An aid for double-lumen intubation.
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Biomedical subjects
Publications and source records attributed to C Aps.
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1 L(-)- and D(+)-bupivacaine in eight different concentrations from 0.06 to 7.69 mmol/l (0.002--0.25%) and physiological saline were given intradermally to seventeen volunteers, using a double-blind technique. 2 Local colour changes were observed as 'nil', 'pink' or 'pale' and analgesia to pinprick was assessed every 10 min to give an estimate of apparent in vivo potency and duration of action (50% recovery). 3 Both isomers were vasodilator in all cases at 7.69 mmol/l, but the incidence of vasodilatation waned with decreasing concentration, more rapidly with L(-)-than with D(+)-bupivacaine. 4 Only L(-)-bupivacaine showed a vasoconstrictor effect. This was maximal at a concentration of 0.48 mmol/l, when the incidence of pallor was 92%. 5 L(-)-bupivacaine had a longer duration of analgesic action than the (D+)-isomer from 0.48-3.84 mmol/l; this was reflected in a higher apparent in vivo potency.
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Plasma lignocaine concentrations were measured during and after lignocaine infusions administered for suppressing ventricular dysrhythmias. Twenty-four patients with a primary diagnosis of acute myocardial infarction without gross circulatory disturbance received, after a bolus of lignocaine, either 4 mg/min for 30 minutes, 2 mg/min for two hours, then 1 mg/min thereafter or 1 mg/min throughout. The higher dose regimen produced continous therapeutic levels of lignocaine, which were achieved only after four hours by the lower dose. On the other hand, in patients who had undergone cardiac surgery and who had circulatory and heptic dysfunction the lower dose regimen achieved therapeutic levels early. The plasma half life was longer in the surgical group (P less than 0.02). The higher initial infusion rate is recommended for patients with acute myocardial infarction without gross circulatory impairment.
In a double-blind trial bupivacaine 0.125, 0.25 and 0.5% and lignocaine 0.5, 1 and 2% were given intradermally to 31 volunteers. Vasoconstriction was observed more frequently at low concentrations of each drug, and vasodilatation at high concentrations. These observations were highly significant (P less than 0.001). Duration of action was unaffected by concentration, except in the case of bupivacaine 0.5%, the effect of which was longer lasting than that of other solutions.
A suitable combination of anaesthetic and surgical techniques has allowed the safe management of post-operative cardiac surgical patients to be conducted in a surgical recovery area rather than in the intensive care ward. The results of the first 103 patients so managed (aged 49 +/- 10.7 years) are presented. Coronary artery bypass grafts were performed on 98 patients, 4 patients underwent repair of atrial septal defect and on 1 patient a pulmonary valvotomy was performed. The complications and their management are described.
The efficacy of heparin reversal was investigated in 35 patients undergoing open-heart surgery. A total protamine sulphate dose of 3.0 mgs/kg was administered in divided doses and given as a continuous infusion. On this regime complete heparin neutralisation was observed 10 min after decannulation, but heparin levels were again detectable in 29% of cases 2 hours later. This phenomenon was found to correlate with the total circulating load of heparin to be neutralised. All cases with detectable postoperative heparin levels had in-vivo protamine sulphate: heparin ratios of less than 1.6. These data suggest that in-vitro assays of protamine sulphate neutralisation of heparin may seriously underestimate the required dose of protamine sulphate following open-heart surgery.
Fast-tracking in cardiac surgery evolved as the pressure on bed space in intensive therapy units (ITU) grew and clinical management improved. It relies on achieving a patient condition that allows for earlier extubation and postoperative management in alternative facilities to the ITU.