits after resuscitation from cardiac arrest in rats.

Study Objective: The purpose of this study was to determine the prevalence of hypoglycemia and describe the clinical variables associated with hypoglycemia in children receiving resuscitation care., Methods: A cross-sectional study of consecutive children receiving resuscitation care in an emergency department was performed. Rapid glucose testing was prospectively established as one of the initial resuscitation steps, and clinical variables were obtained from a retrospective chart review. The setting was an urban children's hospital ED (Level II trauma center) with a census of 31, 000 per year and a 10% admission rate. The patient population consisted of children (birth to 20 years of age) receiving resuscitation care for altered consciousness, status epilepticus, respiratory failure, cardiac failure, and cardiopulmonary arrest., Results: Over a 1-year period, 49 nontrauma-related children received resuscitation care. Nine (18%; 95% confidence interval 8.7 to 32.2) were hypoglycemic (glucose level

Study Objective: Early countershock of ventricular fibrillation (VF) has been shown to improve immediate and long-term outcome of out-of-hospital cardiac arrest. However, studies indicate that countershock of prolonged VF most commonly results in asystole or a nonperfusing bradyarrhythmia (pulseless electrical activity [PEA]), which rarely respond to current therapy. The cause of these postcountershock rhythm disturbances is not well understood but may be related to electrical injury of the globally ischemic myocardium or to local metabolic abnormalities that impair impulse formation and cardiac contraction. The purpose of this study was to evaluate changes in serum potassium and free calcium homeostasis during cardiac arrest and advanced cardiac life support (ACLS) interventions., Methods: After sedation, intubation, anesthesia, and instrumentation, VF was induced in 13 dogs. After 7.5 minutes of VF, animals were immediately countershocked, standard closed-chest CPR was initiated, and epinephrine was administered (1 mg in repeated doses if necessary)., Results: Ten animals could not be resuscitated despite 20 minutes of ACLS interventions. In these animals, a progressive increase in serum potassium was observed from the onset of ACLS to the termination of resuscitation efforts (4.3+/-.6 to 6.0+/-.8 mEq/L, P<.01). A significant increase was observed within 10 minutes of beginning ACLS measures. This was accompanied by a decrease in ionized calcium concentration over the same period (4.95+/-.40 to 3.44 mg/dL, P<.01). The decrease in ionized calcium was significant within 5 minutes of ACLS interventions. Nine of these 10 animals had either postcountershock asystole or PEA at the termination of resuscitative efforts. The increase in potassium was not related to acidemia. Successfully resuscitated animals did not demonstrate these electrolyte changes., Conclusion: Ionized hypocalcemia and hyperkalemia occur during prolonged resuscitative efforts and may be related to dysfunctional transcellular ionic transport mechanisms. These cations play important roles in cardiac electrical and contractile activity and may play a role in refractory postcountershock rhythm disturbances.

Little information is available about the effects of CPR in children, although it is known that the outcomes are dismal. Examples of unanswered questions include which advanced life support (ALS) procedures should be performed out-of-hospital, whether high-dose epinephrine improves survival, and the true prevalence of ventricular fibrillation as a presenting rhythm. Children differ from adults as to the cause and pathophysiology of cardiopulmonary arrest, but prehospital EMS and hospital resuscitation teams were initially designed for the care of adults. Because pediatric cardiopulmonary arrest is rare, prospective data are difficult to gather, and there are few large published studies. The purpose of this collective review was to review the current body of knowledge regarding survival rates and outcomes in pediatric CPR and, based on this review, to outline a course for future research.

Study Objective: Studies indicate that ventricular tachycardia (VT) and ventricular fibrillation (VF) are no longer the most common rhythms initially documented in out-of-hospital sudden cardiac death. Although the outcome from asystole and rhythms designated as pulseless electrical activity (PEA) is reported as poor (approximately 1% survival), resuscitative efforts for these patients are still encouraged. The purpose of this study was to determine the potential contribution that this patient group makes to overall survivorship., Methods: During this 2-year prospective study, all patients in cardiopulmonary arrest who were transported to the study institution after out-of-hospital Advanced Cardiac Life Support (ACLS) interventions were considered eligible for inclusion. Patients younger than 18 years of age and those in posttraumatic arrest were excluded. Age, sex, first-documented arrest rhythm, presence of a witness to the arrest, performance of bystander CPR, survival to hospital discharge, and functional status at discharge were recorded., Results: A total of 197 patients met the inclusion criteria. The initial rhythm was VF/VT in 59 (30%; 95% confidence interval [CI], 24% to 37%) and asystole/PEA in 138 (70%; 95% CI, 64% to 76%). There was 1 hospital survivor in the VT/VF group; 9 patients (7%; 95% CI, 4% to 13%) in the asystole/PEA group survived to hospital discharge. Of the asystole/PEA survivors, 100% (95% CI, 66% to 100%) had a witnessed arrest and 56% (95% CI, 21% to 86%) received bystander CPR. Fifty-six percent (95% CI, 21% to 86%) of the asystole/PEA survivors were discharged at a functional level equivalent to that preceding arrest., Conclusion: In this study, patients in asystole/PEA comprised 90% of the survivors. The outcome for patients with asystole/PEA whose arrest was witnessed and who received bystander CPR may be greater than previously estimated and supports the current practice of initiating aggressive out-of-hospital ACLS in this patient group.

Study Objective: To examine the effects of moderate hypothermia (33 degrees C), induced by surface cooling in the ED and maintained for 12 hours in the ICU, on patients with anoxic brain injury after out-of-hospital cardiac arrest., Methods: We conducted the study in a teaching hospital in Melbourne, Victoria, Australia. Participants were 22 adults who remained unconscious after return of spontaneous circulation following out-of-hospital cardiac arrest. This treatment group was studied prospectively, and a control group of 22 similar patients was studied by retrospective chart review. Moderate hypothermia (33 degrees C) was induced in the ED by means of surface cooling and maintained for 12 hours in the ICU with rewarming to normothermia over 6 hours; control patients were maintained at normothermia., Results: There were no significant adverse effects of induced hypothermia. Cardiovascular changes included decreased pulse rate, but there were no significant differences in mean arterial blood pressure between the two groups. Small increases in serum potassium and decreases in pH at 18 hours in the hypothermic patients compared with normothermic controls were of no clinical significance. There were no septic complications. There was a significant increase in the number of patients with good outcome (Glasgow Outcome Coma Scale category 1 or 2) with induced hypothermia (11 of 22, versus 3 of 22 for normothermic controls; P<.05), and the mortality rate was significantly lower (10 of 22 versus 17 of 22; P<.05)., Conclusion: Compared with historical normothermic controls, outcome was significantly improved and there was no increase in complications when moderate hypothermia was induced in comatose survivors of out-of-hospital cardiac arrest and maintained for 12 hours. Larger, prospective, randomized, controlled studies of induced moderate hypothermia in comatose survivors of out-of-hospital cardiac arrest are warranted.

Brain damage accompanying cardiac arrest and resuscitation is frequent and devastating. Neurons in the hippocampus CA1 and CA4 zones and cortical layers III and V are selectively vulnerable to death after injury by ischemia and reperfusion. Ultrastructural evidence indicates that most of the structural damage is associated with reperfusion, during which the vulnerable neurons develop disaggregation of polyribosomes, peroxidative damage to unsaturated fatty acids in the plasma membrane, and prominent alterations in the structure of the Golgi apparatus that is responsible for membrane assembly. Reperfusion is also associated with vulnerable neurons with prominent production of messenger RNAs for stress proteins and for the proteins of the activator protein-1 complex, but these vulnerable neurons fail to efficiently translate these messages into the proteins. The inhibition of protein synthesis during reperfusion involves alteration of translation initiation factors, specifically serine phosphorylation of the alpha-subunit of eukaryotic initiation factor-2 (elF-2 alpha). Growth factors--in particular, insulin--have the potential to reverse phosphorylation of elF-2 alpha, promote effective translation of the mRNA transcripts generated in response to ischemia and reperfusion, enhance neuronal defenses against radicals, and stimulate lipid synthesis and membrane repair. There is now substantial evidence that the insulin-class growth factors have neuron-sparing effects against damage by radicals and ischemia and reperfusion. This new knowledge may provide a fundamental basis for a rational approach to "cerebral resuscitation" that will allow substantial amelioration of the often dismal neurologic outcome now associated with resuscitation from cardiac arrest.

Objective: Monomorphic ventricular tachycardia (MVT) is the most common form of prehospital ventricular tachycardia (VT). Recent literature suggests that polymorphic ventricular tachycardia (PVT) is more common during cardiopulmonary arrest than previously thought but responds poorly to advanced cardiac life support (ACLS) therapy. We undertook this study to determine the prevalence, response to therapy, and outcome of both MVT and PVT in the prehospital sudden cardiac death victim., Design: Retrospective prehospital chart review from 1987 to 1991., Setting: Municipal, fire department-based, multitiered emergency medical system serving a population of approximately one million., Participants: Adult patients older than 18 years experiencing prehospital, nontraumatic cardiopulmonary arrest with VT occurring at any time during the resuscitation. VT was defined as PVT if the QRS-complex configuration was not stable when viewed in a single electrocardiographic lead (ie, episodic changing of the QRS-complex electrical axis, amplitude, or both or the presence of more than two QRS-complex morphologies). Outcome was defined in terms of both the presence or absence of spontaneous circulation at the end of the prehospital phase of care and ultimate outcome (survival to hospital discharge or death). Four hundred seventy-six patients met entry criteria; 37 patients were excluded because of incomplete medical records, and 439 patients were used for data analysis., Interventions: ACLS therapy based on the 1987 American Heart Association guidelines., Results: MVT occurred in 323 patients (73.6%), with 119 (36.8%) showing return of spontaneous circulation (ROSC) in the prehospital setting; 35 MVT patients (10.8%) survived to hospital discharge. PVT occurred in 116 patients (26.4%), with 48 (41.4%) showing ROSC in the prehospital setting; 15 PVT patients (12.9%) survived to hospital discharge. The use of ACLS therapy (defibrillation, endotracheal intubation, medication usage) between the two rhythm groups was not statistically different. The P values for ROSC, ultimate outcome, and use of ACLS therapy were all not significant., Conclusion: We conclude that PVT is a common rhythm occurring in prehospital cardiopulmonary arrest that responds as well as MVT to ACLS therapy. Until prospective data are available, standard ACLS therapy should be used in all forms of prehospital VT occurring during cardiopulmonary arrest.

Study Objective: Recent studies suggest that norepinephrine-induced hypertension early after cardiac arrest ameliorates cerebral hypoperfusion and improves neurologic outcome. The purpose of this study was to evaluate the effects of early norepinephrine-induced hypertension on postresuscitation myocardial blood flow and oxygen use., Design: Prospective, controlled laboratory study., Participants: Ten swine., Interventions: All animals underwent 10 minutes of ventricular fibrillation cardiac arrest followed by 5 minutes of low-flow cardiopulmonary bypass (10 mL/kg.min), norepinephrine (0.12 mg/kg), and defibrillation. Animals then were assigned to a hypertension group (mean aortic pressure, 95 mm Hg) or a control group (mean aortic pressure, 75 mm Hg) by titrating a norepinephrine infusion to attain the prescribed aortic pressure., Results: Myocardial blood flow, perfusion pressure, and oxygen metabolism were compared between groups at different times using analysis of variance with a post-hoc Tukey test. Groups had similar myocardial blood flow during ventricular fibrillation, total defibrillation energy, and time to restoration of spontaneous circulation. Fifteen minutes after restoration of spontaneous circulation, the hypertension group had significantly elevated myocardial blood flow, 965 +/- 314 mL/min.100 g versus 325 +/- 67 mL/min.100 g in the control group (P < .001), myocardial oxygen consumption of 51.2 +/- 26.9 mL O2/min.100 g versus 6.4 +/- 3.4 mL O2/min.100 g (P < .001), and myocardial oxygen extraction of 46% +/- 20% versus 14% +/- 4% (P < .01)., Conclusion: In the early resuscitation period, increasing the norepinephrine dose to induce mild hypertension significantly increases oxygen use in the postischemic myocardium.

The simplest, most easily determined, and most easily understood outcomes after cardiac arrest are survival and awakening. Awakening is defined by the patient's being able to follow commands or produce comprehensible speech. Both occur at specific times, thus lending themselves to life-table analyses. Unfortunately, these simple measures are not adequate to characterize the disability that may be present in those who survive and awaken after cardiac arrest. For such patients, measures of independence are needed. These measures often require longer follow-up, direct contact with patients, and a greater understanding of the instrument to be used than for the simple measures. Investigators must decide based on the goals of a particular study what outcomes are most appropriate and the amount of resources that they are willing to devote to outcome assessment. As initial steps in resuscitation research, there may be more to gain from studies of large numbers of patients evaluated with simple measures than small numbers of patients evaluated intensively with more detailed measures.

Study Objectives: To determine the appropriate diagnostic workup of the emergency department patient with an uncomplicated cocaine-related grand mal seizure., Design Setting: Retrospective analysis. A city and county ED with 45,000 selected visits per year., Type of Participants: Thirty-seven patients with acute grand mal seizure after cocaine exposure were studied. All had historical or laboratory evidence of cocaine use and no history of prior seizure disorder., Interventions: The diagnostic workup varied among patients. Most received computed head tomography (35), whereas fewer received-ECG (18), EEG (16), and lumbar puncture (six)., Measurements and Main Results: Thirty-three patients with an uncomplicated cocaine-related seizure had an unremarkable series of diagnostic tests. The four patients with remarkable neurologic manifestations were compared with the remainder of patients who were without neurologic abnormalities. Comparison of groups by route of cocaine intake revealed no significant difference in the time interval to seizure (P = .761)., Conclusion: Diagnostic workup probably is not indicated for the patient experiencing a cocaine-related generalized seizure who will recover promptly and have a normal postictal examination.

Study Background: Free or ionized calcium (Ca+2) is known to play a critical role in normal cardiovascular function, and Ca+2 administration in the setting of ionized hypocalcemia has been shown to improve indexes of cardiac function. The value of Ca+2 administration in the setting of cardiac arrest and resuscitation is unproven and controversial, in large part because ionized Ca+2 levels during cardiac arrest and resuscitation have not been adequately studied and exogenous calcium therapy may worsen ischemic cellular injury., Study Purpose: To measure free calcium during prolonged cardiac arrest and CPR in a canine model., Methods and Measurements: Central arterial and venous catheters were positioned in nine dogs, and ventricular fibrillation (VF) was induced electrically. After seven and one-half minutes of VF, countershocks were administered, and CPR was initiated and performed in accordance with current recommendations for 20 minutes. At five-minute intervals during resuscitation efforts, arterial pH, ionized Ca+2, and lactate as well as aortic pressure were measured., Results: During resuscitation, average systolic arterial pressure was 50 mm Hg. Within five minutes of instituting CPR, ionized Ca+2 significantly decreased from control values (5.1 +/- 0.1 at control to 4.0 +/- 0.1 mg/dL); after 20 minutes of attempted resuscitation, it averaged 3.2 +/- 0.2 mg/dL (P less than .05 vs control). There was no change in total Ca+2 during the arrest period (9.2 +/- 0.5 at control to 8.6 +/- 0.8 mg/dL at 27.5 minutes). Arterial lactate significantly increased throughout the arrest and resuscitation period (1.9 +/- 0.2 at control to 7.5 +/- 0.4 mM/L at 27.5 minutes). A significant correlation was demonstrated between ionized Ca+2 and lactate concentrations (r = -.72, P less than .001) but not between ionized calcium and pH (r = -.22, P greater than .20)., Conclusion: Ionized hypocalcemia occurs during prolonged cardiac arrest and resuscitation, and ionized hypocalcemia during prolonged arrest and resuscitation may be due to binding by lactate, as has been demonstrated in vitro.

Study Objective: Carbicarb, sodium bicarbonate, and 5% dextrose were compared for effects on resuscitability in a canine model of electromechanical dissociation after ventricular fibrillation., Design/interventions: 21 healthy mongrel dogs were anesthetized with pentobarbital, intubated, and mechanically supported. They were instrumented to measure heart rate, arterial pressure, pulmonary artery pressure, right atrial pressure, cardiac output, and arterial and mixed venous blood gases. The dogs were then subjected to a protocol that consisted of three successive CPR episodes. During each episode they were treated with repeated injections of one of the three substances, randomly chosen. After two minutes of ventricular fibrillation and four minutes of electromechanical dissociation, CPR was started with a thumper (rate, 60; duty cycle, 50%). If recovery was not obtained after five minutes of CPR, 1 mEq/kg carbicarb or sodium bicarbonate or 5 mL D5W was injected in the right atrium. Half the dose of the same substance was injected every five minutes thereafter; 1 mg epinephrine was also injected every five minutes until recovery. Hemodynamic and gasometric evaluations were performed five and 20 minutes after recovery. This later evaluation served as baseline for the next CPR episode., Measurements and Main Results: The duration and success rates of CPR are similar in the three CPR groups. Hemodynamic parameters were also similar during recovery. Bicarbicarb and sodium bicarbonate increased bicarbonate levels and corrected pH in the arterial and mixed venous blood. There was no difference in the blood gas values after carbicarb and sodium bicarbonate., Conclusion: In this model of cardiac arrest, carbicarb was not superior to sodium bicarbonate in the correction of metabolic acidosis during CPR.

Study Objective: To define the time course of myocardial ischemic injury using high-energy phosphate (HEP) depletion and the cessation of lactate production as metabolic markers., Setting: Data were collected in a laboratory animal model., Type of Participants: Ten immature mixed breed swine weighing 23.2 +/- 3.5 kg., Design: After thoracotomy, transmural myocardial biopsies were taken in vivo during normal sinus rhythm and at designated times during ventricular fibrillation with total circulatory arrest (VF-TCA)., Measurements and Main Results: Frozen tissue samples were analyzed for adenine nucleotides, by high-performance liquid chromatography, and lactate by enzymatic assay. At five minutes of VF-TCA, myocardial adenosine triphosphate averaged 50% of control. At 15 minutes of VF-TCA, 89% of animals had myocardial adenosine triphosphate levels above 20% of control and adenylate charge ratio above 0.60. With more than 30 minutes of VF-TCA, all animals had adenosine triphosphate levels below 10% of control and adenylate charge ratio below 0.30. In addition, myocardial lactate levels plateaued after 30 minutes of VF-TCA, indicating the cessation of lactate production., Conclusion: These results suggest that the myocardium can tolerate VF-TCA for as long as 15 minutes without irreversible injury; however, post-ischemic myocardial dysfunction may occur after as little as five minutes of VF-TCA. With more than 30 minutes of VF-TCA, myocardial injury is likely to be irreversible.

Study Objective: Animal studies suggest that the standard dose of epinephrine (SDE) for treatment of cardiac arrest in human beings may be too low. We compared the outcome after SDE with that after high-dose epinephrine (HDE) in children with refractory cardiac arrest., Design: Prospective intervention versus historic control groups., Type of Participants: Two similar groups of 20 consecutive patients each (median ages, 2.5 and 3 years) with witnessed cardiac arrest who remained in arrest after at least two SDEs (0.01 mg/kg)., Interventions: Treatment with an additional SDE versus HDE (0.2 mg/kg)., Measurements and Main Results: The rates of return of spontaneous circulation and long-term survival were compared. Fourteen of the HDE group (70%) had return of spontaneous circulation, whereas none of the SDE group did (P less than .001). Eight children survived to discharge after HDE, and three were neurologically intact at follow-up. No significant toxicity from HDE was observed., Conclusion: HDE provided a higher return of spontaneous circulation rate and a better long-term outcome than SDE in our series of pediatric cardiac arrest. HDE may warrant incorporation into standard resuscitation protocols at an early enough point to prevent irreversible brain injury.

A study was undertaken to determine the pattern of arterial blood gas (ABG) concentration in the canine model undergoing prolonged cardiopulmonary resuscitation (CPR) from fibrillatory arrest, and to determine the importance of acid base abnormalities in predicting resuscitation. Ventricular fibrillation was induced electrically in 12 dogs. CPR was begun at 3 minutes and continued for 27 minutes, at which time the dogs were defibrillated. ABG samples were taken at 0, 8, 18, and 28 minutes of ventricular fibrillation. Seven of the 12 dogs were resuscitated successfully. There was no difference in pH, PCO2, or PO2 between the survivors and nonsurvivors at any of the points measured. A pattern of pH and PCO2 abnormalities was noted in each dog over 30 minutes. Each developed a respiratory alkalosis that peaked at 8 minutes. During the next 22 minutes the pH gradually declined. This combination of respiratory alkalosis and metabolic acidosis resulted in normalization of the pH at about 18 minutes of fibrillation. We concluded that when adequate ventilation is provided in the canine model undergoing CPR, significant arterial acidemia does not occur for at least 18 minutes. Further, acid base abnormalities did not correlate with successful resuscitation.

We investigated the use of transvenous (TV) and transmyocardial (TM) pacemakers in the emergency department (ED) in 54 adult patients (42 men and 12 women) with bradyasystolic cardiac arrest. Down time prior to cardiopulmonary resuscitation (CPR) was 4.8 +/- 4.3 minutes. Time in the ED prior to pacer insertion was 26.9 +/- 17.7 minutes. Electrical capture rate was 63%. Pulse developed in 5%. Only 1.2% were admitted, and none was discharged alive. There was no significant difference in capture rate for TV versus TM pacers or in capture rate whether the pacer was inserted early or late after ED arrival. We conclude that ED pacer insertion for such patients does not alter survival rates.

Standard external CPR (SECPR) steps A, B, and C can maintain the brain's viability if started immediately, but not after prolonged arrest times. "New CPR" (simultaneous ventilation-compression CPR, SVC-CPR) is not suitable for basic life support, and may not be physiologically superior to optimally performed SECPR. The superiority of interposed abdominal compression CPR (IAC-CPR) over SECPR for basic life support is also uncertain. Open-chest CPR is physiologically superior to all external CPR methods studied thus far. Open-chest CPR should again be taught to physicians, and used more often after prolonged cardiac arrest. In intractable cases of cardiac arrest, particularly after prolonged arrest times or cold water drowning, cardiopulmonary bypass appears promising. After restoration of normal perfusion pressures and blood gases, a brain-oriented intensive care protocol for the support of extracerebral organs leads to better outcome than "usual care." Reflow promoting measures, particularly intracarotid hypertensive hemodilution, ameliorate postarrest brain damage and should be developed for clinical use. Barbiturates have been shown to exert no breakthrough effect on outcome after cardiac arrest, but are safe in the hands of those skilled in advanced intensive care. Barbiturates may be of adjunctive value after prolonged cardiac arrest, particularly when used to suppress seizures, facilitate controlled ventilation, and reduce intracranial pressure. Calcium entry blockers have been shown in animal models to improve hemodynamics and cerebral outcome postarrest, but not consistently.(ABSTRACT TRUNCATED AT 250 WORDS)

We describe a patient with a long history of rheumatoid arthritis who presented in full cardiopulmonary arrest. He was given intracardiac epinephrine. Fibroptic laryngoscopy determined the cause of the arrest to be upper airway obstruction from cricoarytenoid joint ankylosis, a complication of long-standing rheumatoid arthritis. The patient underwent a tracheostomy, recovered uneventfully, and was doing well nine months later. The literature is reviewed, and the pathophysiology, clinical findings, presentations, and treatment of this potentially fatal entity are described.

Our study was performed to determine the pattern of arterial, venous, and cerebral spinal fluid (CSF) acidosis in a canine model of cardiac arrest and resuscitation; and the effect of bicarbonate treatment on arterial, venous, and CSF acidosis. Animals were instrumented to sample arterial blood, mixed venous blood, and CSF through a cisternal catheter. Following six minutes of ventricular fibrillation, manual CPR efforts were begun and continued for 30 minutes of cardiac arrest. Arterial, mixed venous, and CS fluids were sampled at baseline, six, 12, 18, 24, 27, and 30 minutes. Ten experimental dogs received sodium bicarbonate (2 mEq/kg) at 20 minutes of cardiac arrest, while ten animals in the control group received no alkali treatment. The experimental group showed a significantly higher arterial (7.79 +/- 0.20 vs 7.46 +/- 0.16 at 30 minutes) and venous pH (7.34 +/- 0.12 vs 7.19 +/- 0.10 at 24 minutes) following bicarbonate administration. This higher pH occurred despite a concomitant increase in arterial (31 +/- 10 vs 19 +/- 9 mm Hg at 27 minutes; 31 +/- 9 vs 10 +/- 8 at 30 minutes) and venous (104 +/- 30 vs 63 +/- 10 mm Hg at 24 minutes) pCO2. CSF analysis showed a gradually worsening acidosis. However, CSF pH (7.12 +/- 0.14 vs 7.16 +/- 0.23 at 30 minutes) and pCO2 were not significantly changed by the administration of bicarbonate.

Cardiac arrest caused by massive pulmonary embolism is highly refractory to conventional resuscitation. Emergency surgical embolectomy has been considered the only effective intervention. We present the case of a 33-year-old woman who suffered a massive pulmonary embolism with circulatory arrest refractory to one half hour of aggressive CPR. A 10-mg bolus of recombinant tissue-type plasminogen activator was administered through a central line followed by a further 90-mg IV infusion over two hours. Rapid hemodynamic and clinical improvement followed the bolus dose. The patient was discharged later without neurological or other sequelae. This is the first reported case of successful thrombolytic therapy of massive pulmonary embolism during prolonged CPR.

Cerebral blood flow (CBF) with conventional closed-chest cardiopulmonary resuscitation (CCPR) has been measured at only 2% to 11% of prearrest values. The purpose of our study was to determine whether the peripheral administration of higher doses of epinephrine than currently recommended during CCPR following a prolonged cardiac arrest improves CBF compared to CCPR using a standard dose of epinephrine. Fifteen swine were randomized to receive CCPR plus 0.02 mg/kg, 0.2 mg/kg, or 2.0 mg/kg epinephrine through a peripheral IV line following a ten-minute cardiopulmonary arrest and three minutes of CCPR. Regional CBF measurements were made by radionuclide microsphere technique during normal sinus rhythm (NSR), CCPR, and following epinephrine administration. The adjusted regional blood flows (in mL/min/100 g) following epinephrine administration for the 0.02-, 0.2-, and 2.0-mg/kg groups were, respectively, left cerebral cortex (3.3, 13.1, 11.8); right cerebral cortex (3.9, 13.8, 12.2); cerebellum (9.2, 32.0, 33.1); midbrain/pons (9.9, 32.1, 32.3); medulla (10.6, 61.5, 54.2); and cervical spinal cord (12.2, 53.8, 35.8). In this swine model, 0.2 mg/kg and 2.0 mg/kg epinephrine significantly increased regional CBF over that seen with standard doses. Because neuronal survival is dependent on flow rates of 10 to 15 mL/min/100 g, this preliminary evidence suggests that these higher doses of epinephrine may help improve neurological outcome in CCPR.

ECG patterns observed during cardiac arrest were analyzed in 261 comatose cardiac arrest survivors. Forty-seven patients (18%) exhibited electromechanical dissociation (EMD) at some point before restoration of stable spontaneous circulation. These patients had a higher mortality (P = .05) and a lower rate of cerebral recovery (P = .01) during the one-year follow-up than study patients who did not exhibit EMD. Patients who developed EMD subsequent to defibrillation had better outcome than patients presenting with EMD. Multivariate analysis revealed that age more than 70 years old (P = .007), pulmonary disease (P less than .001), diabetes (P = .013, in-hospital arrests only), and prearrest hypoxemia (P = .013, outside-hospital arrests only) were independently predictive of the occurrence of EMD. Although the generalizability of these findings is limited, they may offer new clues to the pathophysiology of EMD.

Despite advances in the understanding of the pathophysiology of cerebral ischemia, no single brain resuscitation therapy has yet been shown to be clinically superior to brain-oriented intensive care. Basic concepts in cardiopulmonary-cerebral resuscitation (CPCR) are discussed, as are two specific phases of CPCR, cerebral preservation and cerebral resuscitation. Cerebral preservation is initiated during cardiac arrest (ie, prior to restoration of spontaneous circulation [ROSC]) and includes use of artificial perfusion techniques and drugs to produce cerebral perfusion during this phase. Cerebral resuscitation is brain-oriented therapy initiated after ROSC. Pharmacologic agents currently under study for cerebral resuscitation include the barbiturates, calcium antagonists, and iron chelators. With respect to defining efficacy of the pharmacologic agents, the concept of therapeutic window is important. Although no agent has been proven clinically, several appear to be promising.

Calcium chloride has been advocated since the 1920s for resuscitation of asystole and ventricular fibrillation. Most reports have been anecdotal, and have failed to substantiate its effectiveness. In two large retrospective series with a collective experience of 181 patients, investigators reviewed the effectiveness of calcium chloride in asystole and did not support its use. A prospective, randomized, double-blind study comparing calcium chloride with saline in the prehospital setting was done. Patients with trauma or pediatric arrests were excluded. During the period from October 1982 to October 1983, a total of 32 patients with witnessed arrests presented with a rhythm of asystole and were refractory to epinephrine, bicarbonate, and atropine. The rate of successful resuscitation in the calcium group was 5.6% (1/18), and there were no successful resuscitations (0/14) in the saline group (P = .37). A successful resuscitation was defined as conveyance of a patient with a rhythm and pulse to an emergency department. Groups were analyzed for sex, age, cardiac history, and cardiac drugs, and there were no statistically significant differences. No patient who was successfully resuscitated in the field was discharged alive from the hospital. Calcium chloride is of no value in resuscitating refractory asystole in the prehospital cardiac arrest setting.

Access to an ambulance service trained to provide only basic cardiac life support (BCLS) and adjunctive ventilation with oxygen provided the opportunity to study cardiac rhythms during BCLS in patients with circulatory arrest. Holter monitoring was attempted in 43 patients. Technically adequate traces throughout transport to hospital were obtained in 21. The average monitored time was 11.9 minutes. A tachydysrhythmia (mainly VF/VT) was initially found in 10, heart block or bradycardia in 9, and asystole in 2 persons. During BCLS, six patients with bradycardic rhythms converted temporarily to VF. The first ECG tracing obtained in the hospital revealed, however, that only five were still in a tachydysrhythmia and 15 were asystolic. These data demonstrate that important rhythm changes occur when BCLS is continued for several minutes during circulatory arrest. Although some bradycardic rhythms convert to VF, the VF is not sustained. After an average of 12 minutes, 90% of those initially in bradycardic rhythm and 50% of those initially in VF/VT were asystolic. This study provides further evidence that BCLS does not prevent cardiac deterioration.

This prehospital prospective, controlled study was conducted to determine if prehospital cardiac pacing affects survival. The study involved 239 patients, 226 pulseless, nonbreathing patients (rhythms of asystole and electromechanical dissociation with heart rates less than 70) and 13 patients with hemodynamically significant bradycardia (heart rate less than 60; blood pressure less than 90 mm Hg; not responding to atropine). Patients were assigned to treatment or control groups on an every-other-day basis. One hundred three patients were treated with an external cardiac pacing device; 22 (21.4%) were resuscitated (arrival at admitting hospital with pulse and blood pressure) and seven (6.8%) were saved (survival to hospital discharge). One hundred thirty-six patients were not paced and served as controls; 28 (20.6%) were resuscitated (P = .90) and six (4.4%) were saved (P = .71). Analysis of pacing times showed increased resuscitation in patients paced early. All surviving paced patients were paced in 17 minutes or less. Analysis of rhythm subgroups showed no significant difference in the resuscitation or survival rates of paced and control groups for primary asystole, primary electromechanical dissociation, and secondary asystole and electromechanical dissociation occurring after countershock treatment of ventricular fibrillation when compared respectively. However, among patients with hypotensive bradycardia, six of six paced patients were resuscitated and five were saved, while only two of seven controls were resuscitated (P = .01) and one was saved (P = .01). Interpretation of the bradycardic patient data is limited by inequalities noted between control and treatment groups with regard to the administration of isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

We hypothesize that brain injury from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. We conducted a study to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron in low-molecular-weight species (LMWS iron) used the o-phenanthroline test on an ultrafiltered (molecular weight less than 30,000) tissue sample; malondialdehyde (MDA), a product of lipid peroxidation, in brain tissue was assayed by the thiobarbituric acid test (TBA). Samples of the parietal cortex from 11 nonischemic control dogs (Group 1) had LMWS iron levels of 9.6 +/- 4.9 nmol/100 mg tissue and MDA levels of 7.7 +/- 2.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 15 minutes of cardiac arrest (Group 2) had LMWS iron levels of 9.3 +/- 3.1 nmol/100 mg tissue and MDA levels of 6.1 +/- 1.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 45 minutes of cardiac arrest (Group 3) had LMWS iron levels of 6.7 +/- 3.3 nmol/100 mg tissue and MDA levels of 5.6 +/- 0.4 nmol/100 mg tissue. There was no significant difference among the three groups for either LMWS iron or MDA. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 4). Following resuscitation the chest was closed and the dogs were given intensive care for two hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium dichloroacetate (DCA) has been shown to lower elevated serum lactate levels produced by hypoxia, exercise, and phenformin. We conducted a study to investigate the effect of DCA treatment on lactic acidosis following resuscitation from asphyxial cardiac arrest. Conditioned dogs were anesthetized with pentobarbital (30 mg/kg), endotracheally intubated, and mechanically ventilated to maintain an arterial pCO2 of 30 to 40 mm Hg. Asphyxial cardiac arrest was produced by endotracheal tube occlusion for six to eight minutes. After five minutes of cardiac arrest, the endotracheal tube was unclamped and closed-chest CPR was begun. Six animals received DCA 100 mg/kg IV push after one minute of CPR. Control animals (n = 6) received an equal volume of saline. CPR was continued until the return of a spontaneous pulse, when mechanical ventilation was resumed. Arterial and venous blood gases, glucose, and lactate levels were obtained at baseline and 15, 30, 45, 60, 90, and 120 minutes after resuscitation. Mean arterial blood pressure, pulse, and glucose, and venous and arterial blood gases were similar in both groups throughout the study. By 45 minutes after resuscitation, the DCA-treated group showed a significantly faster rate of decline in lactate levels that continued to the final sampling period. By 90 minutes, arterial lactate in DCA animals was not significantly different from baseline (pre-arrest) values. DCA given during cardiac arrest will cause a more rapid normalization of arterial lactate after successful resuscitation. Further studies are needed to evaluate the effects of lowered lactic acid on survival and neurological outcome following cardiac arrest.

We studied the development of acidosis, as measured by blood gases, in a convenience sample of 16 patients undergoing five minutes of closed-chest CPR (CC-CPR) followed by five minutes of open-chest CPR (OC-CPR). To eliminate the influence of variable pCO2 on serum pH, all blood gas values were adjusted to a pCO2 of 40 mm Hg. Adjusted pH fell a mean of 0.09 U (SEM +/- 0.03, P = .02) with five minutes of CC-CPR and then 0.05 U (SEM +/- 0.02, P = .05) with five minutes of OC-CPR. The decline in adjusted pH during CC-CPR was statistically comparable to the decline that occurred during OC-CPR. The development of acidosis as measured by blood gases does not appear to be significantly different for patients undergoing five minutes of CC-CPR versus five minutes of OC-CPR when OC-CPR follows CC-CPR.

Sixty-five patients who arrived in the emergency department in cardiac arrest were studied prospectively to determine whether central venous pH could be used as an accurate predictor of arterial pH in prolonged cardiac arrest. Central venous and arterial access were obtained as soon as possible after arrival in the emergency department. Simultaneous arterial and venous samples were drawn and sent for blood gas analysis. Under normal conditions, central venous pH (pHcv) approximates arterial pH (pHa). In prolonged cardiac arrest, however, our data reveal a mean pHa of 7.31 +/- 0.25 and a mean pHcv of 7.08 +/- 0.19. There was moderate correlation between pHa and pHcv when all patients were considered (r = .69, P less than .01). The correlation was excellent, however, in the subgroup of 15 patients who had a pulse at some point during resuscitation (r = .95, P less than .01). In 13 of these 15 patients the acid base status would have been managed correctly based on the predicted pHa (pHcv + 0.12 correction factor). The pHcv was also valuable in identifying a second subgroup of patients who required no further bicarbonate therapy; all patients who had a pHcv greater than or equal to 7.15 had a pHa greater than 7.30 (21 patients). The central venous pH was found to be a useful index of arterial pH when applied to a definable subset of patients, which in this study constituted 45% of all patients in prolonged cardiac arrest.

We tested the hypothesis that polymorphonuclear leukocytes (neutrophils) contribute to morbidity and mortality in a canine model of cardiac arrest-induced central nervous system ischemia. Circulating neutrophils were depleted by administration of a neutrophil-specific sheep immune serum before a ten-minute cardiac arrest in ten experimental animals. Ischemic damage measured by a neurologic deficit score in these animals was compared with that in 12 animals that received either vehicle control or nonimmune sheep serum. Animals receiving immune serum averaged 89% depletion of neutrophils immediately after resuscitation (neutrophils +/- SEM: 703 +/- 123/mm3 after antiserum versus 6,384 +/- 1,171/mm3 before immune serum) and 70% depletion over the first three hours after resuscitation. Neurologic deficit scores assessed at one, two, six, 12, and 24 hours after arrest did not vary between depleted dogs and controls. Overall survival time in neutrophil-depleted dogs was less than in controls (15.5 +/- 1.3 versus 19.5 +/- 1.3 hours; P = .04). These results suggest that neutrophils may not contribute to clinically important central nervous system dysfunction after resuscitation from a ten-minute cardiac arrest.

The development and increasing use of the automatic implantable cardioverter defibrillator (AICD) represents a major therapeutic advance for management of recurrent ventricular tachycardia and ventricular fibrillation. However, the AICD sensing functions that determine appropriate energy discharge may complicate resuscitation from cardiac arrest. This care report illustrates a properly functioning AICD interfering with the resuscitation of a 67-year-old man. In the presence of persistent ventricular tachycardia and ventricular fibrillation or successful conversion to a supraventricular tachycardia with pulses that exceed the rate cutoff, it may be helpful to inactivate the AICD with a magnet to prevent unneeded discharges during resuscitation and stabilization.

Pulseless idioventricular rhythm (PIVR) is a slow electrical rhythm of ventricular origin without mechanical activity, and it is associated with a mortality rate that approaches 100%. In 1976 high-dose corticosteroids were advocated as beneficial in the treatment of PIVR. A critical review of the early literature suggests that the favorable outcome may have been attributable to variables other than treatment with high-dose steroids. Recent prospective clinical trials have not confirmed the salutory effect of steroids in this dysrhythmia.

We studied a clinically realistic field-to-hospital scenario in dogs with four-minute ventricular fibrillation (VF) cardiac arrest followed by 30-minute standard external CPR basic life support (BLS). At the end of this 34-minute insult, cardiopulmonary bypass (CPB) was used for early defibrillation and assisted circulation for one hour (n = 10). Recovery was compared with that of control dogs (n = 10) in which standard CPR with advanced life support (ALS) for another 30 minutes was used for restoration of spontaneous circulation (ROSC). Both groups had hemodilution and heparinization; controlled blood pressure, blood gases, ventilation, and other parameters for 20 hours; and intensive care to 72 hours. During CPR-BLS of 30 minutes in both groups signs of cerebral viability returned. CPB achieved ROSC more successfully (ten of ten vs five of ten CPR-ALS controls) (P less than .02); and more rapidly, with less defibrillation energy (first countershock in eight of ten) and with less epinephrine (P less than .01). CPB improved 72-hour survival (seven of ten vs three of ten controls) (P less than .05). Between two and 24 hours, of those with ROSC, cardiac complications killed three of ten CPB dogs (after weaning), and two of five CPR-ALS dogs (NS). All seven CPB survivors to 72 hours were neurologically normal; of the three CPR-ALS survivors, one remained with severe neurologic deficit and two were neurologically normal (seven of ten CPB vs two of ten controls, P = .025). Starting CPR-BLS within four minutes of arrest can maintain cerebral viability.(ABSTRACT TRUNCATED AT 250 WORDS)