Hypertensive emergencies

Abstract

A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage. Most patients presenting with hypertensive emergency have chronic hypertension, although the disorder can present in previously normotensive individuals, particularly when associated with pre-eclampsia or acute glomerulonephritis. The pathophysiological mechanisms causing acute hypertensive endothelial failure are complex and incompletely understood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous vasodilator mechanisms, upregulation of proinflammatory mediators including vascular cell adhesion molecules, and release of local vasoconstrictors such as endothelin 1. Magnetic resonance imaging has demonstrated a characteristic hypertensive posterior leucoencephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital lobes; this syndrome is potentially reversible with appropriate prompt treatment. Generally, the therapeutic approach is dictated by the particular presentation and end-organ complications. Parenteral therapy is generally preferred, and strategies include use of sodium nitroprusside, beta-blockers, labetelol, or calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy. Novel therapies include the peripheral dopamine-receptor agonist, fenoldapam, and may include endothelin-1 antagonists.

Experimental Intracerebral Hemorrhage: Avoiding Pitfalls in Translational Research

“…While stroke-prone, spontaneous hypertensive rats are useful for studying stroke, they tend to develop ischemic stroke and, when hemorrhage occurs, this is usually secondary to hemorrhagic transformation of an infarct (Sadoshima et al, 1981). In humans, chronic hypertension is a major risk factor for ICH, and recent evidence suggests that development of an acute hypertensive episode superimposed on chronic hypertension may trigger ICH, possibly through activation of the reninangiotensin and sympathetic nervous systems (Metoki et al, 2006;Vaughan and Delanty, 2000). A new model of ICH in hypertensive mice has thus been proposed (Wakisaka et al, 2010).…”

Dialysis disequilibrium leading to posterior reversible encephalopathy syndrome in chronic renal failure

“…Cerebral auto regulation keeps blood flow constant, and protects the brain during changes in blood pressure; but, a sudden and severe increase in blood pressure can impair auto regulation, and this impairment can lead to arteriolar vasodilatation and endothelial dysfunction. As a result, plasma and red blood cells migrate to the extravascular space from the intravascular space, thereby engendering vasogenic edema [7]. Both these hypothesis fit in the clinical context of PRES, where hypertension or hypertensive urgency plays a major role in the midst of other complications.…”

Severe Hypertension and Bradycardia Secondary to Midodrine Overdose

“…However, there has only been one case noted of central nervous system depression by the midodrine manufacturer product information, with no other details mentioned [9]. Another possibility is that our patient developed an acute hypertensive encephalopathy, but other features of hypertensive encephalopathy including headache [11] could not be confirmed in our patient due to her altered conscious state. This is less likely as hypertensive encephalopathy typically starts 12 h after a sustained blood pressure increase, whereas our patient had only been hypertensive for a few hours.…”