Worthley L I
Arch Surg. 1986 Oct;121(10):1195-8. doi: 10.1001/archsurg.1986.01400100107020.
During a seven-year period, 15 patients admitted to an intensive care unit with a metabolic alkalosis resistant to saline and potassium chloride infusions and with an arterial pH of greater than 7.44 and arterial carbon dioxide pressure (PaCO2) of greater than 50 mm Hg, while breathing spontaneously, were given hydrochloric acid at 200 mmol/24 h through a central venous line until the arterial pH had decreased to less than 7.36 or PaCO2 had decreased to less than 40 mm Hg. Five patients without respiratory failure had a significant decrease in PaCO2, pH, bicarbonate Ion (HCO3-), and base excess (BE). Four patients with acute respiratory failure had a significant decrease in PaCO2, HCO3-, and BE and an increase in arterial oxygen pressure, indicating that in both of these patient groups alveolar ventilation had improved. Six patients with chronic respiratory failure had a significant decrease in pH, HCO3-, and BE, although there was no significant change in PaCO2, indicating that in this patient group alveolar ventilation could not be consistently increased in response to a reduction in arterial pH.
在七年期间,15名入住重症监护病房的患者,存在对输注生理盐水和氯化钾抵抗的代谢性碱中毒,动脉血pH大于7.44,动脉二氧化碳分压(PaCO2)大于50 mmHg,在自主呼吸时,通过中心静脉导管以200 mmol/24小时的剂量给予盐酸,直至动脉血pH降至小于7.36或PaCO2降至小于40 mmHg。5名无呼吸衰竭的患者的PaCO2、pH、碳酸氢根离子(HCO3-)和碱剩余(BE)显著降低。4名急性呼吸衰竭患者的PaCO2、HCO3-和BE显著降低,动脉血氧分压升高,表明这两组患者的肺泡通气均有所改善。6名慢性呼吸衰竭患者的pH、HCO3-和BE显著降低,尽管PaCO2无显著变化,表明该组患者不能因动脉血pH降低而持续增加肺泡通气。