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H J Eberlein

Publications and source records attributed to H J Eberlein.

At least 37 records · Page 2Linked to original sources
PubMed1981

[Monitoring of cerebral electrical activity during cardiac surgery (author's transl)].

Continuous recording of cerebral activity by the Cerebral Function Monitor is a useful supplementation to anaesthetic monitoring in cardiac surgery. It is a simple and reliable method for early detection of cerebral damage during heart surgery and in other situations with possible cerebral impairment. The operating principles of the Cerebral Function Monitor and the interpretation of the electrical activity tracings are presented. Therapeutic considerations to minimize or to prevent anoxic brain damage are offered.

Age Factors↗
PubMed1980

Enflurane today.

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Chemical and Drug Induced Liver Injury↗
PubMed1980

Comparison of intravenous acetylsalicylic acid and dipyrone in postoperative pain: an interim report.

1 In 17 gynaecological patients with postoperative pain the analgesic efficacy of intravenous lysine salicylate 1.8 g (corresponding to acetylsalicylic acid (ASA) 1.0 g) and dipyrone 1.0 g were compared in a double-blind randomized study. 2 In the ASA group, mean pain relief and pain intensity difference scores reached a maximum 30 min after drug administration and remained at this level for the next 90 minutes. 3 In the dipyrone group, these scores reached their peak 60 min after drug administration and seemed to fall off during the next hour. 4 The mean pain relief and intensity difference scores were greater following aspirin than dipyrone. However, firm conclusions cannot be drawn from the results of this small study.

Adult↗
PubMed1978

[The influence of sodiumnitroprusside on the oxyhaemoglobin dissociation curve in vitro (author's transl)].

Blood from 16 donors was incubated with 3 microgram sodiumnitroprusside (SNP)/ml blood and the PO2 for halfsaturation of haemoglobin at standard pH and temperature was measured. There was no significant shift of the oxygen dissociation curve. Erythrocyte 2, 3 DPG and met-Hb concentrations did not show significant differences between SNP-treated and control blood. Although the red cells and the haemoglobin are involved in the metabolism of SNP, in clinical doses SNP does not alter the oxygen affinity.

Diphosphoglyceric Acids↗
PubMed1977

Effects of althesin, etomidate and fentanyl on haemodynamics and myocardial oxygen consumption in man.

The acute effects of althesin, etomidate and fentanyl upon haemodynamics, myocardial contractility and oxygen comsumption of the heart were studied in healthy premedicated patients (n = 15) lightly anaesthetized with N2O-O2 (ratio 2:1), 0.3 volumes per cent of halothane and isoflurane respectively. All individuals were ventilated at a normal level. The patients (n = 9) in the halothane group received etomidate 0.3 mg/kg and 20 minutes later althesin 0.075 ml/kg intravenously. In a second group of 6 patients on isoflurane fentanyl 0.01 mg/kg was given. Etomidate did not affect the cardiovascular system significantly. While the decrease in blood pressure after althesin (24 per cent) was the result of a reduction in total peripheral resistance (32 per cent), hypotension associated with fentanyl (23 per cent) was caused by diminished output due to bradycardia (18 per cent). Load data,heart rate, and maximum dp/dt indicated moderate negative inotropic properties only of althesin. Using the complex haemodynamic parameter developed by Bretschneider the myocardial oxygen consumption was calculated. The energy demand of the heart decreased with etomidate, althesin and fentanyl by 14 per cent, 16 per cent and 32 per cent respectively. It is concluded that the risk of cardiovascular depression at induction in patients with impaired myocardial performance and coronary insufficiency can be minimized with etomidate and/or fentanyl.

Adult↗
PubMed1977

Antagonism of morphine with naloxone in dogs: cardiovascular effects with special reference to the coronary circulation.

The cardiovascular effects of naloxone 15 microgram/kg following morphine 2.0 mg/kg were studied in closed-chest dogs during light nitrous oxide-halothane anaesthesia. The bolus injection of naloxone caused an increase in heart rate (73%), cardiac output (20%) and mean arterial pressure (20%). Total peripheral resistance was unaffected. LV dP/dt max and LV dP/dt max/IP increased by 25% and 14% respectively, but positive inotropic effects could not be shown when load data, heart rate and the decrease in left ventricular ejection fraction (22%) were taken into consideration. The cardiovascular stimulation resulted in an increase in myocardial oxygen demand (66%) which was met by an increase in coronary blood flow (59%). The data suggest that the antagonism of narcotics with high doses of naloxone may impair the myocardial oxygen supply in patients suffering from coronary insufficiency. It is concluded that naloxone should be titrated for each patient to ensure adequate reversal of respiratory depression and to avoid circulatory stress.

Animals↗
PubMed1977

[Influence of modern inhalation anaesthetics on haemodynamics, myocardial contractility, left ventricular volumes and myocardial oxygen supply (author's transl)].

The cardiocirculatory responses to equianaesthetic concentrations (MAC 0.5 and MAC 1.0 plus 67% N2O) of halothane, methoxyflurane, enflurane and isoflurane were studied in a total of 35 closed-chest dogs during ventilation controlled to produce normocapnia. Each anaesthetic produced a dose-related decrease in mean arterial pressure and in values reflecting cardiac function. These included cardiac output, stroke volume, left ventricular max dp/dt and ejection fraction. Isoflurane seemed slightly less depressant to the heart than the other 3 anaesthetics. Total peripheral resistance remained nearly unaffected during halothane and methoxyflurane anaesthesia but decreased significantly with MAC 1.0 enflurane and isoflurane. There was no change in heart rate at low anaesthetic concentrations. The deeper levels of anaesthesia were associated with moderate increases in heart rate. In spite of the obvious depression of myocardial contractility there was a fall in pulmonary artery and left ventricular end-diastolic pressures and in left ventricular end-diastolic volumes with each of the agents. We take this as an expression of decreased ventricular filling resulted from pooling of blood in peripheral capacitive vessels. With the exception of isoflurane, each of the other three anaesthetics reduced coronary blood flow. Coronary vascular resistance was not substantially influenced by halothane and methoxyflurane, but decreased with MAC 1.0 enflurane and isoflurane. Myocardial oxygen availability was always found to be adequate. Isoflurane even produced a significant rise in coronary venous oxygen saturation indicating coronary vasodilation. Parallel with the depression in cardiac performance and blood pressure as two of the main predictors of energy demand, myocardial oxygen consumption was found to be significantly reduced by each of the anaesthetics. The ratio of the external work of the left ventricle to its oxygen consumption indicated that myocardial efficiency deterioated. The clinical implications are discussed.

Anesthetics↗
PubMed1977

[Effect of high dosages of morphine and meperidine on haemodynamics, coronary blood flow and myocardial oxygen consumption in comparison to fentanyl and piritramide (author's transl)].

Although morphine is one of the oldest drugs known to man, it has only recently been used in large doses as an anesthetic agent. The main advantage is the cardiovascular stability. The purpose of this investigation was to study the circulatory response to high equianalgesic doses of morphine and meperidine. In 10 closed chest dogs during normoventilation and light background-anaesthesia (0.5 Vol. % halthane; N2O:O2 = 2:1) 2.0 mg/kg morphine and 15.0 mg/kg meperidine were given at random. Morphine produced a decrease in mean arterial blood pressure by 28%, which was paralleled by an identical fall in total peripheral resistance. No negative inotropic effects were found. In contrast to this, the severe hypotension developing with meperidine (decrease in blood pressure by 54%) was the result of peripheral vasodilatation (46%) and of myocardial depression indicated by a sharp drop in dp/dtmax (59%), dp/dtmax/IP (14%) and in left ventricular ejection fraction (33%). Utilizing the thermodilution technique, the cardiac output remained largely unaffected with both narcotic analgesics, as the increase in heart rate (morphine 27%; meperidine 101%) compensated for the fall in stroke volume (morphine 19%; meperidine 55%). In spite of the altered haemodynamics there was no change in the myocardial energy demand, which was adequately met by the coronary blood flow measured with the pressure-difference technique. Both, morphine and meperidine, produced initially an increase in coronary blood flow and coronary venous oxygen saturation indicating coronary vasodilation. While the mechanism for the change in cardiovascular status with high doses of morphine is vasodilatation probably due to histamine release, the results of this study suggest a peripheral as well as a central (myocardial depression) site of action with meperidine. The results obtained from this study were compared with the data from a previous investigation on equianalgesic doses of fentanyl and piritramide and their clinical implications were discussed.

Animals↗
PubMed1976

Haemodynamics and myocardial oxygen consumption during isoflurane (forane) anaesthesia in geriatric patients.

The influence of isoflurane on haemodynamics and myocardial oxygen consumption was examined in seven geriatric patients under conditions of controlled ventilation and a normal arterial carbon dioxide tension. During isoflurane/nitrous oxide in oxygen anaesthesia (0.75 and 1.5 vol% inspired isoflurane) no significant changes occurred in cardiac output, stroke volume, heart rate, central venous and pulmonary artery pressure. Arterial pressure decreased, as did total peripheral resistance. A reduction in left ventricular maximum dp/dt (18-39%) was, at least in part, a result of changes in loading conditions. Total body (CaO2--CVO2) and base excess values remained within the normal range. We consider that the oxygen supply was adequate to meet the metabolic demands of the body as a whole. Myocardial oxygen consumption decreased by 25% during 0.75 vol% inspired isoflurane and by 43.5% with deepening of anaesthesia (1.5 vol% isoflurane).

Anesthesia, Inhalation↗
PubMed1975

[Anaesthetic management of patients with hyperdynamic circulation in hepatic cirrhosis (author's transl)].

Cirrhosis of the liver is frequently associated with arterial hypoxaemia and a hyperdynamic state of the systemic circulation. The hypoxaemia and the circulatory changes probably have a common aetiology, namely, shynting in the systemic and pulmonary vascular beds. Experiences in two well-documented cases suggest that anaesthetic agents may increase arteriovenous shunting and hypoxaemia in patients with hepatic cirrhosis. A plan for preanaesthetic identification and anaesthetic management in this type of patients is outlined.

Adult↗
PubMed1975

[Cardiovascular effects of the new inhalation anaesthetic isoflurane in man (author's transl)].

Cardiovascular responses to isoflurane (forane)-nitrous oxide-oxygen anaesthesia were studied in seven older premedicated patients. Anaesthesia was induced with the new non-barbiturate induction agen etomidate. All patients were intubated and mechanically ventilated to maintain normal PaCO2. Clinical concentrations of isoflurane (0.75 and 1.5 vol.-% inspiratory) decreased mean arterial pressure 22%-42%. Only small reductions in cardiac output and stroke volume were seen. Heart rate, central venous and pulmonary artery pressure remained nearly unaffected. The major cause of the arterial hypotension was a fall in total peripheral resistance by 36% as anaesthesia deepened. Left ventricular maximum dp/dt and load data indicated that isoflurane also possesses negative inotropic properties. Tension-time-index and total body oxygen consumption decreased by 47% and 20% respectively. AVDO2 values remained within the normal range. We take this to mean that the oxygen supply was adequate to meet the metabolic demands of the body as a whole. This was corroborated by the finding that base excess did not change significantly. Conclusions considering the use of isoflurane in patients with diminished cardiovascular reserve are drawn.

Adult↗
PubMed1975

[Effects of glucagon on systemic circulation, coronary blood flow and myocardial oxygen consumption in the anesthetized dog (author's transl)].

The systemic and coronary hemodynamic effects of 10, 20, 40 and 80 mug/kg glucagon have been studied in 9 anesthetized normoventilated closed-chest dogs. Intravenous administration of this agent produced a dose-related increase in the average coronary blood flow between 19% (10 mug/kg) and 49% (80 mug/kg). Coronary vascular resistance decreased by between 16% (10 mug/kg) and 39% (80 mug/kg). A--V O2 difference 1 min after the administration of glucagon no changes in myocardial oxygen extraction were observed after 5, 10 and 20 min. The calculated myocardial oxygen consumption rose up to 50% after 80 mug/kg glucagon. We conclude that the increase in coronary blood flow and the decrease in coronary resistance are mainly secondary to the metabolic effects of the increased myocardial contractility and heart rate, and that there is only an initial direct vasodilating effect on the coronary vessels.

Animals↗