Articles: general-anesthesia.
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Anesthesia and analgesia · Aug 1994
Changes in heart rate variability under propofol anesthesia: a possible explanation for propofol-induced bradycardia.
We propose to study the bradycardia associated with propofol anesthesia. Ten women undergoing laparoscopy for benign disease were studied using ambulatory electrocardiogram monitoring. Anesthesia was induced with an intravenous bolus of propofol and maintained with an infusion. ⋯ We conclude that high-frequency variability reflects parasympathetic tone. Propofol anesthesia reduces parasympathetic tone to a lesser degree than sympathetic tone. This autonomic milieu predisposes the patient to developing bradycardia in response to parasympathetic stimuli.
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We have assessed the effect of lengthening the expiratory limb of an Ayre's T-piece from 0.5 to 10 m for ventilation with a Nuffield series 200 ventilator and Newton valve, as this equipment is potentially suitable for infants and young children during anaesthesia for magnetic resonance imaging (MRI). We used lung models with compliances and resistances representative of the respiratory system with intubated trachea of a neonate, infant and child weighing 15-20 kg. The effects on ventilation were small, being greatest with the largest lung model where the longer T-piece resulted in a reduction in tidal volume from 261 to 236 ml and an increase in intrinsic and extrinsic positive end-expiratory pressure from 0.20 to 0.32 kPa and from 0.14 to 0.25 kPa, respectively. Such changes are unlikely to be clinically important and can be obviated by using the ventilator with the standard valve in children weighing 15-20 kg.
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Randomized Controlled Trial Clinical Trial
[The arterial blood gas change in anesthetized patients with apnea: disadvantage of hyperventilation before intubation].
We studied the arterial blood gas changes during 4 minute apnea period without using constant oxygen flow under anesthesia. Fifteen adult surgical patients (ASA PS 1 or 2, 21-49 years of age) were randomly divided into 3 groups by ETCO2 before the start of apnea (group I: 40 mmHg, group II: 30 mmHg, group III: 20 mmHg). In addition, each patient was monitored with pulse oximetry, ECG, blood pressure, FIO2 and ETCO2. ⋯ In conclusion, the rate of rise of PaCO2 in anesthetized patients with apnea was logarithmic and there was no correlation with pre-apnea ETCO2. The rate of SpO2 decrease was significant in hyperventilated group (III). Thus, hyperventilation applied before the endotracheal intubation is not of benefit to the oxygenation of healthy humans.