Percutaneous methanol intoxication: case report.
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Biomedical subjects
Publications and source records attributed to T Adanir.
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BACKGROUND AND OBJECTIVE: To determine if there is any significant difference between the effects of desflurane, isoflurane and sevoflurane on the QT interval, QT dispersion, heart rate corrected QT interval and QTc dispersion of the electrocardiogram. METHODS: The study was conducted in a prospective, double blind and randomized manner in a teaching hospital. Ninety ASA I patients, aged 16-50 yr, undergoing general anaesthesia for noncardiac surgery were studied. RESULTS: There was no significant change in QT intervals during the study in any group (P > 0.05). QT dispersion in the sevoflurane group 49+/-14 ms vs. 37+/-10 ms; in the desflurane group 55+/-16 and 62+/-21 ms vs. 35+/-14 ms and in the isoflurane group 54+/-26 and 59+/-24 ms vs. 42+/-19 ms were significantly increased at 3 and 10 min after 1 MAC of steady end-tidal anaesthetic concentration compared with baseline values (P < 0.05). QTc values in the sevoflurane group were 444+/-24 and 435+/-2 1ms vs. 413+/-19 ms (P < 0.05), in the isoflurane group were 450+/-26 and 455+/-34 ms vs. 416+/-34 ms (P < 0.05), in the desflurane group were 450+/-26 and 455+/-34 ms vs. 416+/-34 ms (P < 0.05) at 3 and 10 min after reaching 1 MAC of anaesthetic concentration and significantly increased compared with baseline values. QTc dispersion increased significantly with sevoflurane 62+/-14 ms vs. 45+/-16 ms (P < 0.05); isoflurane 70+/-36 ms at 3 min and 75+/-36 ms at 10 min after reaching 1 MAC of anaesthetic concentration vs. 50+/-24 ms (P < 0.05); desflurane 67+/-25 ms at 3 min and 74+/-27 ms at 10 min after 1 MAC concentration vs. 41+/-22 ms (P < 0.05). CONCLUSION: Sevoflurane, isoflurane and desflurane all prolonged QTd, QTc and QTcd but there were no significant intergroup differences.
Cardiopulmonary bypass (CPB) produces an inflammatory response due to the interaction of blood with a foreign body surface. The lungs are most affected by this inflammatory response. Pentoxifylline (PTX), a phosphodiesterase inhibitor and an inhibitor of leukocyte activation, is used to minimize damage in lungs where leukocytes play an important role. Twenty patients with mitral valve stenosis with planned mitral valve surgery were included in the study. The ten patients receiving pentoxifylline (PTX group) were administered 400 mg PTX orally TID for 3 days preoperatively and, following anesthetic induction, a 300 mg PTX infusion was given. The ten patients receiving no PTX were the control group (CT). Platelet and leukocyte counts, mean pulmonary arterial pressure (mPAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI), pulmonary vascular resistance (PVR), alveolar-arterial PO2 gradient (AaDO2) were measured just before and after CPB, and 2 h postoperatively. The number of the leukocytes increased in the blood samples drawn 15 min after CPB in both groups and 2 h postoperatively showed no statistical change. The number of platelets had decreased significantly at the end of the CPB in both groups and, 2 h postoperatively, there was a further decrease in the blood count in the control group (P < 0.05). There was no significant difference in either the preoperative or postoperative PAP, PAWP, and CI. Pulmonary vascular resistance increased in both groups following the CPB (CT, before: 136 +/- 44, after: 177 +/- 94 dyne. sec.cm-5; PTX, before: 151 +/- 82, after 182 +/- 43 dynes.sec.cm-5). Two hours postoperatively, a considerable increase continued in the control group (CT 219 +/- 170 dynes.sec. cm-5), while there was an insignificant increase in the PTX group (PTX 193 +/- 51 dynes.sec.cm-5) (P < 0.05). The alveolar-arterial PO2 gradient increased after the CPB in both groups but a moderate decrease was observed 2 h postoperatively. In lung biopsy specimens taken before and after the CPB, there was marked leukocyte sequestration in the control group, whereas the number of leukocytes was seen to be insignificant in the PTX group (P < 0.005). This dosage regimen of PTX inhibits the postoperative increase in PVR and greatly minimized leukocyte sequestration in the lung due to CPB.