Severely Increased Blood Pressure In The ED: Treating The Mercury? Rick Blubaugh, D.O. Cornerstone Physician’s Management Group Skaggs Community Health Center Branson, MO Case History 50 y/o male History of hypertension Hasn’t taken meds in 1 year C/O headache & malaise for 2 days Exam: remarkable only for BP 210/120 & grade I retinopathy Questions For EP Is patient stable? Is further WU indicated? & if so, what? Does pt require immediate intervention? & if so, what? Does pt require admission or monitoring, or if D/C’d, how soon should he be seen in follow up? Background Prolonged & severely increased BP causes cerebral, cardiovascular, and renal disease (Target Organs). Morbidity & mortality can be improved with treatment Limited data concerning acutely elevated blood pressure Physiology Affects heart, brain, kidneys, & large arteries Chronic HTN causes right shift in pressure flow autoregulation curve When BP decreases, cerebral vasodilation occurs When BP increases, constriction occurs Cerebral perfusion pressure remains constant despite fluctations in MAP Normal individuals: cerebral blood flow remains constant for MAP of 60-150mmHg When MAP decreases to less than lower limits of autoregulation, the brain becomes hypoperfused & cerebral hypoxia occurs. MAP = Diastolic + 1/3 (Systolic – Diastolic) Cerebral perfusion pressure = MAP – Intracranial pressure Chronic hypertension: lower limit of autoreguation is increased Autoregulation might fail at MAPs well tolerated in normotensive individuals Lower limit of autoregulation is approximately 25% of MAP Therefore, MAP should not be lowered by more than 20-25% Autoregulation Curve Fig. 4. Gao, E. et al. Am J Physiol Heart Circ Physiol 274: H1023-H1031 1998 Copyright ©1998 American Physiological Society Clinical Evaluation BP 180/110: immediate or evaluation within 1 week (Joint National CommitteeVI Guidelines) Recheck BP: many spontaneously reduce Seated, arm at level of heart, both arms Automated cuff inaccurate in A-Fib or irreg Manage pain or underlying causes Fundoscopic exam: retinal hemorrage or papilledema Cardiovascuar exam: Identify heart failure Neuro exam: LOC, visual fields, motor & sensory deficits Serum creatinine ECG Med History including OTC Urine drug screen: cocaine, amphetamine Stratification of Hypertensive Events Emergent Urgent Uncontrolled hypertension Hypertensive Emergency Rapid, progressive decompensation or damage of target organs Hypertensive encephalopathy, or brain hemorrage Acute aortic dissection, acute LV failure, AMI, unstable angina, symptomatic aortic aneurysm. Acute glomerulonephritis,kidney transplant Hypertensive Emergency Pheochromocytoma Sympathomimetic use Severe burns Severe epistaxis Eclampsia/preeclampsia Requires immediate (1-2 hours) BP reduction Parenteral agent Nitroprusside – most events Labetalol – intracranial disorders (does not dilate cerebral vessels) B- blockers – aortic dissection (blocks reflex tachycardia) Oral agents – should not be used (limited data, high failure rates, not titratable, uncontrolled hypotension) Emergent Blood Pressure Reduction Should not exceed 20%-25% of pretreatment BP 1st 30-60 Min: Reduce MAP to 110-115 Further reduction over next 24 hours Hemorrhagic & Ischemic CVA When systolic BP is reduced, cerebral autoregulation might fail leading to extension of CVA Some believe that elevated MAP is protective in CVA AHA: reduce BP in CVA only when MAP is > 130mm Hg or SBP > 220 mm Hg Esmolol & labetalol are good choices Nipride – cerebral vasodilation Cardiovascular Emergencies CHF – nitroprusside & ACE inhibitor ACS – nitroglycerine – reduce BP to normal levels Aortic Dissection – nitroprusside + Bblocker. Hypertensive Urgency Controversial History of prior target organ disease (CHF, CAD, angina, renal insuff, TIA, or CVA) Treatment strategy should be initiated in ED, although BP does not necessarily need to be reduced in ED Reliance on specific numbers is inadequate Hypertensive Urgency VA Cooperative Study: no adverse outcomes within first 3 months in patients who had DBP 115-130mm Hg No evidence to support practice of treating hypertension by reducing BP acutely in ED Numerous reports of adverse outcomes with acute, rapid reduction of BP in ED. Uncontrolled Hypertension Asymptomatic elevated BP without evidence of target organ disease Represents majority of patients with elevated BP in ED Goal: lifelong BP control Treat pain or infection Refer for recheck after primary problem resolved ( 1 week) Uncontrolled Hypertension If patient has quit taking antihypertensive meds – then restart them 1/3 of patients in ED with DBP > 95 mmHg were normotensive at follow-up Initial Oral Drug Choices Case Revisited Tx: analgesia for headache Lab: Serum creatinine, UA, ECG CT: if findings on H&P suggest CNS involvement If history or CT scan shows prior CVA, then patient qualifies as hypertensive urgency – justifying initiation of maintenance treatment Best regimen is one that previously worked Otherwise – diuretic & B-blocker Follow up in 1 week or observation Case If clinical exam & work up is negative & BP remains elevated after resolution of headache, then patient is stratified as uncontrolled hypertension Follow –up with PCP Summary Hypertensive Emergency – rapidy, progressive end-organ damage. Needs parenteral meds & ICU Caution in cerebrovascular events Summary Hypertensive Urgency – BP elevated > 180/110 & history of end- organ disease. Initiate oral meds & short term follow up or observation Uncontrolled Hypertension – asymptomatic Referral to PCP & education