Improved survival and reduced myocardial necrosis with cardiopulmonary bypass reperfusion in a canine model of coronary occlusion and cardiac arrest

STUDY QUESTION: Does cardiopulmonary bypass (CPB) improve resuscitation rates and limit infarct size after cardiac arrest and acute myocardial infarction? DESIGN: Controlled randomized trial with all animals undergoing left anterior descending coronary artery occlusion and subsequent ventricular fibrillation and resuscitation. All animals were supported for four hours after resuscitation in an intensive care setting. INTERVENTION: Group 1 (eight) was resuscitated with standard external CPR and advanced life support. Group 2 (eight) was resuscitated with CPB. MEASUREMENTS AND MAIN RESULTS: Group hemodynamic, resuscitation variables, number resuscitated, and number of four-hour survivors were compared. Ischemic and necrotic myocardial weights were determined with histochemical staining techniques in four-hour survivors. Infarct size was measured as the ratio of necrotic weight to ischemic weight. Significantly fewer dogs were resuscitated in group 1 (four of eight) than in group 2 (eight of eight) (P less than .05). Group 2 survivors required significantly less epinephrine and lidocaine than group 1 survivors (P less than .05) and higher aortic diastolic and coronary perfusion pressures after CPB (P less than .001). The ratio of myocardial necrotic weight to ischemic weight at four hours was 0.82 +/- 0.25 in group 1 and 0.22 +/- 0.25 in group 2 (P less than .05). However, collateral blood flow was not measured in this study. CONCLUSION: This pilot study further substantiates the improvement in resuscitation rates obtainable with CPB. CPB may also limit infarct size during the postresuscitation period and requires further study.     

Comparison of standard external CPR, open-chest CPR, and cardiopulmonary bypass in a canine myocardial infarct model

STUDY OBJECTIVES: After cardiac arrest, open-chest CPR (OCCPR) and cardiopulmonary bypass (CPB) have demonstrated higher resuscitation rates when compared individually with standard external CPR (SECPR). We compared all three techniques in a canine myocardial infarct ventricular fibrillation model. TYPE OF PARTICIPANTS: Twenty-six mongrel dogs were block-randomized to receive SECPR and advanced life support (nine), CPB (nine), or OCCPR (eight). DESIGN AND INTERVENTIONS: All dogs received left anterior descending coronary artery occlusion followed by four minutes of ventricular fibrillation without CPR and eight minutes of Thumper CPR. At 12 minutes, dogs received one of three resuscitation techniques. After resuscitation, all animals received four hours of intensive care. Animals that were resuscitated had histochemical determination of ischemic and necrotic myocardial areas. MEASUREMENTS: Intravascular pressures were measured and coronary perfusion pressure was calculated during baseline, cardiac arrest, resuscitation, and postresuscitation periods. Percent necrotic myocardium, percent ischemic myocardium, and necrotic-to-ischemic ratios were determined for resuscitated animals. Epinephrine dosage and number of countershocks were determined for each group. MAIN RESULTS: Nine of nine CPB and six of nine OCCPR, compared with two of eight SECPR animals, were resuscitated (P less than .01). Three of nine CPB and OCCPR and two of eight SECPR dogs survived to four hours (P = NS). Coronary perfusion pressure two minutes after institution of technique was significantly higher with CPB (75 +/- 37 mm Hg) and OCCPR (56 +/- 31 mm Hg) than in SECPR animals (16 +/- 16 mm Hg, P less than .04). Epinephrine required for resuscitation was significantly less with CPB (0.10 +/- 0.02 mg/kg) than for SECPR (0.28 +/- 0.11 mg/kg, P less than .002). The ratio of necrotic to ischemic myocardium at four hours was significantly lower with CPB (0.15 +/- 0.31) and OCCPR (0.39 +/- 0.25) than for SECPR (1.16 +/- 0.31, P less than .02). CONCLUSION: OCCPR and CPB produce higher coronary perfusion pressures and improved resuscitation rates from ventricular fibrillation when compared with SECPR in this canine myocardial infarct cardiac arrest model. CPB and OCCPR yielded similar resuscitation results, although less epinephrine was required with CPB.     

Neurologic benefits from the use of early cardiopulmonary resuscitation

The efficacy of bystander CPR in resuscitation from cardiac arrest when defibrillation is available within five to six minutes has been questioned. Epidemiologic studies from different cities have shown conflicting results. We conducted a study to determine the effect of early CPR versus no CPR on resuscitability, 24-hour survival, and neurologic deficit in an animal model of cardiac arrest. Twenty-two mongrel dogs were subjected to five minutes of electrically induced ventricular fibrillation. In 11 dogs, closed-chest massage and ventilation with room air was begun immediately and was continued for five minutes. The other 11 dogs received no CPR. At five minutes defibrillation was attempted and advanced cardiac life support (ACLS) protocols were followed until the animal was resuscitated or died. No statistical difference in resuscitability or 24-hour survival between the two groups was demonstrated. Eight of 11 "early CPR" animals were resuscitated and survived 24 hours; six of 11 "no CPR" dogs were resuscitated, and five lived for 24 hours. A significant difference was demonstrated by the Student t test in neurologic deficit and ease of resuscitation. "Early CPR" dogs had no neurologic deficit, while "no CPR" dogs had a 41% deficit (P less than .01). "Early CPR" dogs were resuscitated in significantly less time once ACLS was started (29 versus 317 seconds), and required less electrical energy (100 versus 560 J), fewer countershocks (1.3 versus 4.0), and less epinephrine (0.1 versus 1.7 mg) than did "no CPR" animals. In this animal model of cardiac arrest, early CPR was shown to be beneficial to neurologic function and ease of resuscitation, even when ACLS was provided within five minutes.     

Comparison of epinephrine and phenylephrine for resuscitation and neurologic outcome of cardiac arrest in dogs

A study was done comparing resuscitability and 24-hour neurologic outcome in fibrillating dogs that were treated with either phenylephrine (a primary alpha agonist) or epinephrine. Ventricular fibrillation was induced electrically in 18 dogs. After three minutes, standard CPR was instituted using a mechanical resuscitator. Dogs were given phenylephrine or epinephrine at nine minutes and defibrillation was attempted at 12 minutes. Dogs underwent hemodynamic monitoring and pharmacologic support, if necessary, for an additional 90 minutes. At four, eight, 12, and 24 hours, a standard neurologic examination was performed and deficit scores were assigned by an observer blinded to the drug given. Fourteen of the 18 dogs were resuscitated. There were no statistically significant differences in the epinephrine- or phenylephrine-treated groups with regard to number of animals resuscitated, time and interventions required for resuscitation, initial cardiac rhythm post resuscitation, or occurrence of ventricular fibrillation during resuscitation. No differences were found in arterial, central venous, or myocardial perfusion pressures during CPR. Phenylephrine-treated dogs tended to have higher mean pressures in the critical care period (15 to 30 minutes), although this was not significant. Total neurologic deficit scores were 127.8 +/- 83.8 for the phenylephrine-treated group and 129.4 +/- 87.4 for the epinephrine group. No significant differences were found in the level of consciousness, cranial nerve function, motor skills, or general behavior scores. We conclude that there is no difference in neurologic or cardiovascular outcome when phenylephrine is compared to epinephrine in a canine model of cardiac arrest and cardiopulmonary resuscitation.     

Cardiopulmonary bypass after cardiac arrest and prolonged closed-chest CPR in dogs

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)     

Cardiopulmonary bypass in a model of acute myocardial infarction and cardiac arrest

Cardiopulmonary bypass (CPB) reperfusion has demonstrated improved resuscitation rates in ventricular fibrillation cardiac arrest models. To investigate the effectiveness of CPB reperfusion in an ischemic cardiac arrest setting, simulating the clinical scenario of myocardial ischemia preceding sudden cardiac death, we developed a canine model of acute myocardial infarction followed by ventricular fibrillation. Sixteen dogs were randomly assigned to two groups. Group 1 (eight) had ventricular fibrillation induced without left anterior descending coronary artery occlusion. Group 2 (eight) had a thrombogenic copper coil placed in the left anterior descending artery and showed ECG evidence of acute myocardial infarction before induction of ventricular fibrillation. CPR commenced after eight minutes of ventricular fibrillation. Epinephrine 0.05 mg/kg and NaHCO3 1.0 mEq/kg were administered at ten minutes. CPB was begun at 12 minutes and continued for one hour. Myocardial ischemic and necrotic areas were determined in four-hour survivors by dual histochemical staining. All animals were resuscitated; all eight group 1 and six of eight group 2 animals survived to four hours. With the onset of CPB, coronary perfusion pressures increased significantly by 68.6 +/- 31.8 (SD) mm Hg in group 1 and 56.2 +/- 34.6 mm Hg in group 2 over those obtained with CPR (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Survival with full neurologic recovery and no cerebral pathology after prolonged cardiopulmonary resuscitation with vasopressin in pigs

OBJECTIVES: We sought to determine the effects of vasopressin and saline placebo in comparison with epinephrine on neurologic recovery and possible cerebral pathology in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). BACKGROUND: It is unknown whether increased cerebral blood flow during CPR with vasopressin is beneficial with regard to neurologic recovery or detrimental owing to complications such as cerebral edema after return of spontaneous circulation. METHODS: After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive every 5 min either vasopressin (0.4, 0.4 and 0.8 U/kg; n = 6), epinephrine (45, 45 and 200 microg/kg; n = 6) or saline placebo (n = 5). The mean value +/- SEM of aortic diastolic pressure was significantly (p < 0.05) higher 90 s after each of three vasopressin versus epinephrine versus saline placebo injections (60 +/- 3 vs. 45 +/- 3 vs. 29 +/- 2 mm Hg; 49 +/- 5 vs. 27 +/- 3 vs. 23 +/- 1 mm Hg; and 50 +/- 6 vs. 21 +/- 3 vs. 16 +/- 3 mm Hg, respectively). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve return of spontaneous circulation. RESULTS: All the pigs that received epinephrine and saline placebo died, whereas all pigs on vasopressin survived (p < 0.05). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology. CONCLUSIONS: During prolonged CPR, repeated vasopressin administration, but not epinephrine or saline placebo, ensured long-term survival with full neurologic recovery and no cerebral pathology in this porcine CPR model.     

Use of cardiopulmonary bypass, high-dose epinephrine, and standard-dose epinephrine in resuscitation from post-countershock electromechanical dissociation.

STUDY OBJECTIVE: To determine the effects of cardiopulmonary bypass with standard-dose epinephrine, high-dose epinephrine, and standard-dose epinephrine on perfusion pressures, myocardial blood flow, and resuscitation from post-countershock electromechanical dissociation. DESIGN: Prospective, controlled laboratory investigation using a canine cardiac arrest model randomized to receive one of three resuscitation therapies. INTERVENTIONS: After the production of post-countershock electromechanical dissociation, 25 animals received ten minutes of basic CPR and were randomized to receive cardiopulmonary bypass with standard-dose epinephrine, high-dose epinephrine, or standard-dose epinephrine. MEASUREMENTS AND MAIN RESULTS: Myocardial blood flow was measured using a colored microsphere technique at baseline, during basic CPR, and after intervention. Immediate and two-hour resuscitation rates were determined for each group. Return of spontaneous circulation was achieved in eight of eight cardiopulmonary bypass with standard-dose epinephrine compared with four of eight high-dose epinephrine and three of eight standard-dose epinephrine animals (P less than .04). One animal was resuscitated with CPR alone and was excluded. Survival to two hours was achieved in five of eight cardiopulmonary bypass with standard-dose epinephrine, four of eight high-dose epinephrine, and three of eight standard-dose epinephrine animals (NS). Coronary perfusion pressure increased significantly in the cardiopulmonary bypass with standard-dose epinephrine group when compared with the other groups (cardiopulmonary bypass with standard-dose epinephrine, 76 +/- 45 mm Hg; high-dose epinephrine, 24 +/- 12 mm Hg; standard-dose epinephrine, 3 +/- 14 mm Hg; P less than .005). Myocardial blood flow was higher in cardiopulmonary bypass with standard-dose epinephrine and high-dose epinephrine animals compared with standard-dose epinephrine animals but did not reach statistical significance. Cardiac output increased during cardiopulmonary bypass with standard-dose epinephrine (P = .001) and standard-dose epinephrine (NS) compared with basic CPR but decreased after epinephrine administration in the high-dose epinephrine group (NS). CONCLUSION: Resuscitation from electromechanical dissociation was improved with cardiopulmonary bypass and epinephrine compared with high-dose epinephrine or standard-dose epinephrine alone. However, there was no difference in survival between groups. Cardiopulmonary bypass with standard-dose epinephrine resulted in higher cardiac output, coronary perfusion pressure, and a trend toward higher myocardial blood flow. A short period of cardiopulmonary bypass with epinephrine after prolonged post-countershock electromechanical dissociation cardiac arrest can re-establish sufficient circulation to effect successful early resuscitation.     

Resuscitation of dogs from cold-water submersion using cardiopulmonary bypass

In cold-water drowning, attempts at restoration of spontaneous circulation (ROSC) by external cardiopulmonary resuscitation (CPR) often fail. We explored the longest period of asphyxial cardiac arrest from cold-water submersion (without inhalation of water) from which ROSC is possible using cardiopulmonary bypass (CPB). In 19 lightly anesthetized dogs the tracheal tube was clamped (simulating laryngospasm) and the dogs were immersed in ice water from 20, 40, 60, 90, or 120 minutes. Cardiac arrest occurred after six to 11 minutes of submersion. At start of resuscitation, rectal temperature ranged from 21 C (after 60 minutes) to 34 C (after 20 minutes of submersion), and cerebral temperature was between 7 C (after 120 minutes) and 27 C (after 20 minutes submersion). Resuscitation attempts were performed according to protocol in 16 dogs, using only CPB by venoarterial pumping with an oxygenator and a heat exchanger. Priming was with 400 to 800 mL Dextran 40 and Ringer's solution 1:1 plus heparin. CPB flows were 10 mL/kg/min, and they increased to achieve normotension and return of rectal temperature to 32 C. After one-half to three hours, of CPB, ROSC was successful in 75%. This percentage included one of three dogs after 90 minutes submersion, but not in the one dog after 120 minutes submersion. Spontaneous breathing and EEG activity returned in 56% at two to 24 hours, after 20 to 90 minutes of submersion. Failure of ROSC attempts apparently were due to clotting in large vessels during arrest and capillary leakage during reperfusion. CPB is effective for ROSC after prolonged hypothermic cardiac arrest, and it should be evaluated in animal outcome studies.     

Early amelioration of neurologic deficit by lidoflazine after fifteen minutes of cardiopulmonary arrest in dogs

A prospective, controlled, blind study was done to test the effect of a calcium entry blocker on the neurologic integrity of dogs after cardiopulmonary arrest. Ten male mongrel dogs were anesthetized, prepared with sterile technique, and instrumented for pulmonary arterial (PA) and systematic arterial pressure monitoring. A left thoracotomy and pericardotomy were performed. Cardiac arrest was produced by injecting KCl (1 mEq/kg) through the PA line, and the respirator was stopped. Full arrest was maintained for 15 minutes. Thereafter, the dogs were resuscitated with ventilation, internal massage, fluids, bicarbonate, epinephrine, and internal defibrillation. All dogs were resuscitated within 6 to 10 minutes. Five control dogs received saline placebo, and five dogs were treated with lidoflazine (1 mg/kg) IV drip immediately post resuscitation. All dogs were scored neurologically every two hours by a deficit grading scale. All treated dogs had spontaneous ventilation, reactive pupils and corneals, voluntary movements, and responses to tactile stimulation at 12 hours post resuscitation. Four of five control dogs had maximum deficit scores without improvement. The difference in neurologic scores between the treated and control groups became increasingly divergent with time, and was statistically significant (P less than .05) by four hours post resuscitation. Thus the calcium antagonist lidoflazine produces improvement in neurologic recovery in the first 12 hours after cardiopulmonary arrest in dogs.     

Lactic acidosis during closed-chest CPR in dogs

Survival after out-of-hospital cardiac arrest is intimately related to the time from cardiovascular collapse to the initiation of CPR, or downtime. Furthermore, the reperfusion technique that optimizes coronary and cerebral blood flow after cardiac arrest may also be dependent on downtime. Peak blood lactate levels have been shown to be unchanged throughout resuscitation and predictive of downtime in dogs subjected to cardiopulmonary arrest and open cardiac massage. The purpose of this study was to determine the course of arterial lactate levels in dogs subjected to a fibrillatory cardiopulmonary arrest and conventional closed-chest CPR (CCPR). Fourteen dogs were subjected to five minutes of cardiopulmonary arrest and 30 minutes of CCPR. Resuscitation was performed according to a standardized protocol. Arterial lactic acid samples were collected at timed intervals throughout the experiment. Mean arterial lactic acid levels increased significantly with each sampling interval during 30 minutes of CCPR (overall P less than .05). In nine dogs successfully resuscitated, there were no significant differences in mean arterial lactic acid levels after the return of spontaneous circulation (ROSC). Open-chest resuscitation after five minutes of ventricular fibrillation in dogs results in peak lactic acid levels that do not change significantly once internal cardiac massage is initiated. In contrast, CCPR in similarly arrested dogs does not appear to provide adequate tissue oxygenation and/or perfusion to prevent continuous lactic acid accumulation.     

Twenty-four hour survival in a canine model of cardiac arrest comparing three methods of manual cardiopulmonary resuscitation

Two new modifications of manual cardiopulmonary resuscitation, high impulse compression at a rate of 120/min and interposed abdominal compression at a rate of 60/min, have been reported to produce better hemodynamic responses than standard cardiopulmonary resuscitation at 60/min. However, the effect of these two new methods on initial resuscitation success and 24 hour survival is unknown. In this study, 30 mongrel dogs were divided into three equal groups, each treated with one of three types of manual cardiopulmonary resuscitation. Ventricular fibrillation was induced electrically in morphinized, endotracheally intubated dogs emerging from halothane anesthesia. After 3 minutes of circulatory arrest without intervention, one of the three techniques of manual cardiopulmonary resuscitation was begun, and continued for 17 minutes. Defibrillation was performed at 20 minutes. Successful resuscitation was defined as a mean arterial blood pressure of at least 60 mm Hg, without chest compressions, 10 minutes after the initial defibrillation attempt. Intensive care was provided for 2 hours, including hemodynamic and respiratory monitoring, and drug intervention when required. Twenty-four hour survival and neurologic deficit were used as critical measures of outcome. Ten of 30 animals survived 24 hours with a mean neurologic deficit score of 5% (normal = 0, brain dead = 100). There was no difference in initial resuscitation success, 24 hour survival or neurologic deficit of the survivors among the three manual cardiopulmonary resuscitation methods. Aortic diastolic and calculated coronary perfusion pressures were similar for all three methods. Well performed standard manual cardiopulmonary resuscitation is as effective as these modified versions (high impulse compression and interposed abdominal compression) when compared in the same animal model.     

Immediate countershock versus cardiopulmonary resuscitation before countershock in a 5-minute swine model of ventricular fibrillation arrest

STUDY OBJECTIVE: Prior laboratory and clinical studies demonstrate that cardiopulmonary resuscitation (CPR) preceding countershock of prolonged ventricular fibrillation (VF) increases the likelihood of successful cardiac resuscitation. The lower limit of VF duration at which time preshock CPR provides no benefit has not been specifically studied. The purpose of this study was to compare countershock and cardiac resuscitation outcome between immediate countershock of VF of 5-minute duration and CPR without drug therapy before countershock in a swine model. METHODS: VF was induced in anesthetized and instrumented swine. After 5 minutes of VF, animals received 1 of 2 treatments. Animals in group 1, a "historical" control group (n=20), received immediate countershock followed by CPR and repeated shocks if needed. Group 2 animals (n=11) received CPR for 90 seconds preceding countershock, then continued CPR and repeated countershock if necessary. Drugs were not administered to either group, and resuscitation efforts were discontinued if a perfusing rhythm was not restored within 10 minutes of the first countershock. First shock success rate (defined as termination of VF), the number of shocks required to terminate VF, and the cardiac resuscitation rate were compared between groups. RESULTS: The first shock terminated VF in 13 of 20 group 1 animals and 2 of 11 group 2 animals (P =.023). All but 1 animal in group 1 developed pulseless electrical activity after countershock. All but 1 animal in group 1 were eventually successfully resuscitated with CPR and repeated shocks if necessary. Four group 2 animals could not be resuscitated (P =.042). CONCLUSION: Although effective in improving outcome of prolonged VF, CPR preceding countershock of VF of 5-minute duration does not improve the response to the first shock, decrease the incidence of postshock pulseless electrical activity, or the rate of return of circulation. In this study, CPR preceding countershock resulted in a significantly lower cardiac resuscitation rate.     

Survival and neurologic outcome after cardiopulmonary resuscitation with four different chest compression-ventilation ratios

STUDY OBJECTIVE: The optimal ratio of chest compressions to ventilations during cardiopulmonary resuscitation (CPR) is unknown. We determine 24-hour survival and neurologic outcome, comparing 4 different chest compression-ventilation CPR ratios in a porcine model of prolonged cardiac arrest and bystander CPR. METHODS: Forty swine were instrumented and subjected to 3 minutes of ventricular fibrillation followed by 12 minutes of CPR by using 1 of 4 models of chest compression-ventilation ratios as follows: (1) standard CPR with a ratio of 15:2; (2) CC-CPR, chest compressions only with no ventilations for 12 minutes; (3) 50:5-CPR, CPR with a ratio of 50:5 compressions to ventilations, as advocated by authorities in Great Britain; and (4) 100:2-CPR, 4 minutes of chest compressions only followed by CPR with a ratio of 100:2 compressions to ventilations. CPR was followed by standard advanced cardiac life support, 1 hour of critical care, and 24 hours of observation, followed by a neurologic evaluation. RESULTS: There were no statistically significant differences in 24-hour survival among the 4 groups (standard CPR, 7/10; CC-CPR, 7/10; 50:5-CPR, 8/10; 100:2-CPR, 9/10). There were significant differences in 24-hour neurologic function, as evaluated by using the swine cerebral performance category scale. The animals receiving 100:2-CPR had significantly better neurologic function at 24 hours than the standard CPR group with a 15:2 ratio (1.5 versus 2.5; P =.007). The 100:2-CPR group also had better neurologic function than the CC-CPR group, which received chest compressions with no ventilations (1.5 versus 2.3; P =.027). Coronary perfusion pressures, aortic pressures, and myocardial and kidney blood flows were not significantly different among the groups. Coronary perfusion pressure as an integrated area under the curve was significantly better in the CC-CPR group than in the standard CPR group (P =.04). Minute ventilation and PaO (2) were significantly lower in the CC-CPR group. CONCLUSION: In this experimental model of bystander CPR, the group receiving compressions only for 4 minutes followed by a compression-ventilation ratio of 100:2 achieved better neurologic outcome than the group receiving standard CPR and CC-CPR. Consideration of alternative chest compression-ventilation ratios might be appropriate.     

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.     

Good neurological recovery after rescue thrombolysis of presumed pulmonary embolism despite prior 100 minutes CPR

We reported the case of a 70-year-old man who was admitted to neurologic wards for recurrent syncope for 3 years. Unfortunately, just 2 hours after his admission, he suddenly collapsed and failed to return of spontaneous circulation (ROSC) after a 100-minute standard cardiopulmonary resuscitation (CPR). Fortunately, he was timely suspected to have pulmonary embolism (PE) based on his sedentary lifestyle, elevated D-dimer and markedly enlarged right ventricle chamber on bedside echocardiography. After a rescue thrombolytic alteplase therapy, he was successfully resuscitated and good neurological recovery was achieved.     

Cardiac resuscitability with cardiopulmonary bypass after increasing ventricular fibrillation times in dogs

Previous studies in dogs have shown resuscitation from prolonged cardiac arrest to conscious survival to be more effective with the use of cardiopulmonary bypass (CPB) than with standard advanced cardiac life support. This study compared cardiovascular resuscitability with CPB only after varying periods of cardiac arrest without artificial circulatory support in a canine model. Group 1 (ten) was subjected to ventricular fibrillation for 15 minutes; group 2 (ten) for 20 minutes; and group 3 (ten) for 30 minutes. All received total CPB after ventricular fibrillation without advanced cardiac life support to defibrillation at two to five minutes and partial CPB to four hours. In all three groups CPB with epinephrine generated normal coronary perfusion pressure and increased ventricular fibrillation amplitude significantly. In groups 1 and 2, CPB reperfusion allowed for successful defibrillation in less than five minutes, weaning from CPB in all dogs at four hours, and stable spontaneous circulation thereafter. In group 3, only five of ten dogs could be weaned from bypass at four hours, and all died early with myocardial necroses. It was concluded that CPB may be of value in the setting of prolonged cardiac arrest when advanced cardiac life support has not been provided or is unable to restore spontaneous heart-beat.     

CPR for patients labeled DNR: the role of the limited aggressive therapy order

Patients who sustain a cardiac arrest have a less than 20% chance of surviving to hospital discharge. Patients may request do-not-resuscitate (DNR) orders if they believe that their chances for a meaningful recovery after cardiopulmonary arrest are low. However, in some identifiable circumstances, cardiopulmonary resuscitation (CPR) has a higher chance of success and lower likelihood of neurologic impairment. The probability of survival from a cardiac arrest influences patients' wishes regarding resuscitation; thus, when CPR has a higher likelihood of success, patients' expressed preferences for treatment as contained within a DNR order may not accurately reflect their intended goals. Patients should be offered the option of consenting to CPR for "higher-success" situations, including a witnessed cardiopulmonary arrest in which the initial cardiac rhythm is ventricular tachycardia or fibrillation, cardiac arrest in the operating room, and cardiac arrest resulting from a readily identifiable iatrogenic cause. This new level of resuscitation could be called a "limited aggressive therapy" order.     

Guidelines for discontinuing prehospital CPR in the emergency department--a review

We provide information that we believe should allow the establishment of rational guidelines for discontinuing, with physician supervision, unsuccessful prehospital CPR. Goldberg has advocated that CPR be terminated only after evidence of brain or cardiac death has persisted for more than one hour of adequately applied advanced CPR. This recommendation was made for inhospital resuscitation and does not reflect the limited capabilities of basic and advanced CPR techniques to sustain life outside the hospital. In addition, White and associates have demonstrated that after resuscitation from prolonged cardiac arrest, cerebral cortical blood flow is reduced severely. This state of hypoperfusion may last up to 18 hours. Because this condition can result in extensive neurologic damage, it may explain the poor survival rates after prolonged resuscitation. We propose that CPR be terminated in the ED when, despite adequate rescue attempts (intubation, defibrillation, IV medications, CCCM en route) by those responding at the scene of cardiac arrest, intrinsic cardiac activity has not been achieved in patients brought to the hospital with asystole or bradyarrhythmia. Additionally patients who have had advanced prehospital CPR for more than 45 minutes without generation of any intrinsic cardiac activity are not resuscitatable by current standard techniques, and CPR may be discontinued. These criteria must not be used for victims of hypothermia before a core temperature of 35 C to 36.1 C is achieved by active core rewarming during CPR. The available data suggest that if these criteria are implemented, many unproductive hospital-based resuscitative efforts can be eliminated without jeopardizing potential survivors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.