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Anesth Analg. 2010 Feb 1;110(2):321-8. doi: 10.1213/ANE.0b013e3181c6fd12. Epub 2009 Dec 11.

Impaired autoregulation of cerebral blood flow during rewarming from hypothermic cardiopulmonary bypass and its potential association with stroke.

Author information

1
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.

Abstract

BACKGROUND:

Patient rewarming after hypothermic cardiopulmonary bypass (CPB) has been linked to brain injury after cardiac surgery. In this study, we evaluated whether cooling and then rewarming of body temperature during CPB in adult patients is associated with alterations in cerebral blood flow (CBF)-blood pressure autoregulation.

METHODS:

One hundred twenty-seven adult patients undergoing CPB during cardiac surgery had transcranial Doppler monitoring of the right and left middle cerebral artery blood flow velocity. Eleven patients undergoing CPB who had arterial inflow maintained at >35 degrees C served as controls. The mean velocity index (Mx) was calculated as a moving, linear correlation coefficient between slow waves of middle cerebral artery blood flow velocity and mean arterial blood pressure. Intact CBF-blood pressure autoregulation is associated with an Mx that approaches 0. Impaired autoregulation results in an increasing Mx approaching 1.0. Comparisons of time-averaged Mx values were made between the following periods: before CPB (baseline), during the cooling and rewarming phases of CPB, and after CPB. The number of patients in each phase of CPB with an Mx >4.0, indicative of impaired CBF autoregulation, was determined.

RESULTS:

During cooling, Mx (left, 0.29 +/- 0.18; right, 0.28 +/- 0.18 [mean +/- SD]) was greater than that at baseline (left, 0.17 +/- 0.21; right, 0.17 +/- 0.20; P <or= 0.0001). Mx increased during the rewarming phase of CPB (left, 0.40 +/- 0.19; right, 0.39 +/- 0.19) compared with baseline (P <or= 0.001) and the cooling phase (P <or= 0.0001), indicating impaired CBF autoregulation. After CPB, Mx (left, 0.27 +/- 0.20; right, 0.28 +/- 0.21) was higher than at baseline (left, P = 0.0004; right, P = 0.0003), no different than during the cooling phase, but lower than during rewarming (left, P <or= 0.0001; right, P <or= 0.0005). Forty-three patients (34%) had an Mx >or=0.4 during the cooling phase of CPB and 68 (53%) had an average Mx >or=0.4 during rewarming. Nine of the 11 warm controls had an average Mx >or=0.4 during the entire CPB period. There were 7 strokes and 1 TIA after surgery. All strokes were in patients with Mx >or= 0.4 during rewarming (P = 0.015). The unadjusted odds ratio for any neurologic event (stroke or transient ischemic attack) for patients with Mx >or= 0.4 during rewarming was 6.57 (95% confidence interval, 0.79 to 55.0, P < 0.08).

CONCLUSIONS:

Hypothermic CPB is associated with abnormal CBF-blood pressure autoregulation that is worsened with rewarming. We found a high rate of strokes in patients with evidence of impaired CBF autoregulation. Whether a pressure-passive CBF state during rewarming is associated with risk for ischemic brain injury requires further investigation.

PMID:
20008083
PMCID:
PMC5516214
DOI:
10.1213/ANE.0b013e3181c6fd12
[Indexed for MEDLINE]
Free PMC Article

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