The majority of patients with respiratory failure seen in our institution developed it as part of multiple organ failure complicated by other organ failures such as renal or hepatic failure. The alleviation of pulmonary interstitial edema has been one of the most important therapeutic approaches since pulmonary edema is considered to be the main cause of impaired pulmonary function in patients with nultiple organ failure.
However, the treatment of interstitial edema is difficult especially when it is associated with renal failure. We applied continuous hemofiltration (CHF) or continuous hemodiafiltrayion (CHDF) in the treatment of 59 patients with respiratory failure complicated by renal failure between January 1988 and March 1993. We studied the changes in the levels of F_IO₂ and PEEP needed to obtain acceptable PaO₂ and cumulative water balance (CWB) levels following CHF/CHDF treatment for 3 consecutive days. The levels of F_IO₂ and PEEP decreased significantly as did the respiratory index following CHF/CHDF treatment, indicating an improvement in oxygenation. The average of CWB during the 3 days of the study period was 2282ml on negative balance. However, the CVP showed no significant changes, suggesting that CHF/CHDF can remove pulmonary interstitial edema without causing remarkable changes in the circulating blood volume. We conclude that CHF/CHDF is an effective method for reducing pulmonary edema in the treatment of the patients with simultaneous respiratory and renal failure.

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The relationships between the speed of deterioration in severe asthma attack and clinical characteristics as measured by arterial blood gas values, duration of mechanical ventilation needed, and course of peak inspiratory pressure (PIP) during mechanical ventilation were studied. Twenty-six patients with severe bronchial asthma who underwent mechanical ventilation were classified into 3 groups according to the time interval from the first symptoms of asthma attack to endotracheal intubation: rapid onset group-(ROG: n=9, <3hr), intermediate onset group-IOG (n=9, ≥3hr, but <24hr) and slow onset group-(SOG: n=8, ≥24hr). Mechanical ventilation was adapted in order to achieve optimal tidal volume, respiratory frequency, and inspiratory flow rate compatible with PIP 50cmH₂O or under. Sedatives (diazepam, midazolam) and muscle relaxants (pancuronium, vecuronium) were given intravenously while mechanical ventilation was performed.
ROG showed severe mixed acidosis with extreme hypercapnia (pH=7.01±0.17 (mean±SD), PaCO₂=106±31mmHg, BE=-8.9±7.6mEq·l^-1), high incidence of respiratory arrest, and deeply altered consciousness on admission. Blood gas values of ROG were significantly different from those of SOG (pH=7.23±0.10, PaCO₂=69±10mmHg, BE=-0.9±6.1mEq·l^-1: p<0.05). PIP at the start of mechanical ventilation was high (39±9cmH₂O), but between 30 minutes and 8 hours after the start of mechanical ventilation it suddenly dropped showing no further sign of increased airway responsiveness. One patient in ROG developed subcutaneous emphysema. ROG was characterized by rapid recovery with shorter duration of mechanical ventilation (10±8hr)than IOG (59±26hr) or SOG (63±29hr) (p<0.01).
IOG showed higher PIP at the start of mechanical ventilation than SOG (42±8cmH₂O versus 31±5cmH₂O: p<0.05) and needed prolonged ventilatory support due to long-standing high PIP and/or airway hyper-responsiveness. Three patients in IOG developed subcutaneous emphysema.
In contrast SOG did not show high PIP during mechanical ventilation, but needed prolonged ventilatory support because of a large amount of secretion in the airway and/or hypoxemia.
These findings indicate that there are significant differences in the clinical features and pathogenesis of airway narrowing between the 3 groups, and ROG and IOG have a higher incidence of pulmonary barotrauma due to severe airway narrowing during mechanical ventilation.

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We measured serial changes in myosin light chain-I (MLC-I) in 19 patients undergoing coronary recanalization for evolving myocardial infarction to elucidate whether analysis of MLC-I release kinetics is useful for the evaluation of myocardial salvage following coronary recanalization therapy.
All patients had a left anterior descending artery lesion (#6 or #7 according to the American Heart Association classification) in the infarction related artery, and received intravenous or intracoronary administration of tissue plasminogen activator or urokinase within 6 hours after the onset except for 3 cases with spontaneous recanalization and 2 cases with direct percutaneus transluminal coronary angioplasty (PTCA). Six control patients with left anterior descending artery lesions in the infarction related artery were given conventional therapy using intravenous urokinase without emergent coronary angiography.
The release kinetics of MLC-I following coronary recanalization therapy were divided into three patterns. Group A (n=7) showed two peaks with a larger first peak and a smaller second peak. Group B (n=5) showed two peaks with a smaller first peak and a larger second peak. Group C (n=7) showed a single late peak pattern of MLC-I release kinetics. The time need to obtain recanalization on coronary angiography was significantly longer in Group A compared to Groups B and C (5.72±1.11, n=6 vs 3.84+0.80 hours n=6, p<0.05). The left ventricular ejection fraction (LVEF) at the convalescent stage in Group A was significantly lower than that in Groups B and C (44.4+13 vs 62.0+15.0%, p<0.05).
Patients showing a two-peaked pattern with a larger first peak were consistent with patients with late repertused, less salvaged, and more depressed left ventricular function at the convalescent stage. MLC-I release kinetics were influenced by the wash-out phenomenon in cases of late reperfusion.

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The present study was undertaken to investigate hepatocellular and systemic energy metabolism in critically ill patients with liver failure. The arterial ketone body ratio (AKBR), total ketone bodies, pyruvate/lactate, energy expenditure and respiratory quotient were measured in 43 patients with septic hepatic faliure, 16 patients with acute type fulminant hepatitis and 13 patients with subacute type fulminant hepatitis who were treated in the ICU. The results showed that deterioration of metabolism developed in both the liver and the whole body in septic hepatic failure and that metabolic derangement took place only within the liver in fulminant hepatitis. Hepatocellular metabolic dysfunction developed diffusely in the whole liver in acute type fulminant hepatitis, but only in parts of the liver in subacute type fulminant hepatitis. The main energy substrate in septic hepatic failure was fat and in fulminant hepatitis was glucose.
These results suggest that critically ill patients with hepatic failure present a variety of symptoms and metabolic changes and that it is of the utmost importance to measure various metabolic parameters to establish nutritional support based on each patients metabolic changes.

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The effect of changes in position (supine to lateral) on the hemodynamics of patients with acute myocardial infarction (AMI) during the acute phase were observed.
Blood pressure and heart rate were measured automatically with blood pressure and heart rate monitors in 61 patients with AMI. Measurements were taken during each of three positions; supine, right lateral and left lateral, every 5 minutes. The measurements were carried out from 0.6 to 55 hours (mean 17.0) after CCU admission.
Pressure-rate product (PRP) and systolic blood pressure (sBP) did not change significantly in the three positions. However, sBP decreased by more than 15% in 6 patients. This was considered due to hemodynamic instability from neurohumoral dysregulation. In addition, 78.7% of patients complained of lumbago in the supine position.
These results suggest that nurses may safely change the postures of patients from supine to laleral to alleviate the patient's back pain, during the acute phase. However, care must be taken for the serious decrease in sBP in the lateral position.

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A case of pseudohypoxemia due to acute leukemia is reported. A male patient was admitted with severe anemia and was diagnosed as having both myelodysplastic syndrome and left renal cancer. Respiratory failure occurred after renal tumor resection and led to disturbance of consciousness. After intubation, his consciousness became clear and a pulsoximeter indicated 98% O₂ saturation. However, blood gas analysis at that time showed a PaO₂ 41mmHg and SaO₂ 79%.
Acute leukemia secondary to myelodysplastic syndrome was diagnosed because his white blood cell count was 257×10³·mm^-3. The partial oxygen pressure of arterial blood kept at room temperature was 103mmHg just after sampling and decreased to 85mmHg after 2 minutes, 69mmHg after 5 minutes, 52mmHg after 10 minutes, and 36mmHg after 30 minutes. When the white blood cell count decreased to less than 37×10³·mm^-3 during chemotherapy, a decay in oxygen tension was not observed. Thus, extreme leukocytosis secondary to leukemia can cause spurious hypoxemia. Special attention must be paid to blood gas analysis in patients with leukemia.

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