Nizet Tessa A C, Heijdra Yvonne F, van den Elshout Frank J J, van de Ven Marjo J T, Bosch Frank H, Mulder Paul H, Folgering Hans Th M
Department of Pulmonary, Rijnstate Hospital Arnhem, Arnhem, The Netherlands.
Clin Physiol Funct Imaging. 2009 Nov;29(6):392-9. doi: 10.1111/j.1475-097X.2009.00878.x. Epub 2009 Jul 10.
Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO(2)). Acute metabolic acidosis was induced by administration of ammonium chloride (NH(4)Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33.2 +/- 11.5 years; FEV(1) 108.3 +/- 16.2% predicted), 14 asthma patients (5 male; age 48.1 +/- 16.1 years; FEV(1) 101.6 +/- 15.3% predicted), and 15 moderate to severe COPD patients (9 male; age 62.8 +/- 6.8 years; FEV(1) 50.0 +/- 11.8% predicted). An acute metabolic acidemia of BE -3.1 mmol x L(-1) was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference -0.1 kPa x sec x L(-1) [95%-CI: -0.1 - -0.02]. In COPD patients PaCO(2) was significantly lowered during metabolic acidemia (mean difference -1.73 mmHg [-3.0 - -0.08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure.
哮喘和慢性阻塞性肺疾病(COPD)中的呼吸肌疲劳会导致伴有高碳酸血症的呼吸衰竭,进而引发呼吸性酸中毒。急性代谢性酸中毒的治疗性诱导会进一步增加呼吸驱动力,因此可能减轻通气衰竭和高碳酸血症。另一方面,已知急性代谢性酸中毒也会对(呼吸)肌功能产生负面影响,因此可能导致呼吸衰竭恶化。此外,我们推断,由于呼吸肌功能已经受损,与哮喘患者和健康受试者相比,代谢性酸中毒对COPD患者呼吸肌力量和呼吸肌耐力的影响可能更明显。在本研究中,研究了代谢性酸中毒对周围肌肉力量、周围肌肉耐力、气道阻力和动脉二氧化碳张力(PaCO₂)的影响。通过给予氯化铵(NH₄Cl)诱导急性代谢性酸中毒。研究了代谢性酸中毒对吸气和呼气肌力量以及呼吸肌耐力的影响。在15名健康受试者(4名男性;年龄33.2±11.5岁;FEV₁为预测值的108.3±16.2%)、14名哮喘患者(5名男性;年龄48.1±16.1岁;FEV₁为预测值的101.6±15.3%)和15名中度至重度COPD患者(9名男性;年龄62.8±6.8岁;FEV₁为预测值的50.0±11.8%)中,采用随机、安慰剂对照的交叉设计进行了研究。诱导出了碱剩余为-3.1 mmol·L⁻¹的急性代谢性酸血症。急性代谢性酸血症分别未显著影响呼吸肌和周围肌肉的力量或耐力。在所有受试者中,代谢性酸血症诱导后气道阻力显著降低(平均差值-0.1 kPa·sec·L⁻¹ [95%可信区间:-0.1 - -0.02])。在COPD患者中,代谢性酸血症期间PaCO₂显著降低(平均差值-