Jugular bulb saturation and cognitive dysfunction after cardiopulmonary bypass.

Inadequate cerebral oxygenation during cardiopulmonary bypass may lead to postoperative cognitive dysfunction in patients undergoing cardiac operations. A psychological test battery was administered to 255 patients before cardiac operation and just before hospital discharge. Postoperative impairment was defined as a decline of more than one standard deviation in 20% of tests. Variables significantly (p < 0.05) associated with postoperative cognitive impairment are baseline psychometric scores, largest arterial-venous oxygen difference, and years of education. Jugular bulb hemoglobin saturation is significant if it replaces arterial-venous oxygen difference in the model. Factors correlated with jugular bulb saturation at normothermia were cerebral metabolic rate of oxygen consumption (r = -0.6; p < 0.0005), cerebral blood flow (r = 0.4; p < 0.0005), oxygen delivery (r = 0.4; p < 0.0005), and mean arterial pressure (r = 0.15; p < 0.05). Three measures were significantly related to desaturation at normothermia and at hypothermia as well: greater cerebral oxygen extraction, greater arterial-venous oxygen difference, and lower ratio of cerebral blood flow to arterial-venous oxygen difference. We conclude that cerebral venous desaturation occurs during cardiopulmonary bypass in 17% to 23% of people and is associated with impaired postoperative cognitive test performance.

Effect of aging on cerebral autoregulation during cardiopulmonary bypass. Association with postoperative cognitive dysfunction.

BACKGROUND: Age is a predictor of cognitive dysfunction after cardiac surgery, but the mechanism is unknown. The purpose of our study was to determine whether age-related decrements in cognition are associated with cerebral blood flow (CBF) autoregulation during cardiopulmonary bypass (CPB). METHODS AND RESULTS: Cognitive function testing was completed before surgery and before hospital discharge in 215 patients undergoing elective coronary artery bypass grafting (CABG) surgery. The battery consisted of seven tests with nine measures designed to evaluate memory, mood changes, and visuomotor speed and function. Pressure-flow and metabolic-flow cerebral autoregulation during hypothermic cardiopulmonary bypass were determined using the 133Xe clearance CBF method and radial artery and jugular bulb effluent to calculate cerebral metabolic rate (CMRO2) and cerebral AV difference (C[AV]O2). Pressure-flow autoregulation was tested by using two CBF measurements at stable hypothermia: one at stable mean arterial pressure (MAP) and the second 15 minutes later when MAP had increased or decreased > or = 20%. Metabolism-flow autoregulation was tested by varying the temperature (CMRO2) and measuring the coupling of CBF and CMRO2. Individual patient autoregulation was correlated with changes in cognitive measures. Cognitive performance declined in 6 of 9 measures after CABG surgery. Age predicted cognitive decline in 7 of 9 measures; short-term memory showed the greatest effect of age. Pressure-flow autoregulation during hypothermic CPB showed a small but significant (P < .0001) effect of pressure on CBF. There was no effect of age on the slope of CBF response to changes in MAP (pressure-flow autoregulation). There was a major effect of temperature on CBF during CPB (P < .0001). Coupling CBF and CMRO2 with changing temperature was unaffected by age. Changes in cognition were not associated with measures of cerebral autoregulation. However, increasing C(AV)O2 is associated with cognitive deficits in 5 of 9 measures; these associations were independent of age. CONCLUSIONS: Increased age predisposes to impaired cognition after cardiac surgery. This decline in cognitive function in the elderly is not associated with age-related changes in cerebral blood flow autoregulation. The association of increased oxygen extraction with decline in some measures of cognitive function suggests that an imbalance in cerebral tissue oxygen supply, which is unrelated to age, contributes to acute cognitive dysfunction after cardiac surgery. Cognitive dysfunction after CPB in the elderly cannot be explained by impaired CBF autoregulation.

Hemodilution induces stable changes in global cardiovascular and regional myocardial function.

The cardiovascular responses associated with isovolemic hemodilution have been described. However, the stability of these responses over time remains controversial. We hypothesized that the hemodynamic responses to isovolemic hemodilution are stable over time. Nine fentanyl-midazolam-anesthetized dogs were monitored to follow global cardiovascular and regional myocardial function. Isovolemic hemodilution was performed to a moderate (hemoglobin = 7.5 g%) target hemodilutional state that was maintained for 4 h. Data were obtained at each hemodilutional state and each hour during the 4-h period of sustained moderate hemodilution. During acute hemodilution, cardiac output increased from 2.6 +/- 0.5 L/min to 3.0 +/- 0.5 L/min (P < 0.05) and mean coronary flow increased from 20.8 +/- 2.4 mL/min to 31.4 +/- 5.5 mL/min (P < 0.05). Cardiac output and mean coronary flow remained elevated during the extended hemodilutional period. In addition, norepinephrine increased from 586 +/- 152 pg/mL to 1135 +/- 247 pg/mL (P < 0.05) during acute isovolemic hemodilution and remained at this increased level during extended hemodilution. Epinephrine levels did not change with hemodilution. Compensatory mechanisms such as increases in cardiac output and mean coronary flow observed during acute hemodilution persist during extended periods of hemodilution.

Cerebral blood flow and metabolism during cardiopulmonary bypass.

Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.

Is esmolol cardioprotective? Tolerance of pacing tachycardia, acute afterloading and hemodilution in dogs with coronary stenosis.

OBJECTIVES: The aim of this study was to determine whether esmolol, an ultrashort-acting beta-adrenergic antagonist, possesses cardioprotective properties unrelated to a concomitant decrease in heart rate. BACKGROUND: Previous studies have demonstrated beneficial effects of beta-adrenergic blocking agents with unchanged heart rates. METHODS: The effect of esmolol (100 micrograms/kg per min) on the response of global cardiovascular and regional myocardial contractile function (sonomicrometry) to pacing-induced tachycardia and acute left ventricular afterloading was assessed in dogs with a critical stenosis of the left anterior descending coronary artery (LAD). These responses were observed at the baseline hemoglobin level (12.5 +/- 0.3 g/100 ml) as well as after hemodilution-induced mild regional contractile dysfunction (7.4 +/- 0.4 g/100 ml) in the area supplied by this artery (LAD area). Data were analyzed by using a repeated measures multivariate analysis of variance with complete block design treating pacing rate and afterloading, respectively, as the repeated measure. RESULTS: Esmolol decreased the maximal first derivative of left ventricular pressure (dP/dtmax); global cardiovascular and regional myocardial contractile function were otherwise unchanged. Esmolol did not alter the response of global cardiovascular or regional myocardial function to pacing-induced tachycardia or to acute left ventricular afterloading, both at the baseline hemoglobin level as well as during mild hemodilution-induced LAD area contractile dysfunction. CONCLUSIONS: At an infusion rate of 100 micrograms/kg per min we were unable to demonstrate cardioprotective esmolol effects in a canine model of critical coronary stenosis with controlled heart rate and identical loading conditions.

Warming during cardiopulmonary bypass is associated with jugular bulb desaturation.

The objective of this study was to characterize cerebral venous effluent during normothermic nonpulsatile cardiopulmonary bypass. Thirty-one (23%) of 133 patients met desaturation criteria (defined as jugular bulb venous oxygen saturation less than or equal to 50% or jugular bulb venous oxygen tension less than or equal to 25 mm Hg) during normothermic cardiopulmonary bypass (after hypothermic cardiopulmonary bypass at 27 degrees to 28 degrees C). Cerebral blood flow, calculated using xenon 133 clearance methodology, was significantly (p less than 0.005) higher in the saturated group (33.7 +/- 10.3 mL.100 g-1.min-1) than in the desaturated group (26.2 +/- 6.9 mL.100 g-1.min-1), whereas the cerebral metabolic rate for oxygen was significantly lower (p less than 0.005) in the saturated group (1.28 +/- 0.39 mL.100 g-.min-1) than in the desaturated group (1.52 +/- 0.36 mL.100 g-1.min-1) at normothermia. The arteriovenous oxygen difference at normothermia was lower in the saturated group (3.92 +/- 1.12 mL/dL) than in the desaturated group (5.97 +/- 1.05 mL/dL). Neuropsychological testing was performed in 74 of the 133 patients preoperatively and on day 7 postoperatively. There was a general decline in mean scores of all tests postoperatively in both groups with no significant difference between the groups. We conclude that cerebral venous desaturation represents a global imbalance in cerebral oxygen supply-demand that occurs during normothermic cardiopulmonary bypass and may represent transient cerebral ischemia. These episodes, however, are not associated with impared neuropsychological test performance as compared with the performance of patients with no evidence of desaturation.