Plasma epinephrine levels in resuscitation with cardiopulmonary bypass

Since the highest plasma epinephrine levels have been recorded during resuscitation, we evaluated the isolated effect of cardiac arrest upon adrenomedullary secretion. We determined plasma epinephrine in dogs resuscitated with cardiopulmonary bypass (CPB) after cardiac arrest periods of 12 (CPB-12; n = 4) or 16 min (CPB-16; n = 5). Through 2 h of CPB and the following 6 h of critical care, there was no difference between CPB-12 and CPB-16 regarding most cardiopulmonary functional variables. Plasma epinephrine was markedly elevated immediately after initiation of CPB (p less than .01 at 1 min CPB vs. basal) and returned rapidly to basal concentrations. Comparison of plasma epinephrine levels between CPB and standard CPR groups showed that responses to cardiac arrest were similar (p greater than .05 at 1 min CPB vs. 11.5 min CPR). We conclude that cardiac arrest is the main or sole determinant of the plasma epinephrine elevation of resuscitation.     

窒息家兔心肺复苏疗效与血浆内皮素变化的关系

目的探讨窒息家兔心肺复苏(cardiopulmonaryresuscitation,CPR)疗效与血浆内皮素(endothelin,ET)变化的关系。方法对62只家兔均在呼气末夹闭气管8min,造成窒息性心脏停搏模型后,开始人工胸外心脏按压及机械通气,期间不用任何药物,复苏5min内恢复自主循环(restorationof spontaneouscirculation,ROSC)的家兔定义为常规CPR成功;对5min内未能ROSC者再随机分为两组,分别给予肾上腺素(0.2mg kg)和加压素(0.8U kg)静脉注射,并继续行常规CPR。分别在窒息前和CPR15、60、120min采血测血浆ET浓度。结果常规CPR的家兔ROSC率为24.16%(1562),加用肾上腺素和加压素后总的ROSC率提高到48.39%(3062)。对常规CPR失败的家兔而言,肾上腺素疗效明显优于加压素(ROSC率分别为54.16%和8.70%,P=0.001)。但复苏成功组和复苏失败组家兔血浆ET的比较,差异无显著性。结论对窒息性心脏停搏的家兔CPR时应用肾上腺素或加压素可提高ROSC率,但肾上腺素疗效明显优于加压素。窒息家兔CPR疗效与血浆内皮素变化无明显相关关系。     

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.     

The effect of cardiopulmonary bypass resuscitation on cardiac arrest induced lactic acidosis in dogs

The adequacy of end organ blood flow following a cardiac arrest varies depending on the artificial reperfusion technique utilized and may critically affect patient outcome. Both oxygen consumption (VO2) and arterial lactate values have previously been used to assess tissue perfusion. Cardiopulmonary bypass resuscitation (CPB) is a reperfusion technique capable of providing near normal end organ blood flow. The purpose of this investigation was to study the effect of femoro-femoral veno-arterial CPB resuscitation compared to standard CPR on VO2 and arterial lactic acid values after a prolonged cardiac arrest. Ten mongrel dogs were electrically fibrillated and left in cardiopulmonary arrest without therapy for 12 min. Resuscitation was attempted according to a standardized protocol utilizing either CPB (n = 5) or standard external CPR (n = 5). Oxygen consumption values and arterial lactic acid samples were obtained at baseline, at timed intervals throughout resuscitation and after return of spontaneous circulation in successfully resuscitated dogs. Baseline hemodynamic and biochemical measurements were similar in both treatment groups (P greater than 0.05). Oxygen consumption (440 +/- 50 ml/min/M2) and mean arterial lactic acid values (7.44 +/- 2.25 mmol/l) were significantly higher at 1 min of resuscitation in CPB-treated dogs compared to dogs treated with CPR (60 +/- 10 ml/min/M2) (3.16 +/- 0.69 mmol/l) respectively (P less than 0.05). Mean arterial lactic acid values rose significantly at each sampling interval during CPR (P less than 0.05) but began to decrease after 5 min of resuscitation in the CPB animals and were not significantly different than baseline after 60 min of bypass (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Periodic acceleration (pGz) CPR in a swine model of asphyxia induced cardiac arrest. Short-term hemodynamic comparisons

BACKGROUND: Asphyxia is one of the most common causes of pediatric cardiac arrest, and becoming a more frequently recognized cause in adults. Periodic acceleration (pGz) is a novel method of cardiopulmonary resuscitation (CPR). pGz is achieved by rapid motion of the supine body headward-footward that generates adequate perfusion and ventilation during cardiac arrest. In a swine ventricular fibrillation cardiac arrest model, pGz produced a higher return of spontaneous circulation (ROSC), superior neurological outcome, less echocardiography evidence of post resuscitation myocardial stunning, and decreased indices of tissue injury. In contrast to standard chest compression CPR, pGz does not produce rib fractures. We investigated the feasibility of pGz in severe asphyxia cardiac arrest and assessed whether beneficial effects seen in the VF model of cardiac arrest could be realized. METHODS AND RESULTS: Sixteen swine weight 4+/-1 kg were anesthetized, tracheally intubated, and instrumented to measure, hemodynamics and echocardiography. Asphyxia was induced by occlusion of the tracheal tube. After loss of aortic pulsations (median time 10 min) animals were observed for three additional minutes following which all were in cardiac arrest. The animals were then randomized to receive 10 min of pGz or standard chest compression ventilation performed with a commercial device (Thumper). A single dose of epinephrine (adrenaline) and sodium bicarbonate were given and defibrillation attempted if appropriate for a maximum of 10 min. Both groups received fractional inspired O2 concentration of 100% during CPR and after resuscitation. Four animals in each group (50%) had an initial ROSC, however only two of the four initial survivors remained alive 3h after ROSC. There were no significant differences in blood pressure, coronary perfusion pressure during CPR and after early ROSC between groups. pGz treated animals had significantly lower pulmonary artery pressure; 20+/-4 mmHg compared to Thumper 46+/-5 mmHg, 30 min after ROSC (p<0.01). Surviving animals in both groups had severe myocardial dysfunction at 30 min after ROSC. At necropsy, 25% of the Thumper treated animals had rib fractures, while none occurred in the pGz group. CONCLUSIONS: In a lethal model of asphyxia cardiac arrest, pGz is equivalent to standard CPR, with respect to acute outcomes and resuscitation survival rates but is associated with significantly lower pulmonary artery pressures and does not produce traumatic rib fractures.     

Myocardial perfusion pressure: a predictor of 24-hour survival during prolonged cardiac arrest in dogs

Myocardial perfusion pressure, defined as the aortic diastolic pressure minus the right atrial diastolic pressure, correlates with coronary blood flow during cardiopulmonary resuscitation (CPR) and predicts initial resuscitation success. Whether this hemodynamic parameter can predict 24-h survival is not known. We examined the relationship between myocardial perfusion pressure and 24-h survival in 60 dogs that underwent prolonged (20 min) ventricular fibrillation and CPR. Forty-two (70%) animals were initially resuscitated and 20 (33%) survived for 24 h. Myocardial perfusion pressure was significantly greater when measured at 5, 10, 15 and 20 min of ventricular fibrillation in the resuscitated animals than in the non-resuscitated animals (P less than 0.01). Likewise, the myocardial perfusion pressure was also greater in the animals that survived 24 h than in animals that were resuscitated, but died before 24 h (P less than 0.02). Myocardial perfusion pressure measured after 10 min of CPR was 11 +/- 2 mmHg in animals never resuscitated, 20 +/- 3 mmHg in those resuscitated that died before 24 h and 29 +/- 2 mmHg in those that survived 24 h (P less than 0.05). A myocardial perfusion pressure at 10 min of CPR of 20 mmHg or less is an excellent predictor of poor survival (negative predictive value = 96%). Myocardial perfusion pressure is a useful index of CPR effectiveness and therefore may be a useful guide in helping to optimize resuscitation efforts.     

Combination drug therapy with vasopressin,adrenaline (epinephrine) and nitroglycerin improves vital organ blood flow in a porcine model of ventricular fibrillation

There is increasing evidence that the combination of epinephrine (adrenaline) with vasopressin may be superior to either epinephrine or vasopressin alone for treatment of cardiac arrest. However, the optimal combination, and dosage of cardiovascular drugs to minimize side effects, and to improve outcome has yet to be found. We therefore evaluated whether the combination of vasopressin plus epinephrine plus nitroglycerin (EVN), would improve vital organ blood flow during cardiopulmonary resuscitation (CPR) when compared with epinephrine (EPI) alone. After 4 min of ventricular fibrillation (VF) and 4 min of standard CPR, pigs were randomized to the combination of epinephrine (45 microg/kg) plus vasopressin (0.4 U/kg) plus nitroglycerin (7.5 microg/kg; n=12), or epinephrine (40 microg/kg; n=12) alone. Cerebral and myocardial blood flow was measured with radiolabeled microspheres. Defibrillation was attempted after 19 min of VF including 15 min of CPR. Mean+/-SEM coronary perfusion pressures were significantly (P < 0.01) higher 5 min after EVN vs. EPI alone (34+/-3 vs. 24+/-3 mmHg, respectively). At the same time, mean+/-SEM left ventricular, and global cerebral blood flow was also significantly (P < 0.05) higher after EVN vs. EPI alone (0.78+/-0.11 vs. 0.48+/-0.08 ml/min/g; and 0.37+/-0.05 vs. 0.22+/-0.0 3 ml/min/g, respectively). Spontaneous circulation was restored in 11 of 12 animals in the EVN group vs. 6 of 12 swine after EPI alone (P = N.S.). In conclusion, the combination of EVN significantly improved vital organ blood flow during CPR compared with EPI alone. Addition of nitroglycerin to the combination of low dose epinephrine with vasopressin during cardiac arrest may be beneficial.     

Two-stage resuscitation of the cat brain after prolonged cardiac arrest

Following prolonged cardiac arrest, reperfusion of the brain is endangered by the low blood perfusion pressure during the early resuscitation phase. In order to avoid low perfusion brain injury, a two-stage resuscitation protocol was applied to cats submitted to 30 min potassium chloride induced cardiac arrest: first, the heart was resuscitated, followed — after stabilisation of blood pressure — by recirculation of the brain. During cardiac resuscitation the brain was disconnected from the general circulation by inflating a pneumatic cuff around the neck. The results were compared with the outcome of conventional one-stage resuscitation following 15 min cardiac arrest. Cardiac resuscitation was successful in 5 out of 8 animals with 15 min and in 6 out of 13 animals with 30 min cardiac arrest. In successfully resuscitated animals of both groups, brain energy metabolism recovered to normal within 3 h although two-stage resuscitation increased brain ischemia time to 37–61 min. Twostage resuscitation, in consequence, is a promising approach for revival of the brain after prolonged cardiac arrest.     

Effects of naloxone on the adrenomedullary response during and after cardiopulmonary resuscitation in dogs

To determine the effects of naloxone, an opiate antagonist, on the adrenomedullary response to cardiac arrest, plasma epinephrine and norepinephrine levels were measured before, during, and after cardiac arrest in dogs. Ventricular fibrillation was induced in 12 dogs anesthetized with pentobarital sodium (30 mg/kg) and standard American Heart Association cardiopulmonary resuscitation (CPR) was begun using a mechanical device. At 6.5 minutes of CPR, naloxone (10 mg/kg) or 0.9% saline (10 ml) was given intravenously. At 12 minutes of CPR, the cardiac ventricles were electrically defibrillated. Plasma epinephrine and norepinephrine levels were measured before ventricular fibrillation; at 2.5, 4.5, 9.5, and 11.5, minutes of CPR; and at 5, 10, 15, and 20 minutes after resuscitation. Epinephrine and norepinephrine increased from prearrest levels of 3.66 +/- 0.67 (+/- SE) and 24.02 +/- 3.67 ng/ml to 66.67 +/- 9.65 and 74.00 +/- 9.91 ng/ml, respectively, at 4.5 minutes of CPR. After resuscitation, norepinephrine levels remained slightly elevated, while epinephrine fell to prearrest levels. Naloxone did not cause a significant change in either epinephrine or norepinephrine from 6.5 minutes of CPR (time of treatment) through 20 minutes postresuscitation. In addition, naloxone had no effect on either the end-diastolic pressure difference during CPR or resuscitation outcome. We conclude that cardiac arrest causes significant increases in plasma epinephrine and norepinephrine levels, which remain elevated for the duration of the arrest, and that naloxone has no effect on these levels.     

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.     

Sympathetic responses in out-of-hospital cardiac arrest

To determine the clinical relevance of the sympathetic response to out-of-hospital cardiac arrest, we measured plasma concentrations of catecholamine and cortisol in ten such arrested patients on their arrival. The duration of cardiac arrest was estimated from 9 to 200 min before basic life support was initiated by ambulance personnel. Two of the patients developed spontaneous pulses in response to ALS and were resuscitated, and the others were not, although the length and the extent of ALS were not different between the two groups. Plasma concentrations of epinephrine (EN), norepinephrine (NE) and cortisol prior to ALS in both groups were markedly elevated. In particular, the patients who never regained spontaneous pulses showed 58-fold and 12-fold increase in the plasma EN and NE levels, respectively, which were much higher than those in the resuscitated cases; 8- and 1.7-fold increase, respectively. These massive EN and NE discharges correlated well with the arrest time (r = 0.96 and 0.94, respectively) and the degree of acidosis (r = -0.82 and -0.82, respectively).     

Simultaneous sterno-thoracic cardiopulmonary resuscitation improves short-term survival rate in canine cardiac arrests

We have reported previously that simultaneous sterno-thoracic cardiopulmonary resuscitation (SST-CPR) using a device that compresses the sternum and constricts the thorax circumferentially during a compression systole that can be achieved using standard cardiopulmonary resuscitation (STD-CPR). This study was designed to assess whether SST-CPR improves the survival rate of dogs with cardiac arrest compared with STD-CPR. Twenty-nine mongrel dogs (19-31 kg) were enrolled in this study. After 4 min of ventricular fibrillation induced by an AC current, animals were randomized to be resuscitated by either STD-CPR (n=15) or SST-CPR (n=14). Defibrillation was attempted 10 min after the induction of cardiac arrest. Standard advanced cardiac life support was started if defibrillation was unsuccessful. Aortic blood pressure, coronary perfusion pressure, and end tidal CO(2) tension were measured during CPR and the post-resuscitation period. Survival was determined 12 h after the induction of cardiac arrest. SST-CPR resulted in a significantly (P<0.001) higher systolic arterial pressure (91+/-47 vs 47+/-24 mmHg), diastolic pressure (43+/-24 vs 17+/-10 mmHg), coronary perfusion pressure (35+/-25 vs 13+/-9 mmHg), and end tidal CO(2) tension (9+/-4 vs 3+/-2 mmHg). Two of 15 animals (13%) resuscitated by STD-CPR and seven of 14 animals (50%) resuscitated by SST-CPR survived for 12 h after cardiac arrest (P<0.05). In conclusion, SST-CPR improves the short-term survival rate in canine cardiac arrest compared with STD-CPR.     

Cardiac resuscitation by extracorporeal circulation after failure of conventional CPR

After cardiac arrest, return of cardiac function and effective circulation are contingent on prompt restoration of myocardial blood flow. Because conventional closed-chest CPR has limited hemodynamic efficiency, we investigated venoarterial ECC utilizing peripheral vascular access as an alternative for cardiac resuscitation. Ventricular fibrillation was induced in domestic pigs by alternating current delivered to the endocardium of the right ventricle. Conventional closed-chest CPR was begun after 10 minutes. In each instance, precordial compression and external defibrillation failed to restore a viable rhythm. ECC was begun at 15 minutes at an average flow rate of 183 ml/kg/min. In each of eight animals, sinus rhythm was restored. In six of these eight animals, spontaneous circulation was reestablished after an average interval of 152 minutes. When epinephrine was administered concomitantly with ECC in an additional eight animals so as to maintain mean aortic pressure between 60 and 100 mm Hg, sinus rhythm and spontaneous circulation were reestablished in each pig after an average of only 23 minutes. The effects of ECC in conjunction with epinephrine were then compared with those of conventional precordial compression in conjunction with epinephrine (sham ECC). In contrast to ECC, which successfully resuscitated each of five animals, none of five sham ECC-treated animals was resuscitated by continued precordial compression and maximal doses of epinephrine (p less than 0.01). We conclude that ECC in conjunction with epinephrine emerges as a highly effective experimental intervention for resuscitation when conventional techniques of precordial compression and external defibrillation fail to reverse cardiac arrest.     

Inspiratory-cycle Instillation of Endotracheal Epinephrine in Porcine Arrest

Objective : To compare timed inspiratory-cycle endotracheal (ET) instillation of epinephrine (EPI) with instillation during apnea during CPR. Methods : Prospective randomized laboratory comparison of two ET-EPI instillation techniques in 24 preadolescent anesthetized and paralyzed Yucatan swine (mean weight 10.3 ± 1.5 kg) with apnea-induced hypoxic and hypercarbic cardiopulmonary arrest. After 8 minutes of cardiopulmonary arrest and 1 minute of CPR, 500 μg (50 ± 7 μg/kg) of radiolabeled ET EPI was either administered timed to a ventilator inspira-tory cycle (IN, n= 15) or injected during apnea (DA, n= 9) using a monitoring lumen built into the sidewall of the ET tube. Injection technique was carefully controlled regarding ET-tube position, dilution, flush, and pressure-limited mechanical ventilations. CPR was resumed and continued for 5 minutes. If resuscitation occurred, monitoring was continued for one hour. Outcome variables included pulmonary EPI distribution pattern (DIST), plasma exogenous and total EPI levels, successful resuscitation, and hemodynamic response. Results : Bilateral DIST occurred in 58% of the pigs, with significantly more bilateral DISTs for IN versus DA pigs (p = 0.01). Plasma radio-labeled exogenous EPI counts were significantly greater for IN versus DA pigs(p = 0.03). Total plasma EPI levels rose significantly above baseline over time within each group, but showed no difference between the IN and DA groups at any time point. Successful resuscitation occurred in 21% of the pigs, with no difference between IN and DA pigs (p = 0.38). Conclusion : When other aspects of ET EPI instillation are optimized and controlled during porcine hypoxic-hypercarbic arrest, timed inspiratory-cycle instillation of ET EPI (50 μg/kg) results in an improved bilateral DIST and greater exogenous EPI absorption. However, in this severe pediatric asphyxial arrest model using a 50- μg/kg dose, inspiratory-cycle instillation does not improve the resuscitation rate or hemodynamic response over currently recommended instillation during apnea.     

Vasopressin decreases endogenous catecholamine plasma concentrations during cardiopulmonary resuscitation in pigs

OBJECTIVE: The purpose of this study was to evaluate the effect of vasopressin vs. saline placebo on catecholamine plasma concentrations during cardiopulmonary resuscitation (CPR). DESIGN: Prospective, randomized laboratory investigation by using an established porcine CPR model with instrumentation for measurement of hemodynamic variables, vital organ blood flow, and return of spontaneous circulation. SETTING: University hospital laboratory. SUBJECTS: Sixteen domestic pigs. INTERVENTIONS: After 15 mins of untreated cardiac arrest and 3 mins of CPR, 16 pigs were randomized to be treated with either 0.8 U/kg vasopressin (n = 8) or placebo (normal saline; n = 8). Arterial epinephrine and norepinephrine plasma concentrations were sampled at prearrest, after 1.5 mins of chest compressions, and at 1.5 mins and 5 mins after drug administration during CPR. MEASUREMENTS AND MAIN RESULTS: In comparison with placebo pigs at 1.5 and 5 mins after drug administration, animals resuscitated with vasopressin had significantly (p < .01) higher mean +/- SEM left ventricular myocardial (131+/-27 vs. 10+/-1 mL x mins(-1) x 100 g(-1) and 62+/-13 vs. 9+/-2 mL x mins(-1) x 100 g(-1)); total cerebral (90+/-8 vs. 14+/-3 mL x mins(-1) x 100 g(-1) and 51+/-4 vs. 12+/-2 mL x mins(-1) x 100 g(-1)); and adrenal gland perfusion (299+/-36 vs. 38+/-7 mL x mins(-1) x 100 g(-1) and 194+/-23 vs. 29+/-5 mL x mins(-1) x 100 g(-1)). Significantly lower mean +/- SEM epinephrine concentrations in the vasopressin pigs compared with the placebo group were measured 1.5 mins and 5 mins after drug administration, (24167+/-7919 vs. 80223+/-19391 pg/mL [p < .01] and 8346+/-1454 vs. 71345+/-10758 pg/mL [p < .01]). Mean +/- SEM norepinephrine plasma concentrations in the vasopressin animals in comparison with placebo were at 1.5 and 5 mins after drug administration significantly lower (41729+/-13918 vs. 82756+/-9904 pg/mL [p = .01] and 10642+/-3193 vs. 62170+/-8797 pg/mL [p < .01]). CONCLUSIONS: Administration of vasopressin during CPR resulted in significantly superior vital organ blood flow, but significantly decreased endogenous catecholamine plasma concentrations when compared with placebo.     

Arterial pH and carbon dioxide tension as indicators of tissue perfusion during cardiac arrest in a canine model.

BACKGROUND AND METHODS: Previous studies have shown that Paco2 and end-tidal CO2 reflect coronary artery perfusion pressures during cardiac arrest. We investigated the relationship of coronary artery perfusion pressure to central arterial pH and Paco2 values during resuscitation from cardiac arrest in a canine model. Twenty-four mongrel dogs were block randomized to three different resuscitation groups after induction of ventricular fibrillation and cardiac arrest: a) standard cardiopulmonary resuscitation (CPR) and advanced life support (n = 8); b) cardiopulmonary bypass (n = 8); or c) open-chest CPR (n = 8). Central arterial blood gases and perfusion pressures were monitored during cardiac arrest and during resuscitation. RESULTS: Prearrest blood gases and hemodynamic values were similar between groups. Sixteen dogs from all three groups were successfully resuscitated. Survivors had significantly higher coronary artery perfusion pressure (p = .03), Paco2 (p = .015), and lower pH (p = .01) values than nonsurvivors. There was no correlation of pH and Paco2 during mechanical external CPR. However, after institution of the different resuscitation techniques, pH and Paco2 each showed a statistically significant correlation (r2 = .50 and .33, respectively) with coronary artery perfusion pressure. CONCLUSIONS: Central arterial pH and Paco2 monitoring during cardiac arrest may reflect the adequacy of tissue perfusion during resuscitation and may predict resuscitation outcome from ventricular fibrillation.     

Hypercarbic acidosis reduces cardiac resuscitability

BACKGROUND AND METHODS: Marked increases in myocardial hypercarbia and acidosis accompany cardiac arrest and resuscitation. To investigate whether hypercarbic acidosis independent of oxygenation is of itself detrimental to cardiac resuscitation, three groups of six Sprague-Dawley rats were ventilated with gas mixtures containing concentrations of inspired CO2 (FICO2) of 0.0, 0.3, or 0.5, with oxygen fractions held constant at 0.5. After 4 mins of ventricular fibrillation, mechanical chest compressions were initiated with a pneumatic thumper; 2 mins later, transthoracic defibrillation was attempted. RESULTS: Each animal ventilated with FICO2 of 0.0 or 0.3 was successfully resuscitated. However, none of the animals ventilated with FICO2 of 0.5, in which aortic pH was less than 6.67 and aortic PCO2 was greater than 200 torr (greater than 26.7 kPa), was resuscitated (p less than .001). This finding contrasted with a second control group of seven identically treated animals which, in the absence of cardiac arrest, demonstrated no adverse effects after ventilation with an FICO2 of 0.5. CONCLUSIONS: Increases in FICO2 to levels of 0.5 under conditions of constant arterial oxygenation and controlled coronary perfusion pressure preclude successful resuscitation in this rodent model of CPR.     

H ANDBOOK OF U RGENT C ARE M EDICINE , 2 ND E DITION

Abstract

Background. Hyperglycemia is common in the early period following resuscitation from cardiac arrest and has been shown to be a predictor of neurologic outcome in retrospective studies. Objective. To evaluate neurologic outcome and early postarrest hyperglycemia in a swine cardiac arrest model. Methods. Electrically induced ventricular fibrillation cardiac arrest was induced in 22 anesthetized and instrumented swine. After 7 minutes, cardiopulmonary resuscitation (CPR) and Advanced Cardiac Life Support were initiated. Twenty-one animals were resuscitated and plasma glucose concentration was measured at intervals for 60 minutes after resuscitation. The animals were observed for 72 hours and the neurologic score was determined at 24-hour intervals. Results. Ten animals had a peak plasma glucose value ≥226 mg/dL during the initial 60 minutes after resuscitation. The neurologic scores at 72 hours in these animals (mean score = 0, mean overall cerebral performance category = 1) were the same as those in the animals with a peak plasma glucose value <226 mg/dL. The end-tidal carbon dioxide (CO₂) values measured during CPR, times to restoration of spontaneous circulation, and epinephrine doses were not significantly different between the animals with a peak glucose concentration ≥226 mg/dL and those with lower values. The sample size afforded a power of 95% to detect a 50-point difference from the lowest score (0 points) of the porcine neurologic outcome scale. Conclusion. In this standard porcine model of witnessed out-of-hospital cardiac arrest, early postresuscitation stress hyperglycemia did not appear to affect neurologic outcome. During the prehospital phase of treatment and transport, treatment of hyperglycemia by emergency medical services providers may not be warranted.     

Quality of cardiopulmonary resuscitation before and during transport in out-of-hospital cardiac arrest

AIM OF THE STUDY: To evaluate quality of cardiopulmonary resuscitation (CPR) performed during transport after out-of-hospital cardiac arrest. MATERIALS AND METHODS: Retrospective, observational study of all non-traumatic cardiac arrest patients older than 18 years who received CPR both before and during transport between May 2003 and December 2006 from the community run EMS system in Oslo. Chest compressions and ventilations were detected from impedance changes in routinely collected ECG signals, and hands-off ratio calculated as time without chest compressions divided by total CPR time. RESULTS: Seventy-five of 787 consecutive out-of-hospital cardiac arrest patients met the inclusion criteria. Quality data were available from 36 of 66 patients receiving manual CPR and 7 of 9 receiving mechanical CPR. CPR was performed for mean 21+/-11 min before and 12+/-8 min during transport. With manual CPR hands-off ratio increased from 0.19+/-0.09 on-scene to 0.27+/-0.15 (p=0.002) during transport. Compression and ventilation rates were unchanged causing a reduction in compressions per minute from 94+/-14 min(-1) to 82+/-19 min(-1) (p=0.001). Quality was significantly better with mechanical than manual CPR. Four patients (5%) survived to hospital discharge; two with manual CPR (Cerebral performance categories (CPC) 1 and 2), and two with mechanical CPR (CPC scores 3 and 4). No discharged patients had any spontaneous circulation during transport. CONCLUSIONS: The fraction of time without chest compressions increased during transport of out-of-hospital cardiac arrest patients. Every effort should therefore be made to stabilise patients on-scene before transport to hospital, but all transport with ongoing CPR is not futile.     

End-tidal CO2 as a guide to successful cardiopulmonary resuscitation: a preliminary report

Utilizing a well-established porcine model of cardiac arrest, we found that end-tidal CO2 concentration (ETCO2) strikingly decreased to approximately 24% of control levels, immediately after cardiac arrest and before precordial compression. During precordial compression, ETCO2 progressively increased to 46% of control values in successfully resuscitated animals but only to 26% in animals which failed to respond to resuscitation efforts. After successful resuscitation, ETCO2 rapidly returned to baseline values. These data indicate that ETCO2 may be a useful monitor for assessing the adequacy of CPR.