Hypertensive Crises. Controlling high blood pressure prevents disease. Recognition and Management of Acute Hypertensive Emergencies

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1 Controlling high blood pressure prevents disease Recognition and Management of Acute Hypertensive Emergencies David idweiner, M.D. Co-holder, C. Craig and Audrae Tisher Chair in Nephrology Functional Genomics University of Florida College of Medicine and NF/SGVHS Arch Int Med 157:2413, Those at greatest risk benefit the most JNC-7 BP Classifications Classification SBP DBP Normal < 120 <80 Prehypertension Stage I Stage II Hypertensive crisis > 180 >120 Arch Int Med 157:2413, Two types of hypertensive crisis Long-term survival is bad in patients with hypertensive emergency Hypertensive emergency Hypertension causing acute end-organ damage Hypertensive urgency Hypertension not causing acute end-organ damage, (Typically y causes severe anxiety, particularly in the physicians) Predictors of shorter survival Renal damage Proteinuria BUN > 28 mg/dl Creatinine > 2.2 mg/dl LVH by ECG Causes of death Renal failure (39.7%), Stroke (23.8%), Myocardial infarction (11.1%) Heart failure (10.3%) Median Survival (Months) J Hypertens 13:915-24, University of Florida College of Medicine Page 1

2 Patients with hypertensive emergencies have hypertension-related and other chronic conditions Antihypertensive use in week prior to presentation 90% 82% 80% 70% 60% 50% 40% 60% 50% 40% 30% 46% 54% 32% 31% 24% 22% 30% 20% 19% 17% 10% 0% 10% 9% 15% 16% 20% 20% 15% 12% 10% 0% 2% 2% Acad Emerg Med 7:653-62, Acad Emerg Med 7:653-62, Hypertensive Emergency What are the typical presentations? What should you do - JNC-7 Guidelines Acute pulmonary edema, 37% Intracerebral or SAH, 5% Encephalopathy, 16% ACS, 12% Aortic dissection, 2% Eclampsia, 5% Ischemic CVA, 25% The initial goal of therapy in hypertensive emergencies is to Reduce mean arterial BP by no more than 25% within the first hour, Then, if stable, To 160/ mmhg within the next 2-6 hours. But, which is worse Risk of ACUTE hypertension-induced tissue damage Risk of ACUTELY decreased tissue perfusion due to decreased BP How solid is the data for these recommendations? In depth Cochrane review, It was definitively disappointing No RCT evidence to answer the question: Does antihypertensive therapy, as compared to placebo or no treatment, Change mortality and morbidity in patients with hypertensive emergencies? Patient #1 Mr. XYZ is a 72 yo gentleman who presents to the ED with acute onset of left arm weakness 4 hours earlier. The event occurred while he was putting on the 15 th hole, he missed his putt, and he complains about missing the putt. He tells you he has a h/o HTN and DM and that his HTN is treated with a β-blocker and an ACE-I. He took his β-blocker this morning (to help his putting!). He did not take his ACE-I (he worries about getting lightheaded while playing golf on a hot day) J Hum Hypertens 22: , University of Florida College of Medicine Page 2

3 Patient #1 Physical examination BP 187/121; HR 84; RR 20 (wnl) Left arm weakness, with increased DTR in the biceps Is this a hypertensive emergency? Yes, very hypertensive Yes, has acute end-organ damage Should you Lower the BP? Raise the BP? Hypertensive emergency in the setting of an acute CVA Elevated BP, in the short-term, may maintain ischemic tissue perfusion BP decreases ~20 mmhg in first 24 hr in the absence of therapy JD Blumenfeld, et al, AJH 14: , Correlation between BP and outcome in stroke patients Excessive BP change (1st 24 hrs) worsens outcome 90% 100% 57% 80% 54% 30% 60% 49% 13% 24% 40% Increase 20% 14% 11% Decrease >20 Decrease % SBP change in 1 st Early neurologic Poor neurologic Mortality, 3 deterioration outcome month 24 hours Stroke 33: , J Castillo, et al, Stroke 35:520-7, Clinical trials of BP management in acute stroke Effect of early candesartan on events after CVA Calcium channel blockers Ineffective Cochrane Database of Systematic Reviews 2000; Issue 1. Outcome worsened Cerebrovascular Diseases 1994;4: Stroke 2000;31: β-receptor antagonists Outcome worsened BMJ 1988;296: Lisinopril or labetalol vs placebo Decreased mortality, but no effect on functional status Lancet 2009;8: ARB s No effect on functional outcome at 3 months, but improved mortality and vascular events at 10 months Stroke 2003;34: No improvement in any measure at t6 months, and dincreased risk of poor functional outcome with ARB use Lancet 377:741-50, Trial of stopping meds! No difference between stopping or continuing meds on outcomes Lancet Neurol 2010; 9:62-5. Lancet 377:741-50, 2011 University of Florida College of Medicine Page 3

4 Effect of early candesartan on events after CVA Recent (2011) editorial The results of the 2011 ARB trial are also consistent with the results of ten previous trials of blood-pressurelowering drugs in independent populations with acute stroke. Clinicians should therefore not be prescribing blood- pressure-lowering drugs with the first week of acute stroke in routine practice. Lancet 377:741-50, 2011 Lancet 377:696-8, Stroke and hypertension summary BP > 185/110 Yes Bring it down some (Labetalol, Nicardipine); Keep it down Yes No Reperfusion Therapy? Take a deep breath, Relax. No need for emergent therapy No Yes Bring it down slowly % in 1 st day BP > 220/120 No Take a deep breath, Relax What to do in the setting of an acute ischemic CVA Patient is eligible for acute reperfusion intervention SDP > 185 or DBP > 110 Labetalol 10 to 20 mg IV over 1 to 2 minutes, may repeat once; or Nitropaste 1 to 2 inches; or Nicardipine infusion 5 mg/h, titrate up by 2.5 mg/h at 5- to 15-minute intervals, maximum dose 15 mg/h; when desired blood pressure attained, reduce to 3 mg/h If blood pressure does not decline and remains >185/110 mm Hg, do not administer thrombolytics BP management pressure during and after treatment acute reperfusion Monitor blood pressure every 15 minutes during treatment and then for another 2 hours, then every 30 minutes for 6 hours, and then every hour for 16 hours Systolic 180 to 230 mm Hg or diastolic 105 to 120 mm Hg Labetalol 10 mg IV over 1 to 2 minutes, may repeat every 10 to 20 minutes, maximum dose of 300 mg; or Labetalol 10 mg IV followed by an infusion at 2 to 8 mg/min Systolic 230 mm Hg or diastolic 121 to 140 mm Hg Labetalol 10 mg IV over 1 to 2 minutes, may repeat every 10 to 20 minutes, maximum dose of 300 mg; or Labetalol 10 mg IV followed by an infusion at 2 to 8 mg/min; or Nicardipine infusion, 5 mg/h, titrate up to desired effect by increasing 2.5 mg/h every 5 minutes to maximum of 15 mg/h If blood pressure not controlled, consider sodium nitroprusside BP management if no reperfusion therapy SBP 220 and DBP 120 Relax, take a deep breath and do nothing Continue existing meds SBP > 220 or DBP > 120 Lower BP cautiously Reasonable goal 15-25% within the first day Restart oral medications, titrate carefully my recommendations University of Florida College of Medicine Page 4

5 Patient #2 Mrs. ABC is the 69 yo wife of Mr. XYZ who, on the same day, while playing tennis had acute onset of precordial tightness, diaphoresis and shortness of breath. She has a h/o HTN and DM; her HTN is treated with a β- blocker and an ACE-I I. She did not take either her β-blocker or ACE-I this morning (she worries about getting light-headed while playing tennis) Patient #2 EKG reveals acute ST-T wave changes Troponin is elevated BP 187/121; HR 84; RR 20 (wnl) What should you do about her BP? Hypertensive emergency and ACS Patient #3 Elevated BP increases myocardial O 2 demand Treatment goal Decrease myocardial O 2 demand while increasing O 2 delivery β-blockers Labetalol Nitroglycerin Avoid Nitroprusside Coronary steal Enalaprilat Unpredictable effect on BP Nicardipine Reflex tachycardia and increased myocardial O 2 demand Mr. DEF, their 45 yo son has worsening dyspnea for four days. He has non-ischemic cardiomyopathy, EF 15%. Because of work pressure, he has been drinking large amounts of coffee, using Adderal for ADHD and has not been taking his β-blocker, ACE-I and diuretic (they make him tired). BP 187/121; HR 84; RR 20 (wnl) Hypertensive emergency and CHF Patient #4 Hypertension increases afterload Decreases cardiac output Increases pre-load Causes development of pulmonary edema Treatment goal decrease afterload and preload Nitroprusside Needs arterial line ACE-I IV enalaprilat Avoid Nicardipine Reflex tachycardia, may decrease myocardial contractility Hydralazine Increased cardiac work β-blockers Decreased myocardial contractility Mrs. HIJ, their 44 yo daughter, on the same day, comes in with acute onset of back pain. She has Marfan s syndrome. Physical examination reveals 187/121; HR 84; RR 20 (wnl) BP in legs is 102/72 University of Florida College of Medicine Page 5

6 Aortic dissection and hypertension Critical to reduce both BP and dp/dt β-blocker, must be initial therapy (reduces both) Labetalol Metoprolol Esmolol Large volume load ( ml/kg/hr) Vasodilator, if needed, to reduce BP Nitroprusside Patient #5 Ms. KLM is the 24 yo granddaughter who, on the same day, while visiting her family, gets her BP checked and is found to have a BP of 187/121. She has a long-history of SLE Laboratory studies: BUN/Cr; 47/2.38 Hgb, 10.2 Haptoglobin, <10 Platelets, 47K Hypertensive emergency and renal involvement Labetalol Nicardipine Fenoldopam Nitroprusside Short-term only, < 48 hr! Patient #6 Mr. NOP is Mrs. ABC s brother While visiting her in the hospital, he has his VS checked 187/121; HR 84; RR 20 (wnl) He has a history of HTN and DM He did not take either his ACE-I or β-blocker today because he was hurrying to come visit her Physical exam, screening laboratory studies (renal function panel, CBC, U/A) All unremarkable What should you do? Differentiate hypertensive urgency from hypertensive emergency Is there acute end-organ damage? If not, then hypertensive urgency Does NOT require, or even need in most cases, hospital admission Key to treatment: This is a long-term problem, not a short-term problem Take a deep breath and relax Headache and anxiety are NOT end-organ damage Treating hypertensive urgency Restart meds, if discontinued or not current Add a new medication or increase dose of existing medication Arrange out-patient follow-up, preferably in 1-2 days Avoid clonidine! University of Florida College of Medicine Page 6

7 My favorite meds for hypertensive emergency Drug Dose Onset Duration Special indications Nitroprusside µg/kg/min Immediate 1-2 min Need arterial line; 48 hr limit with renal failure Nicardipine 5 mg/hr, titrate up by 5-10 min Caution with CAD 2.5 mg/h at 5- to 15- minute intervals, to max 15 min, but can be >4 hr Labetalol mg IV q 10 min mg/min 5-10 min 3-6 hr Avoid with CHF Enalaprilat mg q6hr min 6-12 hr Avoid with ACS, response variable depending on level of renin NTG µg/min 2-5 min 5-10 min Useful with ACS My less favorite meds for hypertensive emergency Drug Dose Onset Duration Special indications Fenoldopam < 5 min 30 min µg/kg/min Hydralazine mg IV min 1-4 hr Eclampsia mg IM min 4-6 hr Esmolol min min Aortic dissection µg/kg/min / Phentolamine 5-15 mg IV 1-2 min min Pheochromocytoma University of Florida College of Medicine Page 7