Gorini M, Misuri G, Corrado A, Duranti R, Iandelli I, De Paola E, Scano G
Unità di Terapia Intensiva Polmonare e Fisiopatologia Toracica, Ospedale di Careggi, Firenze, Italy.
Thorax. 1996 Jul;51(7):677-83. doi: 10.1136/thx.51.7.677.
The factors leading to chronic hypercapnia and rapid shallow breathing in patients with severe chronic obstructive pulmonary disease (COPD) are not completely understood. In this study the interrelations between chronic carbon dioxide retention, breathing pattern, dyspnoea, and the pressure required for breathing relative to inspiratory muscle strength in stable COPD patients with severe airflow obstruction were studied.
Thirty patients with COPD in a clinically stable condition with forced expiratory volume in one second (FEV1) of < 1 litre were studied. In each patient the following parameters were assessed: (1) dyspnoea scale rating, (2) inspiratory muscle strength by measuring minimal pleural pressure (PPLmin), and (3) tidal volume (VT), flow, pleural pressure swing (PPLsw), total lung resistance (RL), dynamic lung elastance (ELdyn), and positive end expiratory alveolar pressure (PEEPi) during resting breathing.
Arterial carbon dioxide tension (PaCO2) related directly to RL/PPLmin, and ELdyn/PPLmin, and inversely to VT and PPLmin. There was no relationship between PaCO2 and functional residual capacity (FRC), total lung capacity (TLC), or minute ventilation. PEEPi was similar in eucapnic and hypercapnic patients. Expressing PaCO2 as a combined function of VT and PPLmin (stepwise multiple regression analysis) explained 71% of the variance in PaCO2. Tidal volume was directly related to inspiratory time (TI), and TI was inversely related to the pressure required for breathing relative to inspiratory muscle strength (PPLsw, %PPLmin). There was an association between the severity of dyspnoea and both the increase in PPLsw (%PPLmin) and the shortening in TI.
The results indicate that, in stable patients with COPD with severe airflow obstruction, hypercapnia is associated with shallow breathing and inspiratory muscle weakness, and rapid and shallow breathing appears to be linked to both a marked increase in the pressure required for breathing relative to inspiratory muscle strength and to the severity of the breathlessness.
导致重度慢性阻塞性肺疾病（COPD）患者出现慢性高碳酸血症和呼吸浅快的因素尚未完全明确。本研究探讨了稳定期重度气流受限的COPD患者慢性二氧化碳潴留、呼吸模式、呼吸困难以及相对于吸气肌力量的呼吸所需压力之间的相互关系。
对30例临床稳定、一秒用力呼气容积（FEV1）<1升的COPD患者进行研究。评估每位患者的以下参数：（1）呼吸困难量表评分；（2）通过测量最小胸膜压力（PPLmin）评估吸气肌力量；（3）静息呼吸时的潮气量（VT）、流速、胸膜压力波动（PPLsw）、总肺阻力（RL）、动态肺弹性（ELdyn）和呼气末肺泡正压（PEEPi）。
动脉血二氧化碳分压（PaCO2）与RL/PPLmin、ELdyn/PPLmin直接相关，与VT和PPLmin呈负相关。PaCO2与功能残气量（FRC）、肺总量（TLC）或分钟通气量之间无相关性。在二氧化碳正常和高碳酸血症患者中，PEEPi相似。将PaCO2表示为VT和PPLmin的联合函数（逐步多元回归分析）可解释PaCO2变异的71%。潮气量与吸气时间（TI）直接相关，TI与相对于吸气肌力量的呼吸所需压力（PPLsw，%PPLmin）呈负相关。呼吸困难的严重程度与PPLsw（%PPLmin）增加和TI缩短均有关联。
结果表明，在稳定期重度气流受限的COPD患者中，高碳酸血症与呼吸浅快和吸气肌无力有关，而呼吸浅快似乎与相对于吸气肌力量的呼吸所需压力显著增加以及呼吸困难的严重程度均有关。
