Regional blood flow during closed-chest cardiac resuscitation in rats
Institute of Critical Care Medicine, University of Health Sciences, Chicago Medical School, Illinois 60064.Journal of Applied Physiology (Impact Factor: 3.06). 01/1993; 74(1):147-52.
Quantitative measurement of regional blood flow during cardiac arrest and resuscitation has been confined to large animals. We report on a rodent model utilizing radioactive microspheres during cardiac arrest and resuscitation for investigation of regional blood flow. Ventricular fibrillation was electrically induced in 10 pentobarbital-anesthetized Sprague-Dawley rats. Resuscitation was attempted by precordial compression followed by external direct current countershock. During precordial compression, cardiac output corresponded to 12% of prearrest flow. Similarly low flows were observed in the myocardium and brain. However, much lower flows were observed in the adrenal glands, kidneys, intra-abdominal viscera, skin, and skeletal muscle. Five of ten animals were successfully resuscitated. During precordial compression, resuscitated animals had significantly higher cardiac output (13.1 +/- 4.1 vs. 8.6 +/- 1.46 ml/min), myocardial blood flow (0.70 +/- 0.24 vs. 0.22 +/- 0.15 ml.min-1.g-1), cerebral blood flow (0.17 +/- 0.04 vs. 0.06 +/- 0.02 ml.min-1.g-1), and adrenal blood flow (1.09 +/- 0.60 vs. 0.27 +/- 0.16 ml.min-1.g-1). Thirty minutes after successful resuscitation, cardiac output and myocardial, cerebral, renal, and adrenal blood flows and blood flow to splanchnic viscera (with the exception of the spleen) had returned to > or = 70% of prearrest flows. These studies confirm the conclusion of earlier investigations in larger animals that visceral blood flow during cardiac arrest and precordial compression is preferentially distributed to the brain and myocardium. Successful cardiac resuscitation is contingent on threshold levels of myocardial blood flow that exceed 0.4 ml.min-1.g-1.
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ABSTRACT: Evaluation of the effects of nimodipine administration during and after cardiopulmonary resuscitation (CPR) on oxygen delivery and consumption was the aim of this study. A randomized double-blind study in 32 anesthetized domestic pigs was performed. After 5 minutes of ventricular fibrillation (VF) and 5 minutes of external CPR, epinephrine (50 micrograms/kg) and either nimodipine or placebo (10 micrograms/kg bolus, 1 microgram/kg/min continuously throughout 4 hours of observation) were administered. One minute later (equal to 11 minutes VF), the first countershock was given. If this failed to restore spontaneous circulation, epinephrine and countershocks were repeated for a maximum of 30 minutes. Eleven of 12 nimodipine- and 7 of 14 placebo-treated pigs could be resuscitated successfully and survived the observation period (P < .05). Hemodynamic responses to nimodipine were characterized by significant decreases in systemic vascular resistance and mean arterial pressure from 10 minutes after restoration of spontaneous circulation onwards with consequent significant increases in cardiac output. Median systemic oxygen delivery indices (DO2I) in nimodipine-treated pigs were significantly higher at all measuring points when compared with placebo-treated animals. Median systemic oxygen consumption indices (VO2I) did not differ significantly between groups. Median oxygen extraction ratios in nimodipine-treated pigs were in the same range as prearrest and were lower when compared with placebo-treated pigs (at 30 minutes P < .05 and at 120 minutes P < .01). DO2I and VO2I were poorly correlated in all pigs treated with nimodipine and in 3 of 7 animals treated with placebo, suggesting supply independency in these animals. This difference between groups was significant (P < .05). Our findings suggest that in nimodipine-treated animals, a lower oxygen deficit or a better redistribution of regional blood flow occurred after circulatory arrest and resuscitation.Journal of Critical Care 03/1994; 9(1):18-24. DOI:10.1016/0883-9441(94)90029-9 · 2.00 Impact Factor
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ABSTRACT: We describe the case of a 6-month-old achondroplastic baby who underwent foramen magnum decompression to relieve congenital cervical cord compression. During the procedure, acute hypotension occurred secondary to cord compression, and following attempts to alleviate this, torrential haemorrhage ensued and air was entrained into the circulation through large venous channels in the surgical field. This resulted in an asystolic cardiac arrest from which the baby was resuscitated whilst remaining in the prone position. Haemorrhage remained difficult to control and a second episode of air embolism occurred 5min later leading to a profound bradycardia and hypotension again requiring full cardiorespiratory resuscitation in the prone position. In total, 11 min elapsed before an adequate spontaneous cardiac output was re-established. The procedure was abandoned and the patient transferred to the intensive care unit for postoperative management. An electroencephalogram performed after 24 h was reported as normal, and clinically the child made a full neurological recovery.Anaesthesia 03/1995; 50(4):348 - 350. DOI:10.1111/j.1365-2044.1995.tb04615.x · 3.38 Impact Factor
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ABSTRACT: To evaluate the efficacy of conventional threshold levels of coronary perfusion pressure and end-tidal CO2 as predictors of resuscitability after prolonged cardiac arrest. Prospective, randomized, controlled animal study. University research laboratory. Twenty-one Sprague-Dawley rats, including three groups of seven animals in each group. Ventricular fibrillation was untreated for 9, 12, or 15 mins. After an additional 5-min interval of precordial compression, external direct current defibrillation was attempted. All animals were successfully resuscitated after 9 mins of ventricular fibrillation but less than one half of the animals were successfully resuscitated after 15 mins of ventricular fibrillation. Each of seven animals survived for 24 hrs after 9 mins of untreated ventricular fibrillation but none of the animals survived after 15 mins of ventricular fibrillation. In this experimental setting, neither coronary perfusion pressure nor end-tidal CO2 produced by precordial compression was predictive of outcomes when the animals underwent progressively longer intervals of untreated cardiac arrest. The efficacy of precordial compression--as measured by coronary perfusion pressure and end-tidal CO2 concentration after prolongation of untreated cardiac arrest--was not overtly compromised. However, the previously established critical threshold levels of coronary perfusion pressure and end-tidal CO2 failed as predictors of resuscitability after prolonged intervals of untreated cardiac arrest.Critical Care Medicine 08/1995; 23(7):1233-6. DOI:10.1097/00003246-199507000-00013 · 6.31 Impact Factor
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