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J W Gethmann

Publications and source records attributed to J W Gethmann.

16 recordsLinked to original sources
PubMed1979

[High doses of thiopental for therapy of post-ischaemic anoxia of the brain. A case report (author's transl)].

The case of a 7-year-old child is presented, who suffered circulatory arrest during induction of anaesthesia for surgery for a posterior fossa tumour. A brain ischaemia lasting 6 minutes duration had to be assumed. After restoration of circulation, 825 mg ethiopenta were administered in order to ameliorate a possible post-ischaemic anoxia of the brain according to a protocol by Safar [18]. 11 hours after circulatory arrest the child awoke. Except for a more pronounced left sided hemiparesis and paresis of the left n. abducens no additional neurological deficit was observed compared to the neurological status before induction of anaesthesia.

Anesthesia↗
PubMed1976

[Effect of high dosages of fentanyl and piritramide upon haemodynamics, coronary blood flow and myocardial oxygen consumption (author's transl)].

High dosages of narcotic analgesics are frequently utilized as the sole anaesthetic agents for patients requiring open-heart surgery. The purpose of this study was to investigate the effect of high dosages of fentanyl and piritramide upon the cardiovascular system. In anaesthetized dogs (N2O:O2=2:1; 0.5 vol% halothane) 0.03 mg/kg fentanyl (=8) and 1.5 mg/kg piritramide (n=8) respectively were given intravenously as a bolus. After the administration of fentanyl there was a slight decrease in blood pressure (10%). The hypotension was the result of a decrease in cardiac output (thermodilution technique) by 13% due to bradycardia. Total peripheral resistance and myocardial contractility remained unaffected. Similar effects were only found late after injection of piritramide, since there was an initial cardiovascular response to piritramide characterized by a marked fall in blood pressure (29%). The major cause of arterial hypotension was peripheral vasodilatation. Load data and the decrease in max dp/dt however indicated also a slight myocardial depression. The altered haemodynamics led to a decrease in myocardial oxygen consumption with both narcotics, which was nearly paralleled by a reduction in coronary blood flow. The narrowing of arteriovenous oxygen difference of the heart proved coronary dilatatory properties of fentanyl and especially of piritramide. This study indicated that high dosages of fentanyl have advantages in comparison to high dosages of piritramide. The clinical implications of the results are discussed.

Animals↗
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

[The effect of ketamine on haemodynamics and myocardial oxygen consumption in anaesthetized dogs (author's transl)].

Ketamine is an induction agent. This experimental study was designed to investigate the immediate effects of ketamine upon haemodynamics, inotropism and myocardial oxygen consumption during induction. In a circulatory steady state of a piritramide - nitrous oxide - oxygen basic anaesthesia normoventilated dogs (n = 8) received intravenous injections of 5.0 and 10.0 mg/kg ketamine within 30 sec at random. Immediately after administration of 10.0 mg/kg ketamine the cardiac output (thermo dilution method) rose (27%) on account of tachycardia while the total peripheral resistance (40%) and the mean arterial pressure (23%) decreased. The decrease in stroke volume (37%) and the inotropic parameter dp/dt max (42%) as well as the increase in the end-diastolic left ventricular pressure (31%) and in the pressure of the pulmonary artery (11%) suggest considerable myocardial depressor properties of ketamine. The change in haemodynamics was paralleled with an increase in myocardial oxygen consumption (47%), which was initially met by an increase in coronary blood flow (25%) and an additional oxygen utilization (20%). The increase in arterio-coronary venous oxygen difference is believed to be due to a constriction of the coronary arteries after ketamine. Since external cardiac work remained unchanged,while myocardial contractility and myocardial wall tension (Psyst) decreased, the increase in heart rate (63%) explains the rise in myocardial oxygen consumption. The efficiency of cardiac work, which is defined as the ratio of myocardial displacement work to myocardial energy demand, decreased (31%) and illustrated the uneconomic work of the heart under the influence of ketamine. The clinical utilization of the data obtained from this study are discussed.

Animals↗
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↗
PubMedDate not supplied

Blood pH and PaCO2 as chemical factors in myocardial blood flow control.

The effect of metabolic and hypercapnic acidosis on myocardial blood flow was studied during intravenous infusions of hydrochloric acid solutions (n = 12) and during passive ventilation with 5% CO2 (n = 5) in anaesthetized, closed chest dogs. Below a pH of 7.2 metabolic acidosis at normal arterial CO2-tensions caused an increase of coronary blood flow and a decrease of coronary vascular resistance associated with a narrowed myocardial arteriovenous O2-difference, indicating vasodilation at unchanged myocardial oxygen consumption. In propranolol-pretreated dogs myocardial blood flow and coronary oxygen AV difference remained unaffected, suggesting that the coronary dilatory effect of metabolic acidemia involves beta adrenergic stimulation. Coronary vasodilation induced by increasing arterial pCO2 was found to the significantly greater as compared with the dilatory effect of metabolic acidosis at the same blood pH level. Blocking of beta receptors did not reduce the coronary response to increased arterial CO2-tensions. It is concluded that the coronary vasodilation observed during hypercapnic acidosis is neither mediated by a beta adrenergic stimulation nor dependent of the concomitant change in blood pH. The possible sites of the coronary dilatory actions of increased arterial CO2-tensions are discussed.

Acidosis↗
PubMedDate not supplied

Comparison of the immediate effects of etomidate, propanidid and thiopentone on haemodynamics, coronary bloodflow and myocardial oxygen consumption.

Since cardiovascular depression at induction is among the most common complications of anesthesia this comparative study was undertaken. Unpremedicated dogs (n = 16) were induced with 3 mg/kg piritramide i.v. and normoventilated (N2O/O2 = 2/1). In 8 animals 0.8 and 1.6 mg/kg Etomidate and 5.0 and 10.0 mg/kg thiopentone and in 8 further dogs 5.0 and 10.0 mg/kg Propanidid were tested. Equipotent doses of Thiopentone and Propanidid caused a marked myocardial depression, which was seen in a decrease in stroke volume and max dp/dt and in an increase of leftventricular end-diastolic pressure and pulmonary arterial pressure. The increased myocardial O2- cosumption mainly due to the rise in heart rate was covered after Thiopentone by an increase of coronary bloodflow (measured with a pitot-catheter) and an increase of arterio-coronaryvenous difference in oxygen. As the latter decreased after Propanidid, it appeared that Propanidid has coronary dilatory properties. The results demonstrated the uneconomic work of the heart under the influence of Thiopentone and Propanidid. In contrast to this the cardiovascular system after Etomidate remained nearly unaffected. The data of this study suggest the use of Etomidate rather than Thiopentone and Propanidid in cases of shock syndrome, heart and/or coronary insufficiency.

Anesthetics↗