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: 3.43). 01/1993; 74(1):147-52.
Source: PubMed

ABSTRACT 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: Objectives Several studies in patients who underwent open heart surgery found that myocardial ischemic damage was reduced by potassium cardioplegia combined with lidocaine infusion. The authors evaluated the effects of potassium/lidocaine-induced cardiac standstill during conventional cardiopulmonary resuscitation (CPR) on myocardial injury and left ventricular dysfunction after resuscitation from prolonged ventricular fibrillation (VF) cardiac arrest in a pig model.Methods Ventricular fibrillation was induced in 16 pigs, and circulatory arrest was maintained for 14 minutes. Animals were then resuscitated by standard CPR. Animals were randomized at the start of CPR to receive 20 mL of saline (control group) or 0.9 mEq/kg potassium chloride and 1.2 mg/kg lidocaine diluted to 20 mL (K-lido group).ResultsSeven animals in each group achieved return of spontaneous circulation (ROSC; p = 1.000). Four of the K-lido group animals (50%) achieved ROSC without countershock. Resuscitated animals in the K-lido group required fewer countershocks (p = 0.004), smaller doses of epinephrine (p = 0.009), and shorter durations of CPR (p = 0.004) than did the control group. The uncorrected troponin-I at 4 hours after ROSC was lower in the K-lido group compared with the control group (2.82 ng/mL, 95% confidence interval [CI] = 1.07 to 3.38 ng/mL vs. 6.55 ng/mL, 95% CI = 4.84 to 13.30 ng/mL; p = 0.025), although the difference was not significant after Bonferroni correction. The magnitude of reduction in left ventricular ejection fraction (LVEF) between baseline and 1 hour after ROSC was significantly lower in the K-lido group (26.5%, SD ± 6.1% vs. 39.1%, SD ± 6.8%; p = 0.004).Conclusions In a pig model of untreated VF cardiac arrest for 14 minutes, resuscitation with potassium/lidocaine-induced cardiac standstill during conventional CPR tended to reduce myocardial injury and decreased the severity of postresuscitation myocardial dysfunction significantly.ResumenObjetivosVarios estudios en pacientes en los que se llevó a cabo una cirugía a corazón abierto documentaron que el daño isquémico del miocardio se redujo por la infusión cardiopléjica de potasio combinada con lidocaína. Se evaluaron los efectos de la lidocaína y el potasio en la parada cardiaca inducida, durante la resucitación cardiopulmonar (RCP) convencional (RCP), en la lesión miocárdica y la disfunción ventricular izquierda tras la RCP de la parada cardiaca por fibrilación ventricular (FV) prolongada en un modelo de cerdo.MetodologíaSe indujo fibrilación ventricular en dieciséis cerdos, y se mantuvo la parada cardiorrespiratoria durante 14 minutos. Los animales fueron entonces resucitados mediante RCP convencional. Los animales se aleatorizaron a recibir 20 mL de salino (grupo control) o 0,9 mEq/kg de potasio clorhídrico y 1,2 mg/kg de lidocaína diluidos a 20 mL (grupo Lido-K), al inicio de la RCP.ResultadosSiete animales en cada grupo consiguieron la recuperación de la circulación espontánea (RCE) (p = 1,000). Cuatro de los animales del grupo Lido-K (50%) alcanzaron la RCE sin choques eléctricos. Los animales resucitados del grupo Lido-K requirieron menor número de choques eléctricos (p = 0,004), menor dosis de adrenalina (p = 0,009), y menor duración de la RCP (p = 0,004) que el grupo control. La troponina-I a las 4 horas tras RCE fue menor en el grupo Lido-K en comparación con el grupo control (2,82 ng/mL [IC 95% = 1,07 a 3,38 ng/mL] frente 6,55 ng/mL [IC 95% = 4,84 a 13,30 ng/mL] p = 0,025), aunque la diferencia no fue significativa tras la corrección de Bonferroni. La magnitud de la reducción en la fracción de eyección del ventrículo izquierdo entre el momento inicial y una hora tras la RCE fue significativamente menor en el grupo Lido-K (26,5% [DE ±6,1%] vs. 39,1% [DE ±6,8%]; p = 0,004).ConclusionesEn un modelo cerdo de parada cardiaca por FV en cerdos no tratada durante 14 minutos, el uso de lidocaína y potasio durante la RCP convencional tendió a reducir la lesión miocárdica y disminuyó la gravedad de la disfunción miocárdica tras la RCP de forma significativa.
    Academic Emergency Medicine 04/2014; 21(4). · 2.20 Impact Factor
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    ABSTRACT: BACKGROUND: There has been controversy over whether a short period of cardiopulmonary resuscitation (CPR) prior to defibrillation improves survival in patients who experienced a sudden cardiac arrest. However, there have been no reports about whether CPR restores the myocardial energy source during prolonged ventricular fibrillation (VF). The aim of this study is to investigate the effect of CPR in restoring myocardial high energy phosphates during prolonged VF. METHODS AND RESULTS: Seventy-two adult male Sprague-Dawley rats were used in this study. Baseline adenosine triphosphate (ATP) and adenosine diphosphate (ADP) prior to induction of VF were measured in nine rats, the No-VF group. Sixty-three rats were subjected to 4min of untreated VF. Animals were then randomized into two groups: No-CPR (n=37) and CPR (n=26). In the No-CPR group, ATPs and ADPs were measured at 4min (No-CPR4), 6min (No-CPR6), 8min (No-CPR8) or 10min (No-CPR10) after the induction of VF. The CPR group received 2min (CPR2), 4min (CPR4) or 6min (CPR6) of mechanical chest compressions before ATP was measured. Myocardial ATP (nmol/mg protein) was decreased as VF duration was prolonged (No-VF: 5.49±1.71, No-CPR4: 4.27±1.58, No-CPR6: 4.13±1.31, No-CPR8: 3.77±1.42, No-CPR10: 3.52±0.90, p<0.05 between each of No-CPRs vs. No-VF). Two minutes of CPR restored myocardial ATP to the level of No-VF group (5.27±1.67nmol/mg protein in CPR2, p>0.05 vs. No-VF group). However, myocardial ATP (nmol/mg protein) decreased if the duration of CPR was longer than 2min (CPR4: 3.77±1.05, CPR6: 3.49±1.08, p<0.05 between CPR4 and CPR6 vs. No-VF). CONCLUSIONS: CPR for 2min helps to maintain myocardial ATP after prolonged VF.
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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.
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