Mutch W A, Harms S, Lefevre G R, Graham M R, Girling L G, Kowalski S E
Department of Anesthesia and Neuroanesthesia Research Laboratory, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Crit Care Med. 2000 Jul;28(7):2457-64. doi: 10.1097/00003246-200007000-00045.
We compared biologically variable ventilation (BVV) (as previously described) (1) with conventional control mode ventilation (CV) in a model of acute respiratory distress syndrome (ARDS) both at 10 cm H2O positive end-expiratory pressure.
Randomized, controlled, prospective study.
University research laboratory.
Farm-raised 3- to 4-month-old swine.
Oleic acid (OA) was infused at 0.2 mL/kg/hr with FIO2 = 0.5 and 5 cm H2O positive end-expiratory pressure until PaO2 was < or =60 mm Hg; then all animals were placed on an additional 5 cm H2O positive end-expiratory pressure for the next 4 hrs. Animals were assigned randomly to continue CV (n = 9) or to have CV computer controlled to deliver BVV (variable respiratory rate and tidal volume; n = 8). Hemodynamic, expired gas, airway pressure, and volume data were obtained at baseline (before OA), immediately after OA, and then at 60-min intervals for 4 hrs.
At 4 hrs after OA injury, significantly higher PaO2 (213+/-17 vs. 123+/-47 mm Hg; mean+/-SD), lower shunt fraction (6%+/-1% vs. 18%+/-14%), and lower PaCO2 (50+/-8 vs. 65+/-11 mm Hg) were seen with BVV than with CV. Respiratory system compliance was greater by experiment completion with BVV (0.37+/-0.05 vs. 0.31+/-0.08 mL/cm H2O/kg). The improvements in oxygenation, CO2 elimination, and respiratory mechanics occurred without a significant increase in either mean airway pressure (14.3+/-0.9 vs. 14.9+/-1.1 cm H2O) or mean peak airway pressure (39.3+/-3.5 vs. 44.5+/-7.2 cm H2O) with BVV. The oxygen index increased five-fold with OA injury and decreased to significantly lower levels over time with BVV.
In this model of ARDS, BVV with 10 cm H2O positive end-expiratory pressure improved arterial oxygenation over and above that seen with CV with positive end-expiratory pressure alone. Proposed mechanisms for BVV efficacy are discussed.
我们在急性呼吸窘迫综合征(ARDS)模型中,于呼气末正压为10 cm H₂O时,将生物可变通气(BVV)(如前所述)与传统控制模式通气(CV)进行比较。
随机、对照、前瞻性研究。
大学研究实验室。
农场饲养的3至4月龄猪。
以0.2 mL/kg/小时的速度输注油酸(OA),吸入氧分数(FIO₂)= 0.5,呼气末正压为5 cm H₂O,直至动脉血氧分压(PaO₂)≤60 mmHg;然后在接下来的4小时内,所有动物呼气末正压增加5 cm H₂O。动物被随机分配继续接受CV(n = 9)或通过计算机控制CV以实现BVV(呼吸频率和潮气量可变;n = 8)。在基线(OA前)、OA后即刻以及随后4小时内每隔60分钟获取血流动力学、呼出气体、气道压力和容积数据。
在OA损伤后4小时,与CV相比,BVV组的PaO₂显著更高(213±17 vs. 123±47 mmHg;均值±标准差),分流分数更低(6%±1% vs. 18%±14%),PaCO₂更低(50±8 vs. 65±11 mmHg)。到实验结束时,BVV组的呼吸系统顺应性更高(0.37±0.05 vs. 0.31±0.08 mL/cm H₂O/kg)。在氧合、二氧化碳清除和呼吸力学方面的改善,并未伴随BVV组平均气道压力(14.3±0.9 vs. 14.9±1.1 cm H₂O)或平均气道峰压(39.3±3.5 vs. 44.5±7.2 cm H₂O)的显著增加。随着OA损伤,氧指数增加了五倍,随着时间推移,BVV使其降至显著更低水平。
在该ARDS模型中,呼气末正压为10 cm H₂O时,BVV相比仅采用呼气末正压的CV能更好地改善动脉氧合。文中讨论了BVV疗效的可能机制。