Susceptibility to upper airway obstruction during partial neuromuscular block.

BACKGROUND: Airway obstruction after anesthesia may be caused or exaggerated by residual neuromuscular block, with loss of muscle support for collapsible upper airway structures. METHODS: Six male volunteers were studied before treatment, during stable partial neuromuscular block with vecuronium at a mean train-of-four (TOF) ratio of 50% (95% CI, 36-61%), and after reversal by neostigmine. Catheter-mounted transducers were placed in the pharynx and esophagus to estimate, respectively, the upper airway resistance, and the work of breathing (calculated as the time integral of the inspiratory pressure developed by the respiratory muscles, esophageal pressure time product) during quiet breathing, during breathing 5% carbon dioxide, and while breathing with an inspiratory resistor. Breathing with pressure at the airway opening held at pressures from -5 to 40 cm H2O were also tested to assess airway collapsibility. RESULTS: Although breathing through a resistor increased upper airway resistance from 1.2 (0.67, 1.72) cm H2O x l(-1) x s to 2.5 (1.32, 3.38) cm H2O x l(-1) x s, and carbon dioxide stimulation reduced resistance to 0.8 (0.46, 1.33) cm H2O x l(-1) x s, no effect of partial neuromuscular block (mean TOF ratio, 52%) on upper airway properties could be shown. CONCLUSIONS: Neuromuscular block with a TOF ratio of 50% can be present yet clinically difficult to detect in patients recovering from anesthesia. This degree of block has no effect on airway patency in volunteers, even during challenge. Airway obstruction during recovery from anesthesia thus is more likely to be caused by residual effects of general anesthetic agents or centrally acting analgesics, either alone or perhaps in concert with residual neuromuscular block.

Intubating conditions using cisatracurium after induction of anaesthesia with thiopentone.

We studied tracheal intubation conditions produced by the muscle relaxant, cisatracurium, following induction of anaesthesia with fentanyl (2 micrograms.kg-1) and thiopentone (6 mg.kg-1). Sixty patients were randomly assigned to receive cisatracurium in a single bolus dose of either 0.15 or 0.20 mg.kg-1. Tracheal intubation was commenced 120 s after injection of the relaxant. The mean (SD) time taken to achieve intubation was significantly shorter in the 0.20 mg.kg-1 group (137 (16) s) than the 0.15 mg.kg-1 group (149 (12) s; p < 0.05). The intubating conditions were better after the larger dose. Our results suggest that when anaesthesia is induced using thiopentone, a dose of 0.20 mg.kg-1 of cisatracurium is recommended to ensure satisfactory intubating conditions.

Comparison of the effects of mivacurium on the diaphragm and geniohyoid muscles.

Although subjects often report difficulty with swallowing shortly after receiving neuromuscular blocking agents, difficulty with swallowing during recovery from neuromuscular blocking agents appears to be infrequent. We have used electromyography to compare onset and recovery at the diaphragm and geniohyoid airway muscles after an intubating dose of mivacurium (0.2 mg kg-1) to determine if the geniohyoid muscles were particularly sensitive to neuromuscular blocking agents. Twelve adults undergoing elective surgery were anaesthetized with propofol and fentanyl and the trachea intubated without neuromuscular blocking agents. The left hypoglossal and right phrenic nerves were stimulated with percutaneous needle electrodes and the electromyogram recorded with surface electrodes. EMG responses were measured after a bolus dose of mivacurium 0.2 mg kg-1. Recordings were also made of the mechanical response of the adductor pollicis to supramaximal ulnar nerve stimulation. There was no difference in the rate of onset of block for geniohyoid muscles and the diaphragm, but recovery to 25% and 90% of the control response was shorter at the diaphragm (median 14.5 (95% confidence limits 12.9-15.3) min and 23.8 (21.7-26) min) than at the geniohyoid muscle (19.4 (15.6-20.1) min and 29.2 (26.3-31.4) min), respectively (P < 0.05). When the train-of-four ratio of the mechanical response of the thumb reached 70%, the diaphragm and geniohyoid muscles had recovered completely in all patients.

A comparison of the neuromuscular blocking effects of atracurium, mivacurium, and vecuronium on the adductor pollicis and the orbicularis oculi muscle in humans.

Both the orbicularis oculi (OO) and the adductor pollicis (AP) muscles have been used to indirectly quantify the extent of neuromuscular block of the respiratory muscles. To clarify any differences in response of these muscles to neuromuscular blocking drugs, the effects of two different doses of atracurium, mivacurium, and vecuronium on the AP and OO were studied. A new technique was used to measure the evoked mechanical response of the OO with accelerometry. Fifty premedicated patients were anesthetized with 5-8 mg/kg thiopental and 2 micrograms/kg fentanyl intravenously (i.v.). They were randomly allocated to receive a single dose of either 300 or 500 micrograms/kg atracurium, 150 or 250 micrograms/kg mivacurium, or 60 or 100 micrograms/kg vecuronium i.v. After orotracheal intubation, anesthesia was maintained with nitrous oxide 60% in oxygen, isoflurane 0.5%-1.5% end-tidal, and 1-2 micrograms/kg fentanyl boluses as required. The evoked response of the AP after ulnar nerve stimulation was measured using a force transducer, and that of the OO after facial nerve stimulation was measured with accelerometry using a piezoelectric probe fixed to the eyelid. The following variables were recorded for each muscle: the maximum depression of the first twitch response to the train-of-four (EMAX), the time to achievement of EMAX (TMAX), the time to recovery of the first twitch response to 25%, 50%, 75%, and 90% of control value (TH25, TH50, TH75, and TH90, respectively) and the time to recovery of the train-of-four response to a ratio of 70% (TOF 0.7). The smaller dose of each relaxant was significantly less potent than the larger dose at the OO. TMAX was shorter for the OO than for the AP at the larger dose of each drug. TH 25 was shorter at the OO than at the AP with 0.5 mg/kg atracurium, but there was no significant difference with 0.25 mg/kg atracurium. TH25 and TH50 were both faster at the OO than at the AP with mivacurium, but there was no difference with vecuronium. TOF 0.7 was shorter with the smaller dose of each drug, but there was no difference with the higher doses. It is concluded that it is possible to record the mechanical response of the OO muscle using a noninvasive method. There are differences between the responses of the OO and the AP to neuromuscular blockers that depend upon both the specific drug itself and the dose used.

[Pharmacological treatment of vasospasm in subarachnoid hemorrhage]. / Traitement pharmacologique du vasospasme de l'hémorragie sous-arachnoïdienne.

Pharmacological treatment of vasospasm in subarachnoid haemorrhage (SAH) is founded on prevention and treatment of arterial narrowing and delayed ischaemic deficits. Safety and efficacy of different agents have been studied and trials classified according to the level of evidence proposed by the "Stroke Council" of the American Heart Association. Early intracisternal fibrinolysis can prevent vasospasm (level III to V of evidence, grade C). Pharmacological treatment is based on few drugs. Nimodipine reduces poor outcome related to vasospasm, but does not affect angiographic vessel caliber (level of evidence I and II, grade A). Its use is strongly recommended. Nicardipine decreases symptomatic and angiographic vasospasm, but does not affect outcome (level of evidence I to V, grade B). Tirilazad associated with nimodipine prevents delayed ischaemic deficits due to vasospasm and improves outcome in male patients. Intra-arterial infusion of papaverine associated with transluminal angioplasty can improve symptomatic vasospasm, resistant to conventional therapy (level of evidence IV to V, grade C). Pharmacological treatment of vasospasm associated with specific management founded on pathophysiology of SAH has improved patients outcome.

Laparoscopic cholecystectomy minimally impairs postoperative cardiorespiratory and muscle performance.

Surgery elicits a subjective feeling of postoperative fatigue, at least partly related to an impairment in cardiorespiratory function and muscle performance. Laparoscopic surgery is reported to impair the patient's condition minimally. The aim of this study was to assess exercise performance in patients scheduled for elective laparoscopic cholecystectomy. Nine patients assessed as having American Society of Anesthesiologists (ASA) grade I were enrolled in the study. Subjective feelings of fatigue (measured on a visual analogue scale), and heart rate, systemic arterial pressure oxygen consumption and carbon dioxide production responses to graded exercise testing, were assessed before operation and on days 3 and 10 after operation. There were no significant differences in any of these measurements, at rest or during exercise, between the preoperative and postoperative values. Uncomplicated laparoscopic cholecystectomy does not impair postoperative cardiorespiratory and muscle performance or induce significant postoperative fatigue in patients with ASA I, allowing rapid recovery.

Muscle weakness in intensive care patients: initial manifestation of vitamin D deficiency.

A 72-year-old woman was referred to hospital for obnubilation with general muscle weakness and hypotonia. Biology showed hypocalcemia, hypophosphatemia, increased serum creatine kinase and alkaline phosphatase levels. Brain CT scan, cerebrospinal fluid examination, and electromyogram were normal. Clinical status and electroencephalogram were consistent with non-convulsive generalized status epilepticus. The treatment included clonazepam and CaCl2 and consciousness returned to normal. A treatment with multivitamin infusion containing vitamin D2 was given for 3 weeks. Muscle weakness improved partially. Serum vitamin D3 level was low and osteomalacic myopathy was diagnosed. A treatment was given with 25OH vitamin D3, 50 micrograms per day. Two months later, serum vitamin D3 and creatine kinase levels were normal and the patient could walk without help. We conclude that vitamin D status should be monitored in elderly patients with muscle symptoms and abnormal calcium status. Osteomalacic myopathy should be considered in critically ill patients with muscle symptoms of an unclear cause.

Recovery of the swallowing reflex after propofol anesthesia.

The swallowing reflex is depressed by anesthetics. During recovery from anesthesia the rapid return of laryngeal and upper airway reflexes is important to protect the lower airway from aspiration. This study measures the recovery of the swallowing reflex after propofol anesthesia. Fifteen patients undergoing a colonoscopy under general anesthesia were studied. No premedication was given. Anesthesia was induced with propofol 2 mg/kg followed by an infusion of 10 mg.kg-1.h-1. The swallowing reflex was measured every 3 min after the end of propofol infusion for 30 min. To initiate swallowing, 0.3 mL of distilled water was injected into the pharynx at two different speeds: a slow injection over 3 s, and a bolus injection. The swallowing reflex was determined by measuring the latency period (i.e., time from water injection to start of electromyographic (EMG) activity measured in the glossal muscles). Swallowing activity was determined by integration of the EMG (EMGi) of the glossal muscles during swallowing. The latency periods after slow and bolus injections were significantly increased for the first 12 min after the end of the propofol infusion and returned to control (preanesthetic values) at 24 min. The EMGi was significantly decreased over the first 12 min and returned to control at 21 min. Propofol depresses the swallowing reflex, but complete recovery is rapid. This study suggests that the oral intake could be allowed early after recovery from anesthesia when propofol is used as the sole anesthetic.

Midazolam/propofol but not propofol alone reversibly depress the swallowing reflex.

General anaesthetics depress swallowing and this is a reason to delay oral intake after general anaesthesia. The swallowing reflex was studied 2 h after general anaesthesia for patients undergoing colonoscopy. Forty-one patients were anaesthetized with midazolam 75 micrograms.kg-1 followed by a continuous infusion of propofol and 39 patients with propofol 1.5 mg.kg-1 bolus followed by an infusion. Swallowing reflex was measured by electromyography 2 h after induction of anaesthesia, before and 5 min after the administration of flumazenil (0.2 mg) or placebo. Two h after anaesthesia, the state of consciousness was almost normal in all patients and did not change after flumazenil. At two hours, the latency times for the swallowing reflex in patients treated with propofol alone were of 1.4 +/- 0.4 s and were significantly shorter (P < 0.05) than the value of 1.9 +/- 0.8 s observed in patients who received midazolam with propofol. In the latter group the latency time of the swallowing reflex was significantly reduced following the administration of flumazenil but not placebo. In patients who received propofol without midazolam, the administration of flumazenil or placebo was not associated with significant changes in the latency times. There were also no significant differences in the latency times in the subgroup that received midazolam followed by flumazenil and the propofol alone groups that did or did not receive flumazenil. These results suggest that midazolam still exerts a depressive effect on the swallowing reflex 2 h after its administration despite the recovery of normal consciousness.

Priming doses of atracurium and vecuronium depress swallowing in humans.

The administration of low doses of muscle relaxant may cause peripheral muscular weakness including difficulty in swallowing. In the present study, the effect of priming doses of atracurium and vecuronium on swallowing was studied. Sixty patients undergoing elective surgery under general anesthesia were divided randomly into four groups of 15 patients and received as a priming dose either vecuronium (10 or 15 micrograms/kg) or atracurium (50 or 75 micrograms/kg). Swallowing muscle activity was measured by electromyography using submental surface electrodes. Swallowing was initiated by administration of 0.3 ml distilled water through an oral catheter. Swallowing reflex was determined by measuring the latency time (i.e., time from water administration to start of EMG activity of glossal muscles). Swallowing activity was determined by integration of the EMG of glossal muscles during swallowing. Peripheral muscle strength was determined by hand grip strength. Swallowing reflex activity and peripheral muscle strength were measured before and 3 and 6 min after administration of vecuronium or atracurium. Latency time remained unchanged after any of the priming doses. Integrated EMG decreased significantly (P < .001) 3 and 6 min after all priming doses tested (42-75% of baseline value). Only after atracurium 75 micrograms/kg was the hand grip strength significantly decreased (P < .01). These results suggest that owing to its effect on swallowing, the priming dose should be used with caution.