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Biomedical subjects

R A Steinbrook

Publications and source records attributed to R A Steinbrook.

15 recordsLinked to original sources
PubMed1992

Electrocardiographic R-wave changes during cardiac surgery.

The diagnostic accuracy of exercise electrocardiography has been improved by incorporation of R-wave gain factor to correct the measured ST-segment changes. If marked changes in R-wave amplitude occur in individual patients during cardiac operations, a similar gain factor correction may improve the intraoperative diagnosis of myocardial ischemia. This investigation was designed to determine the frequency and magnitude of intraoperative V5 R-wave amplitude changes during cardiac operations. Electrocardiograms were recorded from 83 patients while patients were awake, anesthetized (baseline), after placement of the Favaloro and Canadian sternal retractors, and at end-operation. Compared with baseline values, placement of the Canadian sternal retractor was associated with a reduction in V5 R-wave amplitude from 15 +/- 1 to 10 +/- 1 mm (mean +/- SEM), in V5 S-wave amplitude from 3.5 +/- 0.4 to 1.7 +/- 0.3 mm, and in absolute ST-segment deviation from 0.50 +/- 0.04 to 0.39 +/- 0.05 mm. Changes in V5 R-wave amplitude were correlated with changes in ST-segment deviation in patients with baseline ST-segment deviations greater than or equal to 0.5 mm (r = 0.55, P = 0.0004, n = 37). Changes associated with the Favaloro retractor and the respiratory cycle were less marked. However, the V5 R-wave amplitude was decreased from 15 +/- 1 to 9 +/- 1 mm at end-operation. In conclusion, sternal spreading with the Canadian retractor was associated with marked reductions in V5 R- and S-wave amplitudes and ST-segment deviations. Marked changes in V5 R-wave amplitude persisted after sternal closure.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1991

Linking mass spectrometers to provide continuing monitoring during system failure.

Although multipatient monitoring with a time-shared mass spectrometer provides considerable cost advantages, failure of one component in a shared system can disrupt gas monitoring at all sites. We describe a simple method for linking two central mass spectrometer systems to provide continual monitoring during failure of one unit, without the need for time-consuming reconfiguration of individual patient sample line and display connections.

Equipment Failure↗
PubMed1991

Respiratory effects of spinal anesthesia: resting ventilation and single-breath CO2 response.

The effects of spinal anesthesia with bupivacaine or lidocaine on resting pulmonary ventilation and on the response to the single-breath carbon dioxide test were studied in 11 unpremedicated patients. Resting end-tidal PCO2 decreased from 34.8 +/- 4.5 (mean +/- SD) to 31.6 +/- 4.6 mm Hg after induction of spinal anesthesia (P = 0.002). The decrease in end-tidal PCO2 correlated negatively with patient age (r = -0.67, P = 0.02) and positively with spinal analgesic level (r = 0.58, P = 0.06). Breath-to-breath variability of ventilation increased during spinal anesthesia. Spinal anesthesia was not associated with statistically significant changes in tidal volume, respiratory rate, minute ventilation, mean inspiratory flow rate, inspiratory duty cycle duration, or the response to the single-breath CO2 test.

Adult↗
PubMed1989

Naloxone does not alter response to hypercapnia or resistive loading in chronic obstructive pulmonary disease.

To assess the role of endogenous opioid peptides in ventilatory control in patients with chronic obstructive lung disease, we measured the ventilatory and mouth occlusion pressure responses to hypercapnia and the compensatory response to an inspiratory resistive load in 11 male patients with COPD before and after intravenous administration of naloxone or placebo on 2 separate days. There were no statistically significant differences between naloxone and placebo administration in any index of ventilatory response to CO2 or resistive loading. When an inspiratory resistive load was added during CO2 rebreathing, minute ventilation at PETCO2 = 50 mm Hg in all 11 patients decreased significantly (p less than 0.05) with placebo and naloxone. In response to the inspiratory resistive load, in eight of the 11 patients mouth occlusion pressure (P0.1) did not increase; these eight subjects were classified as noncompensators. Naloxone did not affect the P0.1 response to inspiratory resistive loading, either in the group as a whole or in the subgroup of eight patients classified as noncompensators. Our study was unable to demonstrate that increased activity of endogenous opioid peptides suppresses the ventilatory response to CO2 or resistive loading in patients with chronic obstructive lung disease.

Aged↗
PubMed1989

Spinal needles.

Explore the source record for details and available documents.

Anesthesia, Spinal↗
PubMed1988

Ventilatory responses to hypercapnia during tetracaine spinal anesthesia.

The effect of spinal anesthesia with hyperbaric tetracaine with epinephrine on resting ventilation and on ventilatory responsiveness to CO2 rebreathing was studied in 10 unpremedicated patients. Resting end-tidal PCO2 (PETCO2) decreased from 37 +/- 3 mmHg (mean +/- SD) to 34 +/- 2 mmHg after induction of spinal anesthesia (p less than 0.05). Minute ventilation (VE) and occlusion pressure (P0.1) at PETCO2 = 55 mmHg increased during spinal anesthesia from 32.0 +/- 12.9 to 40.2 +/- 17.0 l/min and from 5.0 +/- 1.8 to 8.6 +/- 4.7 cmH2O, respectively. The magnitude of the increase in VE during spinal anesthesia correlated inversely with age. Spinal anesthesia was not associated with significant changes in vital capacity, maximal inspiratory pressure, or the slopes of the lines relating VE or P0.1 to PCO2. These results show increased ventilatory responsiveness to CO2 (a parallel leftward shift of the CO2 response curve) with tetracaine spinal anesthesia.

Adult↗
PubMed1988

Ventilatory responses to hypercapnia during bupivacaine spinal anesthesia.

The effect of spinal anesthesia with isobaric 0.5% bupivacaine on ventilatory responsiveness to CO2 rebreathing was studied in ten unpremedicated patients. Minute ventilation (VE) at end-tidal PCO2 = 55 mm Hg increased from 18.7 +/- 6.7 L/min (mean +/- SD) to 22.3 +/- 10.1 L/min after induction of spinal anesthesia (P less than 0.05). Occlusion pressure (P0.1) at PCO2 = 55 mm Hg also increased, from 3.8 +/- 1.5 to 5.0 +/- 1.7 cm H2O (P less than 0.05). Spinal anesthesia was not associated with significant changes in vital capacity, maximal inspiratory pressure, resting end-tidal PCO2, or the slopes or intercepts of the lines relating VE or P0.1 to PCO2. These results show an increased ventilatory responsiveness to CO2 with bupivacaine spinal anesthesia.

Adult↗
PubMed1987

Endogenous opioids and ventilatory adaptation to prolonged hypoxia in goats.

To investigate whether endogenous opioid peptides mediate time-dependent changes in ventilatory control during prolonged hypoxia, we studied four adult goats at rest during 14 days at simulated high altitude in a hypobaric chamber (PB approximately 450 Torr). Arterial PCO2 fell during the first several hours of hypoxia, remained stable over the next 7 days, and then rose slightly (but without statistical significance) by day 14. Ventilatory responsiveness to CO2 increased during the first week of hypoxia. By day 14, while still greater than control, the ventilatory response to CO2 was less than that observed on day 7. Immunoactive beta-endorphin levels in plasma and CSF did not change during the 14-day period. Administration of naloxone on day 14 did not restore the ventilatory response to CO2 to the level observed during the first week of acclimatization. We conclude that in adult goats, time-dependent changes in ventilatory response to CO2 during acclimatization to prolonged hypoxia are not primarily attributable to alterations in endogenous opioid peptide activity.

Adaptation, Physiological↗
PubMed1987

Detection of hypercapnia by normal subjects.

1. To investigate whether changes in PaCO2 can be detected independently of the CO2-induced changes in pulmonary ventilation, we tested five normal subjects for the ability to distinguish different levels of end-tidal PCO2 (PETCO2) while holding minute ventilation constant. 2. Helped by a visual feedback system, the subjects maintained a constant ventilation targeted at a level that was higher than that dictated by the chemical drive at PETCO2 = 50 mmHg (6.7 kPa). End-tidal PCO2 was held at 40 mmHg (5.3 kPa) during the first 2 min of each test trial ('control period'); then, for 4 min ('test period'), PETCO2 was either elevated to 50 mmHg or kept at 40 mmHg. Twelve runs were performed by each subject. 3. In 24 out of the total 30 trials (80%) in which PETCO2 was raised during the test period to 50 mmHg, the subjects detected the changes. There was one false positive result (3%), when PETCO2 kept at 40 mmHg during the test period was reported as different from control. In four out of the five subjects the ability to detect the change in PETCO2 from 40 to 50 mmHg was statistically significant. 4. We conclude that increases in PETCO2 can be detected independently of changes in the absolute level of ventilation.

Carbon Dioxide↗
PubMed1986

Continuous noninvasive monitoring of cardiac output with esophageal Doppler ultrasound during cardiac surgery.

Esophageal Doppler ultrasonography offers a continuous and noninvasive alternative to standard thermodilution cardiac output monitoring. A total of 372 simultaneous measurements of Doppler and thermodilution cardiac output were compared in 16 patients undergoing cardiac surgery. In addition, echocardiographic aortic diameter measurement, necessary for Doppler calibration, was compared with direct surgical measurement in 23 patients. Echocardiographic aortic measurement was often time consuming and correlated poorly (r = 0.31) with surgical measurement. On the other hand, Doppler cardiac output was determined easily and accurately tracked thermodilution cardiac output (R2 = 0.95, common slope coefficient 1.050, by multiple linear regression). Furthermore, Doppler cardiac output was more reproducible, showing less short-term variability than thermodilution cardiac output. The esophageal Doppler technique allows cardiac output monitoring in patients for whom invasive monitoring is not warranted.

Adult↗
PubMed1985

Recurrence of pulsus alternans after fentanyl injection in a patient with aortic stenosis and congestive heart failure.

Following aortic valve replacement in a patient with aortic stenosis and cardiac failure, marked pulsus alternans recurred immediately after intravenous injection of 0.5 mg fentanyl, without concomitant changes in heart rate, mean left atrial pressure, or the electrocardiogram. Pulsus alternans is known to occur in association with heart failure and aortic stenosis, but has not been reported previously in response to anaesthetic drugs. Mechanisms of pulsus alternans are discussed, and the possible contributory role of fentanyl is considered.

Aged↗
PubMed1985

Endogenous opioids and ventilatory responses to hypercapnia in normal humans.

Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

Adult↗
PubMed1985

Endogenous opioids and ventilatory responses to hypoxia in normal humans.

We studied the putative role of endorphins in modulating hypoxic ventilatory responsiveness. In 12 healthy men, minute ventilation (VE)and mouth occlusion pressure (P0.1) responses to progressive isocapnic hypoxia were determined before and after the intravenous administration of the opioid antagonist naloxone (10 mg) or placebo. Plasma levels of beta-endorphin were measured before and after hypoxia. Naloxone did not affect the slopes or x-intercepts of the relationships between either VE or P0.1 and arterial O2 saturation. There was no correlation between the baseline plasma level of beta-endorphin and any measure of responsiveness to hypoxia. Plasma beta-endorphin levels were not affected by either short-term hypoxia or naloxone alone; however, when hypoxia followed naloxone administration, mean +/- SD beta-endorphin increased from 8.0 +/- 8.9 pg/ml to 20.2 +/- 16.6 pg/ml (p less than 0.005). We concluded that endogenous opioids do not have an important modulating influence on hypoxic ventilatory responsiveness in adult human volunteers.

Adult↗