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Byline: V. Sramek (1), I. Novak (1), M. MatAjovic (1), R. Rokyta (1), M. Nalos (1), P. Hora (1), H. Pittrova (1) Keywords: Citrate anticoagulation; Hemofiltration; Hypercalcemia; Thrombocytopenia; Multiple myeloma; Acute renal failure Abstract: A 72-year-old patient with multiple myeloma was admitted to the intensive care unit because of hypercalcemic crisis and acute renal failure. After 7 days of comprehensive therapy including diuretics, steroids, calcitonin, and intermittent hemodialysis (IHD) with low-calcium dialysate, calcium still reached high levels between IHD treatments and thrombocytopenia developed after chemotherapy. CWHDF with calcium-free bicarbonate dialysate was started. Anticoagulation with 2.2 % citrate was performed in order to chelate calcium, and thus treat the hypercalcemia, and to provide regional anticoagulation, and thus reduce the risk of bleeding due to thrombocytopenia. CWHDF with citrate anticoagulation was continued for 6 days, and standard heparin anticoagulation was started when the hypercalcemia and thrombocytopenia abated. Author Affiliation: (1) ICU, Medical Department I, Charles University Hospital Plzen, Alej Svobody 80, 30460, Plzen, Czech Republic Article History: Registration Date: 23/03/2009 Received Date: 03/07/1997 Accepted Date: 04/12/1997

Byline: R. Rokyta (1), I. Novak (1), M. Matejovic (1), V. Sramek (1), P. Hora (1), P. Jindra (2) Author Affiliation: (1) Intensive Care Unit, Department of Internal Medicine I, Charles University Hospital Plzen, Alej Svobody 80, Lochotin, 304 60 Plzen, Czech Republic (2) Department of Hematology and Oncology, Charles University Hospital, Plzen, Czech Republic Article History: Accepted Date: 24/08/2000 Article note: Electronic Publication

Background: Respiratory induced heart rate variability (rHRV) was analysed in mechanically ventilated patients during two levels of sedation and brain death. Our aim was to determine whether rHRV can distinguish between different levels of sedation and especially between brain death and sedated patients., Methods: In this study 30 critically ill and 23 brain death patients were included and four respiratory rates of 15, 12, 8 and 6 breaths per minute, each lasting 5 min were used. Two sedation levels, basal and deep, were performed in the critically ill patients. Heart rate and blood pressure changes induced by ventilation were subsequently detected and analysed., Results: Significant differences were found in rHRV and rHRV adjusted for tidal volume (rHRV/VT) between critically ill and brain death patients during slow breathing at 6 or 8 breaths per minute. The rHRV at 6 breaths per minute was below 15 ms in all brain death subjects except one. The rHRV/VT was lower than 25 ms/l at both 6 and 8 breaths per minute in all brain death patients and simultaneously at 75% of non-brain death patients was higher (specificity 1, sensitivity 0.24). Differences in rHRV and rHRV/VTs between basal and deep sedation were not significant., Conclusions: The main clinical benefit of the study is the finding that rHRV and rHRV/VT during 6 and 8 breaths per minute can differentiate between critically ill and brain death patients. An rHRV/VT exceeding 25 ms/l reliably excludes brain death.

The effect of exercise on gastric mucosal energy status has not been fully elucidated. The aim of this study was to evaluate the impact of submaximal cycling on gastric mucosal energy balance and its relationship to changes in systemic energy status. Ten healthy volunteers (age 20-40 years) were investigated at rest (BL), during 30 min of submaximal exercise (E) on bicycle ergometry and during the 30 min after the completion of cycling. Gastric mucosal PCO(2) ( P(gm)CO(2)) was measured by air tonometry at 10-min intervals and the gastric mucosal-arterial PCO(2) difference ( PCO(2)gap) was calculated. Hemodynamics, arterial blood gases, lactate and pyruvate were also measured. PCO(2)gap significantly increased throughout exercise [BL: 0.2 kPa (median), -0.1-0.6 kPa (25th-75th percentiles); E(10 min): 1.0 kPa, 0.8-1.7 kPa; E(20 min): 1.35 kPa, 0.8-1.8 kPa; E(30 min): 1.5 kPa, 0.9-2.0 kPa]. The early changes in PCO(2)gap ( PCO(2)gap at E(10 min) minus PCO(2)gap at BL) correlated significantly and positively with corresponding changes in arterial lactate ( r(2)=0.58, P<0.05) and lactate-to-pyruvate ratio ( r(2)=0.72, P<0.05). On recovery, all metabolic parameters normalized within 30 min. We conclude that submaximal cycling in volunteers leads to the early derangement of gastric mucosal energy balance. The time course of PCO(2)gap parallels changes in systemic energy status.