Lavie C J, Crocker E F, Key K J, Ferguson T G
South Med J. 1986 Oct;79(10):1296-9. doi: 10.1097/00007611-198610000-00025.
In metabolic alkalosis, a compensatory decrease in alveolar ventilation with hypercapnia has been noted only rarely. We recently managed a patient with gastric outlet obstruction from a duodenal ulcer who survived after arriving in the emergency room comatose with severe hypochloremic metabolic alkalosis, compensatory hypoventilation, and hypercapnia. We know of no report in the English literature of a patient with gastric outlet obstruction having a respiratory acidosis or hypochloremia as severe as that in our patient. Proper understanding of the pathophysiology of primary metabolic alkalosis due to gastric losses is necessary to correct the acid-base abnormalities quickly and to restore normal alveolar ventilation.
在代谢性碱中毒中，伴有高碳酸血症的肺泡通气代偿性降低情况极为罕见。我们最近治疗了一名因十二指肠溃疡导致胃出口梗阻的患者，该患者在进入急诊室时处于昏迷状态，伴有严重的低氯性代谢性碱中毒、代偿性通气不足和高碳酸血症，最终存活下来。据我们所知，英文文献中尚无胃出口梗阻患者出现像我们患者那样严重的呼吸性酸中毒或低氯血症的报道。正确理解因胃失液导致的原发性代谢性碱中毒的病理生理学，对于迅速纠正酸碱异常和恢复正常肺泡通气至关重要。
