Biomedical subjects
Publications and source records attributed to E Jacobsen.
Esophageal peristalsis in the middle and distal esophagus was analyzed in nine healthy people before, during, and after food intake. A significant increase in amplitude of contractions occurred during and after eating. Furthermore, a significant increase in duration and propagation time of contractions occurred in the distal part of the esophagus during food intake.
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The purpose of this study was to investigate the frequency of primary and secondary displacement of central venous catheters. One hundred and two central venous catheters, inserted through a peripheral or a central vein before surgery or in the intensive care unit, were controlled by chest X-ray 5-720 min after insertion. The number of primarily displaced catheters was 27. Of these, the position was corrected in 8. Thereafter, the 83 correctly placed catheters were observed for 4-560 h. The number of X-ray controls was 2-24. The number of secondary displacement was 2, whereas 12 catheters showed minimal secondary displacement. The rate of complication was very low. We conclude that chest X-ray immediately after insertion of central venous catheters is absolutely necessary, but since the number of secondary displacements is very low, daily chest X-ray control is not necessary. We also conclude that the internal jugular vein is the best route for introducing a central venous catheter, since complications are very few and the number of displacements is very low.
The value of transcutaneous oxygen tension (tcPO2) as an oxygen parameter during uncomplicated thoracic anaesthesia was examined in ten patients anaesthetized with oxygen-nitrous oxide and enflurane or flunitrazepam/fentanyl. tcPO2 was measured with the Radiometer TCM-I monitor at 45 degrees C. Measuring interference due to the anaesthetic agents was not observed. tcPO2 was found to be lower than the arterial tension (PaO2) at any inspiratory oxygen fraction (FIO2). When the peroperative readings were related to the preoperative values, no statistically significant difference was found between PaO2 and tcPO2 at FIO2 - 0.5, 0.4 and 0.3 (P greater than 0.3). Linear regression between PaO2 and tcPO2 shows disparity in pre- and peroperative regression. tcPO2 (preoperative) = -2.2 + 1.03 X PaO2 (4 = 0.89) tcPO2 (preoperative) = +3.1 + 0.56 X PaO2 (r = 0.87). This disparity indicates a decrease in the tcPO2/PaO2 ratio with increasing PaO2. It is concluded that tcPO2 cannot substitute for PaO2, but tcPO2 and PaO2 proved to be equally useful as oxygen parameters in the examined patients. Interpretation of tcPO2 during anaesthesia, however, necessitates a preoperative measurement as reference.
The effect of changes in arterial and venous pressures on transcutaneous oxygen tension (tcPO2) were studied in ten young subjects. The tcPo2 electrode was mounted on the foot, and changes in blood pressures were induced by elevating and lowering the foot and by inflating a cuff around the thigh. tcPo2 decreased gradually during elevation at a rate of 1% per mmHg reduction in arterial pressure. tcPo2 increased during dependency and venous stasis, at a rate of 0.5% per mmHg increase in venous pressure. We propose that tcPo2 is a function of the blood flow under the electrode, and that normal blood flow regulation is abolished in the heated tissue under the electrode.
Blood flow regulation in the foot under a heated (43 degrees C) transcutaneous oxygen tension (tcPo2) electrode was studied in six young subjects. Blood flow under the electrode was estimated from the electrical power consumption of the thermostatistically-controlled heating element in the electrode. Changes in arterial and venous pressures, and thereby in perfusion and transmural pressure and blood flow were induced by elevation and lowering of the foot and by venous stasis. tcPo2 was significantly and positively correlated to the blood flow under the electrode, and blood flow neither showed autoregulation nor vasoconstrictor response as judged from the power consumption. In contrast the blood flow in normal unheated skin measured simultaneously by the 133-Xenon technique showed autoregulation as well as vasoconstrictor response. It is concluded that tcPo2 is a parameter determined by many variables, of which the arterial blood pressure is of particular clinical importance.
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The codiscoverer of disulfiram's usefulness for alcoholics reports on the development of Denmark's present system of alcoholism treatment and the treatment facilities.
In 20 patients, aged 19-80 y and without pulmonary or cardiovascular disease, transcutaneous oxygen tension (tcPO2) and arterial oxygen tension (PaO2) were measured. tcPO2 was measured with a Radiometer TCM-1 (transcutaneous oxygen monitor) at 43 C degrees. The age regression for tcPO2 was: tcPO2 = 10.4-0.035 x age (r = 0.406); the corresponding equation for PaO2 was: 13.8-0.053 x age (r = 0.687). The mean difference between tcPO2 and PaO2 was 2.6 kPa (s.d = 0.97) and the ratio tcPO2/PaO2 was 0.8. The accuracy of tcPO2 at the level 5.3-13.2 kPa based on 480 measurements was on the average +/-1.28 kPa (maximum +/-1.73 kPa) at the 95% confidence level. The accuracy of tcPO2 measurements is acceptable for clinical use, and in healthy adults tcPO2 reflects PaO2.
The influence of halothane-oxygen mixtures on three different transcutaneous oxygen electrodes was investigated. The influence of hypotension caused by halothane and halothane-nitroprusside on transcutaneous oxygen tension measurement (tcPO2) in halothane-anaesthetized patients was examined as well. The electrodes differed with respect to polarization voltages (630 mV or 500 mV) and electrolyte composition (silver chloride or silver bromide). A change dependent on halothane concentration was demonstrated in the electrode readings, both with a polarization voltage of 630 mV and with silver bromide as electrolyte. Using an electrode with 500 mV in polarization voltage and silver chloride as electrolyte, no changes were observed in the readings. During induced hypotension, the tcPO2 values fell in proportion to the mean arterial blood pressure. In patients with a mean arterial blood pressure over 11kPa a tcPO2/PaO2 ratio of 0.6 was found. It is concluded that tcPO2 monitoring during halothane anaesthesia can be influenced in at least two ways, apart from changes in PaO2: (1) by oxygen electrode error due to the halothane; and (2) by changes in skin blood flow. In comparison to the changes in tcPO2 due to the haemodynamic effects of halothane anaesthesia, the changes due to halothane error are small.
Eight patients suffering from severe ergotamine-induced peripheral ischaemia were transferred to our institution for hyperbaric oxygen treatment after unsuccessful therapy in the primary hospital. The patients were exposed to 3 ATBS oxygen for 1 hour 2-3 times daily and they were given an epidural block for the purpose of analgesia where there was severe pain. The circulation and vitality of tissue were restored in all patients. One had tarsal amputations performed half a year later. Hyperbaric oxygen in combination with epidural analgesia is recommended in severe cases of ergotism.
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Changes in pulmonary hemodynamics and acid-base balance were recorded during induction of anesthesia using either intravenous administration of barbiturate (28 patients) or inhalation of N2O-O2-halothane (12 patients). The two types of induction resulted in equal elevations of pressures within the pulmonary circulation. The increase, proportional on the two sides of the heart, was most pronounced immediately before endotracheal intubation. Cardiac index decreased before and during intubation but subsequently increased to levels above control values. Systemic blood pressure increased more during barbiturate than during inhalation induction. Changes in acid-base balance were similar during the two types of induction: arterial blood PCO2 and PO2 increased, pH decreased, and standard bicarbonate remained unchanged. Changes in pulmonary arterial mean pressure and central venous pressure were correlated with changes in PACO2. Pulmonary capillary filtration pressure (i.e., pulmonary capillary wedge pressure minus plasma colloid osmotic pressure) was negative in every patient before anesthesia. During induction of anesthesia, filtration presures became positive in half the patients. Observed changes in circulation may have been caused by hypercapnia alone or by a combination of hypercapnia and vescular reflexes associated with instrumentation during intubation. The increased strain on the heart during induction of anesthesia may lead to cardiac failure in patients with diminished cardiac reserve.