Biomedical subjects
Publications and source records attributed to S T Sum-Ping.
We report a 65-year-old male who developed severe methemoglobinemia only on reexposure to benzocaine. The patient needed two awake fiberoptic intubations for emergency surgeries. On the second exposure, the patient was septic and malnourished, and he was taking acetaminophen. He developed a methemoglobin level of 55%. Possible reasons for the methoglobinemia on reexposure are discussed in this report.
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To assess the effect of hemodialysis on protein metabolism, leucine flux was measured in seven patients before, during, and after high efficiency hemodialysis using cuprophane dialyzers and bicarbonate dialysate during a primed-constant infusion of L-[1-13C]leucine. The kinetics [mumol/kg per h, mean +/- SD] are as follows: leucine appearance into the plasma leucine pool was 86 +/- 28, 80 +/- 28, and 85 +/- 25, respectively, before, during, and after dialysis. Leucine appearance into the whole body leucine pool, derived from plasma [1-13C]alpha-ketoisocaproate enrichment, was 118 +/- 31, 118 +/- 31, and 114 +/- 28 before, during, and after dialysis, respectively. In the absence of leucine intake, appearance rate reflects protein degradation, which was clearly unaffected by dialysis. Leucine oxidation rate was 17.3 +/- 7.8 before, decreased to 13.8 +/- 7.8 during, and increased to 18.9 +/- 10.3 after dialysis (P = 0.027). Leucine protein incorporation was 101 +/- 26 before, was reduced to 89 +/- 23 during, and returned to 95 +/- 23 after dialysis (P = 0.13). Leucine net balance, the difference between leucine protein incorporation and leucine release from endogenous degradation, was -17.3 +/- 7.8 before, decreased to -28.5 +/- 11.0 during, and returned to -18.9 +/- 10.3 after dialysis (P < 0.0001). This markedly more negative leucine balance during dialysis was accountable by dialysate leucine loss, which was 14.4 +/- 6.2 mumol/kg per h. These data suggest that hemodialysis using a cuprophane membrane did not acutely induce protein degradation. It was, nevertheless, a net catabolic event because protein synthesis was reduced and amino acid was lost into the dialysate.
BACKGROUND AND METHODS: Previous studies on acute lung injury induced with oleic acid did not attempt to limit the influence of secondary changes on pulmonary circulation, and cardiopulmonary variable data were only collected and processed intermittently. Our study was designed to continuously monitor the following variables in five swine: systemic and pulmonary pressure; mixed venous oxygen saturation (SVO2) and arterial oxygen saturation (SaO2); minute oxygen consumption and CO2 production before, during, and for 4 hr after the infusion of oleic acid. A personal computer was programmed to produce 20-sec updates of deadspace ratio (VD/VT), venous admixture (Qsp/Qt), pulmonary (PVR) and systemic vascular resistance (SVR), and cardiac output (Qt) from these data. RESULTS: During the oleic acid infusion, there were increases in PVR, SVR, heart rate (HR), mean pulmonary arterial pressure (MPAP), Qsp/Qt, and VD/VT, and a decrease in Qt, SaO2, and SVO2. Thirty minutes after the oleic acid infusion, there was a further increase in HR, Qsp/Qt, and VD/VT, while MPAP, PVR, and SVR gradually decreased to pre-oleic acid infusion levels. No further decrease in SaO2, SVO2, and Qt was observed during that time. After the 30-min period, there was no further change in the cardiopulmonary variables. CONCLUSION: Our method of continuous monitoring was able to demonstrate in swine both the dynamic changes during, and stability after, the oleic acid infusion.
The trachea and esophagus of 21 patients were simultaneously intubated to comparatively evaluate methods for detecting esophageal intubation. In succession, the trachea and esophagus were ventilated with the same inspiratory volume of 621 +/- 45 mL (mean +/- SD). Carbon dioxide (CO2) levels, volumes, and temperatures of expired gas were measured from the tracheal and esophageal tubes. End-expired CO2 levels of gases from the trachea and esophagus were 4.9 +/- 0.7% and 0.6 +/- 0.6%, respectively, with CO2 waveforms observed in 7 (33%) patients with esophageal intubations. Volumes expired from the tracheal tube averaged 615 +/- 64 mL and from the esophageal tube 35 +/- 16 mL (P less than 0.001). Peak temperatures of expired gas recorded from the tracheal tube (32.0 +/- 0.73 degrees C) were higher than those from the esophageal tube (27.3 +/- 1.2 degrees C) (P less than 0.001). The shape of temperature waveforms with a correctly placed tracheal tube remained constant with each ventilation, contrary to that obtained from an esophageal tube. Although the occasional detected of CO2 waveforms from an esophageal tube might lead to an incorrect assessment of tube placement, this limitation of CO2 analyzer can be offset by measurement of volume and temperature of expired gas in identifying placement of an endotracheal tube.