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Biomedical subjects

F A Hensley

Publications and source records attributed to F A Hensley.

At least 19 recordsLinked to original sources
PubMed1991

Thiopental as an adjunct to hypothermia for EEG suppression in infants prior to circulatory arrest.

Fifteen infants were studied to evaluate the effect of profound hypothermia (16 degrees C to 18 degrees C) and hypothermia plus thiopental on the electroencephalogram (EEG) prior to circulatory arrest. Mean patient age and weight were 5.5 +/- 1.2 months and 4.9 +/- 0.3 kg, respectively. After core cooling on cardiopulmonary bypass (CPB), all patients received thiopental, 8 mg/kg, 5 minutes prior to circulatory arrest. Satisfactory EEG recordings were obtained for 9 patients, and serum thiopental concentration was measured in 12 patients. Hypothermia (mean venous return temperature, 17.8 degrees C +/- 1.6 degrees C) alone was associated with persistent cerebral electrical activity in 8 of 9 patients (89%). The addition of thiopental, 8 mg/kg, produced an isoelectric EEG in 6 of these 8 patients (75%). Mean circulatory arrest duration was 44 +/- 4 minutes. EEG activity resumed after reinstitution of CPB in all patients. Serum thiopental concentration at the end of CPB was negligible. It is concluded that hypothermia alone often may not produce EEG isoelectricity, and that the associated cerebral metabolic activity may be suppressed by adjunctive use of thiopental.

Blood Proteins↗
PubMed1991

Hemodynamic effects of muscle relaxant drugs during anesthetic induction in patients with mitral or aortic valvular heart disease.

The hemodynamic effects of three nondepolarizing skeletal muscle relaxant drug regimens were compared during the induction of general anesthesia in 64 patients with valvular heart disease using a double-blind protocol. Patients were first stratified according to primary valvular defect (aortic stenosis, aortic regurgitation, mitral stenosis, or mitral regurgitation). Next, patients were randomly allocated to a drug group, either group A (atracurium), group V (vecuronium), or group MP (metocurine plus pancuronium). Data were collected during three periods: awake, postanesthetic induction, and posttracheal intubation. Four cardiovascular variables were designated a priori as primary variables of interest. These were heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI). Patients with mitral stenosis showed two significant hemodynamic differences among muscle relaxant drug groups: (1) CI increased in group A but decreased in group MP between the awake and postinduction measurements (P = 0.032); and (2) SVRI decreased in group A but increased in group MP between the awake and postintubation periods (P = 0.034). In contrast, patients with aortic stenosis, aortic regurgitation, or mitral regurgitation demonstrated no statistically significant difference in cardiovascular responses among drug groups. Further analysis was performed using the following data: (1) other hemodynamic variables; (2) incidence of deviations from cardiovascular stability; and (3) the frequency of cardiovascular drug use. This examination showed no important differences among the muscle relaxant drug groups. The small but significant hemodynamic changes observed in mitral stenosis patients in drug groups A and MP were not noted with vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1989

The effect of a standardized premedication on oxygen saturation in the cardiac patient before transfer to the operating room.

The effect of premedication with morphine and scopolamine on arterial hemoglobin oxygen saturation (SaO2) was measured continuously in 26 undisturbed patients in their hospital rooms before coronary artery bypass surgery. Two hours preoperatively each patient received morphine, 0.1 mg/kg, and scopolamine, 0.2 or 0.4 mg. SaO2 was continuously recorded using pulse oximetry from one-half hour before premedication until 1 1/2 hours after premedication. The lowest SaO2 measured both the evening before surgery and one-half hour before premedication was 95% +/- 0.5% (mean +/- SEM). After administration of premedication, the lowest SaO2 for the patient population decreased to 93% +/- 0.4% (P less than 0.001 compared with that before premedication), and occurred 52 +/- 2 minutes after premedication was given. Two patients (8%) had an SaO2 less than 90% (lowest SaO2 for both was 88%). It is concluded that the dose of morphine/scopolamine premedication used was associated with a low risk of clinically important hypoxemia in the patient population studied.

Adult↗
PubMed1989

Diltiazem withdrawal before coronary artery bypass surgery.

The authors studied the effects of withdrawing oral diltiazem therapy on the subsequent course of coronary artery bypass graft surgery. Patients with severe coronary artery disease were divided into three groups using a prospective, controlled, randomized protocol. In group D (diltiazem-continuation) patients, diltiazem was administered 2.1 +/- 0.1 hours (mean +/- SEM) before anesthetic induction (n = 10). Group DW (diltiazem-withdrawal) patients received their final diltiazem dose 17.3 +/- 2.9 hours before anesthesia (n = 10). Group R was a reference group of patients not receiving diltiazem (n = 11; not randomized). Anesthesia was induced and maintained with fentanyl and pancuronium without use of halogenated anesthetics. No clinically important differences were detected in measured hemodynamics or drug requirements. Group D patients did not have a lower systemic vascular resistance (SVR) index (P greater than 0.31) or mean arterial pressure (P greater than 0.08) compared with group DW. Also, no evidence for a diltiazem withdrawal response was found, because group DW did not have either a higher SVR index (P = 0.99) or a higher pulmonary vascular resistance index (P = 0.99) compared with group R, and no severe myocardial ischemia, coronary artery spasm, or postoperative heart block were seen. Plasma diltiazem concentrations decreased significantly during CPB (P less than 0.0001), but showed overlap between groups D and DW. Plasma diltiazem concentration did not correlate significantly with simultaneous SVR. These data show the benign effects of both diltiazem administration and its acute withdrawal before coronary artery bypass surgery with high-dose fentanyl anesthesia.

Administration, Oral↗
PubMed1988

Carbon dioxide elimination during total cardiopulmonary bypass in infants and children.

The authors measured the rate of carbon dioxide elimination (VCO2) in 25 pediatric patients (age 2 days to 9 yr) during total cardiopulmonary bypass at average venous blood temperatures ranging from 19.5 to 35.9 degrees C. A multiplexed mass spectrometer was connected to the gas inlet and exhaust ports of the bubble oxygenator, and the gas-phase Fick principle was used to determine VCO2. A curvilinear relationship was found between log VCO2 and venous blood temperature, and a quadratic regression equation (r2 = 0.74) was fit to the data. Q10 (the ratio of VCO2 before and after a 10 degree C temperature change) was estimated to be 2.7 or 3.0, depending on the analytic method used. Venous blood temperature as a predictor variable explained a greater proportion of the variability of log VCO2 than did nasopharyngeal or rectal temperatures. Analysis of covariance revealed that total circulatory arrest during bypass (utilized in 10 patients for 34 +/- 4 min, mean +/- SEM) affected the relationship of venous blood temperature with log VCO2, by increasing the y-intercept (P = .008) but not the slope. These data, with associated 95% prediction intervals, define the expected CO2 elimination rates at various temperatures during standard bypass conditions in our patients. Real-time measurement of VCO2 using mass spectrometry can be a useful routine monitor during CPB that may help to assess patient metabolic function, adequacy of perfusion, and oxygenator performance.

Blood Physiological Phenomena↗
PubMed1988

Continuous oxygen saturation monitoring during cardiac catheterization in adults.

Arterial hypoxemia may contribute to morbidity during cardiac catheterization. Therefore, we measured arterial hemoglobin oxygen saturation (SaO2) continuously using pulse oximetry in 29 patients (age range, 21 to 83 years) undergoing cardiac catheterization. Baseline SaO2 was 96 +/- 0.4 percent. All patients had a decrease in SaO2 at some time during the procedure. Eleven patients (38 percent) had episodes of arterial hypoxemia, defined as a decrease in SaO2 below 90 percent. In these 11 patients, the mean number of episodes of hypoxemia was 16 +/- 7, and the mean duration of each episode was 53 +/- 25 seconds. Multiple stepwise regression analysis showed that the minimum SaO2 during catheterization for any patient was significantly associated with the baseline SaO2, duration of the procedure, and end-diastolic volume (EDV) as described by the following regression equation: minimum SaO2 = 46.8 - 0.0580 (duration of procedure in minutes) + 0.5362 (baseline SaO2) - 0.0159 (EDV). Based on our finding of arterial hypoxemia in greater than one third of our patients, we would consider continuous SaO2 monitoring or supplemental oxygen during cardiac catheterization, especially for those patients with poor ventricular function or low resting SaO2 or those expected to have long procedures.

Adult↗
PubMed1987

The effect of halothane/nitrous oxide/oxygen mask induction on arterial hemoglobin saturation in cyanotic heart disease.

The effect of a halothane/nitrous oxide/oxygen mask induction on arterial hemoglobin saturation (SaO2) was studied in 25 patients with cyanotic congenital heart disease. During this induction the SaO2 increased from 80% +/- 2 (mean +/- SEM) in awake patients breathing room air to 86% +/- 1 after induction of anesthesia, with an average increase of 6.8% +/- 2 (absolute) (N = 25; P < .005). Patients were retrospectively divided into two groups, A and B. Group A patients had pulmonic infundibular stenosis (PIS) (N = 13) with the potential for variable pulmonary outflow tract obstruction. These patients had awake SaO, values of 76% +/- 3 that increased significantly after induction to 86% +/- 1, with an average increase of 10% +/- 4 (absolute) (P < .01). Group B patients did not have PIS; they had an awake SaO2 of 83% +/- 2, which rose insignificantly after induction to 87% +/- 1, with an average increase of 4% +/- 2 (absolute) (P > .1). Thus, the significant increase in SaO2 during induction for the entire group was primarily due to the large response of patients with PIS. No correlation was found between SaO2 and systolic blood pressure for the entire study population as well as for groups A and B separately. The lack of correlation between systolic blood pressure and SaO2 may indicate that relaxation of pulmonic infundibular stenosis is an important mechanism explaining the observed increase in SaO2 during anesthetic induction in group A (PIS) patients. Six patients had clinically important decreases in SaO2 during the induction of anesthesia, and airway obstruction was usually the cause. Anesthetic induction with halothane/nitrous oxide/oxygen leads to an increase in SaO2 in patients with many forms of cyanotic heart disease, but especially those with the potential for variable pulmonary outflow tract obstruction.

Adult↗