Pumphead--or not! Does avoiding cardiopulmonary bypass for coronary artery bypass surgery result in less brain damage?
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Biomedical subjects
Publications and source records attributed to R Peter Alston.
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Metabolic acidosis is a frequent complication of cardiopulmonary bypass (CPB). Commonly, its cause is ascribed to hypoperfusion; however, iatrogenic causes, related to the composition and volume of intravascular fluids that are administered, are increasingly being recognized. The aim of this study was to determine if metabolic acidosis during CPB was associated with hypoperfusion, change in strong ion difference (SID) or haemodilution. Forty-nine patients undergoing cardiac surgery using CPB in the Royal Infirmary of Edinburgh (RIE) or the HCI, Clydebank were included in the study. Arterial blood samples were aspirated before induction of anaesthesia and the end of CPB. Samples were subjected to blood gas analysis and measurement of electrolytes and lactate. Changes in concentrations were then calculated. Change variables that were found to be significant (p < 0.1) univariate correlates of the change in hydrogen ion concentration were identified and entered into a multivariate regression model with hydrogen ion concentration at the end of CPB as the outcome variable (r2 = 0.65, p < 0.001). Change variance in hydrogen ion concentration was created by first entering the baseline hydrogen ion concentration into the model. Next, any variance resulting from the respiratory component of acidosis was removed by entering the change in arterial carbon dioxide tension (regression coefficient (beta)=0.67, p < 0.01). Change in SID (beta = -0.34, p < 0.01) and surgical institution (beta = 0.40, p < 0.01) were then found to be predictors of the remaining variance whilst change in concentration of lactate (beta in = 0.16, p = 0.07) and volume of intravascular fluid that was administered (beta = -0.07, p = 0.52) were rejected from the model. These findings suggest that the metabolic acidosis developing during CPB is partially the result of iatrogenic decrease in SID rather than hypoperfusion, as estimated by lactate concentration, or haemodilution.
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OBJECTIVE: Inhibition of cyclooxygenase 2 provides analgesia in ambulatory patients. We prospectively evaluated the safety and efficacy of a newly introduced cyclooxygenase 2 inhibitor in patients undergoing coronary artery bypass grafting surgery through a median sternotomy in a randomized clinical trial. METHODS: A total of 462 patients with New York Heart Association classes I to III who were less than 77 years of age and were from 58 institutions in the United States, Canada, Germany, and the United Kingdom participated in this multicenter, phase III, placebo-controlled, double-blind, randomized, parallel-group trial. Patients were allocated at a ratio of 2:1 to parecoxib/valdecoxib or standard care (control) groups, respectively. Intravenous study drug (40 mg) was administered within 30 minutes after extubation and every 12 hours for a minimum of 3 days. Subsequently, oral treatment at a dose of 40 mg every 12 hours was initiated and administered for a combined total of 14 days. Patient-controlled analgesia with morphine, oral opioids, or acetaminophen was available as required. Assessment of the analgesic efficacy of the study drug was primarily based on morphine and morphine equivalent use. Additional efficacy evaluations included daily pain intensity, patient and physician global evaluation of study medication, and pain effect on quality of life. Clinical adverse events were assessed by the principal investigator at each site from the time of the first dose through the 30-day postdosing period. RESULTS: Patients in the parecoxib/valdecoxib group received significantly less morphine or morphine equivalents than patients in the control group during the 0- to 24-hour (P =.009), 24- to 48-hour (P =.017), 72- to 96-hour (P =.002), 96- to 120-hour (P =.004), and 120- to 144-hour (P =.037) periods. Both patients (P <.001) and physicians (P <.001) evaluated the study medication as significantly better than control therapy. The modified Brief Pain Inventory questionnaire used in the oral dosing period detected significant improvements in the parecoxib/valdecoxib treatment group in 6 of 8 domains tested (eg, current pain, worst pain, and mood) beginning on day 4 and continuing for at least 4 days. Although there were no differences between the groups in overall adverse events, serious adverse events occurred twice as frequently in parecoxib/valdecoxib-treated patients (19.0%, 59/311 patients) than in control patients (9.9%, 15/151 patients; P =.015). Regarding individual serious adverse events, a greater incidence in sternal wound infection was found in the parecoxib/valdecoxib patients (10 [3.2%]) versus control patients (0 [0%]) (P =.035). The incidences of other individual serious adverse events, including cerebrovascular complications, myocardial infarction, and renal dysfunction, were proportionally greater but not significantly different between the groups. CONCLUSIONS: In patients undergoing coronary artery bypass grafting surgery, the cyclooxygenase 2 inhibitor combination, parecoxib/valdecoxib, was effective for postoperative analgesia. However, the 14-day treatment regimen also was associated with an increased incidence of serious adverse events overall and sternal wound infections in particular. Therefore our study raises important concerns requiring their comprehensive evaluation in a large-scale trial before these cyclooxygenase 2 inhibitors are used in patients undergoing coronary artery bypass grafting surgery.
Theoretically, systemic carbon dioxide (VCO2) production should be an alternative means to systemic oxygen uptake (VO2) for estimating the global efficacy of cardiopulmonary bypass (CPB). This study compared two methods of estimating VCO2: Fick's principle and oxygenator exhaust carbon dioxide (CO2) output. Both of these estimates were then compared with VO2. Fifty-one patients (39 male and 12 female) undergoing elective cardiac surgery requiring CPB were studied. Blood sampling was performed and measurements recorded during active cooling, environmental cooling/stable hypothermia and during rewarming. Blood samples were measured for CO2 tension from which content was estimated. VCO2 was calculated as the product of the arteriovenous difference in CO2 content and pump flow rate (Fick's principle), or the fresh gas flow rate and concentration of the oxygenator exhaust CO2 (output technique). Over all measurements, method comparison analysis revealed a large mean bias of 41 (95% confidence intervals (CI) 32-50) mL/min with very wide limits of agreement (-23, 105 mL/min). Regression analysis found that the bias was also proportional to the size of measurement (beta = 0.75 (95% CI 0.55, 0.95)). Although both methods of VCO2 correlated significantly with VO2 (p < 0.01), regression analysis found that the coefficients (beta) of both techniques had wide CI (Fick's principle: beta = 1.37 (95% CI 1.20, 1.54); output technique: beta = 0.58 (95%CI 0.44, 0.71)). In conclusion, both techniques of VCO2 cannot be used interchangeably, and both are imprecisely related to VO2 as estimated by Fick's principle.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.