Malignant hypertension and hypertensive emergencies

Division of Nephrology and Hypertension, Georgetown University Medical Center, Washington, DC 20007, USA.
Journal of the American Society of Nephrology (Impact Factor: 9.34). 02/1998; 9(1):133-42. DOI: 10.1001/jama.228.13.1673
Source: PubMed


Hypertensive emergencies and urgencies are important causes of morbidity and mortality. Malignant hypertension is a hypertensive urgency characterized by grade III/IV retinopathy and widespread endothelial damage. Control of BP is essential in the treatment of these disorders. The effects of hypertension on target organ function need to be balanced against the risks of excessive BP lowering. In hypertensive emergencies, BP should be lowered within minutes with parenteral agents to prevent critical end-organ damage. In hypertensive urgencies, BP can be lowered more slowly over several hours, often with oral agents, to avoid a detrimental fall in BP. The absolute indications for treatment and the optimal therapy depend on the underlying condition.

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    • "FDA-approved dose 5 mg/h; increase at 2.5-mg/h increments every 5 min to a maximum of 15 mg/h 20 mg initial bolus; 20-80 mg repeat boluses or start infusion at 1-2 mg/min, with maximum dose of 300 mg in 24 h Available formulations IV (including premixed, ready-to-use formulation) and oral formulations IV bolus or continuous infusion (stored in a vial for preparation in a larger volume of solution) Key features High vascular selectivity with strong cerebral and coronary vasodilatory activity [20] Reduces systemic vascular resistance while cerebral, renal, and coronary blood flows are maintained [24] [25] [26] [27] Crosses the blood-brain barrier The α 1 -blocking component of labetalol minimized the reductions in cardiac output seen with agents that have only β-blocking activity [28]. "
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    ABSTRACT: Hypertensive emergencies are acute elevations in blood pressure (BP) that occur in the presence of progressive end-organ damage. Hypertensive urgencies, defined as elevated BP without acute end-organ damage, can often be treated with oral agents, whereas hypertensive emergencies are best treated with intravenous titratable agents. However, a lack of head-to-head studies has made it difficult to establish which intravenous drug is most effective in treating hypertensive crises. This systematic review presents a synthesis of published studies that compare the antihypertensive agents nicardipine and labetalol in patients experiencing acute hypertensive crises. A MEDLINE search was conducted using the term "labetalol AND nicardipine AND hypertension." Conference abstracts were searched manually. Ultimately, 10 studies were included, encompassing patients with hypertensive crises across an array of indications and practice environments (stroke, the emergency department, critical care, surgery, pediatrics, and pregnancy). The results of this systematic review show comparable efficacy and safety for nicardipine and labetalol, although nicardipine appears to provide more predictable and consistent BP control than labetalol.
    The American journal of emergency medicine 09/2011; 30(6):981-93. DOI:10.1016/j.ajem.2011.06.040 · 1.27 Impact Factor
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    • "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). The BBB forms a metabolic and physiologic regulatory interface between the peripheral circulation and the brain extracellular fluid. "
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    ABSTRACT: Hypertensive encephalopathy occurs when acute changes in blood pressure cause breakdown of the blood-brain barrier (BBB). Angiotensin II (Ang II) plays a role in this pathophysiology. We determined whether Ang II directly regulates endothelial cell function at the BBB. In BBB microvessel endothelial cells (MECs), the Ang II (100 nmol/L; 0 to 6 h) effects on permeability to (125)I-albumin and transendothelial electrical resistance (TEER) were assessed. Angiotensin II (100 nmol/L) caused significant time-dependent changes in both (125)I-albumin permeability (25%) at 2 h and TEER (-8.87 Omega x cm(2)) at 6 h. Next, MECs were pretreated with the Ang II type 1 (AT(1)) receptor blocker telmisartan (1 micromol/L) or the Ang II type 2 (AT(2)) receptor blocker PD123,319 (1 micromol/L) followed by treatment with Ang II (100 nm). Telmisartan completely inhibited the Ang II-induced increase in (125)I-albumin permeability in MECs whereas PD123,319 had no effect. Using western blot analysis, we showed that MECs express AT(1) receptors but not AT(2) receptors. Treatment with Ang II (100 nmol/L; 0 to 6 h) also increased total protein kinase C activity. In contrast, Ang II had no effect on the expression of occludin, claudin 5, or actin. These results show that Ang II directly modulates transcytotic and paracellular permeability in BBB endothelial cells and could contribute to the pathophysiology of hypertensive encephalopathy.
    Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 01/2009; 29(3):640-7. DOI:10.1038/jcbfm.2008.158 · 5.41 Impact Factor
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    • "Les HTA postopératoires sont en partie liées à une stimulation adrénergique préalable (per-et postopératoire) chez des patients hypertendus chroniques ou non [16]. D'autres facteurs étiologiques sont identifiés : une anomalie du système rénine angiotensine, une dysfonction des barorécepteurs [17], l'interruption d'antihypertenseurs centraux [18]. "
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    ABSTRACT: The severity of hypertensive crises is determined by the presence of target organ damage (acute aortic dissection, hypertensive encephalopathy…) rather than the level of blood pressure. The management of patients with hypertensive emergencies must be ensured in an intensive care unit and must include the intravenous administration of antihypertensive drugs and accurate blood pressure monitoring. Except for acute aortic dissection, the recommended goal of treatment is a reduction of mean arteriel pressure by no more than 20% during the first few hours, because an abrupt fall in blood pressure in patients with preexisting hypertension may induce severe ischaemic injury in major organs as a result of chronic adaptation of autoregulation mechanisms. Hypertension in a context of acute stroke should be treated only rarely and cautiously because of the presence of impaired autoregulation. Recent development concern postoperative hypertension and catecholamine excess (sometimes requiring urgent treatment). Also, malignant hypertension demands special consideration because of risks of permanent blindness and renal failure.
    Réanimation 03/2008; 17(2). DOI:10.1016/j.reaurg.2007.12.004
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