Comparison of shock-first strategy and cardiopulmonary resuscitation-first strategy in a porcine model of prolonged cardiac arrest

Objective

The choice of a shock-first or a cardiopulmonary resuscitation (CPR)-first strategy in the treatment of prolonged cardiac arrest (CA) is still controversial. The purpose of this study was to compare the effects of these strategies on oxygen metabolism and resuscitation outcomes in a porcine model of 8 min CA.

Methods

Ventricular fibrillation (VF) was electrically induced. After 8 min of untreated VF, 24 male inbred Wu-Zhi-Shan miniature pigs were randomized to receive either defibrillation first (ID group) or chest compression first (IC group). In the ID group, a shock was delivered immediately. If the defibrillation attempt failed to attain restoration of spontaneous circulation (ROSC), manual chest compressions were rapidly initiated at a rate of 100 compressions min⁻¹, and the compression-to-ventilation ratio was 30:2. If VF persisted after five cycles of CPR, a second defibrillation attempt was made. In the IC group, chest compressions were delivered first, followed by a shock.

Results

Hemodynamic variables, the VF waveform and blood gas analysis outcomes were recorded. Oxygen metabolism parameters and the amplitude spectrum area (AMSA) of the VF waveform were computed. There were no significant differences in the rate of ROSC and 24 h survival between two groups. The ID group had lower lactic acid levels, higher cardiac output, better oxygen consumption and better oxygen extraction ratio at 4 and 6 h after ROSC than the IC group.

Conclusions

In a porcine model of prolonged CA, the choice of a shock-first or CPR-first strategy did not affect the rate of ROSC and 24 h survival, but the shock-first strategy might result in better hemodynamic status and better oxygen metabolism than the CPR-first strategy at the first 6 h after ROSC.     

Tilting for perfusion: Head-up position during cardiopulmonary resuscitation improves brain flow in a porcine model of cardiac arrest

IntroductionCerebral perfusion is compromised during cardiopulmonary resuscitation (CPR). We hypothesized that beneficial effects of gravity on the venous circulation during CPR performed in the head-up tilt (HUT) position would improve cerebral perfusion compared with supine or head-down tilt (HDT).MethodsTwenty-two pigs were sedated, intubated, anesthetized, paralyzed and placed on a tilt table. After 6 min of untreated ventricular fibrillation (VF) CPR was performed on 14 pigs for 3 min with an automated CPR device called LUCAS (L) plus an impedance threshold device (ITD), followed by 5 min of L-CPR + ITD at 0° supine, 5 min at 30° HUT, and then 5 min at 30° HDT. Microspheres were used to measure organ blood flow in 8 pigs. L-CPR + ITD was performed on 8 additional pigs at 0°, 20°, 30°, 40°, and 50° HUT.ResultsCoronary perfusion pressure was 19 ± 2 mmHg at 0° vs. 30 ± 3 at 30° HUT (p < 0.001) and 10 ± 3 at 30° HDT (p < 0.001). Cerebral perfusion pressure was 19 ± 3 at 0° vs. 35 ± 3 at 30° HUT (p < 0.001) and 4 ± 4 at 30° HDT (p < 0.001). Brain–blood flow was 0.19 ± 0.04 ml min⁻¹ g⁻¹ at 0° vs. 0.27 ± 0.04 at 30° HUT (p = 0.01) and 0.14 ± 0.06 at 30° HDT (p = 0.16). Heart blood flow was not significantly different between interventions. With 0, 10, 20, 30, 40 and 50° HUT, ICP values were 21 ± 2, 16 ± 2, 10 ± 2, 5 ± 2, 0 ± 2, −5 ± 2 respectively, (p < 0.001), CerPP increased linearly (p = 0.001), and CPP remained constant.ConclusionDuring CPR, HDT decreased brain flow whereas HUT significantly lowered ICP and improved cerebral perfusion. Further studies are warranted to explore this new resuscitation concept.     

Comparison of the efficacy of nifekalant and amiodarone in a porcine model of cardiac arrest

Objective

To compare the efficacy of nifekalant and amiodarone in the treatment of cardiac arrest in a porcine model.

Methods

After 4 min of untreated ventricular fibrillation, animals were randomly treated with nifekalant (2 mg kg⁻¹), amiodarone (5 mg kg⁻¹) or saline placebo (n = 12 pigs per group). Precordial compression and ventilation were initiated after drug administration and defibrillation was attempted 2 min later. Hemodynamics were continuously measured for 6 h after successful resuscitation.

Results

Compared with saline, nifekalant and amiodarone equally decreased the number of electric shocks, defibrillation energy, epinephrine dose, and duration of cardiopulmonary resuscitation required for successful resuscitation (P < 0.01). The incidence of restoration of spontaneous circulation (ROSC) and the 24-h survival rate were higher in both antiarrhythmic drug groups (P < 0.05) vs. the saline group. Furthermore, post-resuscitation myocardial dysfunction at 4-6 h after successful resuscitation was improved in animals given antiarrhythmic drugs as compared with the saline group (P < 0.05). There were no differences between nifekalant and amiodarone for any of these parameters.

Conclusion

The effect of nifekalant was similar to that of amiodarone for improving defibrillation efficacy and for the treatment of cardiac arrest. Administration of either nifekalant or amiodarone before defibrillation increased the ROSC and 24-h survival rates and improved post-resuscitation cardiac function in this porcine model.     

A simpler cardiac arrest model in the mouse

OBJECTIVE: Delivering alternating currency (AC) to right ventricular endocardium to induce ventricular fibrillation (VF) in mice is complicated. We tried to validate whether transoesophageal AC stimulation could induce VF and how long AC stimulation had to be sustained to prevent the spontaneous cardioversion of VF in mice. METHODS: A pacing electrode was inserted orally into the oesophagus and AC was delivered to esophagus through the pacing electrode to stimulate the heart and induce VF in 15 mice. The incidence of VF and time of AC stimulation were recorded 4min after onset of VF cardiopulmonary resuscitation (CPR) was started. RESULTS: VF was induced by short AC stimulation in all 15 mice. With the prolongation of AC stimulation, the incidences of spontaneous cardioversion of VF decreased whereas the incidence of pulseless electrical activity (PEA) increased accordingly. Following the termination of prolonged AC stimulation, VF occurred only in 1 of 15 mice, but PEA in 14 of 15 mice. Before CPR 1 of 15 and 12 of 15 animals remained in VF and in PEA, respectively, while 2 of 15 animals developed into asystole. After CPR, 11 of 15 animals were successfully resuscitated. CONCLUSION: VF can be induced by a short period of transoesophageal AC stimulation in mice. However, prolonged AC stimulation is prone to induce PEA other than VF. Nonetheless, the development of a mouse CA model in this manner is simpler and easier, which may have practical significance for facilitating experimental investigation on CA and CPR.     

叹息样呼吸与猪心肺复苏过程中血流动力学变化的研究

目的 研究CPR的病理生理过程,探讨叹息样呼吸对CPR过程中血流动力学的影响.方法 12头北京长白猪,体质量(30±1)kg,麻醉后气管插管,机械通气,连续记录实时呼吸参数.股动脉置管测量主动脉压(AOP),并抽取动脉血;肺动脉漂浮导管置测最右心房压(RAP)及心输出量(CO).以程控电刺激制作室颤(VF)模型.VF4 min后进行标准30:2 CPR 12 min,记录相关参数.结果 CPR过程中pH,PaCO2及乳酸逐渐升高,而PaO2逐渐降低,但PaO2在整个实验过程中均大于50mmHg.10只动物出现叹息样呼吸,但随时间推移逐渐减弱;未出现叹息样乎吸的2只动物均未复苏成功.标准心外按压在多数动物均可产生大干死腔量(VD)的被动通气,但其潮气量随时间推移逐渐减少.因此人工通气在总分钟通气量中所占比例逐渐增加.CO、冠脉灌注压(CPP)与叹息样呼吸分钟通气量(MVg)呈正相关(r分别等于0.736,0.721,P＜0.01);RAP与MVg呈负相关(r=-0.744,P＜0.01).结论 标准CPR能够维持机体12min的氧合;心外按压能够产生大于VD的被动通气;叹息样呼吸可以通过增加CO、CPP及降低RAP产生对自主循环的恢复产生有益的生理作用.

Abstract：

Objective Gasp was defined as a pathology respiration during cardiac arrest. This study was to investigate its effect on hemodynamics during CPR. Method Twelve domestic pigs, weighening (30 ± 1) kg,were anaesthetized. After tracheal intubation and mechanical ventilation, continuous respiratory variables were recorded. An artery catheter was inserted for reference blood samples and measuring aortic artery pressure (AOP).Right atrial pressure (RAP) and cardiac output (CO) were detected by Swan-Ganz catheter. Ventricular fibrillation (VF) was induced by programmed electrical stimulation instruments. After 4 minutes untreated VF, standard 30:2 CPR was done for 12 minutes and the parameters were recorded. Results pH, PaCO2 and lactic acid increased and PaO2 decreased progressively during CPR, whereas PaO2 was up to 50mmHg during the whole protocol. Gasps were observed in 10 animals, but weaken gradually; the left 2 animals with no gasp did not restore of spontaneous circulation (ROSC). Standard CPR could produce passive ventilation more than dead space (VD), but its tidal volume decreased gradually, which led to the percentage of rescue ventilation increased progressively. Positive correlations were found between CO, coronary perfusion pressure (CPP) and minute ventilation of gasps (MVg) (r was 0.736 and 0.721 respectively, both P ＜0.01); negative correlation were found between RAP and MVg (r= -0. 744, P ＜ 0.01). Conclusions Standard CPR could maintain 12 minutes oxygenation of body; compressions could produce enough passive ventilation more than VD; gasps were benefit to ROSC by increasing CO, CPP and decreasing RAP.     

Hemodynamic improvement of a LUCAS 2 automated device by addition of an impedance threshold device in a pig model of cardiac arrest

Introduction

The combination of the LUCAS 2 (L-CPR) automated CPR device and an impedance threshold device (ITD) has been widely implemented in the clinical field. This animal study tested the hypothesis that the addition of an ITD on L-CPR would enhance cerebral and coronary perfusion pressures.

Methods

Ten female pigs (39.0 ± 2.0 kg) were sedated, intubated, anesthetized with isofluorane, and paralyzed with succinylcholine (93.3 μg/kg/min) to inhibit the potential confounding effect of gasping. After 4 min of untreated ventricular fibrillation, 4 min of L-CPR + an active ITD or L-CPR + a sham ITD was initiated and followed by another 4 min of the alternative method of CPR. Systolic blood pressure (SBP), diastolic blood pressure (DBP), diastolic right atrial pressure (RAP), intracranial pressure (ICP), airway pressure, and end tidal CO₂ (ETCO₂) were recorded continuously. Data expressed as mean mmHg ± SD.

Results

Decompression phase airway pressure was significantly lower with L-CPR + active ITD versus L-CPR + sham ITD (−5.3 ± 2.2 vs. −0.5 ± 0.6; p < 0.001). L-CPR + active ITD treatment resulted in significantly improved hemodynamics versus L-CPR + sham ITD: ETCO₂, 35 ± 6 vs. 29 ± 7 (p = 0.015); SBP, 99 ± 9 vs. 93 ± 15 (p = 0.050); DBP, 24 ± 12 vs. 19 ± 15 (p = 0.006); coronary perfusion pressure, 29 ± 8 vs. 26 ± 7 (p = 0.004) and cerebral perfusion pressure, 24 ± 13 vs. 21 ± 12 (p = 0.028).

Conclusions

In pigs undergoing L-CPR the addition of the active ITD significantly reduced intrathoracic pressure and increased vital organ perfusion pressures.     

The effects of changes to the ERC resuscitation guidelines on no flow time and cardiopulmonary resuscitation quality: a randomised controlled study on manikins

AIM OF THE STUDY: The European Resuscitation Council (ERC) guidelines changed in 2005. We investigated the impact of these changes on no flow time and on the quality of cardiopulmonary resuscitation (CPR). MATERIALS AND METHODS: Simulated cardiac arrest (CA) scenarios were managed randomly in manikins using ERC 2000 or 2005 guidelines. Pairs of paramedics/paramedic students treated 34 scenarios with 10min of continuous ventricular fibrillation. The rhythm was analysed and defibrillation shocks were delivered with a semi-automatic defibrillator, and breathing was assisted with a bag-valve-mask; no intravenous medication was given. Time factors related to human intervention and time factors related to device, rhythm analysis, charging and defibrillation were analysed for their contribution to no flow time (time without chest compression). Chest compression quality was also analysed. RESULTS: No flow time (mean+/-S.D.) was 66+/-3% of CA time with ERC 2000 and 32+/-4% with ERC 2005 guidelines (P<0.001). Human factor interventions occupied 114+/-4s (ERC 2000) versus 107+/-4s (ERC 2005) during 600-s scenarios (P=0.237). Device factor interventions took longer using ERC 2000 guidelines: 290+/-19s versus 92+/-15s (P<0.001). The total number of chest compressions was higher with ERC 2005 guidelines (808+/-92s versus 458+/-90s, P<0.001), but the quality of CPR did not differ between the groups. CONCLUSIONS: The use of a single shock sequence with guidelines 2005 has decreased the no flow time during CPR when compared with guidelines 2000 with multiple shocks.     

Ventricular fibrillation induced by transoesophageal cardiac pacing: a new model of cardiac arrest in rats

OBJECTIVE: To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. METHODS: A pacing electrode was inserted orally into the oesophagus and high-frequency ventricular pacing was performed so as to elicit VF in 25 Sprague-Dawley rats. Incidences of VF and time of cardiac pacing were observed and recorded. Four minutes after onset of VF cardiopulmonary resuscitation (CPR) was initiated. RESULTS: A short interval of high-frequency ventricular pacing caused an immediate drop of blood pressure, loss of pulse and increase of right atrial pressure in the same time frame. When the cardiac pacing was terminated, VF was elicited at least once or more than once in all of the 25 rats. However, the VF elicited by the burst stimulation could be defibrillated spontaneously. With the prolongation (120-180 s) of cardiac pacing, the incidence of defibrillation of VF decreased from 100 to 0%. VF persisted in 19 of 25 animals, developed into asystole in 5 of 25 animals and converted into pulseless electrical activity in 1 of 25 animals prior to CPR. Following CPR 22 of 25 animals were resuscitated. CONCLUSIONS: Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.     

Augmentation of tissue perfusion by a novel compression device increases neurologically intact survival in a porcine model of prolonged cardiac arrest

OBJECTIVE: This study was performed to determine the potential efficacy of an automated device with a load-distributing band (AutoPulse, Revivant Corporation), in improving neurologically intact survival after cardiac arrest. DESIGN: Randomized, controlled trial. SETTING: University animal laboratory. SUBJECTS: Forty-four swine (18-23 kg). INTERVENTIONS: Eight minutes after induction of untreated ventricular fibrillation, pigs were randomized to AutoPulse-CPR (A-CPR, n = 22), conventional cardiopulmonary resuscitation (CPR) with 20% anterior-posterior chest displacement (C-CPR20, n = 10) or 30% chest displacement (C-CPR30, n = 12), followed by resuscitation protocol with ventilation, defibrillation and intravenous epinephrine (adrenaline). MEASUREMENTS AND MAIN RESULTS: Aortic and right atrium blood pressure was measured with micromanometers. Regional blood flows were measured with microspheres. Coronary perfusion pressure during A-CPR was significantly higher as compared to C-CPR without epinephrine (A-CPR versus C-CPR20 versus C-CPR30; 16 +/- 1 mmHg versus 7 +/- 2 mmHg versus 11 +/- 2 mmHg, p < 0.05). A-CPR improved both myocardial flow without epinephrine (A-CPR versus C-CPR20 versus C-CPR30; 23% versus 0% versus 4%; percent of baseline, p < 0.05) and cerebral blood flow (40% versus 4% versus 19%, percent of baseline, p < 0.05). Sixteen of 22 animals receiving A-CPR regained spontaneous circulation and survived; 14/22 had normal cerebral performance (CPC 1). Four of 12 animals receiving C-CPR30 regained spontaneous circulation and survived, but only one animal had normal neurological function (14/22 versus 1/12, p < 0.0001). No animal receiving C-CPR20 achieved spontaneous circulation. At necropsy, 67% of C-CPR30 had rib fracture and 33% showed lung injury, while A-CPR and C-CPR20 resulted in no detectable injuries. CONCLUSIONS: Improved hemodynamics with AutoPulse performed CPR results in improved neurologically intact survival without subsequent thoracic or pulmonary injuries in this porcine model of prolonged cardiac arrest.     

Conceptual models of coronary perfusion pressure and their relationship to defibrillation success in a porcine model of prolonged out-of-hospital cardiac arrest

Introduction

The amount of myocardial perfusion required for successful defibrillation after cardiac arrest is unknown. Coronary perfusion pressure (CPP) is a surrogate for myocardial perfusion. One limited clinical study identifies a threshold of 15 mmHg required for return of spontaneous circulation (ROSC). Our exploration of threshold and dose models of CPP during the initial bout of CPR indicates higher levels than previously demonstrated are required. CPP required for shock success throughout on-going resuscitation is unknown and other conceptual models of CPP have not been explored.

Hypothesis

An array of conceptual models of CPP is associated with and predicts defibrillation success throughout resuscitation.

Methods

Data from 6 porcine cardiac arrest studies were pooled. Mean and area under the curve (AUC) CPP were derived for 30-s epochs. Five conceptual models of CPP were analyzed: threshold, delta, cumulative delta, dose, and cumulative dose. Comparative statistics were performed with one-way ANOVA and two-tailed t-test. Regression models assessed CPP trends and prediction of ROSC.

Results

For 316 defibrillation attempts in 124 animals, those resulting in ROSC (n = 75) had significantly higher threshold, delta, cumulative delta, dose, and cumulative dose CPP than those without. All conceptual models except delta CPP had significantly different values across successive defibrillation attempts and all five models were significant predictors of ROSC, along with experimental design.

Conclusions

Threshold, delta, cumulative delta, dose, and cumulative dose CPP predict individual defibrillation success throughout resuscitation.     

新型大鼠心跳骤停和复苏的机械装置

目的研发由电磁阀系统总控制、压缩气体驱动的新型大鼠电刺激诱发心跳骤停和复苏的机械装置,并探讨其有效性和安全性。方法选用Sprague-Dawley雄性大鼠20只,应用自主开发研制的心跳骤停和复苏机械装置,持续交流电经右心室内膜致颤。在6min心室颤动后,开始给予6min的机械胸外按压和同步机械通气,随后双向波经胸体外除颤。结果15只大鼠复苏成功,自主循环恢复率为75%。电刺激后所有大鼠立刻出现心室颤动,3min的电刺激停止后动物持续表现为室颤而没有自发转复心律现象。心肺复苏期间恢复自主循环组其冠状动脉灌注压恒定在24mmHg左右,显著高于未能恢复自主循环组。结论本新型大鼠心跳骤停和心肺复苏装置的有效性和安全性高,可最大限度减少实验的误差,具有一定的推广应用前景。     

亚低温治疗犬心脏骤停复苏后心功能研究

目的 明确亚低温对室颤复苏后犬心功能及心律失常的影响.方法 12头比格犬随机(随机数字法)分成两组(n=6):常温复苏组(37.0±0.2)℃和亚低温组(34.0±0.2)℃,通过快速电刺激诱导室颤,7 min后行心肺复苏,动态观察比较两组犬的心率、左心室收缩力指数、室性心律失常、除颤能量、肾上腺素用量及复苏后1周心超变化.结果 ①与室颤前比较,两组犬左心室收缩力指数在复苏后均有不同程度降低(P＜0.05),但亚低温组下降幅度小于常温组,且心率低于常温组(141±19)次/minvs.(163±31)次/min,P＜0.05.②与常温组比较,亚低温组犬室性心律失常发生的次数明显减少(P＜0.05),但是除颤次数、肾上腺素用量差异无统计学意义(P＞0.05).③复苏后1周,两组犬的心超结果显示,心脏结构及射血分数均恢复正常.结论 亚低温治疗可改善心脏骤停复苏后心肌收缩力,降低室性心律失常发生率.本研究结果提示,亚低温对复苏后心功能有一定的保护作用.     

Recurrent ventricular fibrillation during advanced life support care of patients with prehospital cardiac arrest

AIM OF THE STUDY: The response of recurrent episodes of ventricular fibrillation (VF) to defibrillation shocks has not been systematically studied. We analyzed outcomes from countershocks delivered for VF during advanced life support (ALS) care of patients with out-of-hospital cardiac arrest. METHODS: Cohort of patients with prehospital cardiac arrest presenting with VF, treated by ALS ambulance staff following ERC Guidelines 2000. Biphasic defibrillators provided shocks increasing from 200 to 360J. Recorded signals were analyzed to determine, for each shock, if VF was terminated and if a sustained organized rhythm was restored within 60s. RESULTS: In 465 of the 467 patients enrolled, the initial VF episode was terminated within three shocks: 92%, 61%, and 83% responded to 200J first, 200J second and 360J third shocks, respectively. VF recurred in 48% of patients within 2min of the first episode, and in 74% sometime during prehospital care. In the 175 patients experiencing five or more VF episodes, single shock VF termination dropped from the first to the fifth episode (90-80%, p<0.001) without change in transthoracic impedance, yet the proportion returning to organized rhythms increased (11-42%, p<0.0001). CONCLUSIONS: Repeated refibrillation is common in patients with VF cardiac arrest. The likelihood of countershocks to terminate VF declines for repeated episodes of VF, yet shocks that terminate these episodes result increasingly in a sustained organized rhythm.     

长时程室颤先行心肺复苏对复苏效果的影响及机制研究

目的 比较7 min室颤先行心肺复苏2 min后除颤与直接除颤的复苏效果,并探讨其机制.方法 建立猪闭胸电诱发室颤模型,CPR First组优先心肺复苏2 min后连续三次除颤,Shock First组直接予连续三次除颤,观察冠脉灌注压、室颤波频率和振幅变化,计算除颤成功率和自主循环恢复率.结果 CPR First组先行心肺复苏2 min后可提高初次除颤前的冠脉灌注压、室颤波的频率和振幅, CPR First组比Shock First组有高的除颤成功率和自主循环恢复率(P＜0.05).结论 7 min室颤除颤前先行胸外按压和人工呼吸可明显提高复苏成功率,其机制与增加冠脉灌注,改善心脏能量储备,提高室颤波的频率和振幅有关.     

Available ventilation monitoring methods during pre-hospital cardiopulmonary resuscitation

High quality cardiopulmonary resuscitation (CPR) in the pre-hospital setting has been associated with improved survival rates during cardiopulmonary arrest (CPA). Recent documentation of hyperventilation associated deterioration in hemodynamics during CPR, suggests that guided or controlled ventilation strategies may contribute to improved hemodynamics and increased survival. This article briefly reviews the mechanical methods, advantages, and disadvantages of the available ventilation monitoring methods currently available for clinical use, with an emphasis on pre-hospital implementation. We recommend that more objective measurement of ventilation during CPR be performed, with emphasis on a strategy for measuring both attempted ventilation frequency (f) and delivered tidal volume (VT). The use of improved thoracic impedance pneumography and capnography are appealing for such monitoring because of the widespread availability, but modifications to existing software and clinical data compared to a clinical standard would be required before general acceptance is possible. Other methods listed may offer advantages over these in select circumstances.     

Assessment of a three-phase model of out-of-hospital cardiac arrest in patients with ventricular fibrillation

AIM: Cardiac arrest with ventricular fibrillation (VF) has been divided into three phases in which phase-specific therapy may improve outcome. The aim of this study was to assess the relationship between call-to-shock time, bystander CPR (BCPR), and cardiac arrest outcomes. METHODS: In a retrospective analysis of prospectively-acquired data from witnessed VF out-of-hospital cardiac arrests (OHCA), patients were classified as phases 1, 2, or 3 based on call-to-shock time (<5, 5-8, and >8 min) and further stratified based on performance of BCPR. Groups were compared with regard to survival, neurological outcome, and restoration of spontaneous circulation (ROSC) with defibrillation only (no ALS interventions to achieve sustained ROSC). RESULTS: Survival, neurologically intact survival, and ROSC with defibrillation were different between phases 1 and 2 (p=0.014 and p=0.005, p<0.01) but not between phases 2 and 3. Patients were further classified as having received BCPR (N=111) or no BCPR (N=107). Neurologically intact survival with and without BCPR, respectively, was 61% versus 72% (phase 1), 44% versus 41% (phase 2), and 42% versus 29% (phase 3). ROSC with defibrillation only with and without BCPR, respectively, was 64% versus 56% (phase 1), 37.0% versus 29% (phase 2), and 33% versus 8% (phase 3). ROSC with defibrillation alone was statistically higher in univariate analysis in phase 3 with BCPR (p=0.033) but not in multivariate analysis (p=0.068). CONCLUSIONS: BCPR did not significantly improve survival in any phase of OHCA, though there was a trend toward increased neurologically intact survival and increased ROSC with defibrillation alone in phase 3.     

东菱克栓酶在心脏骤停兔心肺复苏时的治疗作用

目的研究东菱克栓酶能否提高心脏骤停(CA)兔复苏成功率.方法将30只兔随机分成2组,即溶栓组和对照组,所有动物室颤10 min后行心肺复苏(CPR),溶栓组在开始CPR时静脉注射东菱克栓酶0.3 BU/kg.结果溶栓组复苏成功率明显大于对照组(P<0.05),溶栓组24h后仍有3只兔子成活,对照组24h后所有兔子均死亡.结论东菱克栓酶能提高兔心肺复苏成功率.     

A tourniquet assisted cardiopulmonary resuscitation augments myocardial perfusion in a porcine model of cardiac arrest

ObjectiveDuring cardiopulmonary resuscitation (CPR), myocardial blood flow generated by chest compression rarely exceeds 35% of its normal level. Cardiac output generated by chest compression decreases gradually with the prolongation of cardiac arrest and resuscitation. Early studies have demonstrated that myocardial blood flow during CPR is largely dependent on peripheral vascular resistance. In this study, we investigated the effects of chest compression in combination with physical control of peripheral vascular resistance assisted by tourniquets on myocardial blood flow during CPR.MethodsVentricular fibrillation was induced and untreated for 7 min in ten male domestic pigs weighing between 33 and 37 kg. The animals were then randomized to receive CPR alone or a tourniquet assisted CPR (T-CPR). In the CPR alone group, chest compression was performed by a miniaturized mechanical chest compressor. In the T-CPR group, coincident with the start of resuscitation, the thin elastic tourniquets were wrapped around the four limbs from the distal end to the proximal part. After 2 min of CPR, epinephrine (20 μg/kg) was administered via the femoral vein. After 5 min of CPR, defibrillation was attempted by a single 150 J shock. If resuscitation was not successful, CPR was resumed for 2 min before the next defibrillation. The protocol was continued until successful resuscitation or for a total of 15 min. Five minutes after resuscitation, the elastic tourniquets were removed. The resuscitated animals were observed for 2 h.ResultsT-CPR generated significantly greater coronary perfusion pressure, end-tidal carbon dioxide and carotid blood flow. There was no difference in both intrathoracic positive and negative pressures between the two groups. All animals were successfully resuscitated with a single shock in both groups. There were no significant changes in hemodynamics observed in the animals treated in the T-CPR group before-and-after the release of tourniquets at post-resuscitation 5 min.ConclusionsT-CPR improves myocardial and cerebral perfusion during CPR. It may provide a new and convenient method for augmenting myocardial and cerebral blood flow during CPR.