CRITICAL CARE ISSUES FOR THE NEPHROLOGIST: Current Diagnosis and Management of Hypertensive Emergency

Abstract

The appropriate and timely evaluation and treatment of patients with severely elevated blood pressure is essential to avoid serious adverse outcomes. Most importantly, the distinction between a hypertensive emergency (crisis) and urgency needs to be made. A sudden elevation in systolic (SBP) and/or diastolic blood pressure (DBP) that is associated with acute end organ damage (cardiovascular, cerebrovascular, or renal) is defined as a hypertensive crisis or emergency. In contrast, acute elevation in SBP and/or DBP not associated with evidence of end organ damage is defined as hypertensive urgency. In patients with a hypertensive emergency, blood pressure control should be attained as expeditiously as possible with parenteral medications to prevent ongoing and potentially permanent end organ damage. In contrast, with hypertensive urgency, blood pressure control can be achieved with the use of oral medications within 24-48 hours. This paper reviews the management of hypertensive emergencies.

Angiotensin II Modulates BBB Permeability via Activation of the AT1 Receptor in Brain Endothelial Cells

“…Because of its rapid onset, it is suggested that in most cases an initial trigger plus the higher blood pressure activates a positive feedback loop, which stimulates the release of vasoactive mediators (Haas and Marik, 2006;Kitiyakara and Guzman, 1998). Activation of this feedback loop begins a vicious cycle, which leads to continuous organ damage and continuous increases in blood pressure (Haas and Marik, 2006;Kitiyakara and Guzman, 1998). There are many factors, which contribute to the pathophysiology of hypertensive emergency.…”

“…Additionally, Ang II can stimulate the release of other vasoactive and hypertensive compounds such as vasopressin, aldosterone, and catecholamines as well as stimulate the production of proinflammatory cytokines. The latter can themselves mediate opening of the BBB (Haas and Marik, 2006;Kitiyakara and Guzman, 1998;Zhang et al, 2000).…”

“…These include mechanical stress, endothelial dysfunction, oxidative stress and damage with potential release of cytokines, prostaglandins and nitric oxide. The renin-angiotensin system (RAS) in particular plays a critical role in the initiation and maintenance of hypertensive emergencies and in target organ damage (Haas and Marik, 2006;Kitiyakara and Guzman, 1998;Stefansson et al, 2000;Sunder-Plassmann et al, 2002).…”

Intravenous clevidipine for management of hypertension

“…2 The myocardium is the most commonly affected target organ, but encephalopathy, cerebrovascular accidents, acute papilledema, aortic dissection, renal failure, and acute pulmonary edema are frequently associated with severe BP elevation. 3 Predisposing factors for development of a hypertensive crisis include mechanical stress and injury, endothelial damage, renin-angiotensin system activation, and oxidative stress. 3 The predominant insult seems to be a cascade of humoral vasoconstrictors that leads to increased vascular resistance, generating stress and damaging the endothelium, which activates the coagulation cascade and promotes the deposition of fibrin.…”

“…3 Predisposing factors for development of a hypertensive crisis include mechanical stress and injury, endothelial damage, renin-angiotensin system activation, and oxidative stress. 3 The predominant insult seems to be a cascade of humoral vasoconstrictors that leads to increased vascular resistance, generating stress and damaging the endothelium, which activates the coagulation cascade and promotes the deposition of fibrin. These processes result in ischemia, oxidative injury, and further release of vasoactive substances that perpetuate the destructive cycle, culminating in the multiple organ dysfunction that characterizes a hypertensive emergency.…”