Quantum phase in interferometry.
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Biomedical subjects
Publications and source records attributed to H Rauch.
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OBJECTIVE: Commercially available semi-continuous cardiac output (SCCO) monitoring systems are based on the pulsed warm thermodilution technique. There is evidence that SCCO fails to correlate with standard intermittent bolus cardiac output (ICO) in clinical situations with thermal instability in the pulmonary artery. Furthermore, ventilation may potentially influence thermodilution measurements by enhanced respiratory variations in pulmonary artery blood temperature and by cyclic changes in venous return. Therefore, we evaluated the correlation, accuracy and precision of SCCO versus ICO measurements before and after extubation. DESIGN: Prospective cohort study. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS AND PARTICIPANTS: 22 cardiac surgical ICU patients. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: SCCO and ICO data were obtained at nine postoperative time points while the patients were on controlled mechanical ventilation. Further sets of measurements were taken during the weaning phase 20 min before extubation, and 5 min, 20 min and 1 h after extubation. SCCO and ICO measurements yielded 286 data pairs with a range of 1.8-9.9 l/min for SCCO and 1.9-9.8 l/min for ICO. The correlation between SCCO and ICO was highly significant (r = 0.92; p < 0.01), accompanied by a bias of -0.052 l/min and a precision of 0.56 l/min. Correlation, accuracy and precision were not influenced by the mode of respiration. CONCLUSIONS: Our results demonstrate excellent correlation, accuracy and precision between SCCO and ICO measurements in postoperative cardiac surgical ICU patients. We conclude that SCCO monitoring offers a reliable clinical method of cardiac output monitoring in ICU patients following cardiac surgery.
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OBJECTIVE: Continuous thermodilution cardiac output (CCO) measurement was clinically evaluated in patients who underwent coronary revascularization using hypothermic low-flow, low-pressure cardiopulmonary bypass (CPB). DESIGN: Prospective study. SETTING: University hospital setting. PARTICIPANTS: 30 cardiac surgical patients. INTERVENTIONS: CCO was correlated to standard bolus thermodilution cardiac output (ICO) obtained at end-expiration. MEASUREMENTS AND MAIN RESULTS: Measurements were taken at selected time points (n = 18) before anesthesia induction, before CPB, and 5 minutes to 12 hours after CPB. A total of 540 data pairs were thus obtained. ICO ranged from 1.9 to 9.9 L/min, CCO from 1.5 to 9.9 L/min. Correlation between ICO and CCO was highly significant (r = 0.872; p < 0.01), accompanied by an excellent accuracy (bias -0.0213 L) and precision (0.59 L) before CPB and more than 45 minutes after CPB. However, during the first 45 minutes after CPB, there was no correlation (r = 0.273) between ICO and CCO, and ICO tended to be relatively high, whereas CCO measurements showed relatively low values. During the first 45 minutes after hypothermic CPB, but not during the ensuing time period, central blood temperature decreased, which may be interpreted as a lack of thermal equilibration between central and peripheral compartments. It is hypothesized that thermal instability in combination with increased respiratory variations in pulmonary artery blood temperature caused inhomogenous rewarming of different body sites and might be the main reason for the lack of correlation between ICO and CCO. CONCLUSIONS: Despite an excellent correlation, accuracy, and precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB, a lack of correlation in the early phase after CPB has been found. Further investigation is needed to elucidate the underlying cause of these findings and to clarify whether ICO or CCO or both fail to represent the real cardiac output up to 45 minutes after weaning from hypothermic CPB.
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Thirty-five adult cardiac surgical patients received 20 mg dipotassium clorazepate orally the evening before surgery and 2 mg flunitrazepam 60 min before induction of anaesthesia. If anaesthesia was to be induced after 08.30 hours patients received an additional 20 mg dipotassium clorazepate at 06.15 hours. The following measurements were made: peripheral arterial oxygen saturation (Spo2) breathing room air; anxiety by visual analogue scale; degree of sedation; and haemodynamic variables. Mean (Spo2) was 95.9% (SD 1.8%) on the day before surgery and 95.4% (SD 1.5%) on arrival at the operating room. When the operation started after 08.30 hours, mean (Spo2) at 09.00 hours was 96.0% (SD 1.4%). There were no detected episodes of hypoxaemia after premedication. Mean anxiety score decreased significantly from 3.9 (SD 2.6) on the day before surgery to 3.3 (SD 2.1) on arrival at the operating room (patients' score; P < 0.002) and from 4.6 (SD 2.4) to 3.3 (SD 2.0) (anaesthesiologists' score; P < 0.001). Nearly all patients were considered well sedated, which was reflected by normal haemodynamic variables on arrival at the operating room. The combination of clorazepate and flunitrazepam is effective oral premedication for adult cardiac surgery, causing no obvious desaturation even when supplemental oxygen is not given.
Repeated induction of ventricular fibrillation (VF) with circulatory compromise during implantable cardioverter defibrillator (ICD) testing may cause cerebral injury. To test this hypothesis, somatosensory evoked potentials (SEP), a more sensitive marker of injury, were recorded in patients (N = 10) undergoing ICD implantation. SEP were recorded before induction of anesthesia, after induction of anesthesia, before and at several times following induction of VF. Possible modifying factors of the SEP measurements such as anesthetic application, blood pressure, body temperature, and hematocrit remained constant throughout the operations. Central conduction time was unaffected by ICD defibrillation testing. Amplitude of SEP primary complexes was transiently reduced at 34.9% (P < 0.01) by defibrillation testing, but returned to control within 10 minutes after testing. It is concluded that while ICD defibrillation testing may produce transient changes in SEP, there is no evidence of residual cerebral injury.
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The toxic milk mutation (tx) in mice is an autosomal recessive condition that causes a marked hepatic accumulation of copper in adults and severe copper deficiency in the pups of tx/tx dams. We determined the concentration of metallothionein-I (MT-I) mRNA in mutant and normal animals at various stages of development and following administration of copper and zinc. In two tx/tx males the average MT-I mRNA was 329 molecules/pg RNA compared with 38 molecules/pg in normal animals. In fetal and neonatal animals the concentration of MT-I mRNA was generally the same in normal and mutant mice and was independent of copper status. Copper or zinc administration to 7-d-old pups caused a marked induction of MT-I mRNA. There was an increased response to copper administration in one mutant group, but no clear pattern of hyper-induction of the MT gene in tx/tx animals was demonstrated. The elevation of MT-I mRNA in adult toxic milk mice is likely to be a secondary consequence of copper accumulation and not a primary effect of the mutation, because high MT-I mRNA levels would have been observed in the mutant neonates and fetuses. However, the possibility that the tx mutation causes overexpression of MT in post-weaning animals cannot be excluded by these data. The results also show that copper deficiency has no effect on the fetal or neonatal expression of the MT genes.
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