The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure.

BACKGROUND AND OBJECTIVE: Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS: After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS: In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.     

Analysing ventricular fibrillation ECG-signals and predicting defibrillation success during cardiopulmonary resuscitation employing N(alpha)-histograms.

Mean fibrillation frequency may predict defibrillation success during cardiopulmonary resuscitation (CPR). N(alpha)-histogram analysis should be investigated as an alternative. After 4 min of cardiac arrest, and 3 versus 8 min of CPR, 25 pigs received either vasopressin or epinephrine (0.4, 0.4, and 0.8 U/kg vasopressin versus 45, 45, and 200 microg/kg epinephrine) every 5 min with defibrillation at 22 min. Before defibrillation, the N(alpha)-parameter histogramstart/histogramwidth and the mean fibrillation frequency in resuscitated versus non-resuscitated pigs were 2.9+/-0.4 versus 1.7+/-0.5 (P=0.0000005); and 9.5+/-1.7 versus 6.9+/-0.7 (P=0.0003). During the last minute prior to defibrillation, histogramstart/histogramwidth of > or =2.3 versus mean fibrillation frequency > or =8 Hz predicted successful defibrillation with subsequent return of a spontaneous circulation for more than 60 min with sensitivity, specificity, positive predictive value and negative predictive value of 94 versus 82%, 96 versus 89%, 98 versus 93% and 90 versus 74%, respectively. We conclude, that N(alpha)-analysis was superior to mean fibrillation frequency analysis during CPR in predicting defibrillation success, and distinction between vasopressin versus epinephrine effects.     

Prediction of countershock success using single features from multiple ventricular fibrillation frequency bands and feature combinations using neural networks

Targeted defibrillation therapy is needed to optimise survival chances of ventricular fibrillation (VF) patients, but at present VF analysis strategies to optimise defibrillation timing have insufficient predictive power. From 197 patients with in-hospital and out-of-hospital cardiac arrest, 770 electrocardiogram (ECG) recordings of countershock attempts were analysed. Preshock VF ECG features in the time and frequency domain were tested retrospectively for outcome prediction. Using band pass filters, the ECG spectrum was split into various frequency bands of 2-26 Hz bandwidth in the range of 0-26 Hz. Neural networks were used for single feature combinations to optimise prediction of countershock success. Areas under curves (AUC) of receiver operating characteristics (ROC) were used to estimate prediction power of single and combined features. The highest ROC AUC of 0.863 was reached by the median slope in the interval 10-22 Hz resulting in a sensitivity of 95% and a specificity of 50%. The best specificity of 55% at the 95% sensitivity level was reached by power spectrum analysis (PSA) in the 6-26 Hz interval. Neural networks combining single predictive features were unable to increase outcome prediction. Using frequency band segmentation of human VF ECG, several single predictive features with high ROC AUC>0.840 were identified. Combining these single predictive features using neural networks did not further improve outcome prediction in human VF data. This may indicate that various simple VF features, such as median slope already reach the maximum prediction power extractable from VF ECG.     

Preliminary results on the prediction of countershock success with fibrillation power

In a study of artifact-free ventricular fibrillation episodes in 54 patients, 28 of whom experienced return of spontaneous circulation (ROSC), the power of different indicators to predict the ROSC was compared. Taking the average of sensitivity, specificity and positive and negative predictive value, the dominant frequency reaches 76%, the mean amplitude 72% and fibrillation power 71%. There is little correlation between the three indicators.     

Variability in the assessment of advanced life support skills

The number of short 'life support' and emergency care courses available are increasing. Variability in examiner assessments has been reported previously in more traditional types of examinations but there is little data on the reliability of the assessments used on these newer courses. This study evaluated the reliability and consistency of instructor marking for the Resuscitation Council UK Advanced Life Support Course. Twenty five instructors from 15 centres throughout the UK were shown four staged video recorded defibrillation tests (one repeated) and three cardiac arrest simulation tests in order to assess inter-observer and intra-observer variability. These tests form part of the final assessment of competence on an Advanced Life Support course. Significant levels of variability were demonstrated between instructors with poor levels of agreement of 52-80% for defibrillation tests and 52-100% for cardiac arrest simulation tests. There was evidence of differences in the observation/recognition of errors and rating tendencies of instructors. Four instructors made a different pass/fail decision when shown defibrillation test 2 for a second time leading to only moderate levels of intra-observer agreement (kappa=0.43). In conclusion there is significant variability between instructors in the assessment of advanced life support skills, which may undermine the present assessment mechanisms for the advanced life support course. Validation of the assessment tools for the rapidly growing number of life support courses is required with urgent steps to improve reliability where required.     

Initial treatment of ventricular fibrillation: defibrillation or drug therapy

The belief that defibrillation of unwitnessed ventricular fibrillation frequently results in asystole, combined with perceived low survival rates, led to deviation from "standard" advanced cardiac life support (ACLS) by physicians directing paramedics in the field. In nonstandard ACLS, intubation or drug therapy preceded defibrillation. This study retrospectively compared standard and nonstandard ACLS for ventricular fibrillation. The long-term survival rates were 12.3% (7/57) and 3.6% (6/168) for the two forms of ACLS, respectively (p = 0.03). The incidence of postcountershock asystole was 35% and 28% (p = 0.45). The survival rates for patients with a postcountershock rhythm and a pulse were 83% and 17% after standard and nonstandard ACLS (p less than 0.0001). Other factors reported to have a significant effect on survival were compared, and no significant differences (p greater than 0.05) were noted for mean age, sex, cardiopulmonary resuscitation (CPR) initiated by a bystander, ACLS response time, time to CPR, lay-witnessed arrest, or time to definitive care. The significant difference in the time to defibrillation (14 and 26 minutes) was expected. This is the first clinical study to clearly confirm the ACLS recommendation of early defibrillation before drug therapy in ventricular fibrillation.     

Effects of epinephrine in a pig model of hypothermic cardiac arrest and closed-chest cardiopulmonary resuscitation combined with active rewarming

OBJECTIVE: The aim of the current study was to assess the effects of epinephrine in a pig model of hypothermic cardiac arrest followed by closed-chest cardiopulmonary resuscitation combined with active rewarming, simulating the clinical management of an arrested hypothermic patient in a hospital without cardiopulmonary bypass facilities. DESIGN: Prospective, randomized animal study. SETTING: University research laboratory. SUBJECTS: Twelve 12- to 16-week-old domestic pigs. INTERVENTIONS: Pigs were surface cooled to a body core temperature of 28 degrees C. After 4 min of untreated cardiac arrest, manual closed-chest CPR and thoracic lavage with 40 degrees C warmed fluid were started. After 3 min of external chest compression animals were randomly assigned to receive epinephrine (45, 45 and 200 microg/kg) or saline placebo in 5-min intervals. MEASUREMENTS AND MAIN RESULTS: Coronary perfusion pressure was about 15 mmHg in placebo group pigs. Coronary perfusion pressure was significantly higher after epinephrine, but restoration of spontaneous circulation was not more frequent (one of six epinephrine versus three of six saline placebo pigs, P=0.34). After 45 microg/kg epinephrine the arterial PO(2) was significantly lower when compared to the saline placebo. The third 200 microg/kg epinephrine dose resulted in a significantly enhanced mixed venous hypercarbic acidosis. CONCLUSIONS: After a short 4-min period of hypothermic cardiac arrest, epinephrine may not be necessary to maintain coronary perfusion pressure around the threshold usually correlating with successful defibrillation, even during prolonged closed-chest CPR combined with active rewarming. The enhanced mixed venous hypercarbic acidosis in epinephrine-treated animals may support the argument against repeated or high dose epinephrine administration during hypothermic CPR.     

The natural biochemical changes during ventricular fibrillation with cardiopulmonary resuscitation and the onset of postdefibrillation pulseless electrical activity

OBJECTIVE: The objective of this study was to document the biochemical changes during ventricular fibrillation (VF) with cardiopulmonary resuscitation (CPR), and to identify factors associated with postdefibrillation pulseless electrical activity (PD-PEA). BACKGROUND: It has been reliably estimated that as much as 60% of out-of-hospital sudden cardiac death can be attributed to the onset of PD-PEA (Niemann JT, Cruz B, Garner D et al. Immediate countershock versus CPR before countershock in a 5-minute swine model of ventricular fibrillation arrest. Ann Emerg Med 2000;36:543-6). Previous attempts to treat reversible causes of pulseless electrical activity have not been successful clinically (Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Outcome of out-of-hospital postcountershock asystole and pulseless electrical activity versus primary asystole and pulseless electrical activity. Crit Care Med 2001;29:2366-70). METHODS: This investigation used 22 studies on 14 anesthetized pigs breathing 100% oxygen. Ventricular fibrillation was induced with a right ventricular catheter electrode, and the chest was compressed with a pneumatically driven Chest Thumper (Michigan Instruments) (80-100 lb at 60/min). The electrocardiogram and aortic pressure were recorded continuously. Arterial pH, P(O2), P(CO2), Na+, K+, Ca2+, Cl-, SaO2, glucose, hematocrit, and hemoglobin level were measured at selected times. Ventricular defibrillation was achieved with transchest electrodes. RESULTS: Typically, during VF with CPR, mean aortic pressure was 20 to 25 mm Hg. In all cases aortic P(O2) decreased to about 20% of the initial value in 10 minutes, and aortic blood K+ increased by 50% in 6 minutes. By 5 to 8 minutes, the incidence of PD-PEA was 50%. CONCLUSION: Ventricular fibrillation duration, arterial K+, and arterial P(CO2) were statistically correlated with the onset of PD-PEA in this study. In addition, trends suggest an association of mean arterial blood pressure and arterial P(O2) with the onset of PD-PEA.     

Mild hypothermic cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs

BACKGROUND AND METHODS: This study was designed to explore the effect of mild cerebral and systemic hypothermia (34 degrees C) on outcome after prolonged cardiac arrest in dogs. After ventricular fibrillation with no flow of 10 min, and standard external CPR with epinephrine (low flow) from ventricular fibrillation time of 10 to 15 min, defibrillation and restoration of spontaneous normotension were between ventricular fibrillation time of 16 and 20 min. This procedure was followed by controlled ventilation to 20 hr postarrest and intensive care to 72 hr postarrest. In control group 1 (n = 10), core temperature was 37.5 degrees C; in control group 2 (n = 10), cooling was started immediately after restoration of spontaneous normotension; and in group 3 (n = 10), cooling was initiated with start of CPR. Cooling was by clinically feasible methods. RESULTS: Best overall performance categories achieved (1 = normal; 5 = brain death) were better in group 2 (p = .012) and group 3 (p = .005) than in group 1. Best neurologic deficit scores were 36 +/- 14% in group 1, 22 +/- 15% in group 2 (p = .02), and 19 +/- 18% in group 3 (p = .01). Brain histopathologic damage scores were also lower (better) in groups 2 (p = .05) and 3 (p = .03). Myocardial damage was the same in all three groups. CONCLUSION: Mild cerebral hypothermia started during or immediately after external CPR improves neurologic recovery.     

Predicting defibrillation success by 'genetic' programming in patients with out-of-hospital cardiac arrest

BACKGROUND: In some patients with ventricular fibrillation (VF) there may be a better chance of successful defibrillation after a period of chest compression and ventilation before the defibrillation attempt. It is therefore important to know whether a defibrillation attempt will be successful. The predictive power of a model developed by 'genetic' programming (GP) to predict defibrillation success was studied. METHODS AND RESULTS: 203 defibrillations were administered in 47 patients with out-of-hospital cardiac arrest due to a cardiac cause. Maximal amplitude, a total energy of power spectral density, and the Hurst exponent of the VF electrocardiogram (ECG) signal were included in the model developed by GP. Positive and negative likelihood ratios of the model for testing data were 35.5 and 0.00, respectively. Using a model developed by GP on the complete database, 120 of the 124 unsuccessful defibrillations would have been avoided, whereas all of the 79 successful defibrillations would have been administered. CONCLUSION: The VF ECG contains information predictive of defibrillation success. The model developed by GP, including data from the time-domain, frequency-domain and nonlinear dynamics, could reduce the incidence of unsuccessful defibrillations.     

Left Ventricular Function after Monophasic and Biphasic Waveform Defibrillation: The Impact of Cardiopulmonary Resuscitation Time on Contractile Indices

Previous work has suggested that low-energy biphasic waveform defibrillation (BWD) is followed by less post-resuscitation left ventricular (LV) dysfunction when compared with higher-energy monophasic waveform defibrillation (MWD). To the best of the authors' knowledge, the effect of cardiopulmonary resuscitation (CPR) duration and total ischemia time on LV function after countershock, controlling for waveform type, has not been evaluated. OBJECTIVE: To determine the effect of CPR duration on LV function after MWD and BWD. METHODS: VF was electrically induced in anesthetized and instrumented swine. After 5 minutes of VF, the animals were randomized to MWD (n = 22) or one of two BWDs (n = 46). If countershock terminated VF but was followed by a nonperfusing rhythm, conventional manual CPR without drug therapy was performed until restoration of spontaneous circulation (ROSC), defined as a systolic arterial pressure >60 mm Hg for 10 minutes without vasopressor support. Systolic LV pressure (LVP), LV dP/dt (first derivative of pressure measured over time), and cardiac output (CO) were measured at intervals for 60 minutes postresuscitation. CPR times (times to ROSC) and hemodynamic variables for the three groups were compared. Multivariable linear regression was performed to assess the contribution of defibrillation waveform, total joules, and CPR time on LVP, LV dP/dt, and CO at 15, 30, and 60 minutes postresuscitation. RESULTS: When analyzed as groups, significant differences in median number of shocks to terminate VF, total joules, or CPR time were not observed between waveform groups. Regression analysis demonstrated that increasing CPR time was associated with a significant effect on indices of LV function at 15 and 30 minutes postresuscitation. Global LV function was not influenced by waveform type or total joules. CONCLUSIONS: Adjustment for CPR time, a determinant of total myocardial ischemia time, is necessary when defibrillation waveforms are compared for their effect on postresuscitation cardiac function and short-term outcome.     

Decrease in the occurrence of ventricular fibrillation as the initially observed arrhythmia after out-of-hospital cardiac arrest during 11 years in Sweden

Aim: To describe the change in the occurrence of ventricular fibrillation as initially observed arrhythmia among patients suffering from out-of-hospital cardiac arrest in Sweden. Patients: All patients included in the Swedish cardiac arrest registry between 1991 until 2001. The registry covers 85% of the population in Sweden. Methods: All patients with bystander witnessed out-of-hospital cardiac arrest included in the Swedish Cardiac Arrest Registry between 1991 and 2001 from the same ambulance organisation each year were included in the survey. Results: Over 11 years, among patients in Sweden with a bystander witnessed out-of-hospital cardiac arrest in whom cardiopulmonary resuscitation (CPR) was attempted (n=9666), the occurrence of ventricular fibrillation as the initially obseved arrhythmia decreased from 45% in 1991 to 28% in 2001 (P<0.0001) if the arrest occurred at home, and from 57% to 41% if the arrest occurred outside home (P<0.0001). This was found despite the fact that the proportion who received bystander CPR increased from 29% in 1991 to 39% in 2001 if the arrest occurred at home (P<0.0001) and from 54% to 60% if the arrest occurred outside home (NS). There was a significant increase in age among patients with out-of-hospital cardiac arrest at home, no change in the estimated interval between collapse and call but an increase in the interval between call and arrival of the ambulance among patients with out-of-hospital cardiac arrest outside home. Conclusion: During 11 years in Sweden, there was a marked decrease in the proportion of patients found in ventricular fibrillation among patients with a bystander witnessed cardiac arrest regardless whether the arrest occurred at home or outside home. A modest increase in age and interval between call for, and arrival of, the ambulance was associated with these findings.     

犬室颤心脏骤停模型的研究与改进

目的建立一种简单、有效、稳定的犬心脏骤停（CA）模型,为心肺脑复苏的实验研究奠定基础。方法选用健康成年犬30只,体质量（15±2）kg,雌雄不限,麻醉后经右颈外静脉置电极导管至右心室,以5mA电流诱发室颤的方法制作CA模型,根据CA时间不同随机分为CA3 min组、CA5 min组和CA8 min组,每组10只,随后进行电除颤及标准胸外心肺复苏术,比较各组的复苏成功率及存活情况。结果诱颤后所有犬心电图均显示室颤波,动脉血压下降并失去波动;各组自主循环恢复（ROSC）情况为CA 3min组：90％（9／10）、CA5min：80％（8／10）、CA8min：20％（2／10）;ROSC率CA3 min组和CA5 min组比较差异无统计学意义（P〉0.05）,CA8 min组与其他2组之间比较差异具有统计学意义（P〈0.05）;CA3rain组与CA5min、CA8 min组存活时间比较差异有统计学意义（P〈0.05）。结论犬经右心室导管诱发室颤制作的心脏骤停模型稳定且可靠,CA3 min后开始复苏具有较好的ROSC率和存活时间,能满足心肺脑复苏基础研究的需要。     

Comparison of epinephrine and norepinephrine in the treatment of asphyxial or fibrillatory cardiac arrest in a porcine model

Many animal experiments have shown that alpha-receptor stimulation is a prerequisite for the improvement of myocardial perfusion during CPR. As there are no recent reports on the effectiveness of norepinephrine in the treatment of cardiac arrest, we investigated the effectiveness of epinephrine and norepinephrine after asphyxial or ventricular fibrillation cardiac arrest using a porcine model. After 3 min of asphyxial cardiac arrest, seven animals each received either 45 micrograms/kg epinephrine, 45 micrograms/kg norepinephrine, or placebo (controls). All drugs were given blind. All seven animals given epinephrine could be resuscitated after 174 +/- 53 sec, whereas six of seven given norepinephrine could be resuscitated after 473 +/- 116 sec. None of the seven given the placebo could be resuscitated. After 4 min of ventricular fibrillation cardiac arrest, none of the seven animals that received defibrillating countershocks at 4 min without either mechanical measures or drug therapy, and none of the seven that received CPR and countershocks but no drugs, could be resuscitated. In the group that received CPR plus 45 micrograms/kg epinephrine, defibrillation and restoration of spontaneous circulation were achieved in six of seven animals in 667 +/- 216 sec. In the group that received CPR plus 45 micrograms/kg norepinephrine, defibrillation and restoration of spontaneous circulation were achieved in all seven animals in the significantly shorter time of 86 +/- 18 sec. In this porcine model, norepinephrine appeared superior to the same dose of epinephrine in the treatment of ventricular fibrillation, with respect to resuscitation time.     

Diltiazem improves resuscitation from experimental ventricular fibrillation in dogs.

OBJECTIVE: To determine the effect of diltiazem on survival immediately after cardiac arrest and cardiopulmonary resuscitation (CPR) in dogs. DESIGN: Prospective, double-blind, randomized trial. SETTING: Laboratory at a large, university-affiliated medical center. SUBJECTS: Twenty-eight mongrel dogs, weighing 12 to 16 kg. INTERVENTIONS: After the administration of anesthesia, catheters were placed in the pulmonary artery, aortic arch, left ventricle, right ventricle, and great cardiac vein (12 dogs) for sample collection, pressure determinations, and induction of ventricular fibrillation. Dogs were randomized to receive either diltiazem, calcium chloride, or placebo (saline) either before or early during CPR. Dogs underwent 3 mins of unassisted fibrillatory arrest followed by 10 mins of standard CPR using a pneumatic device. After 13 mins of ventricular fibrillation, defibrillation was attempted repeatedly for less than or equal to 10 mins. Successful resuscitation was defined as an organized rhythm with an unassisted systolic BP of greater than 60 mm Hg for greater than or equal to 2 mins. MEASUREMENTS AND MAIN RESULTS: The resuscitation rate was significantly greater in diltiazem-treated animals (100%) than in those dogs receiving calcium (57%) or placebo (29%). Diltiazem-treated animals were resuscitated faster and required fewer defibrillation attempts than did dogs in the other groups. During CPR, coronary artery perfusion pressure and blood gases (arterial, venous, and myocardial) were similar among treatment groups. CONCLUSIONS: Diltiazem improves the resuscitation from experimentally induced ventricular fibrillation when administered before or early during CPR. This response may have important clinical implications in the treatment of patients undergoing cardiac arrest and CPR.     

Adenosine during cardiac arrest and cardiopulmonary resuscitation: a placebo-controlled, randomized trial.

BACKGROUND AND HYPOTHESIS TESTED: The effects of adenosine (100 micrograms/kg/min; n = 7) were examined during rodent cardiopulmonary resuscitation (CPR). Change in coronary artery perfusion pressure, end-tidal PCO2, and arterial acid-base status of anesthetized, male, Sprague-Dawley rats were compared with CPR controls (0.9% sodium chloride; n = 7) and with sham controls (n = 9). Sustained ventricular fibrillation was induced and precordial chest compression was followed by defibrillation. RESULTS: After 6 mins of cardiac arrest, six (86%) of seven adenosine-treated animals were resuscitated after adenosine infusion and four (57%) of seven control animals were resuscitated after sodium chloride infusion. During chest compression, coronary artery perfusion pressure was 7 +/- 2 mm Hg after adenosine, but was 22 +/- 3 mm Hg in the controls (p less than .01). Parallel decreases were observed in mean aortic pressure. Arterial and end-tidal PCO2 significantly (p less than .01) decreased after adenosine. These changes contrasted with a second control group of nine identically prepared animals which, in the absence of ventricular fibrillation and subsequent chest compression, demonstrated no changes in hemodynamic, respiratory, or blood gas variables. CONCLUSIONS: Adenosine decreased coronary artery perfusion pressure. However, despite marked reductions in coronary artery perfusion pressure, survival was not compromised after adenosine infusion in this rodent model of CPR.     

The three-phase model of cardiac arrest as applied to ventricular fibrillation in a large, urban emergency medical services system

BACKGROUND: Cardiac arrest is responsible for significant morbidity and mortality, with consistently poor outcomes despite the rapid availability of prehospital personnel for defibrillation attempts in patients with ventricular fibrillation (VF). Recent evidence suggests a period of cardiopulmonary resuscitation (CPR) prior to defibrillation attempts may improve outcomes in patients with moderate time since collapse (4-10 min). OBJECTIVES: To determine cardiac arrest outcomes in our community and explore the relationship between time since collapse, performance of bystander CPR, and survival. METHODS: Non-traumatic cardiac arrest data were collected prospectively over an 18-month period. Patients were excluded for: age <18 years, a "Do Not Attempt Resuscitation" (DNAR) directive, determination of a non-cardiac etiology for arrest, and an initially recorded rhythm other than VF. Patients were stratified by time since collapse (<4, 4-10, > 10 min, and unknown) and compared with regard to survival and neurological outcome. In addition, patients with and without bystander CPR were compared with regard to survival. RESULTS:: A total of 1141 adult non-traumatic cardiac arrest victims were identified over the 18-month study period. This included 272 patients with VF as the initially recorded rhythm. Of these, 185 had a suspected cardiac etiology for the arrest; survival to hospital discharge was 15% in this group, with 82% of these having a good outcome or only moderate disability. Survival was highest among patients with time since collapse of less than 4 min and decreased with increasing time since collapse. There were no survivors among patients with time since collapse greater than 10 min. Among patients with time since collapse of 4 min or longer, survival was significantly higher with the performance of bystander CPR; there was no survival advantage to bystander CPR among patients with time since collapse less than 4 min. CONCLUSIONS: The performance of bystander CPR prior to defibrillation by EMS personnel is associated with improved survival among patients with time since collapse longer than 4 min but not less than 4 min. These data are consistent with the three-phase model of cardiac arrest.     

Multifocal cerebral blood flow by Xe-CT and global cerebral metabolism after prolonged cardiac arrest in dogs. Reperfusion with open-chest CPR or cardiopulmonary bypass.

Using the stable xenon-enhanced computed tomography (Xe-CT) method in dogs, we studied local, regional and global cerebral blood flow (LCBF, rCBF and gCBF) in two sham experiments and nine cardiac arrest experiments. Within the same experiments without arrest, gCBF and rCBF values were reproducible and stable. LCBF values varied over time. In group I (n = 4), ventricular fibrillation cardiac arrest (no blood flow) of 10 min was reversed by open-chest cardiopulmonary resuscitation (CPR). In group II (n = 5), ventricular fibrillation cardiac arrest of 12.5 min was reversed by brief closed-chest cardiopulmonary bypass. This was followed by controlled ventilation, normotension, normoxia, normocarbia and normothermia to 4 h (n = 7) or 20 h (n = 2) postarrest. The postarrest CBF patterns were similar in both groups. Open-chest CPR during ventricular fibrillation generated near-baseline gCBF and lower LCBF ranges. During postarrest spontaneous circulation, transient diffuse hyperemia was without low-flow regions, longer in brain stem and basal ganglia than in neocortex. During delayed hypoperfusion at 1-4 h postarrest (n = 9), mean gCBF was 44-60% baseline, rCBF in primarily gray matter regions was 15-49 ml/100 cm3 per min and LCBF voxels with trickle-flow and low-flow values, in percent of CT cut area, were increased over baseline. Global CMRO2 (n = 3 of group II) recovered to near baseline values between 1 and 4 h postarrest, while gCBF and O2 delivery were about 50% baseline (mismatching of O2 uptake and O2 delivery).     

Effect of epinephrine on defibrillation in ischemic ventricular fibrillation

Epinephrine is thought to improve the success of defibrillation with countershock therapy. However, a recent study failed to show any effect of epinephrine in dogs with normal coronary arteries undergoing electrically-induced ventricular fibrillation (VF). In the current study, the effects of epinephrine were examined in dogs with coronary occlusion undergoing both spontaneous and electrically-induced fibrillation. Forty pentobarbital-anesthetized dogs were prepared by placing snares around the circumflex and left anterior descending coronary arteries. Fibrillation and subsequent resuscitation were carried out with one coronary artery occluded. Dogs were randomly allocated so that half of the animals underwent spontaneous fibrillation and half were electrically fibrillated. In addition, half received epinephrine (1 mg) during resuscitation and half received normal saline solution (1 ml). After 3 minutes of cardiac arrest, cardiopulmonary resuscitation (CPR) was begun, and 30 seconds later epinephrine or saline were injected. One minute later defibrillation was attempted using successive stored energy doses of 1, 2, 4, 8, 16, and 32 J/kg. Delivered energy and transthoracic impedance were measured for each countershock. Successful defibrillation was defined as conversion to any rhythm other than VF or ventricular tachycardia that degenerated in VF within 10 seconds. No other drugs were given during resuscitation. Neither the type of fibrillation (electrically-induced versus spontaneous) or drug therapy (epinephrine versus placebo) had a significant effect on the incidence of defibrillation or the energy necessary for successful defibrillation. Epinephrine did significantly increase the incidence of resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden cardiac death: directing the scope of resuscitation towards the heart and brain

BACKGROUND: The fundamental goal of cardiopulmonary resuscitation (CPR) is recovery of the heart and the brain. This is best achieved by (1) immediate CPR for coronary and cerebral perfusion, (2) correction of the cause of cardiac arrest, and (3) controlled cardioplegic cardiac reperfusion. Failure of such an integrated therapy may cause permanent brain damage despite cardiac resuscitation. METHODS: This strategy was applied at four centers to 34 sudden cardiac death patients (a) after acute myocardial infarction (n = 20), (b) "intraoperatively" following successful discontinuation of cardiopulmonary bypass (n = 4), and (c) "postoperatively" in the surgical ICU (n = 10). In each witnessed arrest the patient failed to respond to conventional CPR with ACLS interventions, including defibrillation. The cardiac arrest interval was 72 +/- 43 min (20-150 min). Compression and drugs maintained a BP > 60 mmHg to avoid cerebral hypoperfusion. Operating room (OR) transfer was delayed until the blood pressure was monitored. In four patients femoral bypass maintained perfusion while an angiographic diagnosis was made. RESULTS: Management principles included no repeat defibrillation attempts after 10 min of unsuccessful CPR, catheter-monitored peak BP > 60 mmHg during diagnosis and transit to the operating room, left ventricular venting during cardiopulmonary bypass and 20 min global and graft substrate enriched blood cardioplegic reperfusion. Survival was 79.4% with two neurological complications (5.8%). CONCLUSIONS: Recovery without adverse neurological outcomes is possible in a large number of cardiac arrest victims following prolonged manual CPR. Therapy is directed toward maintaining a monitored peak BP above 60 mmHg, determining the nature of the cardiac cause, and correcting it with controlled reperfusion to preserve function.