A new approach to acid-base physiology, presented by Peter A. Stewart, is now accepted not only in experimental but also in some clinical situations. In his approach, changes in hydrogen ion concentration occur in consequence of water dissociation. Furthermore, hydrogen ion concentration is determined by three independent variables: PaCO₂, strong ion difference (SID), and total weak acid. Neither bicarbonate nor hydrogen ion are independent, rather they are controlled by the independent variables. Albumin can work as an acidifying factor, and chloride ion, by changing SID, can play an important role in acid-base balance. Stewart approach can precisely explain “dilution acidosis” and “metabolic acidosis induced by cardiopulmonary bypass” which are hardly explicated with the old method. We believe that Stewart approach helps us to understand complex acid-base physiology.

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BACKGROUND/PURPOSE: We conducted this study as part of the development of CNS-FACE (Coping & Needs Scale for Family Assessment in critical and emergency care settings), which has been designed as a family assessment tool for critical and emergency care settings, and is intended for standard utilization in Japan. The purpose of this study was to develop a complete version of CNS-FACE based on the existing, provisional version of CNS-FACE. METHODS: We studied 274 family members of 248 patients who were hospitalized at emergency/critical care centers, ICUs or CCUs of 9 university and public hospitals. We gathered data using a behavior-evaluation scale consisting of the 53 items of the provisional version of CNS-FACE. Evaluation of response distribution with regard to each item, exploratory-factor analysis, multitrait scaling analysis, G-P analysis, and confirmatory-factor analysis to evaluate needs and coping were performed for data analysis. RESULTS: We developed a complete version of CNS-FACE that contains a behavior-evaluation scale of 46 items. In addition, construct validity was observed with regard to needs and coping.

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We present a rare, nonpenetrating aortic valve injury after blunt chest trauma. A 53-year-old man on a bike collided with a truck and suffered bilateral hemopneumothrax, lung contusions and multiple rib fractures in the chest and many other traumas. Diastolic murmur was recognized with developing heart failure on the 18th day after the accident. An transthoracic echocardiography revealed severe aortic valve regurgitation without left ventricular dilatation and as infectious endocarditis was ruled out by transesophageal echocardiography, blood culture and chest CT, therefore we diagnosed it as a nonpenetrating aortic valve injury with acute onset regurgitation caused by blunt impact. Aortic valve was replaced on the 119th day. Inspection during the surgery made it apparent that the commissure between the non-coronary cusp leaflet and the left coronary cusp leaflet was detached from the aortic wall and neither tear nor avulsion existed in any one of the three cusp leaflets, which was comfirmed by histological examination. To our knowledge, aortic valve injury of this kind has never been reported.
The patient's postoperative course was uneventful and he discharged on the 140th day after the accident.

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In treatment of severely ill asthmatic patients, initial multimodal treatments are inevitable to avoid fatal outcome. We report two severe asthmatic patients who did not respond to inhaled β₂ agonists, but were treated successfully with intravenous isoproterenol and magnesium sulfate. Maximal infusion rate of isoproterenol was 0.16-0.36μg·kg^-1·min^-1, and maximal arterial concentration of ionized magnesium was 0.48-0.83 mmol·l-1. Any signs and symptoms of cardiac ischemia, or muscle weakness were not observed. Magnesium has cardioprotective effects and augments bronchodilation by β₂ agonists in patients with severe, but not mild to moderate, asthma. Intravenous administration of isoproterenol combined with magnesium sulfate would be more effective and safe for the treatment of severe asthma refractory to conventional regimens.

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A 59-year-old man who had undergone cadaveric renal transplantation received immunosuppression therapy with azathiopurine, predonisolone, and tacrolimus for 9 months. The patient complained of dry cough and dyspnea with fever when he saw a doctor and he was hospitalized after wasting one week. A computed tomography showed mild interstitial pneumonia. The patient was tentatively diagnosed as opportunistic infection in a compromized host and treated in empirical way, but he died 4 weeks after admission without any response to our treatment. All of the laboratory tests and pathological findings could not indicate the evidence of any opportunistic infections in the lungs. Azathioprine-induced interstitial pneumonia was a rare complication but a total dose of azathioprine of our patient (15, 750mg) was as much enough as to induce interstitial pneumonia and histologocal findings in autopsy specimen that were usual interstitial pneumonia and diffuse alveolar damage strongly suggested the toxic effects of azathioprine. On the management of respiratory failure in an immunosuppressed host, we should keep in mind azathioprine-induced interstitial pneumonia as well as opportunistic infections.

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A 52-year-old woman, whose blood type was O+, underwent ABO-incompatible living renal transplantation from her AB+ husband. We performed plasma exchange (PE) for three times before transplantation to remove anti-A and anti-B antibodies. The serum anti-A IgG/IgM titers were ×1/×16 and anti-B IgG/IgM titers were ×1/×4, respectively. Tacrolimus, methylprednisolone, antilymphocyte immunoglobulin, deoxyspergualin and mycophenolate mofetil were administered in perioperative period. The function of transplant kidney deteriorated in the first postoperative day despite good urination immediately after the surgery. We diagnosed it as vascular rejection from clinical manifestations (not proven by biopsy) and introduced PE without delay to remove the anti-A and anti-B antibodies. A total of eight PEs in the postoperative period improved kidney function and successfully suppressed antibody titers. The patient was discharged from the ICU on the 13th postoperative day. As a conclusion PE should be performed aggressively when vascular rejection is suspected.

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A 43-year-old man was admitted to our hospital for complete atrioventricular block. Temporary ventricular pacing worked optimally. Transthoracic echocardiography revealed diffuse hypokinesis of left ventricular wall. Calculated left ventricular ejection fraction was 0.28 and measured cardiac index was 2.0l·min^-1·m^-2. The patient was found to have ALT of 9350 IU·l^-1, arterial ketone body ratio of 0.61 and hepaplastin test of 27%. The working diagnosis was acute fulminant myocarditis accompanied by severe hepatic dysfunction. Because the patient's hemodynamics did not improve in response to administration of catecholamines and cardiac index decreased to 1.7l·min^-1·m^-2, percutaneous cardiopulmonary support system (PCPS) and intraaortic balloon pumping (IABP) were induced to treat circulatory insufficiency 12h after admission. Following arrival at the ICU, the patient's trachea was intubated. Plasma exchange combined with continuous hemodiafiltration was induced to treat hepatic and renal dysfunction. On the fifth day, PCPS was successfully discontinued. On the seventh day, IABP catheter was surgically removed and the patient's trachea was successfully extubated. The patient was discharged from hospital three months later. Clinical features and findings of right ventricular endomyocardial biopsy demonstrated acute fulminant myocarditis. We believe that ischemic hepatic injury may play, an important role in the development of severe hepatic dysfunction. We recommend that mechanical circulatory support system should be immediately induced to improve hepatic circulation when patients with acute fulminant myocarditis result in severe hepatic dysfunction.

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