Anesthesia and analgesia
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Anesthesia and analgesia · Dec 2001
How does the plethysmogram derived from the pulse oximeter relate to arterial blood pressure in coronary artery bypass graft patients?
Twenty patients scheduled for coronary artery bypass grafting had their ear and finger oximeter and radial artery blood pressure (Bp(meas)) waveforms collected. The ear and finger pulse oximeter waveforms were analyzed to extract beat-to-beat amplitude and area and width measurements. The Bp(meas) waveforms were analyzed to measured systolic blood pressure (BP), mean BP, and pulse pressure. The correlation coefficient was determined between the derived waveforms from the pulse oximeter and Bp(meas) for the first 10 patients. The ear pulse oximeter width (Width(Ear)) had the best correlation (r = 0.8). Linear regression was done between Width(Ear) and Bp(meas) based on slope (b) and intercept (a) values, BP was calculated (Bp(calc)) in the next 10 patients as: [equation: see text] where i = systolic BP, mean BP, and pulse pressure. The initial bias was too large to be clinically useful. To improve clinical applicability a period of calibration was introduced in which the first 50 readings of Width(Ear) and Bp(meas) for each patient were used to calculate the intercept. After calibration the systolic BP, mean BP and pulse pressure bias values were -2.6, -1.88 and -1.28 mm Hg, and the precision values were 15.9 10.09, and 9.94 mm Hg, respectively. The present attempt to develop a clinically useful method of noninvasive BP measuring was partly successful with the requirement of a calibration period. ⋯ Statistical comparison was made between measured blood pressure (BP) from arterial line and calculated BP derived from ear pulse oximeter waveform in 10 patients undergoing coronary artery bypass graft surgery. Using 62,077 paired readings, the mean difference for systolic BP, mean BP, and pulse pressure between the 2 methods was -2.6, -1.88, and -1.28 mm Hg, respectively.
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Anesthesia and analgesia · Dec 2001
The effects of increasing concentrations of isoflurane and desflurane on pulmonary perfusion and systemic oxygenation during one-lung ventilation in pigs.
During one-lung ventilation (OLV), hypoxic pulmonary vasoconstriction (HPV) reduces venous admixture and attenuates the decrease in arterial oxygen tension by diverting blood from the nonventilated lung to the ventilated lung. In vitro, desflurane and isoflurane depress HPV in a dose-dependent manner. Accordingly, we studied the effects of increasing concentrations of desflurane and isoflurane on pulmonary perfusion, shunt fraction, and PaO(2) during OLV in vivo. Fourteen pigs (30-42 kg) were anesthetized, tracheally intubated, and mechanically ventilated. After placement of femoral arterial and thermodilution pulmonary artery catheters, a left-sided double-lumen tube (DLT) was placed via tracheotomy. After DLT placement, FIO(2) was adjusted at 0.8 and anesthesia was continued in random order with 3 concentrations (0.5, 1.0, and 1.5 minimal alveolar concentrations) of either desflurane or isoflurane. Differential lung perfusion was measured with colored microspheres. All measurements were made after stabilization at each concentration. Whereas mixed venous PO(2), mean arterial pressure, cardiac output, nonventilated lung perfusion, and shunt fraction decreased in a dose-dependent manner, PaO(2) remained unchanged with increasing concentrations of desflurane and isoflurane during OLV. In conclusion, increasing concentration of desflurane and isoflurane did not impair oxygenation during OLV in pigs. ⋯ In an animal model of one-lung ventilation, increasing concentrations of desflurane and isoflurane dose-dependently decreased shunt fraction and perfusion of the nonventilated lung and did not impair oxygenation. The decreases in shunt fraction are likely the result of anesthetic-induced marked decreases in cardiac output and mixed venous saturation.
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Anesthesia and analgesia · Dec 2001
The involvement of the mu-opioid receptor in ketamine-induced respiratory depression and antinociception.
N-methyl-D-aspartate receptor antagonism probably accounts for most of ketamine's anesthetic effects; its analgesic properties are mediated partly via N-methyl-D-aspartate and partly via opioid receptors. We assessed the involvement of the mu-opioid receptor in S(+) ketamine-induced respiratory depression and antinociception by performing dose-response curves in exon 2 mu-opioid receptor knockout mice (MOR(-/-)) and their wild-type littermates (WT). The ventilatory response to increases in inspired CO(2) was measured with whole body plethysmography. Two antinociceptive assays were used: the tail-immersion test and the hotplate test. S(+) ketamine (0, 10, 100, and 200 mg/kg intraperitoneally) caused a dose-dependent respiratory depression in both genotypes, with greater depression observed in WT relative to MOR(-/-) mice. At 200 mg/kg, S(+) ketamine reduced the slope of the hypercapnic ventilatory response by 93% +/- 15% and 49% +/- 6% in WT and MOR(-/-) mice, respectively (P < 0.001). In both genotypes, S(+) ketamine produced a dose-dependent increase in latencies in the hotplate test, with latencies in MOR(-/-) mice smaller compared with those in WT animals (P < 0.05). In contrast to WT mice, MOR(-/-) mice displayed no ketamine-induced antinociception in the tail-immersion test. These results indicate that at supraspinal sites S(+) ketamine interacts with the mu-opioid system. This interaction contributes significantly to S(+) ketamine-induced respiratory depression and supraspinal antinociception. ⋯ The involvement of the mu-opioid receptor system in S(+) ketamine-induced respiratory depression and spinal and supraspinal analgesia was demonstrated by performing experiments in mice lacking the mu-opioid receptor and in mice with intact mu-opioid receptors.