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Biomedical subjects

Yung-Wei Hsu

Publications and source records attributed to Yung-Wei Hsu.

7 recordsLinked to original sources

Changes in hematocrit based on incremental blood sampling: mathematical models perform poorly.

PURPOSE: Excessive blood sampling, with its inherent risks, is of growing concern among clinicians. We performed this study to measure the changes in hematocrit (Hct) during a laboratory investigation where multiple blood samples are collected. The performance of a simple mathematical model, used in clinical practice to predict Hct changes, is evaluated. METHODS: Eight healthy male volunteers participated in this study. The equation Hct(f) = Hct(i)*(EBV-BL)/EBV is used to predict changes in Hct. Where Hct(f) and Hct(i) are, respectively, the final and initial Hct, EBV is the estimated blood volume and BL is the blood loss. RESULTS: Thirty-five pharmacokinetic samples per subject were collected totalling 314 mL of BL. The Hct decreased from 44.2% +/- 2.2% to 39.9% +/- 2.5% (P = 0.001). On average, model predictions tended to have a discrete tendency to underestimate the Hct changes (-0.5% points of bias). While the predictions of the Hct were very accurate in 50% of the subjects, the discrepancy of the Hct predictions was clinically significant in the other 50% of the subjects. CONCLUSION: Consistent with the model prediction, this study demonstrated a significant reduction in the Hct values in healthy subjects undergoing incremental phlebotomy. On average, the model successfully predicted the decrease in Hct. However, the inter- and intra-individual variabilities in the Hct changes are clinically significant. In clinical settings, which are not well controlled environments, the variability is likely to be greater and the clinical use of the model cannot replace the need to monitor the Hct.

Adult↗

The effect of hemodynamic changes induced by propofol induction on cerebral oxygenation in young and elderly patients.

STUDY OBJECTIVE: To investigate the difference of regional cerebral oxygen saturation (rSo2) decrease in response to the decrease in mean arterial blood pressure (MAP) in young and elderly patients. DESIGN: Prospective clinical study. SETTING: Medical center hospital. PATIENTS: Twenty-four American Society of Anesthesiologists physical status I and II patients, 12 of whom were young and the other 12 elderly, scheduled for elective surgery requiring general anesthesia. Patients received propofol 2 mg/kg (young patient group) and propofol 1.5 mg/kg (elderly patient group) as an induction drug. MEASUREMENTS: MAP and rSo2 were recorded continuously for 5 minutes after propofol administration. MAIN RESULTS: MAP values at the second to fifth minutes and rSo2 at the second minute after propofol administration were significantly lower than baseline in both groups (P<.05). The rSo2 decrease was minimal, and the slopes of the rSo2 decrease in response to the MAP decrease in the young and elderly groups were 0.093+/-0.012 (P<.001) and 0.112+/-0.016 (P<.001) (mean+/-SEM), respectively. CONCLUSIONS: After propofol induction, there was no difference between young and elderly patients in rSo2 decrease in response to the decrease in MAP.

Adult↗

Predicting postoperative pain by preoperative pressure pain assessment.

BACKGROUND: The goal of this study was to evaluate whether preoperative pressure pain sensitivity testing is predictive of postoperative surgical pain. METHODS: Female subjects undergoing lower abdominal gynecologic surgery were studied. A pressure algometer was used preoperatively to determine the pressure pain threshold and tolerance. A visual analog scale (VAS) was used to assess postoperative pain. A State-Trait Anxiety Inventory was used to assess patients' anxiety. Subjects received intravenous patient-controlled analgesia for postoperative pain control. The preoperative pain threshold and tolerance were compared with the postoperative VAS pain score and morphine consumption. RESULTS: Forty women were enrolled. Their preoperative pressure pain threshold and tolerance were 141 +/- 65 kPa and 223 +/- 62 kPa, respectively. The VAS pain score in the postanesthesia care unit and at 24 h postoperatively were 81 +/- 24 and 31 +/- 10, respectively. Highly anxious patients had higher VAS pain scores in the postanesthesia care unit (P < 0.05). Pressure pain tolerance was significantly correlated with the VAS at 24 h postoperatively (P < 0.001, r = -0.52). Pressure pain tolerance after fentanyl administration (mean, 272 +/- 68 kPa) correlated significantly with morphine consumption in the first 24 h postoperatively (P < 0.002, r = -0.48). CONCLUSIONS: Assessment of preoperative pressure pain tolerance is significantly correlated with the level of postoperative pain. Pain tolerance assessment after fentanyl was administered and fentanyl sensitivity predicted the dose of analgesics used in the first 24 h after surgery. The algometer is thus a simple, useful tool for predicting postoperative pain and analgesic consumption.

Adult↗

Dexmedetomidine pharmacodynamics: part I: crossover comparison of the respiratory effects of dexmedetomidine and remifentanil in healthy volunteers.

BACKGROUND: Dexmedetomidine, a highly selective alpha2-adrenoceptor agonist used for short-term sedation of mechanically ventilated patients, has minimal effect on ventilation. METHODS: This study compared the respiratory effect of dexmedetomidine to that of remifentanil. The authors measured and compared respiratory responses of six healthy male volunteers during (1) a stepwise target-controlled infusion of remifentanil, (2) a stepwise target-controlled infusion of dexmedetomidine, and (3) a pseudonatural sleep session. RESULTS: Compared with baseline, remifentanil infusions resulted in respiratory depression as evidenced by a decrease in respiratory rate and minute ventilation, respiratory acidosis, and apnea episodes resulting in desaturations. Remifentanil disturbed the natural pattern of breathing and flattened the distribution of ventilatory timing (inspiratory time/ventilatory cycle time). The respiratory effects of dexmedetomidine markedly contrasted with those of remifentanil. When compared with baseline, during dexmedetomidine infusions, the respiratory rate significantly increased, and the overall apnea/hypopnea index significantly decreased. The distribution of inspiratory time/ventilatory cycle time showed an increased peak. In addition, dexmedetomidine seemed to mimic some aspect of natural sleep. While the subjects were breathing a 5% CO2 mixture, hypercapnic arousal phenomena (documented by the Bispectral Index, the electroencephalogram, and sudden increase in the minute ventilation) were observed during dexmedetomidine infusions. Similar phenomena during natural sleep have been reported in the literature. CONCLUSIONS: In comparison with remifentanil, dexmedetomidine infusions (1) did not result in clinically significant respiratory depression, (2) decreased rather than increased the apnea/hypopnea index, and (3) exhibited some similarity with natural sleep.

Adult↗

Dexmedetomidine pharmacodynamics: Part II: Crossover comparison of the analgesic effect of dexmedetomidine and remifentanil in healthy volunteers.

BACKGROUND: Dexmedetomidine is a highly selective alpha2-adrenoceptor agonist used for short-term sedation of mechanically ventilated patients. The analgesic profile of dexmedetomidine has not been fully characterized in humans. METHODS: This study was designed to compare the analgesic responses of six healthy male volunteers during stepwise target-controlled infusions of remifentanil and dexmedetomidine. A computer-controlled thermode was used to deliver painful heat stimuli to the volar side of the forearms of the subjects. Six sequential 5-s stimuli (ranging from 41 degrees to 50 degrees C) were delivered in random order. The recorded visual analog scale was used to fit an Emax model. RESULTS: Compared to baseline, remifentanil infusions resulted in a right shift of the sigmoid curve (increased T50, the temperature producing a visual analog scale score of 50% of the maximal effect, from 46.1 degrees C at baseline to 48.4 degrees and 49.1 degrees C during remifentanil infusions) without a change of the steepness of the curve (identical Hill coefficients gamma during baseline and remifentanil). Compared to baseline, dexmedetomidine infusions resulted in both a right shift of the sigmoid curve (increased T50 to 47.2 degrees C) and a decrease in the steepness of the curve (decreased gamma from 3.24 during baseline and remifentanil infusions to 2.45 during dexmedetomidine infusions). There was no difference in the pain responses between baseline and after recovery from remifentanil infusions (identical T50 and gamma). CONCLUSION: As expected, dexmedetomidine is not as effective an analgesic as the opioid remifentanil. The difference in the quality of the analgesia with remifentanil may be a reflection of a different mechanism of action or a consequence of the sedative effect of dexmedetomidine.

Adult↗

GTPCH is not a rate-limiting factor for hemorrhagic shock-induced hepatic nitric oxide biosynthesis.

BACKGROUND: Hemorrhagic shock upregulates inducible nitric oxide (NO) synthase (iNOS) expression and the resultant NO overproduction. Liver is one of the major organs that is responsible for increased NO production after trauma-hemorrhage and resuscitation. Guanosine triphosphate cyclohydrolase I (GTPCH) is the rate-limiting enzyme for the synthesis of tetrahydrobiopterin (BH4), a necessary co-factor for iNOS activity. Very little is known about the effects of hemorrhagic shock on hepatic GTPCH expression. METHODS: Fifteen male Sprague-Dawley rats were randomly assigned to one of three groups, i.e. a sham instrumented (Sham) group, a sustained hemorrhagic shock (HS) group, and a hemorrhagic shock with resuscitation (HS/RES) group (n = 5 in each group). Controlled hemorrhagic shock was induced and the mean arterial pressure (MAP) was kept between 40-45 mmHg for sixty minutes in both HS and HS/RES groups. Then resuscitation with infusion of shed autologous blood and normal saline was performed in HS/RES group. Microdialysis probes were put in the liver and the right atrium for collection of serial samples. NO concentrations in dialysate samples were measured using chemiluminescence. Hepatic iNOS and GTPCH mRNA concentrations were analyzed using semiquantitative reverse transcription and polymerase chain reaction (RT-PCR). RESULTS: Hemorrhagic shock induced both the hepatic and circulating NO biosynthesis as well as hepatic iNOS mRNA expression. Resuscitation with shed blood/normal saline normalized this upregulation. However, no difference was found in mean hepatic GTPCH mRNA concentrations between groups in this experiment. CONCLUSIONS: We provide the evidence that hemorrhagic shock-induced NO biosynthesis involves upregulation of iNOS transcription in liver tissue and GTPCH transcription is unaffected by either hemorrhagic shock or resuscitation. Furthermore, microdialysis is an ideal technique for serial sampling and that events can be followed.

Animals↗

Cardiac output measurement during cardiac surgery: esophageal Doppler versus pulmonary artery catheter.

BACKGROUND: Bolus thermodilution cardiac output (BCO) measurement has been considered as the "gold standard" for cardiac output (CO) measurement. However, it requires placement of a pulmonary artery (PA) catheter, and questions have been raised regarding the risk/benefit ratio of this invasive technique. Furthermore, great variations between measurements have been reported. Continuous thermodilution CO (CCO) measurement is reported to be a better alternative, but it still requires the placement of a PA catheter. Esophageal echo-Doppler ultrasonography (ED) provides non-invasive continuous measurement of CO (ED-CO). This study was thus designed to compare the agreement between ED-CO and both thermodilution techniques (BCO and CCO). METHODS: Twenty-four patients undergoing primary coronary artery bypass graft surgery were randomized to have a PA catheter placed for measurement of either BCO or CCO. All patients also had an ED probe placed. In Group I patients (n = 12), BCO measurement was carried out every 15 minutes throughout the surgery except during cardiopulmonary bypass, with concurrent ED-CO reading recorded at the same time point. In Group II patients (n = 12), CCO and ED-CO measurements were recorded at the same designated points of time as in Group I. The agreement between methods (BCO vs. ED-CO or CCO vs. ED-CO) was assessed using Bland-Altman method. RESULTS: The range of measured CO of each method was 2.1 to 9.4 l/min for BCO, 2.4 to 9.2 l/min for CCO and 2.3 to 8.9 l/min for ED-CO. ED-CO and CCO had excellent agreement with a linear regression coefficient (r2 value) of 0.846, and a bias (mean difference) and SD of bias of 0.05 +/- 0.49 l/min. In contrast, the agreement between BCO and ED-CO was poorer; correlation was low (r2 value 0.406) and both the bias and SD of bias were high (0.11 +/- 1.12 l/min). Furthermore, BCO measurements had poor reproducibility, whereas both ED-CO and CCO measurements had good reproducibility. CONCLUSIONS: Esophageal echo-Doppler ultrasonography is a satisfactory alternative for cardiac output measurement because it gives a value in good agreement with CCO measurement. With significant between-measurement variations, the accuracy and precision of BCO are uncertain, and it should not be considered as the "gold standard".

Adult↗