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Biomedical subjects

G Singbartl

Publications and source records attributed to G Singbartl.

48 records · Page 3Linked to original sources
PubMed1981

[Head injury and disturbed pulmonary function (author's transl)].

Results compiled from the literature confirm the occurrence of a neurogenic initiated disturbance of pulmonary function. Neurogenic pulmonary oedema is a rare but grave form of neurogenic triggered changes of pulmonary and haemodynamic parameters. Increase of intracranial pressure or cerebral hypoxia, respectively, is the starting point of mechanisms, mediated primarily by the sympathetic nervous system and leading to hypoxaemia accompanying head injury. Pulmonary parameters involved are decreased pulmonary compliance, increased pulmonary right-to-left-shunt as well as disturbances of mechanisms regulating ventilation-perfusion ratio. Moreover, there exists a relationship between the severity of head injury and the degree of hypoxaemia.

Animals↗
PubMed1978

[Risk of general anaesthesia (author's transl)].

95 506 patients who received general anesthesia during the period of 1964--1977 were studied. The account of all actual or possible life threatening complications during the anesthesia is given: oedema of the glottis, air embolism, accidental injection of the wrong drug, respiratory insufficiency, hypoxia, pulmonary oedema, airway occlusion by the cuff, vomiting and aspiration, anaphylactoid reaction, death within 24 hours, death on the table. Deaths not attributable to anaesthesia are listed separately. We have found that in one of every 139 anaesthetics given there was a life threatening complication to the patient. In every 197th anaesthetic there was a clear connection with the anaesthetic technique used. In contrast with the great number of near fatal complications the rate of irreversible damage or mortality connected with general anaesthesia was low.

Adolescent↗
PubMed1976

[Cardiodepressive effects due to ketamine, etomidate, methohexitone and propanidid. A clinical study by means of the systolic-time-intervals (author's transl)].

The cardiodepressive effects of ketamine (1mg/kg), etomidate (0.3mg/kg), methohexitone (1mg/kg) and propanidid (4mg/kg) have been compared by means of the systolic time intervals on patients during a steady-state halothane--N2O:02(1.1)-- anaesthesia. This anaesthesia served as a pharmacological model of reduced myocardial function, and moreover, it should block the centrally-elicited cardiac stimulation by ketamine, thus unmasking the direct negative inotropic action of this anaesthetic. Ketamine and etomidate are of lesser cardiac depressant action than methohexitone or even propanidid. Diazepam (0.2-0.25mg/kg) proved to be able to attenuate or abolish, respectively, the ketamine-induced increases of heart rate and blood pressure in normo- and hypertensive patients, and might therefore be useful for induction anaesthesia in cardiac and coronary risk patients, as proved on two patients with recent myocardial infarction.

Adult↗
PubMed1975

[Ketamine - a cardiovascular stimulating agent with direct cardiodepressant action (author's transl)].

Induction anaesthesia with 2 mg/kg of ketamine causes the well-known increases in heart rate and blood pressure. Simultaneous registration of the systolic-time-intervals (PEPI, LVETTI, PEP/LVET = Q), however, reveals a biphasic effect of ketamine on these contractility-parameters: an initial increase of PEPI and Q, representing a cardiac depressive effect of ketamine, is followed by a decrease of PEPI and Q, indicating a positive inotropic action of ketamine. Injecting the same dose of ketamine during the steady-state of a halothane-N2O:O2-anaesthesia, that causes a depression of the central and peripheral sympathetic activity, however, results in an increase of PEPI and Q, only. Thus, ketamine is a cardiac depressive agent, this effect, however, usually being overlapped by a centrally-induced cardiac stimulation.

Blood Pressure↗