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Angiotensin-converting enzyme activity in serum or bronchoalveolar lavage fluid does not reflect damage of endothelial cells or damage of alveolocapillary integrity in acute pulmonary disease.

SummaryA postoperative cardiac surgical patient developed ventricular Jibrillation immediately after accidental pericardial injection of bupivacaine at room temperature. The possible causes, which include systemic toxicity. local vasoconstriction with myocardial ischaemia. local toxic effect of bupivacaine or local hypothermia, are discussed. Key wordsToxicity; bupivacaine. Anaesthetic techniques. regional; interpleural block. Heart; ventricular fibrillation.The use of interpleural bupivacaine for analgesia in acute and chronic pain has been reported since 1984. The technique is effective after upper abdominal surgery, but only variably so after thoracotomy [I]. It is thought to work by diffusion of local anaesthetic through the parietal pleura and intercostal muscles, thus blocking the intercostal nerves (dermatomes T, to T,J. The recommended doses of bupivacaine for interpleural analgesia are 20--30 ml in a 0.5 to 0.75% concentration. For treatment of postoperative pain which is resistant to opioids, we have used bupivacaine 0.125% injected into the pleural drain while it is briefly clamped. We report a patient where bupivacaine was accidentally injected through a pericardial drain, with resultant ventricular fibrillation. Case historyA 64-year-old man had a history of two myocardial infarctions. Left ventricular function was good but coronary angiography showed triple vessel disease. Uneventful complete surgical revascularisation was performed and a left pleural and a pericardial drain were left in situ. On the first postoperative day the patient was haemodynamically stable and his pain was treated with piritramide 15 mg intramuscularly. However, on the second day the pain was resistant to this treatment and plain bupivacaine 0.125% 20 ml (25 mg) was injected into the clamped left pleural drain. After 15 min the pain had not diminished, therefore it was decided to inject an additional bolus of bupivacaine 0.125% 10 ml (12.5 mg) interpleurally. However this bolus was inadvertently injected into the pericardial drain, at which point the patient developed ventricular fibrillation. A single D C shock was sufficient to restore sinus rhythm and stable haemodynamics and there were no further cardiac or neurological complications. DiscussionSeveral physiological mechanisms can explain the occurrence of ventricular fibrillation after injection of bupivacaine at room temperature into the pericardial sac.First of all, a local toxic reaction of bupivacaine on epicardial fibres, or perhaps rapid absorption into the coronary arteries, could be responsible for life-threatening arrhythmias. The electrophysiological effect of bupivacaine on myocardial cells results from an interaction with the fast sodium channels in the cardiac membrane [2]. This phenomenon decreases the maximum rate of depolarisation, the amplitude and duration of the action potential and shortens the effective refractory period. This may result in unidirectional conduction delay, ventricular arrhythmias and fibrillation.Secondly, rapid systemic absorption ...

1. The presence of histamine and tryptase in serum during and after coronary artery bypass grafting may be an indication of the induction of inflammation. 2. One group of patients received no glucocorticoids and a second group received methylprednisolone before extracorporeal circulation. In the steroid group no effects were seen on the basal levels of histamine (2.84 + 0.12 ng/ml) and tryptase (030 + 0.05 ng/ml) during and after surgery. In the other group two peak levels of histamine were observed: one at 10 min after starting extracorporeal circulation (4.19 +1.79 ng/ml) and another at 4h after surgery (8.26 +4.85 ng/ml). In this group tryptase was only elevated during the period of extracorporeal circulation (1.54+ 0.16 ng/ml). 3. There were no differences between the two groups in complement activation. C3a levels rose to 170 +8% and 180 +10% of the initial value in the steroid and non-steroid group, respectively. 4. It was concluded that during surgery mast cells were activated, but since tryptase levels decreased in the post-operative period, the second increase in the histamine level can be explained by activation of basophils or by an unknown mechanism for the release of histamine but not tryptase by mast cells. 5. In the bronchoalveolar lavage fluid the levels of histamine and tryptase showed no differences between the two groups of patients, but histamine was enhanced compared with normal levels.

The value of monitoring the right precordial lead, V4R, to detect peri-operative ischaemic events during coronary artery surgery was studied in 60 patients. Thirty-four patients had only left-sided coronary disease (Group 1). The other 26 patients had both left-sided occlusive coronary artery disease and significant right-sided occlusive lesions on coronary angiography (Group 2). Lead sensitivity was estimated, assuming that all ST segment changes were true positive responses. Sensitivity using a single lead was greatest for lead V5 in the two groups (73% for Group 1 and 69% for Group 2). Sensitivity in Group 1 for lead II was intermediate (55%), whereas sensitivity for lead V4R was only 9%. In Group 2, on the other hand, lead V4R was 54% sensitive and lead II only 31%. The combination of leads V4R and V5 increased the sensitivity to 92% in Group 2, whereas lead II or V5 combined with V4R failed to improve sensitivity in Group 1. The monitoring of lead V4R allowed detection of 23% of the ischaemic episodes in Group 2 that would have passed undetected if only lead II and V5 were monitored. These results demonstrate the value of an additional right precordial lead during coronary artery bypass grafting in patients with right-sided occlusive disease.