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


METHODS
Prospective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs.


METHODS
University cerebral resuscitation laboratory.


METHODS
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.


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.
Shaffner
D H
DH
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Eleff
S M
SM
Brambrink
A M
AM
Sugimoto
H
H
Izuta
M
M
Koehler
R C
RC
Traystman
R J
RJ
D000136:Acid-Base Equilibrium / Q000502:physiology*; D000244:Adenosine Diphosphate / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004285:Dogs; D004734:Energy Metabolism / Q000502:physiology*; D006323:Heart Arrest / Q000503:physiopathology* / Q000628:therapy; D009682:Magnetic Resonance Spectroscopy; D010100:Oxygen / Q000378:metabolism; D011446:Prospective Studies; D011897:Random Allocation; D012039:Regional Blood Flow; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000503:physiopathology
D000244:Adenosine Diphosphate; D010100:Oxygen