Objective To determine whether use of intermediate acting neuromuscular blocking agents during general anesthesia increases the incidence of postoperative respiratory complications.Design Prospective, propensity score matched cohort study.Setting General teaching hospital in Boston, Massachusetts, United States, 2006-10.Participants 18 579 surgical patients who received intermediate acting neuromuscular blocking agents during surgery were matched by propensity score to 18 579 reference patients who did not receive such agents. Main outcome measuresThe main outcome measures were oxygen desaturation after extubation (hemoglobin oxygen saturation <90% with a decrease in oxygen saturation after extubation of >3%) and reintubations requiring unplanned admission to an intensive care unit within seven days of surgery. We also evaluated effects on these outcome variables of qualitative monitoring of neuromuscular transmission (train-of-four ratio) and reversal of neuromuscular blockade with neostigmine to prevent residual postoperative neuromuscular blockade. ResultsThe use of intermediate acting neuromuscular blocking agents was associated with an increased risk of postoperative desaturation less than 90% after extubation (odds ratio 1.36, 95% confidence interval 1.23 to 1.51) and reintubation requiring unplanned admission to an intensive care unit (1.40, 1.09 to 1.80). Qualitative monitoring of neuromuscular transmission did not decrease this risk and neostigmine reversal increased the risk of postoperative desaturation less than 90% (1.32, 1.20 to 1.46) and reintubation (1.76, 1.38 to 2.26). ConclusionThe use of intermediate acting neuromuscular blocking agents during anesthesia was associated with an increased risk of clinically meaningful respiratory complications. Our data suggest that the strategies used in our trial to prevent residual postoperative neuromuscular blockade should be revisited. IntroductionTens of millions of people worldwide undergo general anesthesia every day. Anesthetists use a wide variety of drugs to establish the reversible state of anesthesia, which is characterised by hypnosis, amnesia, analgesia, hemodynamic stability with control of the stress response, and immobility.1 Deep anesthesia provides all components 2 3 ; however, to achieve immobility with lower levels of anesthetic agents, anesthetists may coadminister curare-type neuromuscular blocking agents. These drugs inhibit neuromuscular transmission from nerves to muscles by competitively blocking the binding of acetylcholine to its postsynaptic receptors at the motor end plate, thereby causing paralysis of the muscle.More than 400 million people receive neuromuscular blocking agents annually (Intercontinental Marketing Services (IMS) RESEARCHHealth, Multinational Integrated Data Analysis System (MIDAS), September 2010), either in the operating theatre to optimize surgical conditions, or in the intensive care unit to facilitate mechanical ventilation in those with patient-ventilator asynchrony. 4 Neuromuscular blocking a...

The authors developed and validated a score for the prediction of postoperative respiratory complications, a simple, 11-point score that can be used preoperatively by anesthesiologists to predict severe postoperative respiratory complications.

In surgical critically ill patients presenting without preexisting impairment of functional mobility, the surgical intensive care unit optimal mobility score is a reliable and valid tool to predict mortality and intensive care unit and hospital length of stay.

Background Procedural sedation is frequently performed in spontaneously breathing patients but hypnotics and opioids decrease respiratory drive and place the upper airway at risk for collapse. Methods In a randomized, controlled, cross-over, pharmaco-physiological study in 12 rats, we conducted acute experiments to compare breathing, and genioglossus electromyogram activity at equianesthetic concentrations of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist that combines potent analgesic with hypnotic action effects, versus propofol. In 10 chronically instrumented rats resting in a plethysmograph, we measured these variables as well as electroencephalography during 5 conditions: quiet wakefulness, non-rapid-eye-movement sleep, rapid eye movement sleep, low-dose (60mg/kg intraperitoneally) and high-dose ketamine anesthesia (125mg/kg intraperitoneally). Results Ketamine anesthesia was associated with markedly increased genioglossus activity (1.5 to 5-fold higher values of genioglossus electromyogram) compared with sleep and propofol induced unconsciousness. Plethysmography revealed a respiratory stimulating effect: higher values of flow rate, respiratory rate, and duty-cycle (effective inspiratory time, 1.5-to-2-fold higher values). During wakefulness and normal sleep, the beta (f=6.51, p=0.04) electroencephalogram power spectrum was an independent predictor of genioglossus activity, indicating an association between electroencephalographic determinants of consciousness and genioglossus activity. Following ketamine administration, electroencephalogram power spectrum and genioglossus electroencephalogram was dissociated (p=0.9 for the relationship between delta/theta power spectrum and genioglossus electromyogram). Conclusions Ketamine is a respiratory stimulant that abolishes the coupling between loss-of-consciousness and upper airway dilator muscle dysfunction in a wide dose-range. Ketamine compared with propofol might help stabilize airway patency during sedation and anesthesia.

In contrast to handgrip strength, MMT reliably predicted in-hospital mortality, duration of mechanical ventilation, SICU LOS, and hospital LOS.

REFERENCE 1. Kor DJ, Talmor D. Anesthesiology and the acute respiratory distress syndrome: an ounce of prevention is worth a pound of cure [editorial].

Neurons of the ventrolateral preoptic nucleus (VLPO) promote sleep and VLPO loss produces insomnia. Previous studies show that general anesthetics including isoflurane activate VLPO neurons, and may contribute to their sedative effects. However, it is not clear to what extent the activation of VLPO neurons contributes to general anesthesia. We tested whether destruction of the VLPO neurons would affect the onset, depth, or recovery from isoflurane's general anesthetic effects. The VLPO was ablated in 25 rats by bilateral local injection of orexin-saporin, and polysomnography was performed to measure baseline sleep loss and responses to isoflurane anesthesia at 1% and 2%. Eight rats received sham (saline) injections. We measured isoflurane effects on time to loss of righting reflex, onset of continuous slow wave activity, and burst suppression; burst-suppression ratio; and time to recovery of righting reflex and desynchronized EEG. VLPO neuron cell loss was quantified by post hoc histology. Loss of VLPO neurons as well as lesion size were associated with cumulative sleep loss (r=0.77 and r=0.62, respectively), and cumulative sleep loss was the strongest predictor of high sensitivity to anesthesia, expressed as decreased time to loss of righting reflex (−0.59), increased burst-suppression ratio (r=0.52), and increased emergence time (r=0.54); an interaction-effect of isoflurane dose was observed (burst-suppression ratio: p<0.001). We conclude that the sleep loss caused by ablation of VLPO neurons sensitizes animals to the general anesthetic effects of isoflurane, but that the sedation produced by VLPO neurons themselves is not required for deep isoflurane anesthesia.

Introduction:To evaluate whether calabadion 1, an acyclic member of the Cucurbit[n]uril family of molecular containers, reverses benzylisoquinoline and steroidal neuromuscular-blocking agent effects. Methods: A total of 60 rats were anesthetized, tracheotomized, and instrumented with IV and arterial catheters. Rocuronium (3.5 mg/kg) or cisatracurium (0.6 mg/kg) was administered and neuromuscular transmission quantified by acceleromyography. Calabadion 1 at 30, 60, and 90 mg/kg (for rocuronium) or 90, 120, and 150 mg/kg (for cisatracurium), or neostigmine/glycopyrrolate at 0.06/0.012 mg/ kg were administered at maximum twitch depression, and renal calabadion 1 elimination was determined by using a 1 H NMR assay. The authors also measured heart rate, arterial blood gas parameters, and arterial blood pressure. Results: After the administration of rocuronium, resumption of spontaneous breathing and recovery of train-of-four ratio to 0.9 were accelerated from 12.3 ± 1.1 and 16.2 ± 3.3 min with placebo to 4.6 ± 1.8 min with neostigmine/glycopyrrolate to 15 ± 8 and 84 ± 33 s with calabadion 1 (90 mg/kg), respectively. After the administration of cisatracurium, recovery of breathing and train-of-four ratio of 0.9 were accelerated from 8.7 ± 2.8 and 9.9 ± 1.7 min with placebo to 2.8 ± 0.8 and 7.6 ± 2