MECHANISMS OF WORSENING GAS-EXCHANGE DURING ACUTE EXACERBATIONS OF CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

This study was undertaken to investigate the mechanisms that determine abnormal gas exchange during acute exacerbations of chronic obstructi ve pulmonary disease (COPD). Thirteen COPD patients, hospitalized beca use of an exacerbation, were studied after admission and 38+/-10 (+/-S D) days after discharge, once they were clinically stable. Measurement s included forced spirometry, arterial blood gas values, minute ventil ation (V'E), cardiac output ((Q) over bar'), oxygen consumption (V'O-2 ), and ventilation/perfusion (V'A/Q(1)) relationships, assessed by the inert gas technique. Exacerbations were characterized by very severe airflow obstruction (forced expiratory volume in one second (FEV1) 0.7 4+/-10.17 vs 0.91+/-0.19 L, during exacerbation and stable conditions, respectively; p=0.01), severe hypoxaemia (ratio between arterial oxyg en tension and inspired oxygen fraction (Pa,O-2/FI,O-2) 32.7+/-7.7 vs 37.6+/-6.9 kPa (245+/-58 vs 282+/-52 mmHg); p=0.01) and hypercapnia (a rterial carbon dioxide tension (Pa,CO2) 6.8+/-1.6 vs 5.9+/-0.8 kPa (51 +/-12 vs 44+/-6 mmHg); p=0.04), V(1)A/Q(1) inequality increased during exacerbation (log SD Q(1), 1.10+/-0.29 vs 0.96+/-0.27; normal less th an or equal to 0.6; p=0.04) as a result of greater perfusion in poorly -ventilated alveoli. Shunt was almost negligible on both measurements. (VE)-E-1 remained essentially unchanged during exacerbation (10.5+/-2 .2 vs 9.2+/-1.8 L.min(-1); p=0.1), whereas both (Q) over bar(1)(6.1+/- 2.4 vs 5.1+/-1.7 L.min(-1); p=0.05) and (VO2)-O-1 (300+/-49 vs 248+/-5 9 mL.min(-1); p=0.03) increased significantly. Worsening of hypoxaemia was explained mainly by the increase both in V'A/Q' inequality and V' O-2, whereas the increase in (Q) over bar' partially counterbalanced t he effect of greater V'O-2 on mixed venous oxygen tension (P (v) over bar,O-2). We conclude that worsening of gas exchange during exacerbati ons of chronic obstructive pulmonary disease is primarily produced by increased ventilation/perfusion inequality, and that this effect is am plified by the decrease of mixed venous oxygen tension that results fr om greater oxygen consumption, presumably because of increased work of the respiratory muscles.