Despite maintaining arterial pressure with phenylephrine, cerebral desaturation occurred with upright positioning. Cerebral oxygen saturation can provide a valuable endpoint when evaluating the effect of vasopressor therapy on cerebral perfusion.

During their first few minutes of immersion in stirred water at 5 and 150 C. the pulmonary ventilation of twelve unclothed men was high, and their end-tidal PCO2 fell. The pCO2 then returned to or a little above its original level but did not greatly exceed it even in working experiments lasting 20 min. in water at 50 C. or 40 min. in water at 150 C. Although work reduced or reversed the initial fall in pCO2, these results therefore do not bear out predictions that the pCO2 would rise to dangerous levels during hard work in cold water, at least in immersions of moderate duration.In water at 37.80 C. the men's heart rates rose steadily, in water at 250 C. they fell and remained low, and in water at 5 and 150 C. they rose and then fell. Repeated immersion at 150 C. reduced or abolished the early respiratory and heart rate responses to immersion and the metabolic response, but did not significantly increase the falls in rectal temperature. Clothing also reduced the reflex responses to immersion. A number of ventricular extrasystoles were observed during the first 2 min. of immersion in water at 150 C., and it is suggested that ventricular fibrillation due to increased venous and arterial pressures, adrenaline, and hyperventilation, may be responsible for some cases of sudden death in cold water. THIS paper describes observations on the end-tidal pCO2, pulmonary ventilation, heart rate, and electrocardiographs of twelve men during immersion in water at temperatures between 5 and 37.80 C. Cotes [1954 and 1955] has reported that the pulmonary ventilation of a man could be predicted from his alveolar pCO2 and deep body temperature, and anticipated that CO2 would accumulate in the body to reach dangerous concentrations during hard work in cold water.Sudden death in cold water without drowning is generally [Simpson, 1958] attributed to vagal arrest of the heart following inhalation of cold water into the naso-pharynx and glottis. However, it has seemed possible that ventricular fibrillation might be responsible for some of these cases; an increase in venous pressure may follow sudden exposure to cold [Bondurant, Hickam and Isley, 1957; Keatinge and McCance, 1957] and a rise in filling pressure may precipitate ventricular fibrillation in isolated hearts [Keatinge, 1959], while adrenaline is known sometimes to cause ventricular fibrillation after chloroform [Levy, 1914] and to facilitate it without chloroform in isolated hearts [Goodford, 1958].The effect of adaptation by repeated immersion in cold water has also been assessed, since the heart rate and blood pressure responses to the immersion of a hand in ice water [Glaser and Whittow, 1957] are reduced by repetition. The design of the experiments and the subjects have been described in the preceding paper.*

From February 1988 until August 1991, 28 patients with prior coronary artery bypass grafting (CABG) received implantable cardioverter defibrillator (ICD) therapy via a subxiphoid approach. Only one patient required conversion to a median sternotomy incision. The mean defibrillation threshold was 11.9 +/- 4.4 J. The mean R wave was 8.2 +/- 3.7 mV. One perioperative death occurred due to heart failure (mortality rate 1/28 [3.50%]). No patient required reexploration for bleeding. The subxiphoid method for ICD electrode implantation is safe and reliable in patients with prior CABG surgery.

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Continuous venovenous haemofiltration is a wellestablished technique in the management of acute renal failure complicating the multi-organ dysfunction syndrome. In most cases this treatment is well tolerated although where lactate-buffered replacement fluids are used there is an implicit assumption that lactate is metabolised quantitatively to carbon dioxide and water. We report the case of a 46-year-old female who presented in acute renal failure requiring renal support following circulatory arrest. During lactate-buffered haemofiltration an increase in arterial lactate concentration was observed, coupled with deteriorating acid-base parameters and a decreasing cardiac output. Substitution of bicarbonatebuffered replacement fluid for lactate resulted in both the correction of the acid-base disturbance and an improvement in cardiovascular haemodynamics.