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患者は26歳,女性.2001年1月7日,過換気発作にて入院した.発作中の動脈血ガス分析ではpH7.536,HCO3—35.7mEq/l,Base excess+12.9mEq/lと代謝性アルカローシスを示し,PCO2は42.2mmHgと正CO2血症を示した.発作消失後にPCO2、は60.9mmHgと著明な高CO2血症を示した.入院前に嘔吐が持続していたこと,入院時に脱水と低K・低Cl血症を認めたことから,胃液喪失による代謝性アルカローシスと代償性高CO2血症と診断した.胃内視鏡と胃透視の結果,潰瘍に伴う幽門狭窄を認め,持続する嘔吐の原因と考えられた.生食+KClの点滴と抗潰瘍剤の内服で約10日後にpH7.388,PCO242.0mmHg,HCO3—25.3mEq/l,BaSe excess+0.7mEq/lとすべて正常化した.代謝性アルカローシスのうえに過換気発作を併発した稀な症例であり,入院時の正CO2血症は代償性高CO2血症が過換気により一過性に偽正常化したものと考えられた.
A 26-year-old woman was admitted because of hyperventilation attack. Arterial blood gas analyses revealed metabolic alkalosis (pH 7.536. HCO3- 35.7mEq/l, Base excess +12.9mEq/l) with normocapnia (PCO2 42.2 mmHg) during attack and marked hypercapnia (PCO2 60.9mmHg) after attack. Based on the persistence of vomiting before admission and laboratory data on admission (dehydration, hypokalemia and hypochloremia), metabolic alkalosis due to gastric juice losses and compensatory hypercapnia were diagnosed. Gastroscopy and gastography revealed pyloric stenosis with ulcers, which was the cause of the vomiting. Arterial blood gas analysis findings were normalized (pH 7.388, PCO2 42.0mmHg, HCO3- 25.3mEq/l, Base excess +0.7 mEq/l) ten days after admission by intravenous infusion of saline plus KCI and oral administration of antiulcer drugs. This is a rare case of metabolic alkalosis associated with hyperventilation attack, and compensatory hypercapnia is thought to have been transiently pseudonormalized by hyperventilation to normocapnia on admission.
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