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

Donald H. Shaffner, Scott M. Eleff, Ansgar Brambrink, Hide Sugimoto, Makoto Izuta, Raymond C. Koehler, Richard J. Traystman

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

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 0, 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.

Original languageEnglish (US)
Pages (from-to)1335-1342
Number of pages8
JournalCritical Care Medicine
Volume27
Issue number7
DOIs
StatePublished - Jul 1999
Externally publishedYes

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Cerebrovascular Circulation
Cardiopulmonary Resuscitation
Adenosine Triphosphate
Dogs
Perfusion
Pressure

Keywords

  • Cardiac arrest
  • Cardiopulmonary resuscitation
  • Cerebral blood flow
  • Dogs
  • Metabolism
  • Spectroscopy, nuclear magnetic resonance
  • Ventricular fibrillation

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs. / Shaffner, Donald H.; Eleff, Scott M.; Brambrink, Ansgar; Sugimoto, Hide; Izuta, Makoto; Koehler, Raymond C.; Traystman, Richard J.

In: Critical Care Medicine, Vol. 27, No. 7, 07.1999, p. 1335-1342.

Research output: Contribution to journalArticle

Shaffner, Donald H. ; Eleff, Scott M. ; Brambrink, Ansgar ; Sugimoto, Hide ; Izuta, Makoto ; Koehler, Raymond C. ; Traystman, Richard J. / Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs. In: Critical Care Medicine. 1999 ; Vol. 27, No. 7. pp. 1335-1342.
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abstract = "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 0, 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.",
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T1 - Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs

AU - Shaffner, Donald H.

AU - Eleff, Scott M.

AU - Brambrink, Ansgar

AU - Sugimoto, Hide

AU - Izuta, Makoto

AU - Koehler, Raymond C.

AU - Traystman, Richard J.

PY - 1999/7

Y1 - 1999/7

N2 - 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 0, 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.

AB - 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 0, 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.

KW - Cardiac arrest

KW - Cardiopulmonary resuscitation

KW - Cerebral blood flow

KW - Dogs

KW - Metabolism

KW - Spectroscopy, nuclear magnetic resonance

KW - Ventricular fibrillation

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