医学
复苏
感染性休克
灌注
临界关闭压力
平均动脉压
血压
休克(循环)
心脏病学
麻醉
血流
自动调节
微循环
内科学
血流动力学
心输出量
败血症
持续无创动脉压
血管阻力
拯救脓毒症运动
静水压力
重症监护
平均血压
脑自动调节
作者
Michael R. Pinsky,Hernando Gómez,Glenn Elmer Hernández Camelo
标识
DOI:10.1093/ajrccm/aamag397
摘要
Tissue autoregulation to match local blood flow to metabolic demands requires both a high enough upstream mean arterial pressure (MAP) and perfusion pressure difference between this MAP and the downstream arteriolar critical closing pressure to drive blood flow into the capillaries whose downstream capillary pressure is approximated as mean systemic filling pressure. The closing pressure to mean systemic pressure difference represents a vascular waterfall such that increases or decreases in mean systemic filling pressure below closing pressure do not alter tissue flow. Tissues autoregulate their blood flow by altering upstream local vasomotor tone to increase or decrease closing pressure. In vasoplegia, like septic shock vascular tone is decreased, often decreasing closing pressure to approximating mean systemic filling pressure. Such conditions abolish autoregulation even if MAP and cardiac output are not decreased. Effective resuscitation from septic shock requires restoration of local vascular waterfalls. Often initial fluid resuscitation and vasopressor infusion restore vascular waterfalls and tissue blood flow. But often it does not. There are few readily available real-time quantitative estimates of tissue perfusion. Presently only capillary refill time (CRT) minors tissue blood flow changes. If initial resuscitation to target MAP values does not restore tissue perfusion and CRT is > 3 seconds, then potentially a vasopressor test to increase MAP to > 75 mmHg may be studied. If vasopressor-induced increases in MAP decreases CRT to < 3 seconds, then it can be continued. If not, then return to prior levels to minimize iatrogenic vasopressor risk. This paper lists unanswered questions that need studying.
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