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二氧化碳诱发惊恐:非心源性胸痛患者的症状及测压评估

CO2 provocation of panic: symptomatic and manometric evaluation in patients with noncardiac chest pain.

作者信息

Stollman N H, Bierman P S, Ribeiro A, Rogers A I

机构信息

University of Miami School of Medicine and Veterans Administration Medical Center, Florida, USA.

出版信息

Am J Gastroenterol. 1997 May;92(5):839-42.

PMID:9149197
Abstract

OBJECTIVES

Occult panic disorder (PD) may underlie 10-43% of chest pain syndromes in patients with normal coronary arteries. A variety of agents, such as intravenous lactate, oral caffeine, and inhaled CO2, has been identified that may provoke panic attacks in susceptible patients. The aims of this study were (1) to better define the relationship between noncardiac chest pain syndromes and panic disorder; and (2) to assess the diagnostic utility of PD provocative testing with inhaled CO2 in eliciting chest pain and/or esophageal manometric disturbances.

METHODS

Fourteen patients with chest pain syndromes and negative coronary angiograms or stress thallium tests were evaluated for PD and underwent (1) standard esophageal manometry followed by continuous manometric recording; (2) inhalation by face mask of room air or 35% CO2, single blinded, in random order; (3) a previously validated Acute Panic Inventory questionnaire administered before and immediately after each inhalation; and (4) Tensilon 10 mg i.v. administration.

RESULTS

Of 14 patients, 8 met DSM-IIIR criteria for panic disorder. Mean Acute Panic Inventory scores (reflecting panic symptoms) increased significantly after CO2 inhalation relative to room air in all patients. Of 14 patients, 8 (4 PD, 4 non-PD) experienced chest pain after CO2 inhalation, whereas no patient had chest pain after room air inhalation. Of 14 patients, 5 had pain with Tensilon (4 of 5 whom responded to CO2). No specific manometric abnormalities occurred during any chest pain episode.

CONCLUSION

CO2 inhalation is as effective as Tensilon in provoking chest pain in patients with noncardiac chest pain. The high prevalence of PD in such patients suggests that CO2 inhalation, a known panicogen, may be useful in evaluating such patients. The mechanism of CO2 induced chest pain remains unknown, but does not appear to be attributable to demonstrable esophageal motility abnormalities.

摘要

目的

隐匿性惊恐障碍(PD)可能是冠状动脉正常的患者中10% - 43%胸痛综合征的潜在病因。已确定多种药物,如静脉注射乳酸盐、口服咖啡因和吸入二氧化碳,可能会诱发易感患者的惊恐发作。本研究的目的是:(1)更好地界定非心源性胸痛综合征与惊恐障碍之间的关系;(2)评估吸入二氧化碳进行PD激发试验在引发胸痛和/或食管测压异常方面的诊断效用。

方法

对14例胸痛综合征且冠状动脉造影或运动铊试验阴性的患者进行PD评估,并接受以下检查:(1)标准食管测压,随后进行连续测压记录;(2)通过面罩以随机顺序单盲吸入室内空气或35%二氧化碳;(3)在每次吸入前和吸入后立即进行一份先前验证过的急性惊恐量表问卷调查;(4)静脉注射10毫克腾喜龙。

结果

14例患者中,8例符合DSM-IIIR惊恐障碍标准。相对于吸入室内空气,所有患者吸入二氧化碳后急性惊恐量表平均得分(反映惊恐症状)显著增加。14例患者中,8例(4例PD患者,4例非PD患者)吸入二氧化碳后出现胸痛,而吸入室内空气后无患者出现胸痛。14例患者中,5例注射腾喜龙后出现疼痛(其中5例中有4例对二氧化碳有反应)。在任何胸痛发作期间均未出现特定的测压异常。

结论

吸入二氧化碳在诱发非心源性胸痛患者胸痛方面与腾喜龙一样有效。此类患者中PD的高患病率表明,已知的致惊恐剂吸入二氧化碳可能有助于评估此类患者。二氧化碳诱发胸痛的机制尚不清楚,但似乎不归因于可证实的食管动力异常。

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