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 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

Brain changes due to hypoxia during light anaesthesia can be prevented by deepening anaesthesia:a study in rats

In anaesthetic practice the risk of cerebral ischemic/hypoxic damage is thought to be attenuated by deep anaesthesia. The rationale is that deeper anaesthesia reduces cerebral oxygen demand more than light anaesthesia, thereby increasing the tolerance to ischemia or hypoxia. However, evidence to support this is scarce. We thus investigated the influence of light versus deep anaesthesia on the responses of rat brains to a period of hypoxia. In the first experiment we exposed adult male Wistar rats to deep or light propofol anaesthesia and then performed [18F]- Fludeoxyglucose (FDG) Positron Emission Tomography (PET) scans to verify the extent of cerebral metabolic suppression. In subsequent experiments, rats were subjected to light/deep propofol anaesthesia and then exposed to a period of hypoxia or ongoing normoxia (n = 9-11 per group). A further 5 rats, not exposed to anaesthesia or hypoxia, served as controls. Four days later a Novel Object Recognition (NOR) test was performed to assess mood and cognition. After another 4 days, the animals were sacrificed for later immunohistochemical analyses of neurogenesis/neuroplasticity (Doublecortin; DCX), Brain Derived Neurotrophic Factor (BDNF) expression and neuroinflammation (Ionized calcium-binding adaptor protein-1; Iba-1) in hippocampal and piriform cortex slices. The hippocampi of rats subjected to hypoxia during light anaesthesia showed lower DCX positivity, and therefore lower neurogenesis, but higher BDNF levels and microglia hyper-ramification. Exploration was reduced, but no significant effect on NOR was observed. In the piriform cortex, higher DCX positivity was observed, associated with neuroplasticity. All these effects were attenuated by deep anaesthesia. Deepening anaesthesia attenuated the brain changes associated with hypoxia. Hypoxia during light anaesthesia had a prolonged effect on the brain, but no impairment in cognitive function was observed. Although reduced hippocampal neurogenesis may be considered unfavourable, higher BDNF expression, associated with microglia hyper-ramification may suggest activation of repair mechanisms. Increased neuroplasticity observed in the piriform cortex supports this, and might reflect a prolonged state of alertness rather than damage

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

Automatic detection of oesophageal intubation based on ventilation pressure waveforms shows high sensitivity and specificity in patients with pulmonary disease

Background: Unrecognised endotracheal tube misplacement in emergency intubations has a reported incidence of up to 17%. Current detection methods have many limitations restricting their reliability and availability in these circumstances. There is therefore a clinical need for a device that is small enough to be practical in emergency situations and that can detect oesophageal intubation within seconds. In a first reported evaluation, we demonstrated an algorithm based on pressure waveform analysis, able to determine tube location with high reliability in healthy patients. The aim of this study was to validate the specificity of the algorithm in patients with abnormal pulmonary compliance, and to demonstrate the reliability of a newly developed small device that incorporates the technology. Materials and methods: Intubated patients with mild to moderate lung injury, admitted to intensive care were included in the study. The device was connected to the endotracheal tube, and three test ventilations were performed in each patient. All diagnostic data were recorded on PC for subsequent specificity/sensitivity analysis. Results and discussion: A total of 105 ventilations in 35 patients with lung injury were analysed. With the threshold D-value of 0.1, the system showed a 100% sensitivity and specificity to diagnose tube location. Conclusion: The algorithm retained its specificity in patients with decreased pulmonary compliance. We also demonstrated the feasibility to integrate sensors and diagnostic hardware in a small, portable hand-held device for convenient use in emergency situations

A novel method to detect accidental oesophageal intubation based on ventilation pressure waveforms

Background: Emergency endotracheal intubation results in accidental oesophageal intubation in up to 17% of patients. This is frequently undetected thereby adding to the morbidity and mortality. No current method to detect accidental oesophageal intubation in an emergency setting is both highly sensitive and specific. We hypothesized that, based on differences between the mechanical properties of the oesophagus and the trachea/lung, ventilation pressures could discriminate between tracheal and oesophageal intubation. Such a technique would potentially not suffer some of the limitations of current methods to detect oesophageal intubation in emergency conditions such as noisy environment (making clinical assessment difficult) or low/no flow states (reducing the applicability of capnometry). The aim of our study was thus to develop and assess a technique that may more rapidly and accurately differentiate oesophageal from tracheal intubation based on airway pressure gradients. Materials and methods: Forty adult patients undergoing elective surgery were included. In 20 patients the trachea was intubated with an endotracheal tube; in 20 patients the oesophagus was purposefully intubated using an Easytube (R) (Rush, Germany). In all patients, a thin air-filled catheter was inserted through the tube lumen until its tip was 1 cm from the distal end, and connected to a pressure transducer. Pressure was recorded simultaneously from a second catheter at the proximal end of the tube. For the first three manual ventilations in each patient, a parameter (D) based on temporal (dP/dt) and spatial (dP/ds) pressure gradients (and reflecting flow divided by elastance) was calculated and evaluated for its ability to discriminate between oesophageal and tracheal intubation. Results and discussion: For all tracheal ventilations, D-values were >0.5 (range 0.6-47.9), while for all oesophageal ventilations D-values wer