Xiaoye Lu

Fluid resuscitation guided by sublingual partial pressure of carbon dioxide during hemorrhagic shock in a porcine model.

ABSTRACT To avoid aggressive fluid resuscitation during hemorrhagic shock, fluid resuscitation is best guided by a specific measurement of tissue perfusion. We investigated whether fluid resuscitation guided by sublingual PCO2 would reduce the amount of resuscitation fluid without compromising the outcomes of hemorrhagic shock. Ten male domestic pigs weighing between 34 and 37 kg were used. Forty-five percent of estimated blood volume was removed during an interval of 1 h. The animals were then randomized to receive fluid resuscitation based on either sublingual PCO2 or blood pressure (BP). In the sublingual PCO2–guided group, resuscitation was initiated when sublingual PCO2 exceeded 70 Torr and stopped when it decreased to 50 Torr. In the BP-guided group, resuscitation was initiated when mean aortic pressure decreased to 60 mmHg and stopped when it increased to 90 mmHg. First, Ringer’s lactate solution (RLS) of 30 mL kg−1 was administered; subsequently, the shed blood was transfused if sublingual PCO2 remained greater than 50 Torr in the sublingual PCO2–guided group or mean aortic pressure was less than 90 mmHg in the BP-guided group. All the animals were monitored for 4 h and observed for an additional 68 h. In the sublingual PCO2–guided group, fluid resuscitation was required in only 40% of the animals. In addition, a significantly lower volume of RLS (170 ± 239 mL, P = 0.005 vs. BP-guided group) was administered without the need for blood infusion in this group. However, in the BP-guided group, all the animals required a significantly larger volume of fluid (955 ± 381 mL), including both RLS and blood. There were no differences in postresuscitation tissue microcirculation, myocardial and neurologic function, and 72-h survival between groups. During hemorrhagic shock, fluid resuscitation guided by sublingual PCO2 significantly reduced the amount of resuscitation fluid without compromising the outcomes of hemorrhagic shock.

The effects of the rate of postresuscitation rewarming following hypothermia on outcomes of cardiopulmonary resuscitation in a rat model.

Objective:To investigate the optimal rewarming rate following therapeutic hypothermia in a rate model of cardiopulmonary resuscitation. Both clinical and laboratory studies have demonstrated that mild therapeutic hypothermia following cardiopulmonary resuscitation improves myocardial and neurologic outcomes of cardiac arrest. However, the optimal rewarming strategy following therapeutic hypothermia remains to be explored. Design:Prospective randomized controlled experimental study. Setting:University-affiliated research institution. Subjects:Twenty-three healthy male Sprague-Dawley rats. Interventions:Four groups of Sprague-Dawley rats were randomized: 1) normothermia group (control), 2) rewarming rate at 2°C/hr, 3) rewarming rate at 1°C/hr, and 4) rewarming rate at 0.5°C/hr. Ventricular fibrillation was induced and untreated for 8 minutes, and defibrillation was attempted after 8 minutes of cardiopulmonary resuscitation. For the 2, 1, and 0.5°C/hr groups, rapid cooling was started at the beginning of cardiopulmonary resuscitation. On reaching the target cooling temperature of 33°C ± 0.2°C, the temperature was maintained with the aid of a cooling blanket until 4 hours after resuscitation. Rewarming was then initiated at the rate of 2.0, 1.0, or 0.5°C/hr, respectively, until the body temperature reached 37°C ±0.2°C. Blood samples were drawn at baseline and postresuscitation of 4, 6, 8, 10, and 12 hours for the measurements of blood gas and serum biomarkers. Measurements and Main Results:Blood temperature significantly decreased in the hypothermic groups from cardiopulmonary resuscitation to postresuscitation 4 hours. Significantly better cardiac output, ejection fraction, myocardial performance index, reduced neurologic deficit scores, and longer duration of survival were observed in the 1 and 0.5°C/hr groups. The increased serum concentration of troponin I, interleukin-6, and tumor necrosis factor-&agr; was partly attenuated in the 1 and 0.5°C/hr groups when compared with the control and 2°C/hr groups. Conclusions:This study demonstrated that the severity of myocardial, cerebral injuries, and inflammatory reaction after cardiopulmonary resuscitation was reduced when mild therapeutic hypothermia was applied. A rewarming rate at 0.5–1°C/hr did not alter the beneficial effects of therapeutic hypothermia. However, a rapid rewarming rate at 2°C/hr abolished the beneficial effects of hypothermia.

Remote ischemic pre- and postconditioning improve postresuscitation myocardial and cerebral function in a rat model of cardiac arrest and resuscitation.

Objectives:Cardiac arrest and resuscitation are models of whole body ischemia reperfusion injury. Postresuscitation myocardial and cerebral dysfunction are major causes of high mortality and morbidity. Remote ischemic postconditioning has been proven to provide potent protection of the heart and brain against ischemia reperfusion injury. In this study, we investigated the effects of remote ischemic postconditioning on postresuscitation myocardial and cerebral function in a rat model of cardiac arrest and resuscitation. Design:Prospective, randomized, controlled experimental study. Setting:University-affiliated animal research institution. Subjects:Twenty-eight healthy male Sprague-Dawley rats. Interventions:The animals were randomized into four groups: 1) remote ischemic preconditioning initiated 40 minutes before induction of ventricular fibrillation, 2) remote ischemic postconditioning initiated coincident with the start of cardiopulmonary resuscitation, 3) remote ischemic postconditioning initiated 5 minutes after successful resuscitation, and 4) control. Remote ischemic pre- and postconditioning was induced by four cycles of 5 minutes of limb ischemia, followed by 5 minutes of reperfusion. Ventricular fibrillation was induced and untreated for 6 minutes while defibrillation was attempted after 8 minutes of cardiopulmonary resuscitation. The animals were then monitored for 4 hours and observed for an additional 68 hours after resuscitation. Measurements and Main Results:Hemodynamic measurements and myocardial function, including cardiac output, left ventricular ejection fraction, and myocardial performance index, were measured at baseline and hourly for 4 hours after resuscitation. Postresuscitation cerebral function was evaluated by neurologic deficit score at 24-hour intervals for a total of 72 hours. Consequently, significantly better myocardial and cerebral function with a longer duration of survival were observed in the three groups treated with remote ischemic pre- and postconditioning. Conclusions:In a rat model of cardiac arrest and resuscitation, remote ischemic pre-and postconditioning attenuated postresuscitation myocardial and cerebral dysfunction and improved the duration of survival.

Improved cardiac and neurologic outcomes with postresuscitation infusion of cannabinoid receptor agonist WIN55, 212-2 depend on hypothermia in a rat model of cardiac arrest.

Objectives:To investigate the mechanisms of improved myocardial and neurological function and survival following IV administration of cannabinoid receptor agonist, WIN55, 212-2 in a rat model of cardiac arrest. Design:Prospective randomized controlled experimental study. Setting:University-affiliated research institute. Subjects:Thirty male Sprague-Dawley rats. Interventions:Ventricular fibrillation was electrically induced in 30 male Sprague-Dawley rats weighing between 450 and 550 g. Cardiopulmonary resuscitation was initiated after 6 minutes of untreated ventricular fibrillation. The precordial compression was performed with a pneumatically driven mechanical chest compressor. No pharmacological agent was used during cardiopulmonary resuscitation. After 8 minutes of cardiopulmonary resuscitation, up to three 2-J defibrillations were attempted. The animals were then randomized into three groups: 1) WIN55, 212-2 hypothermia, 2) WIN55, 212-2 with normal body temperature, and 3) placebo control. Either WIN55, 212-2 (1.0 mg/kg/hr) or saline placebo was continuously infused for 2 hours. Except for the WIN55, 212-2 hypothermia group, the body temperature in the other two groups was maintained at 37.0 ± 0.2°C using an external heating lamp. Postresuscitation myocardial function was measured by echocardiogram. Neurological deficit scores and survival time were observed for up to 72 hours. Measurements and Main Results:Blood temperatures decreased from 37°C to 33°C in 4 hours in animals in WIN55, 212-2 hypothermia group. Myocardial function, as measured by cardiac output, ejection fraction, and myocardial performance index, was significantly impaired in all animals after successful resuscitation when compared with the baseline values. There was a significant improvement in myocardial function in the animals treated with WIN55, 212-2 hypothermia beginning at 1 hour after start of infusion. However, no improvement was observed in the groups of WIN55, 212-2 with normal body temperature and placebo control. WIN55, 212-2 hypothermia group was associated with significantly improved neurologic deficit scores and survival time when compared with placebo control group and WIN55, 212-2 with normal body temperature group. Conclusions:In a rat model of cardiac arrest, better postresuscitation myocardial function, neurological deficit scores, and longer duration of survival were observed by the pharmacologically induced hypothermia with WIN55, 212-2. The improved outcomes of cardiopulmonary resuscitation following administration of WIN55, 212-2 appeared to be the results from its temperature reduction effects.

484: HYPOTHERMIA IMPROVES THE VENTRICULAR FIBRILLATION WAVEFORM DURING CARDIOPULMONARY RESUSCITATION

Introduction: Intra-arrest hypothermia improves the success of defibrillation. In the present study, we investigated whether intra-arrest hypothermia improves ventricular fibrillation (VF) waveform in a rat model of CPR. Methods: Twenty-six male Sprague-Dawley rats were randomized into two groups: n