Shade E, Kawagoe Y, Brower R G, Permutt S, Fessler H E
Division of Pulmonary and Critical Care Medicine, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
J Appl Physiol (1985). 1994 Aug;77(2):819-27. doi: 10.1152/jappl.1994.77.2.819.
Increased end-expiratory lung volume (EELV) and airway resistance are both characteristic features of obstructive lung disease. Increased EELV alone loads the respiratory muscles and may cause respiratory failure, changes that could be reversed by continuous positive airway pressure (CPAP). To study the effects of elevated EELV on respiration without increased airway resistance, we used a mechanical analogue of airway closure to increase EELV in six spontaneously breathing anesthetized dogs. Hyperinflation of 0.84 +/- 0.11 liter for 30 min decreased minute ventilation from 4.8 +/- 0.37 to 3.5 +/- 0.21 l/min and increased arterial PCO2 from 40.3 +/- 1.5 to 73.2 +/- 8.1 Torr (both P < 0.01). Inspiratory work per breath increased 3-fold, work per liter increased 3.7-fold, and work per minute increased 2.8-fold (all P < 0.01). CPAP at 15 cmH2O restored minute ventilation to 4.3 +/- 0.3 l/min and reduced arterial PCO2 to 54 +/- 6.6 Torr (NS vs. baseline). All measurements of inspiratory work were also restored to baseline, but cardiac output was reduced (baseline 3.09 +/- 0.36, hyperinflation 2.71 +/- 0.36, hyperinflation + CPAP 1.94 +/- 0.29 l/min; P < 0.05, baseline vs. hyperinflation + CPAP). We conclude that increases in EELV mimic important features of airway obstruction, increase inspiratory work, and can cause respiratory failure independent of increased airway resistance. This respiratory failure is reversed by CPAP at the potential expense of hemodynamic compromise.
呼气末肺容积（EELV）增加和气道阻力增加都是阻塞性肺疾病的特征性表现。单独的EELV增加会加重呼吸肌负荷并可能导致呼吸衰竭，而持续气道正压通气（CPAP）可以逆转这些变化。为了研究在气道阻力不增加的情况下EELV升高对呼吸的影响，我们使用气道关闭的机械模拟装置在6只自主呼吸的麻醉犬中增加EELV。0.84±0.11升的过度充气持续30分钟，使分钟通气量从4.8±0.37降至3.5±0.21升/分钟，动脉血PCO2从40.3±1.5升至73.2±8.1托（均P<0.01）。每次呼吸的吸气功增加了3倍，每升功增加了3.7倍，每分钟功增加了2.8倍（均P<0.01）。15 cmH2O的CPAP使分钟通气量恢复到4.3±0.3升/分钟，并使动脉血PCO2降至54±6.6托（与基线相比无统计学差异）。所有吸气功测量值也恢复到基线水平，但心输出量降低（基线3.09±0.36，过度充气2.71±0.36，过度充气+CPAP 1.94±0.29升/分钟；P<0.05，基线与过度充气+CPAP相比）。我们得出结论，EELV增加模拟了气道阻塞的重要特征，增加了吸气功，并且可以独立于气道阻力增加而导致呼吸衰竭。这种呼吸衰竭可通过CPAP逆转，但可能以血流动力学受损为代价。
