Convertino Victor A, Ryan Kathy L, Rickards Caroline A, Cooke William H, Idris Ahamed H, Metzger Anja, Holcomb John B, Adams Bruce D, Lurie Keith G
U.S. Army Institute of Surgical Research, Fort Sam Houston, TX, USA.
Crit Care Med. 2007 Apr;35(4):1145-52. doi: 10.1097/01.CCM.0000259464.83188.2C.
To test the hypothesis that an impedance threshold device would increase systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure and delay the onset of symptoms and cardiovascular collapse associated with severe central hypovolemia.
Prospective, randomized, blinded trial design.
Human physiology laboratory.
Nine healthy nonsmoking normotensive subjects (five males, four females).
Central hypovolemia and impending cardiovascular collapse were induced in human volunteers by applying progressive lower body negative pressure (under two experimental conditions: a) while breathing with an impedance threshold device set to open at -7 cm H2O pressure (active impedance threshold device); and b) breathing through a sham impedance threshold device (control).
Systolic blood pressure (79 +/- 5 mm Hg), diastolic blood pressure (57 +/- 3 mm Hg), and mean arterial pressure (65 +/- 4 mm Hg) were lower (p < .02) when subjects (n = 9) breathed through the sham impedance threshold device than when they breathed through the active impedance threshold device at the same time of cardiovascular collapse during sham breathing (102 +/- 3, 77 +/- 3, 87 +/- 3 mm Hg, respectively). Elevated blood pressure was associated with 23% greater lower body negative pressure tolerance using an active impedance threshold device (1639 +/- 220 mm Hg-min) compared with a sham impedance threshold device (1328 +/- 144 mm Hg-min) (p = .02).
Use of an impedance threshold device increased systemic blood pressure and delayed the onset of cardiovascular collapse during severe hypovolemic hypotension in spontaneously breathing human volunteers. This device may provide rapid noninvasive hemodynamic support in patients with hypovolemic hypotension once the blood loss has been controlled but before other definitive therapies are available.
检验以下假设,即阻抗阈值装置可提高收缩压、舒张压和平均动脉压,并延迟与严重中枢性低血容量相关的症状发作和心血管衰竭。
前瞻性、随机、双盲试验设计。
人体生理学实验室。
9名健康、不吸烟的血压正常受试者(5名男性,4名女性)。
通过施加渐进性下肢负压诱导人类志愿者出现中枢性低血容量和即将发生的心血管衰竭(在两种实验条件下:a)使用设置为在-7 cm H2O压力下打开的阻抗阈值装置进行呼吸时(主动阻抗阈值装置);b)通过假阻抗阈值装置进行呼吸(对照)。
在假呼吸期间心血管衰竭的同一时间,当受试者(n = 9)通过假阻抗阈值装置呼吸时,收缩压(79±5 mmHg)、舒张压(57±3 mmHg)和平均动脉压(65±4 mmHg)低于通过主动阻抗阈值装置呼吸时(分别为102±3、77±3、87±3 mmHg)(p <.02)。与假阻抗阈值装置(1328±144 mmHg·min)相比,使用主动阻抗阈值装置时,血压升高与下肢负压耐受性提高23%相关(1639±220 mmHg·min)(p =.02)。
在自主呼吸的人类志愿者中,使用阻抗阈值装置可提高全身血压,并延迟严重低血容量性低血压期间心血管衰竭的发作。一旦失血得到控制但在其他确定性治疗可用之前,该装置可为低血容量性低血压患者提供快速的非侵入性血流动力学支持。