41 research outputs found

    Improved haemodynamic stability and cerebral tissue oxygenation after induction of anaesthesia with sufentanil compared to remifentanil : a randomised controlled trial

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    Background: Balanced anaesthesia with propofol and remifentanil, compared to sufentanil, often decreases mean arterial pressure (MAP), heart rate (HR) and cardiac index (CI), raising concerns on tissue-oxygenation. This distinct haemodynamic suppression might be attenuated by atropine. This double blinded RCT, investigates if induction with propofol-sufentanil results in higher CI and tissue-oxygenation than with propofol-remifentanil and if atropine has more pronounced beneficial effects on CI and tissue-oxygenation in a remifentanil-based anaesthesia. Methods: In seventy patients scheduled for coronary bypass grafting (CABG), anaesthesia was induced and maintained with propofol target controlled infusion (TCI) with a target effect-site concentration (Cet) of 2.0 mu g ml(- 1)and either sufentanil (TCI Cet 0.48 ng ml(- 1)) or remifentanil (TCI Cet 8 ng ml(- 1)). If HR dropped below 60 bpm, methylatropine (1 mg) was administered intravenously. Relative changes (increment ) in MAP, HR, stroke volume (SV), CI and cerebral (SctO(2)) and peripheral (SptO(2)) tissue-oxygenation during induction of anaesthesia and after atropine administration were analysed. Results: The sufentanil group compared to the remifentanil group showed significantly less decrease in MAP (increment = - 23 +/- 13 vs. -36 +/- 13 mmHg), HR (increment = - 5 +/- 7 vs. -10 +/- 10 bpm), SV (increment = - 23 +/- 18 vs. -35 +/- 19 ml) and CI (increment = - 0.8 (- 1.5 to - 0.5) vs. -1.5 (- 2.0 to - 1.1) l min(- 1) m(- 2)), while SctO(2) (increment = 9 +/- 5 vs. 6 +/- 4%) showed more increase with no difference in increment SptO(2) (increment = 8 +/- 7 vs. 8 +/- 8%). Atropine caused higher increment HR (13 (9 to 19) vs. 10 +/- 6 bpm) and increment CI (0.4 +/- 0.4 vs. 0.2 +/- 0.3 l min(- 1) m(- 2)) in sufentanil vs. remifentanil-based anaesthesia, with no difference in increment MAP, increment SV and increment SctO(2) and increment SptO(2). Conclusion: Induction of anaesthesia with propofol and sufentanil results in improved haemodynamic stability and higher SctO(2) compared to propofol and remifentanil in patients having CABG. Administration of atropine might be useful to counteract or prevent the haemodynamic suppression associated with these opioids

    Comparison of renal region, cerebral and peripheral oxygenation for predicting postoperative renal impairment after CABG

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    Patients undergoing coronary artery bypass grafting (CABG) are at risk of developing postoperative renal impairment, amongst others caused by renal ischemia and hypoxia. Intra-operative monitoring of renal region tissue oxygenation (SrtO(2)) might be a useful tool to detect renal hypoxia and predict postoperative renal impairment. Therefore, the aim of this study was to assess the ability of intra-operative SrtO(2) to predict postoperative renal impairment, defined as an increase of serum creatinine concentrations of > 10% from individual baseline, and compare this with the predictive abilities of peripheral and cerebral tissue oxygenation (SptO(2) and SctO(2), respectively) and renal specific tissue deoxygenation. Forty-one patients undergoing elective CABG were included. Near-infrared spectroscopy (NIRS) was used to measure renal region, peripheral (thenar muscle) and cerebral tissue oxygenation during surgery. Renal region specific tissue deoxygenation was defined as a proportionally larger decrease in SrtO(2) than SptO(2). ROC analyses were used to compare predictive abilities. We did not observe an association between tissue oxygenation measured in the renal region and cerebral oxygenation and postoperative renal impairment in this small retrospective study. In contrast, SptO(2) decrease > 10% from baseline was a reasonable predictor with an AUROC of 0.767 (95%CI 0.619 to 0.14; p = 0.010). Tissue oxygenation of the renal region, although non-invasively and continuously available, cannot be used in adults to predict postoperative renal impairment after CABG. Instead, peripheral tissue deoxygenation was able to predict postoperative renal impairment, suggesting that SptO(2) provides a better indication of 'general' tissue oxygenation status. Registered at ClinicalTrials.gov: NCT01347827, first submitted April 27, 2011

    Noninvasive pulse pressure variation and stroke volume variation to predict fluid responsiveness at multiple thresholds : a prospective observational study

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    Pulse pressure variation (PPV) and stroke volume variation (SVV) are dynamic preload variables that can be measured noninvasively to assess fluid responsiveness (FR) in anesthetized patients with mechanical ventilation. Few studies have examined the effectiveness of predicting FR according to the definition of FR, and assessment of inconclusive values of PPV and SVV around the cut-off value (the "grey zone") might improve individual FR prediction. We explored the ability of noninvasive volume clamp derived measurements of PPV and SVV to predict FR using the grey zone approach, and we assessed the influence of multiple thresholds on the predictive ability of the numerical definition of FR. Ninety patients undergoing general surgery were included in this prospective observational study and received a 500 mL fluid bolus as deemed clinically required by the attending anesthesiologist. A minimal relative increase in stroke volume index (a dagger SVI) was used to define FR with different thresholds from 10-25%. The PPV, SVV, and SVI were measured using the NexfinA (R) device that employs noninvasive volume clamp plethysmography. The area under the receiver operator characteristic curve gradually increased for PPV / SVV with higher threshold values (from 0.818 / 0.760 at 10% a dagger SVI to 0.928 / 0.944 at 25% a dagger SVI). The grey zone limits of both PPV and SVV changed from 9-16% (PPV) and 5-13% (SVV) at the 10% a dagger SVI threshold to 18-21% (PPV) and 14-16% (SVV) at the 25% a dagger SVI threshold. Noninvasive PPV and SVV measurements allow an acceptable FR prediction, although the reliability of both variables is dependent on the intended increase in SVI, which improves substantially with concomitant smaller grey zones at higher a dagger SVI thresholds

    Hemodynamics and tissue oxygenation during balanced anesthesia with a high antinociceptive contribution:an observational study

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    BACKGROUND: In particular surgical conditions, a balanced anesthesia with a high-antinociceptive contribution is required. This may induce cardiovascular impairment and thus compromise tissue oxygenation. In this prospective observational study, we investigated the hemodynamic stability and tissue oxygen saturation (StO2) in 40 patients with a high-antinociceptive general anesthesia, goal-directed fluid therapy, and norepinephrine. In addition, optimal surgical conditions and safe and fast emergence are pivotal parts of anesthetic management. METHODS: In high-antinociceptive propofol/remifentanil anesthesia with bispectral index (BIS) between 40 and 60, norepinephrine was administered to maintain mean arterial pressure (MAP) above 80% of individual baseline. Fluid was administered if the ∆ plethysmographic waveform amplitude exceeded 10%. Surgical and recovery conditions, hemodynamic responses, and tissue oxygenation were investigated. RESULTS: Mean (SD) StO2 at the left thenar eminence increased from 83 (6)% before to 86 (4)% 20 min after induction of anesthesia (p <0.05). Cardiac index dropped from 3.0 (0.7) to 2.1 (0.4) L min(-1) (p <0.05), MAP from 109 (16) to 83 (14) mm Hg, and heart rate from 73 (12) to 54 (8) bpm (p <0.05). Thirteen out of 40 patients received a fluid bolus. The median (range) norepinephrine administration rate was 0.05 (0.0-0.10) μg kg(-1) min(-1). After complete akinesia in all patients during surgery, a median (IQR) extubation time of 311 (253-386) s was observed. CONCLUSIONS: This high-antinociceptive balanced anesthesia with goal-directed fluid and vasopressor therapy adequately preserved StO2 and hemodynamic homeostasis. TRIAL REGISTRATION: ISRCTN20153044
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