Cerebral blood flow during cardiopulmonary bypass: Influence of temperature and pH management strategy

W. Cheng, J. F. Hartmann, D. E. Cameron, E. M. Griffiths, Jeffrey Kirsch, R. J. Traystman

Research output: Contribution to journalArticle

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Abstract

Because disordered autoregulation of cerebral blood flow may underlie neurologic injury associated with cardiopulmonary bypass (CPB), we studied the effects of normothermic (37°C) and hypothermic (18°C) CPB on cerebral vascular reactivity in 6 to 8-week-old piglets. Hypothermic CPB animals were subdivided into alpha-stat and pH-stat groups (n = 6 animals each group) according to acid-base management protocol. Cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebral vascular resistance (CVR), and CBF response to hypercapnia were examined before, during, and 1 hour after CPB and used to calculate CVR per millimeter of mercury change in arterial partial pressure of CO2: (CVR(normocapnia) - CVR(hypercapnia))/(PaCO(2 hypercapnia) - PaCO2 normocapnia)). Before CPB, CBF, CMRO2, and vascular reactivity to elevated CO2 were similar in the three groups; these parameters remained unchanged by normothermic CPB. However, during hypothermic CPB, CBF and CMRO2 decreased in both alpha-stat and pH-stat groups; in the alpha-stat group, CBF decreased from 27 ± 5 mL · min-1 · 100 g-1 (normothermic CPB) to 5 ± 1 mL · min-1 · 100 g-1 (hypothermic CPB) (p <0.05) and CMRO2 decreased from 1.8 ± 0.21 to 0.24 ± 0.04 mL · min-1 · 100 g-1 (p <0.05), whereas in the pH-stat group CBF decreased from 28 ± 2 to 9 ± 1 mL · min-1 · 100 g-1 (p <0.05) and CMRO2 decreased from 1.63 ± 0.07 to 0.31 ± 0.09 mL · min-1 · 100 g-1 (p <0.05). Hypercapnic vascular reactivity during hypothermic CPB was abolished during alpha-stat management (0.065 ± 0.013 [normothermic CPB] to -0.010 ± 0.049 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1 [hypothermic CPB]; p = not significant), but was preserved by pH-stat management (0.057 ± 0.009 to 0.113 ± 0.006 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1) (p <0.05). After CPB, there was full recovery of normocapnic CBF, CMRO2, and hypercapnic reactivity in all groups. We conclude that in this model of the immature animal on CPB (1) hypothermic CPB causes a profound decrease in CBF and CMRO2,(2) cerebrovascular reactivity to CO2 is decreased during hypothermic CPB with alpha-stat but not pH-stat management of arterial blood gases, and (3) regardless of method of blood gas management during CPB, CBF, CMRO2, and hypercapnic reactivity are restored to pre-CPB values after CPB.

Original languageEnglish (US)
Pages (from-to)880-886
Number of pages7
JournalAnnals of Thoracic Surgery
Volume59
Issue number4
DOIs
StatePublished - 1995
Externally publishedYes

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Cerebrovascular Circulation
Cardiopulmonary Bypass
Temperature
Vascular Resistance
Hypercapnia
Blood Vessels

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Cerebral blood flow during cardiopulmonary bypass : Influence of temperature and pH management strategy. / Cheng, W.; Hartmann, J. F.; Cameron, D. E.; Griffiths, E. M.; Kirsch, Jeffrey; Traystman, R. J.

In: Annals of Thoracic Surgery, Vol. 59, No. 4, 1995, p. 880-886.

Research output: Contribution to journalArticle

Cheng, W. ; Hartmann, J. F. ; Cameron, D. E. ; Griffiths, E. M. ; Kirsch, Jeffrey ; Traystman, R. J. / Cerebral blood flow during cardiopulmonary bypass : Influence of temperature and pH management strategy. In: Annals of Thoracic Surgery. 1995 ; Vol. 59, No. 4. pp. 880-886.
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abstract = "Because disordered autoregulation of cerebral blood flow may underlie neurologic injury associated with cardiopulmonary bypass (CPB), we studied the effects of normothermic (37°C) and hypothermic (18°C) CPB on cerebral vascular reactivity in 6 to 8-week-old piglets. Hypothermic CPB animals were subdivided into alpha-stat and pH-stat groups (n = 6 animals each group) according to acid-base management protocol. Cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebral vascular resistance (CVR), and CBF response to hypercapnia were examined before, during, and 1 hour after CPB and used to calculate CVR per millimeter of mercury change in arterial partial pressure of CO2: (CVR(normocapnia) - CVR(hypercapnia))/(PaCO(2 hypercapnia) - PaCO2 normocapnia)). Before CPB, CBF, CMRO2, and vascular reactivity to elevated CO2 were similar in the three groups; these parameters remained unchanged by normothermic CPB. However, during hypothermic CPB, CBF and CMRO2 decreased in both alpha-stat and pH-stat groups; in the alpha-stat group, CBF decreased from 27 ± 5 mL · min-1 · 100 g-1 (normothermic CPB) to 5 ± 1 mL · min-1 · 100 g-1 (hypothermic CPB) (p <0.05) and CMRO2 decreased from 1.8 ± 0.21 to 0.24 ± 0.04 mL · min-1 · 100 g-1 (p <0.05), whereas in the pH-stat group CBF decreased from 28 ± 2 to 9 ± 1 mL · min-1 · 100 g-1 (p <0.05) and CMRO2 decreased from 1.63 ± 0.07 to 0.31 ± 0.09 mL · min-1 · 100 g-1 (p <0.05). Hypercapnic vascular reactivity during hypothermic CPB was abolished during alpha-stat management (0.065 ± 0.013 [normothermic CPB] to -0.010 ± 0.049 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1 [hypothermic CPB]; p = not significant), but was preserved by pH-stat management (0.057 ± 0.009 to 0.113 ± 0.006 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1) (p <0.05). After CPB, there was full recovery of normocapnic CBF, CMRO2, and hypercapnic reactivity in all groups. We conclude that in this model of the immature animal on CPB (1) hypothermic CPB causes a profound decrease in CBF and CMRO2,(2) cerebrovascular reactivity to CO2 is decreased during hypothermic CPB with alpha-stat but not pH-stat management of arterial blood gases, and (3) regardless of method of blood gas management during CPB, CBF, CMRO2, and hypercapnic reactivity are restored to pre-CPB values after CPB.",
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T1 - Cerebral blood flow during cardiopulmonary bypass

T2 - Influence of temperature and pH management strategy

AU - Cheng, W.

AU - Hartmann, J. F.

AU - Cameron, D. E.

AU - Griffiths, E. M.

AU - Kirsch, Jeffrey

AU - Traystman, R. J.

PY - 1995

Y1 - 1995

N2 - Because disordered autoregulation of cerebral blood flow may underlie neurologic injury associated with cardiopulmonary bypass (CPB), we studied the effects of normothermic (37°C) and hypothermic (18°C) CPB on cerebral vascular reactivity in 6 to 8-week-old piglets. Hypothermic CPB animals were subdivided into alpha-stat and pH-stat groups (n = 6 animals each group) according to acid-base management protocol. Cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebral vascular resistance (CVR), and CBF response to hypercapnia were examined before, during, and 1 hour after CPB and used to calculate CVR per millimeter of mercury change in arterial partial pressure of CO2: (CVR(normocapnia) - CVR(hypercapnia))/(PaCO(2 hypercapnia) - PaCO2 normocapnia)). Before CPB, CBF, CMRO2, and vascular reactivity to elevated CO2 were similar in the three groups; these parameters remained unchanged by normothermic CPB. However, during hypothermic CPB, CBF and CMRO2 decreased in both alpha-stat and pH-stat groups; in the alpha-stat group, CBF decreased from 27 ± 5 mL · min-1 · 100 g-1 (normothermic CPB) to 5 ± 1 mL · min-1 · 100 g-1 (hypothermic CPB) (p <0.05) and CMRO2 decreased from 1.8 ± 0.21 to 0.24 ± 0.04 mL · min-1 · 100 g-1 (p <0.05), whereas in the pH-stat group CBF decreased from 28 ± 2 to 9 ± 1 mL · min-1 · 100 g-1 (p <0.05) and CMRO2 decreased from 1.63 ± 0.07 to 0.31 ± 0.09 mL · min-1 · 100 g-1 (p <0.05). Hypercapnic vascular reactivity during hypothermic CPB was abolished during alpha-stat management (0.065 ± 0.013 [normothermic CPB] to -0.010 ± 0.049 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1 [hypothermic CPB]; p = not significant), but was preserved by pH-stat management (0.057 ± 0.009 to 0.113 ± 0.006 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1) (p <0.05). After CPB, there was full recovery of normocapnic CBF, CMRO2, and hypercapnic reactivity in all groups. We conclude that in this model of the immature animal on CPB (1) hypothermic CPB causes a profound decrease in CBF and CMRO2,(2) cerebrovascular reactivity to CO2 is decreased during hypothermic CPB with alpha-stat but not pH-stat management of arterial blood gases, and (3) regardless of method of blood gas management during CPB, CBF, CMRO2, and hypercapnic reactivity are restored to pre-CPB values after CPB.

AB - Because disordered autoregulation of cerebral blood flow may underlie neurologic injury associated with cardiopulmonary bypass (CPB), we studied the effects of normothermic (37°C) and hypothermic (18°C) CPB on cerebral vascular reactivity in 6 to 8-week-old piglets. Hypothermic CPB animals were subdivided into alpha-stat and pH-stat groups (n = 6 animals each group) according to acid-base management protocol. Cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebral vascular resistance (CVR), and CBF response to hypercapnia were examined before, during, and 1 hour after CPB and used to calculate CVR per millimeter of mercury change in arterial partial pressure of CO2: (CVR(normocapnia) - CVR(hypercapnia))/(PaCO(2 hypercapnia) - PaCO2 normocapnia)). Before CPB, CBF, CMRO2, and vascular reactivity to elevated CO2 were similar in the three groups; these parameters remained unchanged by normothermic CPB. However, during hypothermic CPB, CBF and CMRO2 decreased in both alpha-stat and pH-stat groups; in the alpha-stat group, CBF decreased from 27 ± 5 mL · min-1 · 100 g-1 (normothermic CPB) to 5 ± 1 mL · min-1 · 100 g-1 (hypothermic CPB) (p <0.05) and CMRO2 decreased from 1.8 ± 0.21 to 0.24 ± 0.04 mL · min-1 · 100 g-1 (p <0.05), whereas in the pH-stat group CBF decreased from 28 ± 2 to 9 ± 1 mL · min-1 · 100 g-1 (p <0.05) and CMRO2 decreased from 1.63 ± 0.07 to 0.31 ± 0.09 mL · min-1 · 100 g-1 (p <0.05). Hypercapnic vascular reactivity during hypothermic CPB was abolished during alpha-stat management (0.065 ± 0.013 [normothermic CPB] to -0.010 ± 0.049 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1 [hypothermic CPB]; p = not significant), but was preserved by pH-stat management (0.057 ± 0.009 to 0.113 ± 0.006 mm Hg · mL-1 · min-1 · 100 g-1 · mm Hg CO2 -1) (p <0.05). After CPB, there was full recovery of normocapnic CBF, CMRO2, and hypercapnic reactivity in all groups. We conclude that in this model of the immature animal on CPB (1) hypothermic CPB causes a profound decrease in CBF and CMRO2,(2) cerebrovascular reactivity to CO2 is decreased during hypothermic CPB with alpha-stat but not pH-stat management of arterial blood gases, and (3) regardless of method of blood gas management during CPB, CBF, CMRO2, and hypercapnic reactivity are restored to pre-CPB values after CPB.

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