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CSC Apr-03 Big Bad Hypertension Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000; 356: 411-17. Key Points: • Hypertensive emergencies are associated with end-organ damage and need to be treated immediately; hypertensive urgencies are asymptomatic but need to be treated within hours • Goal of treatment for hypertensive emergency is reduction of DBP to 100-110 mmHg OR reduction in MAP by 20-25%, whichever is the greater number, over the first 2-6 hours • Both TTP and hypertensive emergency can cause MAHA, renal failure, and altered mental status; TTP is usually not associated with the degree of elevation of BP seen with malignant HTN I. Definitions: What is a hypertensive emergency vs urgency vs malignant hypertension? a. Hypertensive emergency: HTN with evidence of end-organ damage (usually cardiovascular, CNS, or renal) that requires immediate BP control i. CV: MI, aortic dissection, pulmonary edema, CHF ii. CNS: encephalopathy (HA, N/V, progression to AMS/coma), seizures, CVA iii. Renal: acute renal failure, hematuria, proteinuria iv. Optho: retinal hemorrhages or exudates, papilledema b. Hypertensive urgency: HTN that requires control within hours but without evidence of end-organ damage c. Malignant HTN: marked HTN with papilledema, retinal hemorrhages or exudates (basically a subset of hypertensive emergency) II. Causes of hypertensive emergencies a. Essential HTN b. Renal parenchymal disease: Acute GN, TTP/HUS, vasculitis c. Renovascular disease: Renal artery stenosis d. Endocrine: Pheo, Cushing’s, renin-secreting tumor e. Drugs: Cocaine, amphetamines most common; reported with epo, cyclosporine; anti-hypertensive withdrawal f. Pregnancy: Eclampsia g. CNS disorders: head injury, CVA, increased ICP h. Autonomic hyperreactivity: Guillain-Barre, porphyria III. Differentiation from TTP/HUS a. TTP pentad: Microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure, fever, altered mental status. MAHA, ARF, and altered mental status are common manifestations of malignant HTN; thrombocytopenia and fever less common. i. Note that it is UNCOMMON for patients to present with all 5 parts of the pentad; only MAHA and thrombocytopenia without another clear source are truly required for dx b. Differentiation between TTP and malignant HTN: Patients with TTP alone would be unlikely to have the degree of elevation of BP seen in malignant HTN; also, the fundoscopic changes are unique to malignant HTN. Note, however, that TTP is on the list of diseases that can cause malignant HTN; so the two diseases may co-exist IV. Management: Note that these recommendations are more consensus-of-experts quality than true RCT-proven guidelines a. Hypertensive emergencies: Require ICU admission, A-line, and aggressive BP control, usually with IV agents i. Goal is reduction of BP to DBP of 100-110 mmHg (but reduce MAP by no more than 20- 25% of initial) over first 2-6 hrs. Careful monitoring for worsening of CNS status. ii. Rx choices: 1. Sodium nitroprusside (Nypride): Usual first line therapy. Can cause cyanate or thiocyanate toxicity (after 24-48 hours of rx), which is more of a worry in CSC Apr-03 patients with underlying renal or hepatic dysfunction. Onset immediate, duration of action 1-2 minutes. 2. Labetalol: Both alpha- and beta-blocking properties. 3. Fenoldopam: Peripheral D1-receptor agonist that causes direct vasodilation, renal-arterial dilation, and natriuresis. 4. Others: hydralazine, IV nitroglycerin, nicardipine iii. Special situations: 1. Eclampsia: Deliver the baby; MgSO4 2. CVA: More permissive HTN b. Hypertensive urgencies: Can usually be managed by oral agents
