Sevoflurane and propofol anaesthesia differentially modulate the effects of epinephrine and norepinephrine on microcirculatory gastric mucosal oxygenation.

BACKGROUND: Adequate gastrointestinal mucosal oxygenation is regarded to be crucial in the prevention and therapy of critical illness. Epinephrine and norepinephrine are used for perioperative haemodynamic support. However, their per se effects on gastromucosal haemoglobin oxygenation (µHbO(2)) remain unclear. Moreover, respective effects of epinephrine and norepinephrine may be affected by the type of underlying anaesthesia. Thus, we studied the effects of epinephrine and norepinephrine during anaesthesia with sevoflurane or propofol on regional gastromucosal µHbO(2) and systemic O(2)-derived variables. METHODS: In a double-randomized cross-over study, chronically instrumented dogs (n=6 per group) were anaesthetized randomly with sevoflurane or propofol, ventilated, and then randomly received either epinephrine or norepinephrine (0, 0.05, 0.1, and 0.2 µg kg(-1) min(-1)). We measured gastromucosal µHbO(2), systemic haemodynamics, and O(2)-derived variables. RESULTS: During sevoflurane anaesthesia, norepinephrine markedly increased µHbO(2) (P<0.0001) and systemic oxygen transport (DO(2)) (P=0.0006). In contrast, epinephrine failed to increase µHbO(2), despite doubling DO(2) (P=0.0002). During propofol anaesthesia, in contrast to sevoflurane, neither epinephrine nor norepinephrine affected µHbO(2), although epinephrine, but not norepinephrine, again resulted in markedly increased DO(2) (P<0.0001). CONCLUSIONS: The effects of epinephrine and norepinephrine depended on the type of anaesthesia. In addition, regional effects (i.e. µHbO(2)) were not predictable from systemic effects (i.e. DO(2)).

PEEP decreases oxygenation of the intestinal mucosa despite normalization of cardiac output.

OBJECTIVE: To evaluate if normalization of cardiac output reverses the attenuation of local intracapillary hemoglobin saturation (HbO2) of gastric mucosa by PEEP (positive end-expiratory pressure) during IPPV (intermittent positive pressure ventilation). MATERIALS AND METHODS: Four healthy, chronically instrumented, anesthetized dogs were repeatedly studied (n = 7). Local HbO2 of gastric mucosa was measured continuously by tissue lightguide spectrophotometry and cardiac output (CO) was recorded continuously by means of a precalibrated ultrasonic transit time flowmeter chronically implanted around the pulmonary artery. After obtaining baseline values during IPPV and ZEEP (zero end-expiratory pressure) 15 cmH2O PEEP was added. To compensate the reduction of CO during PEEP ventilation, HES (hydroxyethyl starch 6%) was infused until CO reached baseline values during ZEEP. RESULTS: Despite of unimpaired systemic oxygen saturation, PEEP reduced HbO2 of gastric mucosa from 55.1 +/- 4.2% to 42.1 +/- 4.7% (mean +/- SEM) and CO dropped from 67.7 +/- 4.9 ml.kg-1.min-1 to 33.9 +/- 4.6 ml.kg-1.min-1. Whereas infusion of HES during PEEP ventilation normalized CO to 65.1 +/- 6.2 ml.kg-1.min-1, HbO2 reached only 48.1 +/- 3.3%, a statistically significant improvement compared to HbO2 during PEEP ventilation before HES infusion (p < 0.03, Wilcoxon signed rank test), but still below baseline values (p < 0.04). CONCLUSIONS: Our findings demonstrate that the side effects of PEEP ventilation on cardiac output can be compensated by restoring preload, but normalizing CO did not completely normalize HbO2 of the gastric mucosa. This further emphasizes that global measurements of variables of systemic circulation and oxygenation do not necessarily reflect regional abnormalities of tissue oxygenation. Therefore, in view of the importance of tissue hypoxia especially in the splanchnic region in the pathogenesis of multiple organ failure, monitoring of HbO2 of the intestinal mucosa during PEEP ventilation may be particularly useful in the care of the critically ill patient.

[Postoperative reversal of loss of vigilance following midazolam with the use of the antagonist flumazenil (Ro 15-1788). A comparative study with a placebo and the use of EEG-power spectra]. / Postoperative Demaskierung einer überhängenden Vigilanzminderung nach Midazolameinleitung durch den Antagonisten Flumazenil (Ro 15-1788). Eine Vergleichsuntersuchung zur Plazebogabe unter Zuhilfenahme von EEG-Leistungsspektren.

Midazolam, a benzodiazepine with the purportedly shortest half-life of all these compounds, is advocated for the induction of general anesthesia. It is still debatable, however, whether a long-lasting hangover may result in depression of vigilance postoperatively. After midazolam induction (0.18 mg/kg) and enflurane/nitrous oxide/oxygen anesthesia, ten patients received flumazenil (0.8 mg/70 kg) in the postoperative period while another ten received placebo in a double-blind fashion. Continuous recording of EEg activity was performed using the Lifescan monitor, computing the power in the various EEG frequency domains. Additionally, patients were scored with regard to orientation in space and time and their collaboration and comprehension of verbal commands. Compared to placebo, flumazenil induced power in the alpha domain, accompanied by a drop of power in the delta and theta bands. While the increase in alpha activity resolved after 30 min, beta activity increased significantly, an effect that lasted up to the 180th postoperative minute. As with the finding of higher power in the fast-frequency domains, flumazenil patients scored higher with regard to collaboration and comprehension as well as orientation in space and time. 1. When used for induction, midazolam may result in significant depression of vigilance even 120 min after operation. 2. Flumazenil is a specific antagonist with a rapid onset of action. 3. Flumazenil is an antagonist specifically directed to reverse the side-effects of benzodiazepines in a manner similar to naloxone, which is used in opioid overdose.

[Measuring evoked otoacoustic emissions at various times during intubation anesthesia]. / Messung evozierter otoakustischer Emissionen zu verschiedenen Zeitpunkten einer Intubationsnarkose.

Evoked otoacoustic emissions (EOAE) remain intraindividually similar in repeated measurements. After application of medication for general anesthesia no significant changes of EOAE could be seen. Damping of amplitude and energy, mostly seen in the late phase of general anesthesia, might be caused by possible middle ear pressure changes from nitrous oxide. The recording of EOAE under general anesthesia provides an additional method in objective infant hearing evaluation and expands our diagnostic tools in those cases when children do not cooperate.

Effects of thoracic epidural anaesthesia on microvascular gastric mucosal oxygenation in physiological and compromised circulatory conditions in dogs.

BACKGROUND: The effects of thoracic epidural anaesthesia (TEA) on gastric mucosal microvascular haemoglobin oxygenation (microHbO(2)) are unclear. At the splanchnic level, reduction of sympathetic tone may promote vasodilation and increase microHbO(2). However, these splanchnic effects are counteracted by systemic effects of TEA (e.g., decreased cardiac output (CO) and mean arterial pressure (MAP)), thus making the net effect on microHbO(2) difficult to predict. In this respect, effects of TEA on microHbO(2) may differ between physiological and compromised circulatory conditions, and additionally may depend on adequate fluid resuscitation. Furthermore, TEA may alter the relationship between regional microHbO(2) and systemic oxygen-transport (DO(2)). METHODS: Chronically instrumented dogs (flow probes for CO measurement) were anaesthetized, their lungs ventilated and randomly received TEA with lidocaine (n=6) or epidural saline (controls, n=6). Animals were studied under physiological and compromised circulatory conditions (PEEP 10 cm H(2)O), both with and without fluid resuscitation. We measured gastric mucosal microHbO(2) by reflectance spectrophotometry, systemic DO(2), and systemic haemodynamics (CO, MAP). RESULTS: Under physiological conditions, TEA preserved microHbO(2) (47 (3)% and 49 (5)%, mean (sem)) despite significantly decreasing DO(2) (11.3 (0.8) to 10.0 (0.7) ml kg(-1) min(-1)) and MAP (66 (2) to 59 (3) mm Hg). However, during compromised circulatory conditions, TEA aggravated the reduction in microHbO(2) (to 32 (1)%), DO(2) (to 6.7 (0.8) ml kg(-1) min(-1)) and MAP (to 52 (4) mm Hg), compared with controls. During TEA, fluid resuscitation completely restored these variables. TEA preserved the correlation between microHbO(2) and DO(2), compared with controls. CONCLUSIONS: TEA maintains microHbO(2) under physiological conditions, but aggravates the reduction of microHbO(2) induced by cardiocirculatory depression, thereby preserving the relationship between gastric mucosal and systemic oxygenation.