Intensive care medicine
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Intensive care medicine · Jan 1990
Randomized Controlled Trial Comparative Study Clinical TrialThe use of midazolam versus propofol for short-term sedation following coronary artery bypass grafting.
Midazolam and propofol were compared in an open randomized study for postoperative sedation during 12 h of mechanical ventilation in 40 patients following coronary artery bypass grafting. After an intravenous loading dose of midazolam (50 micrograms.kg-1) or propofol (500 micrograms.kg-1), a titrated continuous infusion was administered of midazolam (mean dose 38.1 micrograms.kg-1.h-1 (SEM 2.6)) or propofol (mean dose 909 micrograms.kg-1.h-1 (SEM 100)) together with a narcotic analgesic infusion. During mechanical ventilation midazolam and propofol produced a similar quality of sedation, but recovery (midazolam 66 min (SEM 16); propofol 24 min (SEM 7)) and weaning from the ventilator (midazolam 243 min (SEM 44); propofol 154 min (SEM 33)) where faster with propofol. In the 2 groups administration of an intravenous loading dose caused a significant decrease in mean arterial pressure but hemodynamic tolerance during maintenance infusion was good.
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The management of severe bacterial sepsis is an integral part of intensive care medicine. Early and appropriate treatment with antimicrobials positively affects mortality and significantly reduces the time spent in both intensive care and the hospital. Drug choice is usually made on a "best guess" basis and instituted prior to receipt of appropriate blood, sputum, urine or drainage culture results. ⋯ Several newer agents have been more recently introduced. These drugs include ceftazidime, imipenem/cilastatin, the quinolones and clavulanic acid/semisynthetic penicillin combinations. Other newer drugs currently under evaluation include aztreonam, teicoplanin, the penems and carbapenems.
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Intensive care medicine · Jan 1990
Case ReportsPositive end expiratory pressure and critical oxygenation during transport in ventilated patients.
Transportation of patients critically dependent on positive end expiratory pressure (PEEP) can be problematic, as a patient of ours with adult respiratory distress syndrome (ARDS) and bilateral broncho-pleural fistulae demonstrated. He required intermittent positive pressure ventilation (IPPV) (Siemens 900C) with 100% O2 and PEEP of 2 kPa to maintain his arterial O2 saturation (SaO2) greater than 90%. Severe hypoxemia (SaO2 less than 75%) occurred on change to a portable ventilator (Oxylog, Dräger) with a PEEP value (Ambu 20) at its expiratory port, despite adjusting the valve to 2 kPa, continuing use of 100% O2, and varying the ventilatory pattern. ⋯ A small leak was introduced from the lung resulting in a decrease in PIP, VT, and PEEP. Adjustment of ventilator minute volume to restore PIP to 5 kPa failed to restore PEEP, airway pressure continuing to fall throughout the expiratory pause. PEEP was restored by providing a compensatory flow of O2 of 5 l/min to the system between the Oxylog non-rebreathing valve and the lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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Intensive care medicine · Jan 1990
Case ReportsAccidental hypothermia with cardiac arrest: complete recovery after prolonged resuscitation and rewarming by extracorporeal circulation.
A 51-year-old male remained immersed in sea water (6 degrees C) for 40 min. Brought ashore, the ECG showed asystole. Advanced life support was immediately commenced. ⋯ After 60 min of re-perfusion the patient was be weaned from bypass supported by a high-dose vasopressor infusion and nitroglycerine. He was discharged after 13 days with no evidence of any permanent organ damage. Given the advantage of providing circulatory support, extracorporeal circulation may be useful when rewarming hypothermic victims with cardiac arrest.
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Multiple Organ Failure (MOF) has largely been attributed to bacterial sepsis, though conclusive evidence of an essential role for bacteria and/or their endotoxins is still lacking. On the other hand, MOF and the clinical syndrome of sepsis may be aseptically induced in germ-free animals. This paper reviews the evidence that excessive activation of endogenous humoral mediators and inflammatory cells may cause this highly lethal syndrome.