The incidence of Marfan's syndrome in the general population is thought to be between 1:10,000 and 1:50,000. t Hence it is possible that at some stage during their practising life many anaesthetists will be called upon to treat such a patient. We recently anaesthetized a patient for a cardiac procedure who demonstrated most of the features of this generalised disorder of connective tissue.Case report An 18-year-old male presented to hospital four days after the acute onset of left sided chest and neck pain. The pain was associated with severe dyspnoea, nausea and faintness and lasted about 15 seconds. It was followed by constant, heavy retrosternal chest pain. Similar episodes of diffuse, heavy chest pain were described on several occasions over the previous two years.The patient gave a history of multiple recurrent dislocations of both shoulders and also of a dislocation of his left ankle. He had undergone surgery at the age of 12 for the correction of a severe pectus excavatum deformity, at 15 years of age for osteo-chondritis dissecans of the left knee and at 17 years, for torsion of the fight testis.Examination of this tall (185 cm), thin (62 kg) patient revealed the typical features of Marfan's syndrome; an arm span that was greater than his height, a cathedral palate, winging of the scapulae, ulnar deviation of fire mctacarpophalangeal joints and residual pectus excavatum. He had also an abberant left radial artery, situated on the dorsum of the forearm.There were significant abnormalities on examination of the cardiovascular system. The blood pressure in the left arm was 110160 mmHg and in the right arm 120f70 mmHg. His apex beat was widely displaced to the 7th left intercostal space, mid axillary line. There was an ejection systolic murmur heard to the right of the sternum with a mid-systolic click at the left sternal edge.A chest x-ray showed a prominent and slightly tortu ous aorta with cardiomegaly and a marked thoracic scoliosis. There were no interstitial pulmonary changes. His ECG showed right atrial hypertrophy and large left ventricular complexes. The following day an aortogram was performed, outlining a large false aortic sac with a possible entry site proximal to the innominate artery. The aortic root was not outlined. He was treated with oral CAN J ANAESTH 1987 ! 34:3 / pp311-4

We present three patients with severe ischaemic heart disease who developed profound bradycardia (heart rates of 15 beats.rain "~, 10 beats'rain -t and asystole) at the time of laryngoscopy and spraying of the trachea with topical lidocaine. All patients had received fentanyl 20-30 tzg-kg -j and pancuronlum 0.1-0.13 mg'fcg -t For over 40 years it has been appreciated by anaesthetists that the performance of laryngoscopy and intubation can be accompanied by reflex circulatory responses. With the introduction of the non-depolarizing muscle relaxants in the 1940's and 1950's it was realised that the shift in technique from intubation under deep planes of volatile anaesthesia to the lighter planes made possible by the use of relaxants could predispose the patient to the development of intubation-related arrhythmias, including bradyarrhythmias. 1Consequent upon the increase in understanding of the pathophysiology of isehaemic heart disease, there has been a shift in emphasis towards the importance of hypertension and taehyeardia associated with laryngoscopy and intubation and the subsequent development of myocardial ischaemia. ~ This emphasis has led to the underestimation of the degree and severity of bradycardia which can occur with laryngoscopy and intubation. Key wordsANAESTHESIA'. cardiac', COMPLICATIONS: bradycardia. We therefore would like to present three patients with severe cardiac disease who developed significant bradycardia at the time of laryngoscopy and spraying of the trachea and vocal cords with topical anaesthetic solution. Case reports Case IFifty-four-year-old 64 kg female, with a long past history of hypertension and ischaemic heart disease, was admitted to the coronary care unit with unstable angina. Her medication consisted of propranolol 320 mg daily, hydroehIorthiazide 25 mg daily, amiloride 5 mg daily and isordil 80 mg orally daily. She was commenced on intravenous nitroglycerine for chest pain which continued despite this therapy and was complicated by one episode of sinus arrest lasting six seconds. Coronary angiography revealed triple vessel disease and the patient was scheduled for urgent coronary artery bypass surgery.She was premedicated with morphine 7.5 mg IM, scopolamine 0.3 mg 1M and received 7 mg diazepam IV during insertion of arterial, venous and pulmonary artery catheters. At induction blood pressure (BP) was 150/80 mmHg, heart rate (HR) 48 bpm, mean pulmonary artery pressure (MPAP) 17 mmHg and pulmonary capillary wedge pressure (PCWP) 10 mmHg. Induction of anaesthesia was with fentanyl 1600 Ixg (25 Ixg' kg-~) pancuronium 8 mg and nitrous oxide with 50 per cent oxygen. Following induction her heart rate increased to 65 bpm and BP was 125/70 mmHg. After three minutes of ventilation, laryngoscopy and spraying of the cords with 1 mg-kg -~ of ten per cent lidocaine was followed by progressive bradyeardia to a minimum rate of l0 bpm, The BP fell to 75 mmHg systolic (Figure 1). A precordial thump was given and heart rate recovered to 75 bpm over the following 12 seconds. Subsequen...

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Twenty patients with good ventricular function undergoing coronary artery bypass surgery were studied to determine whether the pre-bypass use of nitrous oxide resulted in any differences in cerebrospinal fluid markers indicative of cerebral ischaemia. All patients were anaesthetised with diazepam, fentanyl and pancuronium, after which ten patients received 50–60% nitrous oxide in oxygen until commencement of bypass, and the remaining patients 100% oxygen. Because of the known effect of nitrous oxide in expanding gaseous bubbles, any neurological dysfunction of gaseous microembolic origin may be worsened in the presence of nitrous oxide. Patients were lumbar punctured 24 hours after cardiopulmonary bypass and cerebrospinal fluid analysed for the following markers of central nervous system ischaemia: creatine kinase, lactate, total protein, noradrenaline, adrenaline and adenylate kinase. There was a statistically significant difference in cerebrospinal fluid lactate between the two groups. There were no statistically significant differences in the other cerebrospinal fluid markers of ischaemia.