Montes de Oca M, Celli B R
Pulmonary Division, Hospital Universitario de Caracas, Universidad Central de Venezuela.
Eur Respir J. 1998 Sep;12(3):666-71. doi: 10.1183/09031936.98.12030666.
The resting mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) and minute ventilation (V'E) and their response to CO2 in patients with chronic obstructive pulmonary disease (COPD) remain controversial. The ventilatory drive and the factors that predict resting arterial CO2 tension (Pa,CO2) were studied in 19 eucapnic and 14 hypercapnic severe COPD patients, and 20 controls. The CO2 response was evaluated by the Read technique. The V'E, and P0.1 as a function of end-tidal CO2 tension (Pet,CO2) was used to study the ventilatory (deltaV'E/deltaPet,CO2) and P0.1 response (deltaP0.1/deltaPet,CO2). In the patients, respiratory muscle function and pleural occlusion pressure 0.1 s after onset of inspiration (Ppl,0.1) were evaluated with simultaneous measurement of pleural (Ppl) and gastric (Pga) pressures. Hypercapnic patients had lower forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and arterial O2 tension (Pa,O2). Resting P0.1 was higher in patients than in controls, whereas deltaP0.1/deltaPet,CO2 was similar in the three groups. There was no difference in resting P0.1 (3.6+/-2.0 versus 4.3+/-2.8 kPa (2.7+/-1.5 versus 3.2+/-2.1 cmH2O), p=0.2) and Ppl,0.1 (1.4+/-2.3 versus 5.2+/-3.3 kPa (4.08+/-1.7 versus 3.9+/-2.5 cmH2O), p=0.22) between eucapnic and hypercapnic COPD, whereas deltaV'E/deltaPet,CO2 was lower in the hypercapnic group (0.29+/-0.24 versus 0.66+/-0.5 L x min(-1) x kPa, p<0.001). By logistic regression only FEVI and increased diaphragmatic load, and not respiratory drive, predicted resting Pa,CO2. Irrespective of CO2 level, baseline central drive (represented by the mouth occlusion and pleural pressures) and CO2 response are preserved in most patients with severe chronic obstructive pulmonary disease. Effective ventilation is inadequate in the more severely obstructed patients and this results in hypercapnia. Neuroventilatory coupling failure is an attractive explanation for chronic hypercapnia in these patients.
慢性阻塞性肺疾病(COPD)患者吸气开始后0.1秒时的静息口腔闭塞压(P0.1)、分钟通气量(V'E)及其对二氧化碳的反应仍存在争议。对19例正常二氧化碳血症和14例高碳酸血症的重度COPD患者以及20名对照组进行了通气驱动和预测静息动脉血二氧化碳分压(Pa,CO2)的因素研究。采用Read技术评估二氧化碳反应。用V'E以及作为呼气末二氧化碳分压(Pet,CO2)函数的P0.1来研究通气反应(deltaV'E/deltaPet,CO2)和P0.1反应(deltaP0.1/deltaPet,CO2)。在患者中,通过同时测量胸膜压(Ppl)和胃内压(Pga)来评估呼吸肌功能以及吸气开始后0.1秒时的胸膜闭塞压(Ppl,0.1)。高碳酸血症患者的用力肺活量(FVC)、一秒用力呼气容积(FEV1)和动脉血氧分压(Pa,O2)较低。患者的静息P0.1高于对照组,而三组的deltaP0.1/deltaPet,CO2相似。正常二氧化碳血症和高碳酸血症的COPD患者在静息P0.1(3.6±2.0与4.3±2.8 kPa(2.7±1.5与3.2±2.1 cmH2O),p = 0.2)和Ppl,0.1(1.4±2.3与5.2±3.3 kPa(4.08±1.7与3.9±2.5 cmH2O),p = 0.22)方面无差异,而高碳酸血症组的deltaV'E/deltaPet,CO2较低(0.29±0.24与0.66±0.5 L·min⁻¹·kPa,p < 0.001)。通过逻辑回归分析,只有FEV1和膈肌负荷增加而非呼吸驱动可预测静息Pa,CO2。无论二氧化碳水平如何,大多数重度慢性阻塞性肺疾病患者的基线中枢驱动(以口腔闭塞压和胸膜压表示)和二氧化碳反应均得以保留。在阻塞更严重的患者中有效通气不足,这导致了高碳酸血症。神经通气耦联衰竭是这些患者慢性高碳酸血症的一个有吸引力的解释。