Romaldini H, Faro S, Stabile C, dos-Santos M L, Ajzen H, Ratto O R
Braz J Med Biol Res. 1982 Dec;15(6):395-404.
Hemodialysis-induced hypoxemia has been explained by several mechanisms: pulmonary microembolization, decreased pulmonary diffusing capacity, fall in alveolar oxygen tension, hypoventilation and ventilation/perfusion abnormalities. The objective of this study was to analyze the factors influencing pulmonary ventilation and gas exchange of 20 patients with chronic renal failure during hemodialysis performed under the following conditions: Group 1 (9 patients) dialyzed against an acetate dialysate with a cuprophan membrane; Group 2 (7 patients) dialyzed against acetate bubbled with CO2 with a cuprophan membrane; Group 3 (4 patients) similar to Group 1, but using a polyacrylonitrile membrane. Arterial and venous blood samples were obtained from the respective lines during the predialysis period (zero), at 30, 60, 120 180 and 240 min of hemodialysis, and 60 min post dialysis (300 min) for the measurement of pH, PCO2, PO2, HCO-3 and total CO2. The minute expired volume (VE), expired fractions of O2 (FEO2) and CO2 (FECO2), O2 consumption (VO2), CO2 elimination through the lungs (VCO2) and dialyzer, respiratory exchange ratio (R), dead space to tidal volume ratio (VD/VT), alveolar ventilation (VA) and alveolar-arterial O2 difference (delta AaPO2) were measured and a leukocyte count was performed for each period of hemodialysis. The patients in Groups 1 and 3 showed a significant drop in ventilation and PaO2, a slight decrease in PAO2 and a significant increase in delta AaPO2. The patients in Groups 1 and 2 showed a significant leukopenia at 30 min of hemodialysis. The volume of CO2 eliminated across the dialyzer was very similar for the three groups of patients. Group 2 did not show any drop in ventilation or PaO2. For Group 2 venous line pH was very low and PCO2 was within the normal range, in contrast to the normal or high pH and low PCO2 shown by Groups 1 and 3. This study indicates that the drop in PaO2 was partially the consequence of a slight decrease in PAO2, but mainly due to the increase in delta AaPO2. Thus the most likely cause of the decrease in PaO2 was the VA/Q imbalance brought about by a drop in ventilation. The drop in ventilation was linked not only to the volume of CO2 eliminated across the dialyzer, but also to the amount of CO2 delivered to the lungs, and to the pH and PCO2 of the venous line.
肺微栓塞、肺弥散能力下降、肺泡氧分压降低、通气不足以及通气/灌注异常。本研究的目的是分析在以下条件下进行血液透析时影响20例慢性肾衰竭患者肺通气和气体交换的因素:第1组(9例患者)使用铜仿膜透析器,以醋酸盐透析液进行透析;第2组(7例患者)使用铜仿膜透析器,以通入二氧化碳的醋酸盐透析液进行透析;第3组(4例患者)与第1组类似,但使用聚丙烯腈膜。在透析前阶段(零时刻)、血液透析30、60、120、180和240分钟时以及透析后60分钟(300分钟),从相应管路采集动脉和静脉血样本,用于测定pH、PCO₂、PO₂、HCO₃⁻和总CO₂。测量每分钟呼出量(VE)、呼出的O₂分数(FEO₂)和CO₂分数(FECO₂)、O₂消耗量(VO₂)、通过肺排出的CO₂量(VCO₂)和透析器排出的CO₂量、呼吸交换率(R)、死腔与潮气量之比(VD/VT)、肺泡通气量(VA)和肺泡 - 动脉血氧分压差(δAaPO₂),并在血液透析的每个阶段进行白细胞计数。第1组和第3组患者的通气量和动脉血氧分压显著下降,肺泡氧分压略有降低,肺泡 - 动脉血氧分压差显著增加。第1组和第2组患者在血液透析30分钟时出现显著白细胞减少。三组患者通过透析器排出的CO₂量非常相似。第2组患者的通气量或动脉血氧分压没有下降。与第1组和第3组显示的正常或高pH值和低PCO₂相反,第2组患者静脉管路的pH值非常低,而PCO₂在正常范围内。本研究表明,动脉血氧分压下降部分是由于肺泡氧分压略有降低,但主要是由于肺泡 - 动脉血氧分压差增加。因此,动脉血氧分压降低最可能的原因是通气量下降导致的通气/血流比例失衡。通气量下降不仅与通过透析器排出的CO₂量有关,还与输送到肺部的CO₂量以及静脉管路的pH值和PCO₂有关。