Inoue Fumiya, Okazaki Yuji, Ichiba Toshihisa, Chiba Takuyo, Namera Akira
Department of Emergency Medicine, Hiroshima City Hiroshima Citizens Hospital, Hiroshima, JPN.
Department of Emergency Medicine, International University of Health and Welfare, Chiba, JPN.
Cureus. 2025 Jun 9;17(6):e85591. doi: 10.7759/cureus.85591. eCollection 2025 Jun.
Respiratory alkalosis due to hyperventilation is a common acid-base disturbance in emergency care settings. While often linked to anxiety or panic attacks, drug-induced causes must also be considered. Caffeine, a widely consumed methylxanthine, is known to induce respiratory alkalosis due to tachypnea in severe overdoses. However, the effects of caffeine at subtoxic serum concentrations are not well characterized, and the possibility of caffeine-induced respiratory alkalosis in the absence of tachypnea is not usually recognized. A 47-year-old underweight female patient with a history of depression presented with general weakness. Her vital signs were stable, and her respiratory rate was 15 breaths per minute. Physical examination revealed carpopedal spasms and extremity weakness. Laboratory tests showed hypokalemia and a venous blood gas with a pH of 7.57 and partial pressure of carbon dioxide (pCO₂) of 27.4 mmHg, consistent with respiratory alkalosis. Despite intravenous electrolyte replacement, respiratory alkalosis persisted for over 20 hours without evidence of tachypnea. Serum caffeine concentration measured by liquid chromatography-mass spectrometry was 13.6 µg/mL at admission and 6.6 µg/mL at 36 hours post-presentation. No other toxic agents were detected. She recovered with supportive care 36 hours after admission. The final diagnosis was caffeine-induced respiratory alkalosis, occurring in the absence of tachypnea and at subtoxic serum caffeine concentrations. This case illustrates that caffeine can provoke respiratory alkalosis through increased tidal volume, even at subtoxic serum concentrations and in the absence of tachypnea. Clinicians should consider caffeine toxicity in the differential diagnosis of unexplained respiratory alkalosis and obtain a detailed history, including dietary and supplement use.
因过度通气导致的呼吸性碱中毒是急诊护理中常见的酸碱平衡紊乱。虽然它常与焦虑或惊恐发作有关,但也必须考虑药物诱发因素。咖啡因是一种广泛食用的甲基黄嘌呤,已知在严重过量摄入时会因呼吸急促导致呼吸性碱中毒。然而,咖啡因在亚中毒血清浓度下的影响尚未得到充分表征,而且在没有呼吸急促的情况下咖啡因诱发呼吸性碱中毒的可能性通常未被认识到。一名47岁体重过轻、有抑郁症病史的女性患者出现全身无力。她的生命体征稳定,呼吸频率为每分钟15次。体格检查发现手足搐搦和肢体无力。实验室检查显示低钾血症,静脉血气分析显示pH值为7.57,二氧化碳分压(pCO₂)为27.4 mmHg,符合呼吸性碱中毒。尽管进行了静脉电解质补充,但呼吸性碱中毒持续了20多个小时,且没有呼吸急促的迹象。入院时通过液相色谱 - 质谱法测得的血清咖啡因浓度为13.6 µg/mL,就诊后36小时为6.6 µg/mL。未检测到其他有毒物质。入院36小时后,她通过支持性治疗康复。最终诊断为咖啡因诱发的呼吸性碱中毒,发生在没有呼吸急促且血清咖啡因浓度处于亚中毒水平的情况下。该病例表明,即使在亚中毒血清浓度且没有呼吸急促的情况下,咖啡因也可通过增加潮气量引发呼吸性碱中毒。临床医生在不明原因呼吸性碱中毒的鉴别诊断中应考虑咖啡因中毒,并获取详细病史,包括饮食和补充剂使用情况。