Halothane anaesthesia and suxamethonium I: the significance of preoperative atropine administration. A double-blind study.

Preoperative administration of atropine was evaluated during induction of halothane anaesthesia with two administrations of suxamethonium 1 mg/kg body weight, 5 min apart. Sixty-eight healthy, adult patients were studied. They were divided into five groups according to dose and route of administration of atropine. ECG was continuously monitored. Serum potassium, pH, PaCO2, PaO2 and standard bicarbonate were measured at appropriate intervals. It was found that neither atropine 0.01 mg/kg body weight given intramuscularly 1 h beofre the anaesthesia nor atropine 0.01 mg/kg body weight given intravenously 5 min prior to induction protected against serious bradycardias (defined as heart rate below 20 beats per minute) following the second dose of suxamethonium. No serious brady-arrhythmias were seen in patients given either a combination of intramuscular and intravenous atropine in the above-mentioned doses or in patients given atropine 0.015 mg/kg body weight intravenously 5 minutes prior to induction. However, a decrease in heart rate to around 40-50 beats per minute occurred in some of these patients. Furthermore, these large doses of atropine caused an increase in heart rate during induction to more than 120 beats per minute in about 50% of the patients and to more than 140 beats per minute in about 25% of the patients. Our results suggest that preoperative administration of atropine does not protect against serious brady-arrhythmias following a second dose of suxamethonium, unless doses of atropine are used which cause tachycarida of considerable degree.

Cardiovascular effects of etomidate used for induction and in combination with fentanyl-pancuronium for maintenance of anaesthesia in patients with valvular heart disease.

The effects of induction of anaesthesia by etomidate 3 mg kg-1 followed by continuous infusion of etomidate 2 mg min-1, fentanyl 0.01 mg.kg-1 and pancuronium 0.1 mg.kg-1 were studied in ten patients with valvular heart disease. No haemodynamic changes were seen injection of etomidate, but after fentanyl was given there was a significant decline in cardiac index (10%), in mean arterial systemic pressure (20%), in systemic vascular resistance (14%), in left ventricular minute work index (27%) and in right ventricular minute work index (21%) compared to the control values. After supplementing with pancuronium, no further significant changes were seen. There was no significant change in the pulmonary vascular resistance during the whole study. In conclusion, it appears that etomidate is a safe intravenous agent, and is worth further study, in particular in patients with minimal cardiac reserve requiring high inspired oxygen tension.

The effects of droperidol and fentanyl on intracranial pressure and cerebral perfusion pressure in neurosurgical patients.

The effects of droperidol and fentanyl on the intracranial pressure (i.c.p.) and cerebral perfusion pressure (c.p.p.) were studied in eight anaesthetized normocapnic patients with intracranial space-occupying lesions. The infection of droperidol resulted in a small and not significant increase in i.c.p. from 24.0 to 27.2 mm Hg, while c.p.p. decreased from 75.9 mm Hg to 57.8 mm Hg, as a result of a decrease in systemic arterial pressure. The addition of fentanyl produced no change in i.c.p., but a further decrease in arterial pressure decreased c.p.p. from 60.4 mm Hg to 47.8 mm Hg. In four patients values of c.p.p. less than 40 mm Hg were obtained. C.p.p. was was increased by hyperventilation in all but one of these patients. It is concluded that droperidol and fentanyl should be used in patients with intracranial hypertension only if hypocapnia has been established and when the arterial pressure is normal or increased.

The permeability of the blood-brain barrier during electrically induced seizures in man.

The blood-brain barrier (BBB) in man was studied during various conditions using the indicator dilution method of Crone [8]. Using 113m In-DTPA as reference substance the extraction, E, of the small test substances 24Na+, 36Cl-, 14C-urea and 14C-thiourea was estimated from the areas under the venous outflow curves following intracarotid slug injection of tracers. Interlaminar diffusion and red cell carriage were taken into consideration when calculating E. Cerebral blood flow (CBF) was measured using the intra-arterial 133Xe-injection method. Twenty-two patients receiving electroconvulsive therapy (ECT) were studied before and during seizures and during hypercapnia. Before seizures the extraction values in % were as follows: ENa+ 1.6, ECl- 1.9, Eurea 3.9 and Ethiourea 7.8; the corresponding values for the permeability-surface area products (PS) in ml/100 g x min were 0.5, 0.3, 0.7, 4.1, respectively. During seizure a decrease of Ethiourea and an increase of PSurea were significant. During hypercapnia PSNa and PSthiourea rose significantly. Due to the similarity of the findings in those two high flow situations it is suggested that the changes of CBF and not the epileptic activity are responsible for the changes in permeability. The mechanism of action may be a stretching of endothelial cells in the cerebral vessels or an opening up of new capillaries, or a combination of both.

Haemodynamic changes during sodium nitroprusside induced hypotension and halothane/nitrous oxide anaesthesia.

The haemodynamic effects of nitroprusside (SNP) were studied in six patients undergoing surgery for intracranial aneurysm under controlled hypotension in endotracheal anaesthesia with halothane-nitrous oxide during hypocapnia. Mean arterial pressure was reduced with SNP from mean 12.25 kPa to mean 8.29 kPa (32%). There were concomitant statistically significant decreases in systemic vascular resistance (-21%), cardiac index (-17%), stroke index (-23%), pulmonary arterial mean pressure (-27%) and pulmonary capillary wedge pressure (-27%). Heart rate, central venous pressure and pulmonary vascular resistance did not change significantly. After the infusion of SNP was discontinued all parameters, except cardiac index and heart rate, returned to values not significantly different from the control values. The hypotension induced by SNP resulted from reductions in cardiac index and systemic vascular resistance. The reduction in cardiac index did not reach a critical level in any of the patients.

The cardiovascular effects of ketamine used for induction of anaesthesia in patients with valvular heart disease.

The effects of induction of anaesthesia by ketamine 2 mg.kg-1 were studied in six patients with valvular heart disease before tracheal intubation and operation. Cardiac index was unaffected because a mean decrease in stroke index was compensated for a mean increase in heart rate. A significant increase was found in mean arterial pressure, pulmonary arterial mean pressure, pulmonary capillary wedge pressure and central venous pressure. Systemic vascular resistance increased, but not significantly, whereas pulmonary vascular resistance increased significantly by more than 150 per cent. Right ventricular minute work index increased in all patients, and the increase was as much as 400 per cent. Left ventricular minute work index increased in four of the six patients, but the magnitude of the increase was not so marked. It is therefore concluded that ketamine causes pronounced pulmonary vasoconstriction and an undesirable strain on the myocardium. Such effects could prove deleterious in patients with limited functional reserve of the right ventricle.

Cardiovascular haemodynamics after induction of anaesthesia with althesin in patients with valvular heart disease.

The haemodynamic effects of the induction of anaesthesia with Althesin 0.1 ml.kg-1 were studied in eight patients with valvular heart disease before tracheal intubation and surgery. A 20 per cent reduction in stroke index was compensated for by an increase in heart rate of similar magnitude. Cardiac index, mean arterial, pulmonary arterial, central venous and pulmonary capillary wedge pressures and systemic vascular resistance were unaffected. Pulmonary vascular resistance declined by nearly 30 per cent. It is therefore conclude that Althesin causes only minimal cardiovascular depression in patients with valvular heart disease.