高血压急症进展因素知之甚少。初见全身血管阻力增加,随后血压升高产生机械应力及内皮损伤,导致血管通透性增加、血小板及凝血级联反应激活、纤维蛋白沉积。这些过程导致缺血及其他血管活性介质释放,产生持续损伤。压力尿钠排泄及肾素血管紧张素系统激活导致了血容量不足,通常可引起血管收缩。高血压急症的显著特征为全身血管收缩导致重要脏器供血不足并后续导致脏器损伤。神经损伤可能表现为视网膜病变、视乳头水肿、脑病、卒中、癫痫或昏迷。胸痛或气促、即将发生或已发病的心梗、主动脉夹层、伴随肺水肿的左心室衰竭说明存在心肌损伤。少尿及氮质血症说明肾功能衰竭。[6]Zampaglione B, Pascale C, Marchisio M, et al. Hypertensive urgencies and emergencies: prevalence and clinical presentation. Hypertension. 1996;27:144-147.http://hyper.ahajournals.org/cgi/content/full/27/1/144http://www.ncbi.nlm.nih.gov/pubmed/8591878?tool=bestpractice.com[13]Kaplan NM. Kaplan's clinical hypertension, 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.[14]Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000;356:411-417.http://www.ncbi.nlm.nih.gov/pubmed/10972386?tool=bestpractice.com[15]Marik PE, Varon J. Hypertensive crises: challenges and management [published correction appears in Chest. 2007;132:1721]. Chest. 2007;131:1949-1962.http://www.edictforpressurecontrol.com/pdf/1949_HypertensiveCrises.pdfhttp://www.ncbi.nlm.nih.gov/pubmed/17565029?tool=bestpractice.com