Luster E A, Baumgartner N, Adams W C, Convertino V A
Physiology Research Branch, AL/AOCY, Brooks Air Force Base, TX 78235-5117, USA.
Aviat Space Environ Med. 1996 Apr;67(4):308-13.
We tested the hypotheses that hypovolemia would result in attenuated elevation in blood pressure, greater baroreflex-mediated tachycardia, and reduced capacity for vasoconstriction during a Valsalva maneuver (VM).
Heart rate (HR) and mean arterial pressure (MAP) were measured beat-by-beat before strain, during a 15-s VM strain at 30 mmHg expiratory pressure, and post-strain. Eight subjects performed three VM trials in each of three postures (supine, sitting, and standing) under two experimental conditions (normovolemic and hypovolemic). Hypovolemia was acutely induced by a bolus injection of 30 mg furosemide. Each experimental condition was conducted on a different day, separated by one week. delta MAP was used in analyses of phase I, late phase II (an indicator of vasoconstriction) and phase III of VM. The ratio delta HR/delta MAP, an index of nonspecific baroreflex control of HR, was used in analysis of early phase II and phase IV of the VM.
Compared to normovolemia, hypovolemia resulted in 12% lower plasma volume (p = 0.0001). delta MAP for both phase I and phase III of the VM differed between postures (p = 0.0132 and p = 0.0003, respectively) and was lower in the hypovolemic condition than in the normovolemic condition for phase I in the standing posture (-5 mmHg, p = 0.0385).
HR and blood pressure responses to alterations in intrathoracic pressure are affected by fluid redistribution (posture change), but not by circulating blood volume. Therefore, our results did not support our hypothesis that hypovolemia would result in attenuated elevation in blood pressure, greater baroreflex-mediated tachycardia, and reduced capacity for vasoconstriction during a Valsalva maneuver. However, moderate hypovolemia can be specifically predicted by the phase I response to a VM performed in the standing posture.
我们检验了以下假设:低血容量会导致血压升高减弱、压力反射介导的心动过速加剧以及瓦尔萨尔瓦动作(VM)期间血管收缩能力降低。
在用力前、30 mmHg呼气压力下进行15秒VM用力期间以及用力后逐搏测量心率(HR)和平均动脉压(MAP)。八名受试者在两种实验条件(血容量正常和低血容量)下于三种姿势(仰卧、坐姿和站立)中各进行三次VM试验。通过静脉推注30 mg呋塞米急性诱导低血容量。每种实验条件在不同日期进行,间隔一周。ΔMAP用于分析VM的I期、II期后期(血管收缩指标)和III期。HR变化率与MAP变化率之比(HR非特异性压力反射控制指数)用于分析VM的II期早期和IV期。
与血容量正常相比,低血容量导致血浆量降低12%(p = 0.0001)。VM的I期和III期的ΔMAP在不同姿势间存在差异(分别为p = 0.0132和p = 0.0003),并且在站立姿势下I期低血容量条件下的ΔMAP低于血容量正常条件(-5 mmHg,p = 0.0385)。
HR和血压对胸内压变化的反应受液体重新分布(姿势改变)影响,但不受循环血容量影响。因此,我们的结果不支持我们的假设,即低血容量会导致瓦尔萨尔瓦动作期间血压升高减弱、压力反射介导的心动过速加剧以及血管收缩能力降低。然而,通过站立姿势下VM的I期反应可特异性预测中度低血容量。