Pfeiffer Birgit, Hachenberg Thomas, Wendt Michael, Marshall Bryan
Department of Anesthesiology and Intensive Care Medicine, Ernst-Moritz-Arndt-University, Greifswald, Germany.
Crit Care Med. 2002 Feb;30(2):285-9. doi: 10.1097/00003246-200202000-00003.
To compare the effects of conventional mechanical ventilation with low-volume, pressure-limited ventilation (LVPLV) and permissive hypercapnia on ventilation-perfusion (V/Q) distributions in patients with acute respiratory distress syndrome. We hypothesized that the advantageous cardiopulmonary effects of LVPLV would be greater in patients with sepsis than in those without sepsis.
Twenty-two patients with acute respiratory distress syndrome were studied (group 1: 12 patients with hyperdynamic sepsis; group 2: 10 nonseptic patients). Intrapulmonary shunt (Qsp/Qt) (percentage of cardiac output), perfusion of "low" V/Q areas (percentage of cardiac output), ventilation of "high" V/Q areas (percentage of total ventilation [VE]), and deadspace ventilation (percentage of VE) were calculated from the retention/excretion data of six inert gases. Data were obtained during conventional mechanical ventilation and during LVPLV.
In group 1, LVPLV increased PaCO(0)rom 38 +/- 6 torr (5.1 +/- 0.8 kPa) to 61 +/- 12 torr (8.1 +/- 1.6 kPa). Qsp/Qt increased from 28 +/- 16% to 36 +/- 17%, whereas Pao2 (84 +/- 15 torr [11.1 +/- 2.0 kPa] vs. 86 +/- 21 torr [11.5 +/- 2.8 kPa]) and Qt (10.6 +/- 2.3 vs. 11.5 +/- 2.5 L x -1) remained unchanged and PVO(2) (40 +/- 4 [5.3 +/- 0.5 kPa] vs. 49 +/- 6 torr [6.5 +/- 0.3]) increased. In group 2, LVPLV increased PaCO(2) from 38 +/- 6 torr (5.1 +/- 0.8 kPa) to 63 +/- 11 torr (8.4 +/- 1.5 kPa). For Qsp/Qt (24 +/- 9% to 34 +/- 16%), the increase was not significant, whereas Qt (7.4 +/- 1.8 vs. 10.2 +/- 2.2 L x -1), PVO(2)(38 +/- 4 torr [5.1 +/- 0.5 kPa] vs. 50 +/- 6 mm Hg [6.7 +/- 0.8 kPa]), and PaO(2) (89 +/- 16 torr [11.9 +/- 2.1 kPa] vs. 98 +/- 19 torr [13.1 +/- 2.5 kPa]) increased. In both groups, the scatter of perfusion distribution (log SDQ) was greater than expected for normal subjects but was not different between the groups or altered by the treatments.
In patients with acute respiratory distress syndrome, LVPLV with permissive hypercapnia, tended to increase Qsp/Qt, without a concomitant decrease of PaO(2). This occurs because, although atelectasis and increased shunt result from the low ventilatory volume, the effects on PaO(2) are offset by increased PVO(2) resulting from the hypercapnic stimulation of cardiac output. This result was independent of the presence or absence of sepsis.
比较传统机械通气、小潮气量压力限制通气（LVPLV）及允许性高碳酸血症对急性呼吸窘迫综合征患者通气/灌注（V/Q）分布的影响。我们假设LVPLV对心肺的有益作用在脓毒症患者中比非脓毒症患者更大。
对22例急性呼吸窘迫综合征患者进行研究（第1组：12例高动力型脓毒症患者；第2组：10例非脓毒症患者）。根据6种惰性气体的潴留/排出数据计算肺内分流（Qsp/Qt）（心输出量的百分比）、“低”V/Q区域的灌注（心输出量的百分比）、“高”V/Q区域的通气（总通气量[VE]的百分比）及死腔通气（VE的百分比）。在传统机械通气和LVPLV期间获取数据。
在第1组中，LVPLV使PaCO₂从38±6托（5.1±0.8千帕）升至61±12托（8.1±1.6千帕）。Qsp/Qt从28±16%升至36±17%，而PaO₂（84±15托[11.1±2.0千帕]对86±21托[11.5±2.8千帕]）和心输出量（10.6±2.3对11.5±2.5升·分钟⁻¹）保持不变，PVO₂（40±4[5.3±0.5千帕]对49±6托[6.5±0.3]）升高。在第2组中，LVPLV使PaCO₂从38±6托（5.1±0.8千帕）升至63±11托（8.4±1.5千帕）。对于Qsp/Qt（24±9%至34±16%），升高不显著，而心输出量（7.4±1.8对10.2±2.2升·分钟⁻¹）、PVO₂（38±4托[5.1±0.5千帕]对50±6毫米汞柱[6.7±0.8千帕]）及PaO₂（89±16托[11.9±2.1千帕]对98±19托[13.1±2.5千帕]）升高。在两组中，灌注分布的离散度（log SDQ）大于正常受试者的预期值，但两组间无差异，且治疗未使其改变。
在急性呼吸窘迫综合征患者中，采用允许性高碳酸血症的LVPLV往往会增加Qsp/Qt，而不会伴随PaO₂降低。出现这种情况是因为，尽管低潮气量会导致肺不张和分流增加，但对PaO₂的影响被高碳酸血症刺激心输出量增加所导致的PVO₂升高所抵消。这一结果与脓毒症的有无无关。
