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Evaluation of biphasic transthoracic defibrillation in an animal model of prolonged ventricular fibrillation.

OBJECTIVES: To determine whether a biphasic defibrillation waveform (BDW) would produce a superior rate of converting prolonged ventricular fibrillation (VF) into a perfusing rhythm and delay the occurrence of asystole and/or pulseless electrical activity (PEA) during the resuscitation attempt, when compared with a monophasic defibrillation waveform (MDW). METHODS: The authors performed a prospective, randomized, blinded experiment using an established swine model of prolonged VF. Thirty-four mixed-breed domestic swine (mean mass 22.9 kg) were sedated (ketamine/xylazine), anesthetized (isoflurane), and intubated. Aortic and femoral venous catheters were placed. ECG was monitored continuously. The animals were shocked into VF (3-s, 100-mA, 60-Hz shock), and were untreated for 8 minutes. Advanced Cardiac Life Support (ACLS) began with 1 minute of standardized (Thumper) chest compressions and ventilation. The animals were randomized to treatment with either BDW or MDW. Standard ACLS protocols were followed. The energy sequence was 2.5 J/kg first, 3.5 J/kg second, and 4.5 J/kg for all subsequent shocks. Outcome variables were time to event of asystole/PEA, return of spontaneous circulation (ROSC), and one-hour survival. Data were analyzed with two-tailed Fisher's exact test and Kaplan-Meier survival plots (alpha = 0.05). RESULTS: ROSC occurred more frequently in the BDW group (7/17) compared with the MDW group (1/17); p = 0.04. Survival analysis showed that the BDW significantly delayed the occurrence of asystole/PEA during the resuscitation attempt when compared with the MDW; log-ranked p = 0.02. One-hour survival rates (5/17 BDW and 1/17 MDW, p = 0.17) did not differ. CONCLUSIONS: BDW resulted in a superior rate of ROSC and delay in the occurrence of asystole/ PEA during the resuscitation attempt when compared with MDW.

Animals↗

Amiodarone attenuates fluoride-induced hyperkalemia in vitro.

UNLABELLED: Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. OBJECTIVES: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. METHODS: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. RESULTS: Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. CONCLUSIONS: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals.

Amiodarone↗

Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model.

UNLABELLED: Refractory ventricular fibrillation (VF) is a complication of severe hypothermia. Despite mixed experimental data, some authors view bretylium as the drug of choice in hypothermic VF. Bretylium was removed from Advanced Cardiac Life Support guidelines, and, to date, efficacy of amiodarone in hypothermia is unknown. OBJECTIVES: To compare defibrillation rates from hypothermic VF after drug therapy with amiodarone, bretylium, and placebo. METHODS: This was a randomized, blinded, and placebo-controlled laboratory experiment. Thirty anesthetized dogs were mechanically ventilated and instrumented to monitor coronary perfusion pressure (CPP), rectal core temperature, and electrocardiogram (ECG). Animals were cooled to 22 degrees C or the onset of spontaneous VF. Ventricular fibrillation was induced as needed with a transthoracic AC current. Cardiopulmonary resuscitation (CPR) was initiated and animals were randomized (n = 10 each group) to receive amiodarone 10 mg/kg (A), bretylium 5 mg/kg (B), or placebo (P) intravenously. CPR was continued while monitoring for chemical defibrillation. Rewarming was limited to removal from the cold environment. After 10 minutes, up to three escalating defibrillatory shocks were administered. Hemodynamic monitoring continued after resuscitation. Return of spontaneous circulation (ROSC) was defined as a sustainable ECG rhythm generating a corresponding arterial pressure tracing lasting a minimum of 15 minutes. Sample size permitted 80% power to detect a 60% difference in conversion rate between groups. RESULTS: CPR was adequate based on CPP > 15 mm Hg in all animals. Mean (+/-SD) CPP was 35.3 +/- 18.8 mm Hg with an overall lower trend in the amiodarone group (p = 0.06). Baseline variables were similar between groups. No instance of chemical defibrillation was noted. There was no significant difference in ROSC rates between groups. Resuscitation rates were: amiodarone = 1/10, bretylium = 4/10, and placebo = 3/10 (p = 0.45). CONCLUSIONS: In this model of severe hypothermic VF, neither amiodarone nor bretylium was significantly better than placebo in improving the resuscitation rate.

Amiodarone↗

Organization of care for acute myocardial infarction in rural and urban hospitals in Kansas.

CONTEXT: One in 4 Americans lives in a rural community and relies on rural hospitals and medical systems for emergent care of acute myocardial infarctions (AMI). The infrastructure and organization of AMI care in rural and urban Kansas hospitals was examined. METHODS: Using a nominal group process, key elements within hospitals that might influence quality of AMI care were identified, including personnel, equipment, organizational systems, and quality improvement activities. These elements were included in a survey of 45 rural and 12 urban Kansas hospitals. FINDINGS: Though emergency 911 systems were widely available in both urban and rural communities, paramedics and advanced cardiac life support were less likely to be available in rural communities. Few rural hospitals were capable of emergent catheterization, angioplasty, or coronary artery bypass surgery; cardiologists, though readily available by phone, were rarely available on-site. Nevertheless, most rural ambulances could not bypass local hospitals. Most rural hospitals transferred the vast majority of their patients to urban medical centers within an average distance of 78 miles. Standardized protocols were used for emergent AMI care in 67% of urban and 62% of rural hospitals. Hospitals included aspirin in 53% and beta-blockers in 28% of either protocols or standing orders. CONCLUSIONS: Although faced with more limited resources, some rural hospitals, like their urban counterparts, have implemented protocols to address emergent care of AMI patients. Nevertheless, many of these protocols omit crucial aspects of AMI care. Rural and urban hospitals should jointly develop systems that assure consistent, rapid delivery of AMI care.

Cardiology Service, Hospital↗

Witnessed arrest, but not delayed bystander cardiopulmonary resuscitation improves prehospital cardiac arrest survival.

INTRODUCTION: This study correlated the effect of witnessing a cardiac arrest and instituting bystander CPR (ByCPR), as a secondary end point in a study evaluating the effect of bicarbonate on survival. METHODS: This prospective, randomised, double blinded clinical intervention trial enrolled 874 prehospital cardiopulmonary arrest patients encountered in a prehospital urban, suburban, and rural regional emergency medical service (EMS) area. This group underwent conventional advanced cardiac life support intervention followed by empiric early administration of sodium bicarbonate (1 mEq/l), monitoring conventional resuscitation parameters. Survival was measured as presence of vital signs on emergency department (ED) arrival. Data were analysed using chi(2) with Pearson correlation and odds ratio where appropriate. RESULTS: The overall survival rate was 13.9% (110 of 792) of prehospital cardiac arrest patients. The mean (SD) time until provision of bystander cardiopulmonary resuscitation (ByCPR) by laymen was 2.08 (2.77) minutes, and basic life support (BLS) by emergency medical technicians was 6.62 (5.73) minutes. There was improved survival noted with witnessed cardiac arrest-a 2.2-fold increase in survival, 18.9% (76 of 402) versus 8.6% (27 of 315) compared with unwitnessed arrests (p<0.001) with a decreased risk ratio of mortality of 0.4534 (95% CI, 0.0857 to 0.1891). The presence of ByCPR occurred in 32% (228 of 716) of patients, but interestingly did not correlate with survival. The survival rate was 18.2% (33 of 181) if ByCPR was performed within two minutes and 12.8% (6 of 47), if performed >two minutes (p = 0.3752). CONCLUSIONS: Survival after prehospital cardiac arrest is more likely when witnessed, but not necessarily when ByCPR was performed by laymen.

Adult↗

Conjunctival oxygen monitoring during cardiopulmonary resuscitation.

The conjunctival oxygen tension (CjO2) sensor is a non-invasive, continuous index of oxygen delivery in the haemodynamically unstable patient. Human and animal studies have indicated that CjO2 reflects cerebral blood flow and oxygenation. Simple insertion, rapid stabilization and reaction time less than 60 s allow use in the initial stages of cardiopulmonary resuscitation (CPR) where invasive monitoring is often impracticable. CjO2 was monitored to assess cerebral oxygenation during CPR of 15 patients in cardiac arrest in the accident and emergency department (A&E). Patients who arrested out of hospital with delay to advanced cardiac life support and died had CjO2 less than 20 mmHg (normal CjO2 50-60 mmHg) on arrival in A&E. CPR with closed chest cardiac massage (closed CPR) produced no improvement in CjO2. Patients who arrested in ventricular fibrillation (VF) in A&E, and survived with no neurological deficit had CjO2 greater than 20 mmHg during CPR. However, further episodes of VF produced an immediate fall in CjO2 which continued, despite closed CPR, until restoration of spontaneous cardiac output (RSCO) determined by a palpable carotid pulse. In survivors with delay from arrest to CPR the rise in CjO2 with RSCO did not occur for up to 10 min. This study suggests that closed CPR has no value in maintaining or improving cerebral oxygenation during cardiac arrest. Further studies are required to determine the precise relationship of CjO2 to cerebral blood flow and oxygenation during CPR using open and closed techniques of cardiac massage. Open chest cardiac massage (open CPR) has been shown to produce near normal cerebral perfusion and if patients are to survive prolonged resuscitation neurologically intact guidelines for open CPR must be reviewed.

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Long term outcome after out-of-hospital cardiac arrest with physician staffed emergency medical services: the Utstein style applied to a midsized urban/suburban area.

OBJECTIVE: To test the effect of a physician staffed advanced cardiac life support (ALS) system on patient outcome following out-of-hospital cardiac arrest. DESIGN: Observational study. SETTING: Two tier basic life support (BLS) and physician staffed ALS services in the midsized urban/suburban area of Heidelberg, Germany. PATIENTS: All patients suffering out-of-hospital cardiac arrest of cardiac aetiology between January 1992 and December 1994 and who were covered by ALS services. INTERVENTIONS: Physician staffed ALS services. MAIN OUTCOME MEASURES: Return of spontaneous circulation, hospital discharge, and one year survival, according to the Utstein style. RESULTS: Of 330 000 inhabitants, 755 suffered from cardiac arrest covered by the Heidelberg ALS services. In 512 patients, cardiopulmonary resuscitation had been initiated. Of 338 patients with cardiac aetiology, return of spontaneous circulation was achieved in 164 patients (49%), 48 (14%) were discharged alive, and 40 (12%) were alive one year later; most of these patients showed good neurological outcome. Thus, 4.85 patients with cardiac aetiology were saved by the ALS services and discharged alive per 100 000 inhabitants a year. Ventricular fibrillation or tachycardia was detected in 106 patients (31%), other cardiac rhythms in 40 (12%), and asystole in 192 (57%). Hospital discharge rates (and one year survival) in these subgroups were 34.0% (29.2%), 12.5% (7.5%), and 3.6% (3.1%), respectively. Discharge rates increased if cardiac arrest was witnessed (bystander, 20.0%; BLS/ALS personnel, 21.4%; non-witnessed arrest, 3.3%; p < 0.01), and if the time period between the alarm and the arrival of the ALS unit was four minutes or less (</= 4 minutes, 30.6%; 4-8 minutes, 10.4%; > 8 minutes, 8. 1%; p < 0.001). In 69 patients with bystander witnessed cardiac arrest with ventricular fibrillation, the discharge rate was 37.7%; 21 patients were alive after one year. CONCLUSIONS: A two tier BLS and physician staffed ALS system is associated with good long term outcome of patients suffering from out-of-hospital cardiac arrest of cardiac aetiology in a midsized urban/suburban area. Further studies, however, are required to assess whether having a physician in the ALS unit is an independent determinant for improved long term outcome.

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Implementation of team training in medical education in Denmark.

In the field of medicine, team training aiming at improving team skills such as leadership, communication, co-operation, and followership at the individual and the team level seems to reduce risk of serious events and therefore increase patient safety. The preferred educational method for this type of training is simulation. Team training is not, however, used routinely in the hospital. In this paper, we describe a framework for the development of a team training course based on need assessment, learning objectives, educational methods including full-scale simulation and evaluations strategies. The use of this framework is illustrated by the present multiprofessional team training in advanced cardiac life support, trauma team training and neonatal resuscitation in Denmark. The challenges of addressing all aspects of team skills, the education of the facilitators, and establishment of evaluation strategies to document the effect of the different types of training on patient safety are discussed.

Curriculum↗

Improving medical emergency team (MET) performance using a novel curriculum and a computerized human patient simulator.

PROBLEM: Advance cardiac life support (ACLS) training does not address coordination of team resources to improve the ability of teams to deliver needed treatments reliably and rapidly. Our objective was to use a human simulation training educational environment to develop multidisciplinary team skills and improve medical emergency team (MET) performance. We report findings of a crisis team training course that is focused on organization. SETTING: Large center for human simulation training at a university affiliated tertiary care hospital. PARTICIPANTS: Ten courses were delivered and 138 clinically experienced individuals were trained (69 critical care nurses, 48 physicians, and 21 respiratory therapists). All participants were ACLS trained and experienced in responding to cardiac arrest situations. COURSE DESIGN: Each course had four components: (1) a web based presentation and pretest before the course; (2) a brief reinforcing didactic session on the day of the course; (3) three of five different simulated scenarios; each followed by (4) debriefing and analysis with the team. Three of five simulator scenarios were used; scenario selection and order was random. Trainees did not repeat any scenario or role during the training. Participants were video recorded to assist debriefing. Debriefing focused on reinforcing organizational aspects of team performance: assuming designated roles independently, completing goals (tasks) assigned to each role, and directed communication. MEASURES FOR IMPROVEMENT: Participants graded their performance of specific organizational and treatment tasks within specified time intervals by consensus. Simulator "survival" depended on supporting oxygenation, ventilation, circulation within 60 seconds, and delivering the definitive treatment within 3 minutes. EFFECTS OF CHANGE: Simulated survival (following predetermined criteria for death) increased from 0% to 89%. The initial team task completion rate was 10-45% and rose to 80-95% during the third session. LESSONS LEARNT: Training multidisciplinary teams to organize using simulation technology is feasible. This preliminary report warrants more detailed inquiry.

Computer Simulation↗

Short-acting beta-adrenergic antagonist esmolol given at reperfusion improves survival after prolonged ventricular fibrillation.

BACKGROUND: High catecholamine concentrations are cytotoxic to cardiac myocytes. We hypothesized that myocardial interstitial catecholamine levels are greatly elevated immediately after long-duration ventricular fibrillation (VF), defibrillation, and reperfusion and that the short-acting beta-antagonist esmolol administered at reperfusion would protect against this catecholamine surge and improve survival. METHODS AND RESULTS: In part 1 of this study, catecholamines from myocardial interstitial fluid (ISF) and aortic and coronary sinus plasma were quantified by use of 3H-labeled radioenzymatic assay in 8 open-chest, anesthetized pigs. Eight minutes of electrically induced VF was followed by internal defibrillation and reperfusion. By 4 minutes of VF, ISF norepinephrine increased significantly, from 1.3+/-0.3 to 7.4+/-2.4 ng/mL. Epinephrine increased significantly, from 0.4+/-0.2 to 1.5+/-0.7 ng/mL. ISF norepinephrine and epinephrine peaked at 219.2+/-92.1 and 63.7+/-25.1 ng/mL after defibrillation and reperfusion and decreased significantly to 12.2+/-3.5 and 6.7+/-3.1 ng/mL 23 minutes after defibrillation. Transcardiac catecholamine changes were similar. In part 2, 8 minutes of VF was followed by external defibrillation in anesthetized, closed-chest pigs. Animals received 1.0 mg/kg esmolol (n=8) or saline (n=8) intravenously at the start of cardiopulmonary resuscitation (CPR). Advanced cardiac life support, including CPR and epinephrine, was delivered to both groups. Esmolol before reperfusion improved return of spontaneous circulation and 4-hour survival (7/8 versus 3/8 survivors, chi2 P<0.05). CONCLUSIONS: Transcardiac and ISF norepinephrine and epinephrine levels are briefly massively elevated after 8 minutes of VF, defibrillation, and reperfusion. A short-acting beta-antagonist administered immediately after defibrillation improves return of spontaneous circulation and 4-hour survival after this prolonged VF.

Adrenergic beta-Antagonists↗

Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest.

BACKGROUND: Blood pressure is severely reduced in patients in cardiac arrest receiving standard cardiopulmonary resuscitation (CPR). Although active compression-decompression (ACD) CPR improves acute hemodynamic parameters, arterial pressures remain suboptimal with this technique. We performed ACD CPR in patients with a new inspiratory threshold valve (ITV) to determine whether lowering intrathoracic pressures during the "relaxation" phase of ACD CPR would enhance venous blood return and overall CPR efficiency. METHODS AND RESULTS: This prospective, randomized, blinded trial was performed in prehospital mobile intensive care units in Paris, France. Patients in nontraumatic cardiac arrest received ACD CPR plus the ITV or ACD CPR alone for 30 minutes during advanced cardiac life support. End tidal CO(2) (ETCO(2)), diastolic blood pressure (DAP) and coronary perfusion pressure, and time to return of spontaneous circulation (ROSC) were measured. Groups were similar with respect to age, gender, and initial rhythm. Mean maximal ETCO(2), coronary perfusion pressure, and DAP values, respectively (in mm Hg), were 13.1+/-0.9, 25.0+/-1.4, and 36.5+/-1.5 with ACD CPR alone versus 19.1+/-1.0, 43.3+/-1.6, and 56.4+/-1.7 with ACD plus valve (P<0.001 between groups). ROSC was observed in 2 of 10 patients with ACD CPR alone after 26.5+/-0.7 minutes versus 4 of 11 patients with ACD CPR plus ITV after 19.8+/-2.8 minutes (P<0.05 for time from intubation to ROSC). Conclusions-Use of an inspiratory resistance valve in patients in cardiac arrest receiving ACD CPR increases the efficiency of CPR, leading to diastolic arterial pressures of >50 mm Hg. The long-term benefits of this new CPR technology are under investigation.

Adult↗

Long-term survival with open-chest cardiac massage after ineffective closed-chest compression in a canine preparation.

The ultimate goal of cardiopulmonary resuscitation (CPR) is long-term, neurologically intact survival. This study examined whether open-chest cardiac massage could improve 7 day survival and neurologic function when instituted after the failure of standard closed-chest compression CPR. Twenty-nine mongrel dogs were anesthetized and then instrumented with catheters to monitor right atrial and ascending aortic pressures. Ventricular fibrillation was induced and after 3 min standard CPR was begun. Standard CPR was performed with a Thumper programmed for 2 inch chest compressions at 60/min with a 50% duty cycle. External defibrillation was attempted twice after 15 min of ventricular fibrillation. Unsuccessfully defibrillated animals were randomly assigned to either an additional 2 min of continued closed-chest compressions, or 2 min of open-chest cardiac massage. All animals underwent a period of advanced cardiac life support and were followed until they were resuscitated or died. Follow-up care, including scoring of neurologic deficit, was performed for 7 days. In dogs receiving open-chest cardiac massage there was significantly more immediate resuscitation success (14/14 vs 5/14; p less than .005), 24 hr survival (12/14 vs 4/14; p less than .005), and 7 day survival (11/14 vs 4/14; p less than .02) than in those receiving continued closed-chest compression. Open-chest cardiac massage significantly improved long-term outcome when instituted after 15 min of ineffective closed-chest compression.

Animals↗

Prehospital trial of emergency transcutaneous cardiac pacing.

A prospective alternate-day controlled trial of prehospital transcutaneous cardiac pacing (PACE) of hemodynamically significant bradycardia and asystole was undertaken. All patients had a Glasgow coma scale score of 12 or less. Patients in the control group (n = 101) received standard advanced cardiac life support (ACLS) care. Patients in the pacing group (n = 101) were to receive PACE in addition to standard ACLS treatment; 89 patients were actually paced. The two groups were comparable in terms of age, sex, presenting rhythm, and mean times to cardiopulmonary resuscitation (CPR) and ACLS. For the 144 patients in whom the time of arrest could be estimated, the mean times to CPR and ACLS were 5.3 +/- 4.0 and 10.9 +/- 7.1 min, respectively. For the 65 paced patients in whom the time of arrest could be estimated, the mean time from arrest to pacing was 21.8 +/- 8.8 min (range 2 to 43). Multivariate analysis of outcome variables (presentation to emergency department with a pulse, admission to the hospital, and discharge from the hospital) revealed that an initial rhythm of ventricular tachycardia or fibrillation and a short time to ACLS were correlated with a favorable outcome (p less than .05; logistic regression analysis). A short time to PACE was associated with admission to the hospital (p = .20; logistic regression analysis). The use of a stand-alone transcutaneous pacing device in the prehospital arrest setting was associated with generally long times until pacing and did not appreciably improve outcome. Use of PACE in patients demonstrating prehospital bradycardia without neurologic impairment remains to be evaluated.

Adult↗

Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock.

BACKGROUND: Early countershock of ventricular fibrillation has been shown to improve immediate and long-term outcome of cardiac arrest. However, a number of investigations in the laboratory and in the clinical population indicate that immediate countershock of prolonged ventricular fibrillation most commonly is followed by asystole or a nonperfusing spontaneous cardiac rhythm, neither of which rarely respond to current therapy. The use of epinephrine in doses greater than those currently recommended has recently been shown to improve both cerebral and myocardial perfusion during cardiopulmonary resuscitation (CPR). The purpose of this study was to compare cardiac resuscitation outcome between immediate countershock of prolonged ventricular fibrillation with high-dose epinephrine therapy and conventional CPR before countershock of prolonged ventricular fibrillation in a canine model. METHODS AND RESULTS: After sedation, intubation, induction of anesthesia, and instrumentation, ventricular fibrillation was electrically induced in 28 dogs. After 7.5 minutes of ventricular fibrillation, animals were randomly allocated to two treatment groups: group 1, immediate countershock followed by recommended advanced cardiac life support (ACLS) interventions, or group 2, 0.08 mg/kg epinephrine and manual closed-chest CPR before countershock and ACLS. In both groups, ACLS was continued until a spontaneous perfusing rhythm was restored or for 20 minutes (total arrest time, 27.5 minutes). A spontaneous perfusing rhythm was restored in three of 14 group 1 animals and in nine of 14 group 2 animals (p = 0.014 by sequential analysis method of Whitehead). Coronary perfusion pressure (aortic minus right atrial pressure during CPR diastole) before countershock was significantly greater in group 2 (21 +/- 7 mm Hg) when compared with mean circulatory pressure in group 1 (9 +/- 8, p less than 0.01). CONCLUSIONS: The findings of this study suggest that a brief period of myocardial perfusion before countershock improves cardiac resuscitation outcome from prolonged ventricular fibrillation.

Animals↗

Mild resuscitative hypothermia to improve neurological outcome after cardiac arrest. A clinical feasibility trial. Hypothermia After Cardiac Arrest (HACA) Study Group.

BACKGROUND AND PURPOSE: Recent animal studies showed that mild resuscitative hypothermia improves neurological outcome when applied after cardiac arrest. In a 3-year randomized, prospective, multicenter clinical trial, we hypothesized that mild resuscitative cerebral hypothermia (32 degrees C to 34 degrees C core temperature) would improve neurological outcome after cardiac arrest. METHODS: We lowered patients' temperature after admission to the emergency department and continued cooling for at least 24 hours after arrest in conjunction with advanced cardiac life support. The cooling technique chosen was external head and total body cooling with a cooling device in conjunction with a blanket and a mattress. Infrared tympanic thermometry was monitored before a central pulmonary artery thermistor probe was inserted. RESULTS: In 27 patients (age 58 [interquartile range [IQR] 52 to 64] years; 7 women; estimated "no-flow" duration 6 [IQR 1 to 11] minutes and "low-flow" duration 15 [IQR 9 to 23] minutes; admitted to the emergency department 36 [IQR 24 to 43] minutes after return of spontaneous circulation), we could initiate cooling within 62 (IQR 41 to 75) minutes and achieve a pulmonary artery temperature of 33+/-1 degrees C 287 (IQR 42 to 401) minutes after cardiac arrest. During 24 hours of mild resuscitative hypothermia, no major complications occurred. Passive rewarming >35 degrees C was accomplished within 7 hours. CONCLUSIONS: Mild resuscitative hypothermia in patients is feasible and safe. A clinical multicenter trial might prove that mild hypothermia is a useful method of cerebral resuscitation after global ischemic states.

Brain↗

Electrical induction of ventricular fibrillation for resuscitation from postcountershock pulseless and asystolic cardiac arrests.

BACKGROUND: There is increasing evidence that defibrillation from prolonged ventricular fibrillation (VF) before CPR decreases survival. It remains unclear, however, whether harmful effects are due primarily to initial countershock of ischemic myocardium or to resultant postdefibrillation rhythms (ie, pulseless electrical activity [PEA] or asystole). METHODS AND RESULTS: We induced 15 dogs into 12 minutes of VF and randomized them to 3 groups. Group 1 was defibrillated at 12 minutes and then administered advanced cardiac life support (ACLS); group 2 was allowed to remain in VF and was subsequently defibrillated after 4 minutes of ACLS; group 3 was defibrillated at 12 minutes, electrically refibrillated, and then defibrillated after 4 minutes of ACLS. All group 1 and 3 animals were defibrillated into PEA/asystole at 12 minutes. After 4 minutes of ACLS, group 2 and 3 animals were effectively defibrillated into sinus rhythm. The extension of VF in group 2 and 3 subjects paradoxically resulted in shorter mean resuscitation times (251+/-15 and 245+/-7 seconds, respectively, versus 459+/-66 seconds for group 1; P<0.05) and improved 1-hour survival (10 of 10 group 2 and 3 dogs versus 1 of 5 group 1 dogs; Fisher's exact, P<0.005) compared with more conservatively managed group 1 subjects. CONCLUSIONS: Precountershock CPR during VF appears more conducive to resuscitation than CPR during postcountershock PEA or asystole. The intentional induction of VF may prove useful in the management of PEA and asystolic arrests.

Animals↗

Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest.

BACKGROUND: Despite improving arterial oxygen saturation and pH, bystander cardiopulmonary resuscitation (CPR) with chest compressions plus rescue breathing (CC+RB) has not improved survival from ventricular fibrillation (VF) compared with chest compressions alone (CC) in numerous animal models and 2 clinical investigations. METHODS AND RESULTS: After 3 minutes of untreated VF, 14 swine (32+/-1 kg) were randomly assigned to receive CC+RB or CC for 12 minutes, followed by advanced cardiac life support. All 14 animals survived 24 hours, 13 with good neurological outcome. For the CC+RB group, the aortic relaxation pressures routinely decreased during the 2 rescue breaths. Therefore, the mean coronary perfusion pressure of the first 2 compressions in each compression cycle was lower than those of the final 2 compressions (14+/-1 versus 21+/-2 mm Hg, P<0.001). During each minute of CPR, the number of chest compressions was also lower in the CC+RB group (62+/-1 versus 92+/-1 compressions, P<0.001). Consequently, the integrated coronary perfusion pressure was lower with CC+RB during each minute of CPR (P<0.05 for the first 8 minutes). Moreover, at 2 to 5 minutes of CPR, the median left ventricular blood flow by fluorescent microsphere technique was 60 mL. 100 g(-1). min(-1) with CC+RB versus 96 mL. 100 g(-1). min(-1) with CC, P<0.05. Because the arterial oxygen saturation was higher with CC+RB, the left ventricular myocardial oxygen delivery did not differ. CONCLUSIONS: Interrupting chest compressions for rescue breathing can adversely affect hemodynamics during CPR for VF.

Animals↗

Vasopressor effect of epinephrine with and without dopamine during cardiopulmonary resuscitation.

We prospectively studied nine prehospital cardiac arrest patients (six M, three F; aged 60 +/- 8 yr) to determine the vasopressor response following incremental (1, 3, and 5 mg) doses of intravenous epinephrine given 5 minutes apart with or without dopamine 15 micrograms/kg/min. All patients were in ventricular fibrillation on arrival of the paramedics and were not resuscitated with standard advanced cardiac life support therapy. Cardiopulmonary resuscitation (CPR) was performed with a computerized Thumper at 60 compressions/min with a 50:50 downstroke-to-upstroke ratio. All patients were intubated and received 12 ventilations/min at a fraction of inspired oxygen of 80 percent. Radial artery pressure was monitored through a #20 gauge radial artery catheter inserted by cutdown within ten minutes after arrival at the emergency room. Five patients received epinephrine alone (group A) and four received epinephrine plus dopamine (group B). The patient's age, paramedic response time, arterial blood gases, and initial diastolic blood pressure (BP) did not differ significantly between treatment groups. Baseline systolic BP was significantly higher (p less than 0.01) in group B (68 +/- 10 mm Hg) than in group A (35 +/- 5 mm Hg). Epinephrine produced a dose-dependent vasopressor response in group A, but not in group B. In group A, peak systolic BP following epinephrine 1, 3, and 5 mg was 57 +/- 20, 69 +/- 23, and 76 +/- 27 mm Hg, respectively (p less than 0.05 for 5 mg vs. baseline). No statistically significant difference was observed among the respective values in group B (81 +/- 13, 80 +/- 18, and 78 +/- 19 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗