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惊恐障碍中对急性呼吸性碱中毒的过度代偿反应是由乳酸生成增加所致。

Exaggerated compensatory response to acute respiratory alkalosis in panic disorder is induced by increased lactic acid production.

作者信息

Ueda Yoshiyasu, Aizawa Masayo, Takahashi Atsushi, Fujii Masamitsu, Isaka Yoshitaka

机构信息

Department of Advanced Technology for Transplantation, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

出版信息

Nephrol Dial Transplant. 2009 Mar;24(3):825-8. doi: 10.1093/ndt/gfn585. Epub 2008 Oct 21.

DOI:10.1093/ndt/gfn585
PMID:18940883
Abstract

BACKGROUND

In acute respiratory alkalosis, the severity of alkalaemia is ameliorated by a decrease in plasma [HCO(3)(-)] of 0.2 mEq/L for each 1 mmHg decrease in PaCO(2). Although hyperventilation in panic disorder patients is frequently encountered in outpatients, the drop in plasma [HCO(3)(-)] sometimes surpasses the expectation calculated from the above formula. The quantitative relationship between reduced PaCO(2) and plasma [HCO(3)(-)] in acute respiratory alkalosis has not been studied in panic disorder patients. Our objective was to provide reference data for the compensatory metabolic changes in acute respiratory alkalosis in panic disorder patients.

METHODS

In 34 panic disorder patients with hyperventilation attacks, we measured arterial pH, PaCO(2), plasma [HCO(3)(-)] and lactate on arrival at the emergency room.

RESULTS

For each decrease of 1 mmHg in PaCO(2), plasma [HCO(3)(-)] decreased by 0.41 mEq/L. During hypocapnia, panic disorder patients exhibited larger increases in serum lactate levels (mean +/- SD; 2.59 +/- 1.50 mmol/L, range; 0.78-7.78 mmol/L) than previously reported in non-panic disorder subjects. Plasma lactate accumulation was correlated with PaCO(2) (P < 0.001).

CONCLUSIONS

These results suggest that the compensatory metabolic response to acute respiratory alkalosis is exaggerated by increased lactic acid production in panic disorder patients. Here, we call attention to the diagnosis of acid-base derangements by means of plasma [HCO(3)(-)] and lactate concentration in panic disorder patients.

摘要

背景

在急性呼吸性碱中毒中,动脉血二氧化碳分压(PaCO₂)每降低1 mmHg,血浆[HCO₃⁻]降低0.2 mEq/L,碱血症的严重程度随之改善。尽管惊恐障碍患者的过度通气在门诊患者中很常见,但血浆[HCO₃⁻]的下降有时超过根据上述公式计算的预期。急性呼吸性碱中毒时PaCO₂降低与血浆[HCO₃⁻]之间的定量关系在惊恐障碍患者中尚未得到研究。我们的目的是为惊恐障碍患者急性呼吸性碱中毒的代偿性代谢变化提供参考数据。

方法

对34例有过度通气发作的惊恐障碍患者,在急诊室就诊时测量动脉血pH、PaCO₂、血浆[HCO₃⁻]和乳酸水平。

结果

PaCO₂每降低1 mmHg,血浆[HCO₃⁻]降低0.41 mEq/L。在低碳酸血症期间,惊恐障碍患者血清乳酸水平的升高幅度(均值±标准差;2.59±1.50 mmol/L,范围;0.78 - 7.78 mmol/L)比之前报道的非惊恐障碍患者更大。血浆乳酸积累与PaCO₂相关(P < 0.001)。

结论

这些结果表明,惊恐障碍患者急性呼吸性碱中毒的代偿性代谢反应因乳酸生成增加而被夸大。在此,我们提请注意通过血浆[HCO₃⁻]和乳酸浓度对惊恐障碍患者酸碱紊乱进行诊断。

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