Acta anaesthesiologica Scandinavica
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Acta Anaesthesiol Scand · Feb 1994
Measurement of dead-space in a model lung using an oscillating inspired argon signal.
In a model lung, airways dead-space can be accurately measured using a forced inspired oscillating argon signal, which varies sinusoidally about a mean concentration of 6% v/v with an amplitude of +/- 4% v/v. With sinusoid forcing periods longer than 120 seconds, and at a breathing rate of 13.4 breaths minute-1, the mean airways dead-space can be measured with a standard error of less than 5%. Sinusoid forcing periods shorter than 120 s provided inaccurate estimates of dead-space and so should not be used with this technique.
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Acta Anaesthesiol Scand · Feb 1994
Cardiovascular depression by isoflurane and concomitant thoracic epidural anesthesia is reversed by dopamine.
Interactive effects between exogenous dopamine (DA) and isoflurane (I) combined with thoracic epidural blockade (TEA) were studied in dogs during chloralose anesthesia. The I-TEA intervention per se decreased heart rate (HR; 28%), mean arterial pressure (MAP; 63%), cardiac output (CO; 54%), left ventricular dP/dt (LVdP/dt; 75%) and LVdP/dt/systolic arterial pressure (SAP; 42%). Prior to the I-TEA intervention, dopamine increased MAP, CO, LVdP/dt, LVdP/dt/SAP and stroke volume (SV) already at the dose 10 micrograms.kg-1.min-1 and, additionally, increased mean pulmonary artery pressure (MPAP) at the dose 20 micrograms.kg-1.min-1. ⋯ At the dose 20 micrograms.kg-1.min-1, DA also increased MAP (39%), LVdP/dt (119%), LVdP/dt/SAP (73%), SVR (28%) and MPAP (70%) above levels prior to I-TEA. To conclude, exogenous dopamine effectively and dose-dependently counters cardiovascular depression induced by the anesthetic technique of combining I and TEA. The pressor and systemic vasoconstrictor actions of dopamine are potentiated by conjoint administration of I and TEA.
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Acta Anaesthesiol Scand · Jan 1994
Randomized Controlled Trial Comparative Study Clinical TrialPostoperative nausea and vomiting. A comparison between intravenous and inhalation anaesthesia in breast surgery.
Nausea and vomiting during the first 24 postoperative hours after breast surgery were studied. Ninety patients scheduled for elective breast surgery were randomly assigned to one of three anaesthetic methods: total intravenous anaesthesia with propofol, or propofol or thiopental for induction followed by isoflurane anaesthesia. All three groups received fentanyl for peroperative analgesia. ⋯ Nausea and vomiting were seen in 18 (60%), 13 (43%) and 15 (50%) for the groups propofol-propofol, propofol-isoflurane and thiopental-isoflurane, respectively. In conclusion, every second patient experienced nausea or vomiting after breast surgery, the majority of these emetic symptoms occurring after leaving the postoperative unit. Propofol for induction or as a main anaesthetic did not make any major difference with regard to postoperative nausea or vomiting.
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Acta Anaesthesiol Scand · Jan 1994
Randomized Controlled Trial Clinical TrialEffects of ephedrine and phenylephrine on maternal and fetal atrial natriuretic peptide levels during elective cesarean section.
The effects of ephedrine and phenylephrine on fetal and maternal plasma atrial natriuretic peptide (ANP) concentrations were studied during 30 elective cesarean sections. After induction of spinal anesthesia, reductions from baseline maternal blood pressure were corrected with one of these pressor agents administered in a double-blinded, randomized manner. Immediately following delivery, umbilical artery (UA) ANP concentrations were significantly higher than umbilical vein (UV) concentrations (pg/ml) for both groups (ephedrine, 120.8 +/- 64.0 vs. 86.8 +/- 40.8, phenylephrine, 125.0 +/- 54.2 vs. 72.4 +/- 31.7), but there were no differences between groups for UA and UV ANP levels. ⋯ Postpartum maternal (MV2), UA, and UV blood gas variables (pH, PCO2, and PO2) were also not different between groups. These data suggest that effects of pressor doses of ephedrine (beta and alpha agonist) and phenylephrine (alpha agonist) on maternal and fetal ANP levels are not different. Therefore, 1) assuming these pressor drugs stimulate ANP release, this stimulation is not solely mediated by beta receptors and 2) to the extent that fetal ANP influences feto-placental circulatory homeostasis, the effects of ephedrine and phenylephrine on this regulatory mechanism do not appear to be different.