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

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 (SrtO2) 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 SrtO2 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 (SptO2 and SctO2, 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 SrtO2 than SptO2. 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, SptO2 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 SptO2 provides a better indication of 'general' tissue oxygenation status.Registered at ClinicalTrials.gov: NCT01347827, first submitted April 27, 2011.

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

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 µg 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 (∆) in MAP, HR, stroke volume (SV), CI and cerebral (SctO2) and peripheral (SptO2) 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 (∆ = - 23 ± 13 vs. -36 ± 13 mmHg), HR (∆ = - 5 ± 7 vs. -10 ± 10 bpm), SV (∆ = - 23 ± 18 vs. -35 ± 19 ml) and CI (∆ = - 0.8 (- 1.5 to - 0.5) vs. -1.5 (- 2.0 to - 1.1) l min- 1 m- 2), while SctO2 (∆ = 9 ± 5 vs. 6 ± 4%) showed more increase with no difference in ∆SptO2 (∆ = 8 ± 7 vs. 8 ± 8%). Atropine caused higher ∆HR (13 (9 to 19) vs. 10 ± 6 bpm) and ∆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 ∆MAP, ∆SV and ∆SctO2 and ∆SptO2. CONCLUSION: Induction of anaesthesia with propofol and sufentanil results in improved haemodynamic stability and higher SctO2 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. TRIAL REGISTRATION: Clinicaltrials.gov on June 7, 2013 (trial ID: NCT01871935 ).

Prophylactic atropine administration attenuates the negative haemodynamic effects of induction of anaesthesia with propofol and high-dose remifentanil: A randomised controlled trial.

BACKGROUND: Induction of anaesthesia with propofol and remifentanil often induces unwanted bradycardia and hypotension, raising concerns regarding tissue oxygenation. The electrophysiological cardiac effects of remifentanil can be reversed by atropine. OBJECTIVE: To investigate if prophylactic administration of atropine can attenuate the negative haemodynamic effects of propofol and a high dose of remifentanil during induction of anaesthesia. DESIGN: A double-blind, randomised controlled trial. SETTING: Single-centre, University Medical Center Groningen, The Netherlands. PATIENTS: Sixty euvolaemic patients scheduled for surgery under general anaesthesia. INTERVENTIONS: Anaesthesia was induced and maintained with a target-controlled infusion of propofol with a target effect-site concentration (Ce) of 2.5 µg ml, remifentanil (target-controlled infusion), (Ce 8 ng ml) and cis-atracurium. Methylatropine (500 µg) or 0.9% saline was administered at immediately before induction of anaesthesia. MAIN OUTCOME MEASURES: The changes (Δ) in mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), rate pressure product, cerebral tissue oxygenation and peripheral tissue oxygenation between induction of anaesthesia (T0) and 10 min later (T10). RESULTS: Atropine significantly attenuated the changes in the outcome measures between T0 and T10. Median (inter-quartile range) changes were MAP, Δ = -24 (-40 to -21) vs. Δ = -37 mmHg (-41 to -31) (P = 0.02); HR, Δ = 0 ±â€Š13 vs. -19 ±â€Š11 bpm (P < 0.01); CI, Δ = -0.4 ±â€Š0.7 vs. -0.9 ±â€Š0.6l min m (P < 0.01) and rate pressure product, Δ = -3241 (-5015 to -613) vs. Δ = -5712 mmHg min (-6715 to -3917) (P < 0.01). Cerebral tissue oxygenation and peripheral tissue oxygenation did not change in either group. Maximum HR after atropine was 102 (86 to 116) vs. 85 bpm (76 to 95). CONCLUSION: Administration of atropine, before induction of anaesthesia with propofol and high-dose remifentanil, can significantly reduce the decreases in HR, MAP and CI. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT01871922.

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

BACKGROUND: 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. METHODS: 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 (↑SVI) was used to define FR with different thresholds from 10-25%. The PPV, SVV, and SVI were measured using the Nexfin® device that employs noninvasive volume clamp plethysmography. RESULTS: The area under the receiver operator characteristic curve gradually increased for PPV / SVV with higher threshold values (from 0.818 / 0.760 at 10% ↑SVI to 0.928 / 0.944 at 25% ↑SVI). The grey zone limits of both PPV and SVV changed from 9-16% (PPV) and 5-13% (SVV) at the 10% ↑SVI threshold to 18-21% (PPV) and 14-16% (SVV) at the 25% ↑SVI threshold. CONCLUSION: 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 ↑SVI thresholds.

Differential effects of phenylephrine and norepinephrine on peripheral tissue oxygenation during general anaesthesia: A randomised controlled trial.

BACKGROUND: Phenylephrine and norepinephrine are two vasopressors commonly used to counteract anaesthesia-induced hypotension. Their dissimilar working mechanisms may differentially affect the macro and microcirculation, and ultimately tissue oxygenation. OBJECTIVES: We investigated the differential effect of phenylephrine and norepinephrine on the heart rate (HR), stroke volume (SV), cardiac index (CI), cerebral tissue oxygenation (SctO2) and peripheral tissue oxygenation (SptO2), and rate-pressure product (RPP). DESIGN: A randomised controlled study. SETTING: Single-centre, University Medical Center Groningen, The Netherlands. PATIENTS: Sixty normovolaemic patients under balanced propofol/remifentanil anaesthesia. INTERVENTIONS: If the mean arterial pressure (MAP) dropped below 80% of the awake state value, phenylephrine (100 µg + 0.5 µg kg(-1) min(-1)) or norepinephrine (10 µg + 0.05 µg kg(-1) min(-1)) was administered in a randomised fashion. MAIN OUTCOME MEASURES: MAP, HR, SV, CI, SctO2, SptO2 and rate-pressure product (RPP) analysed from 30 s before drug administration until 240 s thereafter. RESULTS: Phenylephrine and norepinephrine caused an equivalent increase in MAP [Δ = 13 (8 to 22) and Δ = 13 (9 to 19) mmHg, respectively] and SV [Δ = 6 ± 6 and Δ = 5 ± 7 ml, respectively], combined with a significant equivalent decrease in HR (both Δ = -8 ± 6 bpm), CI (both Δ = -0.2 ± 0.3 l min(-1) m(-2)) and SctO2 and an unchanged RPP (Δ = 345 ± 876 and Δ = 537 ± 1076 mmHg min(-1)). However, SptO2 was slightly but statistically significantly (P < 0.05) decreased after norepinephrine [Δ  = -3 (-6 to 0)%] but not after phenylephrine administration [Δ = 0 (-1 to 1)%]. In both groups, SptO2 after vasopressor was still higher than the awake value. CONCLUSION: In normovolaemic patients under balanced propofol/remifentanil anaesthesia, phenylephrine and norepinephrine produced similar clinical effects when used to counteract anaesthesia-induced hypotension. After norepinephrine, a fall in peripheral tissue oxygenation was statistically significant, but its magnitude was not clinically relevant.

Tissue oxygenation as a target for goal-directed therapy in high-risk surgery: a pilot study.

BACKGROUND: Tissue hypoperfusion occurs frequently during surgery and may contribute to postoperative organ dysfunction. There is a need for perioperative treatment protocols aiming at improving tissue oxygenation (StO2). We hypothesised that intra-operative optimisation of StO2 improves tissue perfusion and thus reduces postoperative complications. Furthermore, we evaluated the feasibility of the optimisation algorithm used. METHODS: We randomized 50 high-risk patients, all >65 years with ASA physical status III, who underwent major abdominal surgery under standardized balanced general anesthesia combined with epidural analgesia. Throughout surgery StO2 was monitored at the thenar eminence using near-infrared spectroscopy. All patients were treated according to a standard care algorithm. In addition, patients in the intervention group were treated with dobutamine if necessary to keep or raise StO2 ≥ 80%. Data were recorded continuously and complications were recorded during hospital stay with a maximum of 28 days. RESULTS: The number of complications was not significantly different between groups (11 vs 20; p = 0.23). Eleven patients in the intervention group had no complication, versus 7 in the control group. There was no significant difference between groups in length of stay in ICU or in hospital. Only ten patients in the intervention group received dobutamine. Administration of dobutamine resulted in a moderate 6 [-3 to 10] % increase of StO2. The overall protocol adherence was 94%. CONCLUSIONS: No statistically significant difference in outcome was realized through intraoperative optimization of StO2 values in this pilot study. The protocol used may be considered feasible for clinical practice. Further research is obligatory to define both the optimal StO2 threshold and intervention to treat tissue hypoperfusion. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01342900. Registered 21 April 2011.

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

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.