J. Phipps

Response of cerebral blood flow to phenylephrine infusion during hypothermic cardiopulmonary bypass: influence of PaCO2 management.

Twenty-eight adult patients anesthetized with fentanyl, then subjected to hypothermic cardiopulmonary bypass (CPU), were studied to determine the effect of phenylephrine-induced changes in mean arterial pressure (MAP) on cerebral blood flow (CBF). During CPB patients managed at 28° C with either alpha-stat (temperature-un-corrected PaCo2 = 41 ± 4 mmHg) or pH-stat (temperature-uncorrected PaCo2 = 54 ± 8 mmHg) PaCo2 for blood gas maintenance received phenylephrine to increase MAP ≥ 25% (group A, n = 10; group B, n = 6). To correct for a spontaneous, time-related decline in CBF observed during CPB, two additional groups of patients undergoing CPB were cither managed with the alpha-stat or pH-stat approach, but neither group received phenylephrine and MAP remained unchanged in both groups (group C, n = 6; group D, n = 6). For all patients controlled variables (nasopharyngcal temperature, PaCo2, pump flow, and hematocrit) remained unchanged between measurements. Phenylephrine data were corrected based on the data from groups C and D for the effect of diminishing CBF over time during CPB. In patients in group A CBF was unchanged as MAP rose from 56 ± 7 to 84 ± 8 mmHg. In patients in group B CBF increased 41% as MAP rose from 53 ± 8 to 77 ± 9 mmHg (P < 0.001). During hypothermic CPB normocarbia maintained via the alpha-stat approach at a temperature-uncorrected PaCo2, of ∼40 mmHg preserves cerebral autoregulation; pH-stat management (PaCo2 ∼57 mmHg uncorrected for temperature, or 40 mmHg when corrected to 28°C) causes cerebrovascular changes (i.e., impaired autoregulation) similar to those changes produced by hypercarbia in awake, normothermic patients.

Cerebral Emboli during Cardiac Surgery in Children

Background: Microemboli occur commonly during cardiac surgery in adults, and, when present, increase the risk of neuropsychological deficits. Their incidence and significance during correction of congenital heart disease is unknown. The authors hypothesized that microemboli would occur before bypass with right‐to‐left cardiac shunts and would also occur in large numbers when the aortic crossclamp was released in children during repair of congenital heart defects. Methods: In 25 children studied with carotid artery Doppler, embolic signals were counted and timed in relation to 13 intraoperative events. Patients were classified as either at high risk (obligate right‐to‐left shunt or uncorrected transposition of the great arteries) or at low risk (net left‐to‐right shunt or simple obstructive lesions) for paradoxical (venous to arterial) emboli. Results: The median number of emboli detected was 122 (range, 2–2,664). Forty‐two percent of all emboli were detected within 3 min of release of the aortic crossclamp. The high‐risk group had significantly more emboli (median, 66; range, 0–116) during the time interval before cardiopulmonary bypass than did the low‐risk group (median, 8; range, 0–73), with P < 0.01. There was no significant difference between the high‐and low‐risk groups in the total number of emboli detected. There was no apparent association between number of emboli and gross neurologic deficits. Conclusions: Microemboli can be detected in the carotid arteries of children undergoing repair of congenital heart disease and are especially prevalent immediately after release of the aortic crossclamp. The role of emboli in causing neurologic injury in children undergoing repair of congenital heart disease remains to be determined.

CEREBRAL BLOOD FLOW DECREASES WITH TIME WHEREAS CEREBRAL OXYGEN CONSUMPTION REMAINS STABLE DURING HYPOTHERMIC CARDIOPULMONARY BYPASS IN HUMANS

&NA; Recent investigations demonstrate that cerebral blood flow (CBF) progressively declines during hypothermic, nonpulsatile cardiopulmonary bypass (CPB). If CBF declines because of brain cooling, the cerebral metabolic rate for oxygen (CMRo2) should decline in parallel with the reduction in CBF. Therefore we studied the response of CBF, the cerebral arteriovenous oxygen content difference (A ‐ VDcereO2), and CMRo2 as a function of the duration of CPB in humans. To do this, we compared the cerebrovascular response to changes in the Paco2. Because sequential CBF measurements using xenon 133 (133Xe) clearance must be separated by 15‐25 min, we hypothesized that a time‐dependent decline in CBF would accentuate the CBF reduction caused by a decrease in Paco2, but would blunt the CBF increase associated with a rise in Paco2. We measured CBF in 25 patients and calculated the cerebral arteriovenous oxygen content difference using radial arterial and jugular venous bulb blood samples. Patients were randomly assigned to management within either a lower (32‐48 mm Hg) or higher (50‐71 mm Hg) range of Paco2 uncorrected for temperature. Each patient underwent two randomly ordered sets of measurements, one at a lower Paco2 and the other at a higher Paco2 within the respective ranges. Cerebrovascular responsiveness to changes in Paco2 was calculated as specific reactivity (SR), the change in CBF divided by the change in Paco2, expressed in mL‐100 g−1·min−1·mm Hg−1. In the entire group of 25 subjects, SR was 0.69 ± 0.33 mL·100g−1·min−1·mm Hg−1 (SD) if Paco2 was reduced and 0.10 ± 0.30 mL·100g−1·min−1·mm Hg−1 if Paco2 was increased (P < 0.001). In patients managed within the lower range of Paco2, SR was 0.63 ± 0.31 and 0.21 ± 0.17, respectively, when Paco2 was reduced or increased (P < 0.05), In patients managed within the higher range of Paco2, SR was 0.76 ± 0.38 and −0.01 ± 0.36, respectively, when Paco2 was reduced or increased (P < 0.01). Estimated CMRo2 remained constant within groups from the initial to the repeat measurements. These results confirm a significant time‐dependent decline of CBF during CPB. Moreover, by demonstrating that CMRo2 did not change significantly as Paco2 was altered in either direction, they suggest that the CBF reduction cannot be attributed to progressive brain cooling during stable, hypothermic, nonpulsatile CPB, but must result from an alteration in cerebrovascular resistance.

Sodium Nitroprusside Infusion Does Not Dilate Cerebral Resistance Vessels during Hypothermic Cardiopulmonary Bypass

This study determined whether sodium nitroprusside (SNP) changes cerebral vascular resistance during stable, hypothermic cardiopulmonary bypass (CPB). Cerebral blood flow (CBF) was measured using Xenon clearance in 39 patients anesthetized with fentanyl. In 25 patients (group 1), CBF was measured before and during infusion of SNP at a rate sufficient to reduce mean arterial pressure (MAP) approximately 20%. In 14 other patients (group 2), CBF was measured before and during simultaneous infusion of SNP and phenylephrine; SNP was continued at a rate that had reduced MAP approximately 20% while phenylephrine was added in a dose sufficient to restore MAP to preinfusion levels. Patients within each group were randomized to maintenance of PaCO2 approximately 40 mmHg (groups 1a and 2a), uncorrected for body temperature, or to maintenance of PaCO2 approximately 50 mmHg (groups 1b and 2b). The following variables were maintained within a narrow range: nasopharyngeal temperature (26-29 degrees C), pump oxygenator flow (1.7-2.5 l.min-1.m-2), PaO2 (150-300 mmHg), and Hct (22-28 vol%). In each patient, controlled variables varied no more than +/- 5% between measurements. In group 1a (PaCO2 approximately 40 mmHg), MAP was 86 +/- 9 mmHg (mean +/- SD) before and 65 +/- 8 mmHg during SNP infusion (P less than 0.0001). CBF was 12 +/- 3 ml.100g-1.min-1 before and 10 +/- 2 ml.100(-1).min-1 during SNP infusion (P less than 0.01). In group 1b (PaCO2 approximately 55 mmHg), MAP was 86 +/- 11 mmHg before and 66 +/- 13 mmHg during SNP infusion (P less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)