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Hypertensive Emergencies Alyssa Morris, R3 March 5, 2009 Thanks to Dr Gant! Definitions Hypertensive Emergency • Acute, life threatening, usually a BP> 180/120 • Target organ damage Hypertensive Urgency • Asymptomatic, severe HTN, usually >180/120 • NO target organ damage Hypertensive Emergencies Neurological • Hypertensive Encephalopathy • CVA • SAH • ICH Cardiovascular • MI/ischemia • Acute LV dysfxn • Ao dissection Pulmonary • Acute edema Other • Acute renal failure/insufficiency • Retinopathy • Eclampsia • MAHA Components of BP BP= CO x SVR CO= HR x SV Think of the components as: • CO= heart • BP= arteries • SVR= arterioles CPP=MAP-ICP CASE 1 Hypertensive Encephalopathy Uncommon syndrome Acute and reversible Results from an abrupt, sustained rise of BP that exceeds the limits of cerebral autoregulation of the small resistance arteries in the brain Arises from “breakthrough” hyperperfusion and leakage of fluid thru BBB Clinical Presentation Severe h/a Drowsiness ALOC Vomitting Seizures Focal neuro deficits Blindness Tx Various recommendations 25% over 3-4hrs 10% in first hour, 15% in next 2-3 hours *will not be able to perfuse brain if you drop it too fast or too much CPP=MAP-ICP Drug Options VASODILATORS CALCIUM CHANNEL • Nitroprusside BLOCKERS • Nitroglycerin • Enalaprilat/enalipril • Fenoldopam ALPHA BLOCKERS • Hydralazine • Phentolamine BETA BLOCKERS • Labetalol • Esmolol • Clonidine Nitroprusside Potent smooth muscle relaxing agent Reduces both preload and afterload Rate of onset rapid, duration very short Also a cerebral vasodilator Can increase ICP secondary to increased cerebral blood flow Unstable in UV light, therefore wrapped in tinfoil Infusion at 0.25-0.5ug/kg/min -then increase by 0.5mcg/kg/min Max of 10 mcg/kg/min Nitroglycerine 1) Activates guanylate cyclase 2) Accumulation of cGMP 3) Sequestration of Ca into SR 4) Relaxation of Vascular smooth muscle Dose dependent Low dose: venodilator (preload) High dose: veno and arteriodilator (afterload) Therefore, usually reduce BP by reducing preload and CO Start with 10-20ug/min infusion Titrate up 5-10ug/minQ3-5min Hydralazine Direct arteriolar vasodilator Used to be used as first line in pregnancy htv emergencies Starting dose is 5mg IV Repeat doses of 5-10mg IV every 20 mins to maintain desired BP Complications: • Marked hypotension • Reflex tachycardia (can give angina) • Flushing and nausea • H/a Labetalol Selective α-1 blocker and nonselective β-blocker α:β blockade ratio between 1:3 and 1:7 Not a significant drop in CO like other βB Does not affect cerebral blood flow or renal fxn BP starts to fall in 5-10m, max effect at 30m How much do you guys give? Esmolol Selective β-1 blocker Very short acting Elimination ½ life of 9 minutes No intrinsic sympathomimetic activity Phentolamine α-blocking agent Used for the Mx of catecholamine-induced HTV crisis MAOI, Pheo, Cocaine Immediate effect Effect lasts up to 15 mins 1-5mg IV boluses CASE 2 PRES Posterior reversible encephalopathy syndrome Pathophysiology Cerebral vasospasm leading to cytotoxic edema 2. Vasodilattion leading to vasogenic edema 1. CASE 3 HTN Mx in Ischemic Stroke Stroke. 2007;38:1655-1711. HTN Mx in Ischemic Stroke HTN common in 1st hours after stroke • SBP>160 found in 60% pts with acute ischemic stroke For every 10mmHg raise >180, risk of neurologic deterioration increases by 40% and risk of poor outcome by 23% HTN Mx in Ischemic Stroke Theoretical reasons for lowering BP in stroke • Decrease formation of brain edema • Lessening risk of hemorrhagic transformation of infarction • Preventing further vascular damage • Forestalling early recurrent stroke BUT remember aggressive tx of BP may lead to neurologic worsening by decreasing perfusion pressure to ischemic areas of brain CPP=MAP-ICP CASE 4 HTN Mx in Ischemic Stroke A lot of studies showing harm with reduction of BP Most pts have a decrease in BP a few hours post- stroke w/o intervention Oliveira-Filho et al. Neurology. 2003;61:1047-1051 • Found >90% pts had a decrease in SBP by 28% in 24hrs post-stroke with no intervention Consensus Statement “ emergency administration of antihypertensive agents should be withheld unless DBP>120 and SBP>220” “reasonable goal to decrease blood pressure by 15-25% within 24 hours” This is a case-by-case decision More research needs to be done Case 4 Stroke, 2007;38:2001-2023 HTN Mx in Hemorrhagic Stroke Primary rational for reducing BP is to avoid hemorrhagic expansion from potential sites of bleeding BP is correlated with increased ICP and volume of hemorrhage Difficult to determine whether increased BP is a cause of hemorrhage growth or an effect of increased volumes of ICH and increased ICP HTN Mx in Hemorrhagic Stroke Summary of studies Isolated SBP<210 is not clearly related to hemorrhagic expansion or neurologic worsening Decrease in MAP by 15% does not result in decreased CBF Baseline BP was not associated with growth of ICH in largest prospective study Hemorrhage enlargement occurs more frequently in pts with increased SBP but it is not clear if this is an effect of increased growth of ICH with associated increase in ICP or a contributing cause to the growth of ICH Evidence supports maintaining CPP >60mmHg HTN Bleeds Where do you get HTN bleeds in the brain? 1) Cerebellum 2) Pons 3) Basal ganglia 4) Thalamus Case 4 HTN Mx in Ao Dissection Remember to check BP in legs if you are thinking dissection b/c the flap can give you falsely low BP in arms Want to avoid shear stress and wide pulse pressures Reduce the LV ejection force Goal is to get SBP 90-110 but just do what you can Use labetalol or esmolol Can use nipride after have sufficiently BB b/c will blunt the reflex tachycardia and increased SV Case 6 Drug Summary Nitroprusside • 0.25-0.5ug/kg/min • Inc by 0.5ug/kg/min quickly Nitro • 10-20ug/min • Inc by 5-10ug/min Q3-10min Labetalol • 10-20mg IV Q5-10min • Infusion at 1-2mg/min