Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs.

OBJECTIVES To test the hypothesis that greater cerebral perfusion pressure (CPP) is required to restore cerebral blood flow (CBF), oxygen metabolism, adenosine triphosphate (ATP), and intracellular pH (pHi) levels after variable periods of no-flow than to maintain them when cardiopulmonary resuscitation (CPR) is started immediately. DESIGN Prospective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs. SETTING University cerebral resuscitation laboratory. INTERVENTIONS We used radiolabeled microspheres to determine CBF and magnetic resonance spectroscopy to derive ATP and pHi levels before and during CPR. Ventricular fibrillation was induced, epinephrine administered, and thoracic vest CPR adjusted to provide a CPP of 25 or 35 mm Hg after arrest times of O, 6, or 12 mins. MEASUREMENTS AND MAIN RESULTS When CPR was started immediately after arrest with a CPP of 25 mm Hg, CBF and ATP were 57 +/- 10% and 64 +/- 14% of prearrest (at 10 mins of CPR). In contrast, CBF and ATP were minimally restored with a CPP at 25 mm Hg after a 6-min arrest time (23 +/- 5%, 16 +/- 5%, respectively). With a CPP of 35 mm Hg, extending the no-flow arrest time from 6 to 12 mins reduced reflow from 71 +/- 11% to 37 +/- 7% of pre-arrest and reduced ATP recovery from 60 +/- 11% to 2 +/- 1% of pre-arrest. After 6- or 12-min arrest times, brainstem blood flow was restored more than supratentorial blood flow, but cerebral pHi was never restored. CONCLUSIONS A CPP of 25 mm Hg maintains supratentorial blood flow and ATP at 60% to 70% when CPR starts immediately on arrest, but not after a 6-min delay. A higher CPP of 35 mm Hg is required to restore CBF and ATP when CPR is delayed for 6 mins. After a 12-min delay, even the CPP of 35 mm Hg is unable to restore CBF and ATP. Therefore, increasing the arrest time at these perfusion pressures increases the resistance to reflow sufficient to impair restoration of cerebral ATP.

[1]  R. Nowak,et al.  A technique revisited: hemodynamic comparison of closed- and open-chest cardiac massage during human cardiopulmonary resuscitation. , 1995, Critical care medicine.

[2]  H. Halperin,et al.  A preliminary study of cardiopulmonary resuscitation by circumferential compression of the chest with use of a pneumatic vest. , 1993, The New England journal of medicine.

[3]  M. Goetting,et al.  Simultaneous radial, femoral, and aortic arterial pressures during human cardiopulmonary resuscitation , 1993, Critical care medicine.

[4]  B. Siesjö,et al.  Coupling of Energy Failure and Dissipative K+ Flux during Ischemia: Role of Preischemic Plasma Glucose Concentration , 1993, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[5]  B. Siesjö,et al.  Coupling of cellular energy state and ion homeostasis during recovery following brain ischemia , 1993, Brain Research.

[6]  M. C. Rogers,et al.  Brain bioenergetics during cardiopulmonary resuscitation in dogs. , 1992, Anesthesiology.

[7]  R. Koehler,et al.  Effect of Adrenergic Drugs on Cerebral Blood Flow, Metabolism, and Evoked Potentials After Delayed Cardiopulmonary Resuscitation in Dogs , 1991, Stroke.

[8]  M. Goetting,et al.  Simultaneous aortic, jugular bulb, and right atrial pressures during cardiopulmonary resuscitation in humans. Insights into mechanisms. , 1989, Circulation.

[9]  M. C. Rogers,et al.  Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine. , 1989, Circulation.

[10]  P. Safar,et al.  Effect of cardiac arrest time on cortical cerebral blood flow during subsequent standard external cardiopulmonary resuscitation in rabbits. , 1989, Resuscitation.

[11]  W. Weaver,et al.  Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation. , 1988, Circulation.

[12]  Henry R. Halperin,et al.  Progranmable Pneumatic Generator for Manipulation of Intrathoracic Pressure , 1987, IEEE Transactions on Biomedical Engineering.

[13]  M. C. Rogers,et al.  Beneficial effect of epinephrine infusion on cerebral and myocardial blood flows during CPR. , 1985, Annals of emergency medicine.

[14]  P. Safar,et al.  Cerebral preservation during cardiopulmonary resuscitation , 1985, Critical care medicine.

[15]  M. Weisfeldt,et al.  Transmission of Intrathoracic Pressure to the Intracranial Space during Cardiopulmonary Resuscitation in Dogs , 1985, Circulation research.

[16]  M. C. Rogers,et al.  Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. , 1984, Circulation.

[17]  M. C. Rogers,et al.  Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. , 1983 .

[18]  J I Hoffman,et al.  Blood flow measurements with radionuclide-labeled particles. , 1977, Progress in cardiovascular diseases.