I.V. MIDAZOLAM AS AN INDUCTION AGENT FOR ANAESTHESIA: A STUDY IN VOLUNTEERS

The central nervous and cardiovascular effects of midazolam 0.15 mg kg−1 were studied in 20 healthy, unpremedicated volunteers (10 male and 10 female). No important side-effects were noted and the venous tolerance to midazolam was excellent. Three minutes after injection mean systolic arterial pressure decreased from 121±(SEM) 2 mm Hg to 115±(SEM) 2 mm Hg and diastolic pressure from 78±2 to 70±2 mm Hg (P <0.05), and these effects persisted for at least 20 mm. Heart rate increased from 77±4 beat mm−1 to 90±3 and 88±3 beat mm−1 1 and 3 mm after the injection (P <0.05). Anterograde amnesia (40±3 min duration) and drowsiness (lasting 128±23 mm) were observed in all subjects. Loss of the eyelash reflex and apnoea were observed more often in the male group than in the female subjects. Midazolam 0.15 mg kg−1 was not sufficient to induce anaesthesia reliably in healthy unpretnedicated volunteer

Fatal myocardial infarction after lung resection in a patient with prophylactic preoperative coronary stenting†

In this report we present the case of a 77-yr-old man who underwent resection of the upper lobe of the left lung for a carcinoma, six weeks after percutaneous transluminal coronary angioplasty (PTCA) with stenting of the left anterior descending (LAD) and circumflex coronary arteries. Antiplatelet therapy with clopidogrel was interrupted two weeks before surgery to allow for epidural catheter placement and to minimize haemorrhage. The surgical procedure was uneventful. In the immediate postoperative period, however, the patient suffered severe myocardial ischaemia. Emergency coronary angiography showed complete thrombotic occlusion of the LAD stent. In spite of successful recanalization, reinfarction occurred and the patient died in cardiogenic shock. Prophylactic preoperative coronary stenting may put the patient at risk of stent thrombosis if surgery cannot be postponed for three months. In such cases, other strategies such as perioperative β-blockade for preoperative cardiac management should be considered. Br J Anaesth 2004; 92: 743-

Fatal myocardial infarction after lung resection in a patient with prophylactic preoperative coronary stenting.

In this report we present the case of a 77-yr-old man who underwent resection of the upper lobe of the left lung for a carcinoma, six weeks after percutaneous transluminal coronary angioplasty (PTCA) with stenting of the left anterior descending (LAD) and circumflex coronary arteries. Antiplatelet therapy with clopidogrel was interrupted two weeks before surgery to allow for epidural catheter placement and to minimize haemorrhage. The surgical procedure was uneventful. In the immediate postoperative period, however, the patient suffered severe myocardial ischaemia. Emergency coronary angiography showed complete thrombotic occlusion of the LAD stent. In spite of successful recanalization, reinfarction occurred and the patient died in cardiogenic shock. Prophylactic preoperative coronary stenting may put the patient at risk of stent thrombosis if surgery cannot be postponed for three months. In such cases, other strategies such as perioperative beta-blockade for preoperative cardiac management should be considered

Effect of clonidine on ICP and on the hemodynamic responses to nociceptive stimuli in patients with brain tumors

The effect of clonidine on intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), heart rate (HR), and drug requirements was studied in 24 patients scheduled for elective cerebral tumor resection (ICP &lt; or = 20 mm Hg). The patients were randomly assigned to one of two groups: Group P (placebo), 12 patients; Group C (clonidine 3 micrograms/kg 10 min before induction), 12 patients. In all patients, anesthesia was induced with a propofol infusion (500 micrograms/kg/min) combined with fentanyl 2 micrograms/kg, lidocaine 1.5 mg/kg, and vecuronium 0.1 mg/kg. Propofol was also used for maintenance. During the preinduction period, clonidine had no effect on ICP or HR, but in clonidine-treated patients, MAP and CPP decreased significantly in comparison to those of the placebo group. During induction, ICP and HR were stable and similar in both groups. MAP and CPP remained significantly lower in Group C. At intubation and Mayfield clamp application, ICP increased in both groups, with similar values at all times. MAP increased in both groups at intubation, Mayfield clamp application, and incision, staying lower, however, in Group C. CPP followed a pattern similar to that of MAP. Propofol requirements up to the 20th min were lower in Group C than in Group P (2.08 +/- 0.83 vs. 3.3 +/- 0.7 mg/kg, p &lt; 0.05). Finally, throughout the study, eight patients in Group C versus two in Group P had a CPP value &lt; 60 mm Hg for &gt; or = 1 min (p &lt; 0.05).(ABSTRACT TRUNCATED AT 250 WORDS