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Vicki Groo, Pharm.D.

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Vicki Groo, Pharm.D. Define hypertensive crisis and describe differences between hypertensive urgency and hypertensive emergency Describe causes of hypertensive crisis Discuss pathophysiology of hypertensive
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Vicki Groo, Pharm.D. Define hypertensive crisis and describe differences between hypertensive urgency and hypertensive emergency Describe causes of hypertensive crisis Discuss pathophysiology of hypertensive crisis Compare and contrast treatment options for hypertensive crisis Design a treatment plan for a given patient with hypertensive crisis Hypertension SBP 140 mmhg and/or DBP 90 mmhg Stage 1 Hypertension SBP and/or DBP Stage 2 Hypertension SBP 160 mmhg and/or DBP 100 mmhg Hypertensive Crisis SBP 180 mmhg or DBP 120 mmhg Causes Medication nonadherence Illicit drug use (i.e. cocaine, amphetamines) Withdrawal (i.e. clonidine rebound) Mechanism is poorly understood, but likely initiated by abrupt increase in SVR Increase in BP causes endothelial injury and mechanical stress Increased permeability, activation of coagulation cascade and platelets, and fibrin deposition Marik PE. Chest 2007; 131(6): Hypertensive Urgency Severe elevations in blood pressure NO evidence of target organ dysfunction, but may be symptomatic BP may be lowered over several hours to days NOT life threatening Oral therapy Hypertensive Emergency Severe elevations in blood pressure Evidence of ACUTE target organ dysfunction BP must be lowered (not necessarily to normal) immediately Potentially life threatening IV therapy Hypertensive encephalopathy (MS changes, confusion) Stroke (focal speech or motor impairment) Dissecting aortic aneurysm (chest pain radiating to back, unequal pulses) ACS = Acute Coronary Syndromes CP = chest pain SOB = shortness of breath MS = mental status ACS (CP, SOB, cardiac enzymes, EKG changes) Acute heart failure (SOB, pulmonary edema) ARF ( Cr, BUN, UOP) Varon J. Drugs 2008;68(3): Accessed 11/24/08. Symptoms Chest pain (27%) Dyspnea (22%) Neurologic deficits (21%) Organ dysfunction uncommon with DBP 130 mmhg Except in children and pregnant women Rate of increase of BP may be more important than absolute level Marik PE. Chest 2007; 131(6): Thorough patient history Hypertensive history Antihypertensive medications and adherence Use of recreational drugs Confirmation of BP in both arms with proper size cuff Physical exam Pulses, ascultation of lungs, heart, renal arteries Neurologic and fundoscopic exam Treatment goal Lower BP slowly over hours Oral medications recommended Avoid immediate release nifedipine, SL captopril, or high dose oral medications Rapid BP reduction may be associated with significant morbidity CPP = MAP ICP (normal ~ 80 mmhg) 2/jorg=clinics&source=&sp= &sid=0/N/646416/f jpg. Accessed 11/25/08 Captopril mg PO Labetalol mg PO Clonidine mg PO Rebound effect in noncompliant patients Consider adjustment of oral medications Caution: Loading with oral agents may lead to delayed drop in BP Restart medications in noncompliant patients Follow-up in 2-3 days Treatment goal Reverse target-organ damage Reduce MAP by up to 25% within minutes to few hours Further reduce MAP to mmhg over next 2-6 hours Convert to oral medication regimen once condition stabilized Chobanian, et al. Hypertension 2003;42: Vasodilators Sodium nitroprusside Nitroglycerin Nicardipine Fenoldopam Enalaprilat Adrenergic Inhibitors Esmolol Labetalol Phentolamine Agent Dose Special Indications Avoid in. Nitroprusside mcg/kg/min Most hypertensive emergencies; pulmonary edema Nitroglycerin mcg/min Acute coronary syndromes (ACS); pulmonary edema Nicardipine 5-15 mg/h Most hypertensive emergencies; encephalopathy Fenoldopam mcg/kg/min Enalaprilat 1.25 mg q6h up to 5 mg q6h Esmolol mcg/kg/min Labetalol mg IV q 10 min or 1-2 mg/min Most hypertensive emergencies Left ventricular failure Aortic dissection; perioperative HTN Most hypertensive urgencies Phentolamine 5-20 mg IV bolus Catecholamine excess Caution in ARF or ICP; use only with beta blocker (BB) in aortic dissection Use only with BB in aortic dissection Acute HF or ACS Glaucoma ACS Acute HF Immediate release nifedipine (PO or SL) May cause unexpected precipitous drop in BP Reports of stroke and AMI Sudden decrease in BP in setting of acute ischemic stroke Disruption in autoregulation may worsen neurologic deficits Use of vasodilator without beta blocker in acute aortic dissection Achieve beta blockade (HR ~60 bpm) before adding vasodilator Goal SBP mmhg Hypertensive urgency is non-life threatening, but may be symptomatic Can be treated over several days with oral medications Hypertensive emergency is life-threatening with acute target-organ damage BP must be lowered by 25% in first hour IV infusion therapy with rapid onset and short duration preferred
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