Hypertensive Emergencies Trevor Langhan PGY3 November 10 2005

Hypertensive Emergencies Trevor Langhan PGY-3 November 10, 2005

Objectives n n n Discuss cases of hypertension in ED How to lower BP and when not to do it How low is too low? Or too fast?

Receptor sites n n n alpha-receptor Vasoconstriction iris dilation intestinal relaxation intestinal sphincter contraction bladder sphincter contraction n n beta-receptor vasodilation (b 2) cardioacceleration (b 1) intestinal relaxation (b 2) uterus relaxation(b 2) bronchodilation (b 2)

quiz

Nitroprusside CON PRO n n n Vasodilator Direct effect on smooth muscle Dose related BP reduction Drug of choice for most HTN emergencies Rapid onset Short duration n n Increase ICP Metabolized to thiocyanate by KD n cyanide can build up n ARF and prolonged use n Avoid in pregnancy Must be IV n Unstable in UV light n Must be wrapped Supine to prevent orthostasis S/E due to decreased BP and vasodilation

Fenoldopam PRO n n n Peripheral dopamine agonist Improves renal function Rapid action Does not cross blood brain barrier Hypotension less often CON n Tachycardia, flushing and h/a may occur

nitroglycerin PRO n n Vasodilating agent n venous Decreases LVEDP Reduces BP by decreasing preload and CO Sublingual or IV CON n n Limit to pts with cardiac ischemia or pulmonary edema Hypotension with pts who have RV dysfunction

hydralazine PRO n n Direct arterial vasodilator Historically used ++ in PIH and eclampsia CON n n Reflex tachycardia May provoke angina Flushing, n/v, h/a Chronic use results in lupus like syndrome

Beta-blockers - labetalol PRO n n n Selective alpha 1 and nonselective beta blocker IV or oral No reflex tachycardia Less uncontrolled drops in BP May not need ICU Good for aortic dissection or cardiac ischemia CON n n IV use has deep orthostasis Supine post admin x 2 -3 hours No effect on renal or cerebral blood flow Contraindicated: n Heart block n CHF n Asthma n pheo

Beta-blockers - esmolol PRO n n Ultra short acting Selective beta 1 Little BP effects Good for reflex tachy CON n n n Thrombophlebitis Tissue necrosis Contraindicated: n Heart block n CHF n Asthma n Pheo n cocaine

alpha-blockers - phentolamine PRO n n Alpha-blocker Use in catecholamine HTN crisis: n Pheo n MAOI crisis n cocaine CON n Reflex tachycardia

nicardipine PRO n n n IV CCB Titratable Less negative inotropy Less tachycardia Mostly vasodilator Safe in pregnancy CON n n n Caution in poor LV fxn Liver metabolism H/a, flushing, tachycardia

Enalaprilat/enalipril PRO n n n IV ace-I Infrequent hypotension Increasing evidence for use in cardiac n Remodeling CON n n n Not dose related May precipitate ischemia if MAP drop too steep Angioedema Cough ARF Toxic in 1 st trimester

quiz - fin

§Hypertension § § § What is normal BP? § SBP < 140 § DBP < 90 What is hypertension? § SBP >160 § DBP >100 Anything in between GRAY.

§Hypertension § Possible cardiovascular causes of increased BP: § Loss of vessel elasticity with age § Coarctation of aorta § Delayed femoral pulses § Hypertensive upper extremities § Bruit in upper back

§Hypertension § Endocrine causes for elevated BP: § § Pheo Excess steroids § Often iatrogenic § Cushings § Look for hypokalemia § Volume overload from Na retention

§Hypertension § Other causes include: § § § § Withdrawal of sedative drugs § Et. OH, benzo Tyramine toxicity in MAO-I patients Aortic dissection Sympathomimmetic drug intoxication Withdrawal of clonidine or beta blocking agents Reno-vascular disease Renin-angiotensin system abnormality

§Hypertension § HTN will present to the ED in a variety of ways: § 1. Hypertensive crisis/emergency § 2. Hypertensive urgency § 3. Mild hypertension without EOD § 4. Transient hypertension

Malignant hypertension n n Malignant hypertension: Term no-longer used Prognosis of this d/o has changed much since first introduced in 1928 1 -2/100 000 people in developed countries 1 year survival has increased n <22% in 1939 – 90 % in recent series Only age and renal function at presentation are independent markers of prognosis

§Hypertensive Emergency § § Also called hypertensive crisis Elevated blood pressure § signs of acute damage to target organs § Brain § Eyes § Heart § kidneys

§Hypertensive Emergency § § Malignant hypertension § Hypertensive encephalopathy § Microangiopathic hemolytic anemia § Acute renal failure Eclampsia/preeclampsia Aortic dissection HTN in setting of: § MI § Left ventricular failure § Bleeding § Thrombolytic therapy

§Hypertensive Urgency § § § Blood pressure elevation is an imminent risk for target-organ damage No acute end organ damage but risk is high if BP elevation continues Relative increase in BP more important than specific numbers

• Hypertensive Emergency n Rosen’s states: n True medical emergencies n Immediate reduction of BP in 1 hour

§Pathophysiology § § Mild to moderate increase in BP leads to initial vasoconstriction “autoregulation” § Maintains perfusion at relatively stable level § Prevents increased pressure from being transmitted downstream to smaller vessels As BP further increases, autoregulation fails Elevated BP disrupts vasc endothelium, causing narrowing

§Pathophysiology § § Chronic increase in BP causes arteriolar hypertrophy Will decrease the amount of pressure passed on to more distal vessels § Chronically hypertense people need diastolic BP’s >130 for symptoms § Normotensive people can have hypertensive crisis at DBP > 100

§Case 1 § § § 45 y male c/o 12 hour history of SOBOE, mild chest heaviness Vomiting, drowsy Bi-frontal headache Blurred vision both eyes BP 240/150, HR 102, RR 16, sats 95%

§Case 1 § § § PMHx: ? HTN, was on a “water pill” many years ago. No DM, no CAD, generally healthy Labs normal, except Creat: 150 Inx? DDx? Mgnt?

Hypertensive Emergency

Hypertensive Emergency

Hypertensive Encephalopathy § § Cerebral edema: § breakthrough hyper-perfusion from severe and sudden increase BP § BP has exceeded the capacity of autoregulation § vessels that can’t accommodate the pressure § leakage and edema (fibrinoid necrosis) Autoregulation must be considered during treatment § Hypertrophied vessels can’t vasodilate § caution with lowering blood pressure § Avoid relative hypoperfusion

Hypertensive Encephalopathy § § True medical emergency Is an acute presentation, but reversible Progression of untreated cerebral edema leads to coma and death Admission and invasive BP monitoring is the recommended mainstay of therapy

Hypertensive Encephalopathy § Test: § 1) BP 140/90 § What is MAP? § What is goal MAP § 2) BP 240/140 § What is MAP? § What is goal MAP? Approx- 110 Goal – 85 Approx – 175 Goal - 130

Hypertensive Encephalopathy § § § First hour goals: § Reduce MAP by 25% § Keeping DBP > 110 mm. Hg Goal at 4 -6 hours: § Reduction to pt’s normal BP What agents? § Nitroprusside - titratable, easy off, potential toxicity § labetalol – alpha and beta blocker

§Case 2 § § § 67 y female known CAD, DM, smoker, atrial fib. Presents with c/o weakness left side BP 160/100, HR 94, RR 14, sats 99% O/E left facial droop, markedly weak left upper/lower extremity EKG: a fib, nil acute Chest exam unremarkable

§Case 2 § § Management? How do you treat her elevated BP?

§Stroke syndromes § § Most patients with this presentation are ischemic strokes (85%) not hemorrhagic Likely don’t have acutely elevated BP May have mild to moderate BP elevation ***CAUTION*** § lowering BP as watershed area sensitive to hypoperfusion § Lowering BP may worsen ischemic brain injury

§Stroke syndromes § Rarely stoke with grossly elevated DBP > 140 § But a contraindication to t. PA is a BP >185/110 § § Patients receiving reperfusion therapy may require a lowering of BP Titrate labetalol slowly to achieve decrease in MAP by a max of 20%

§Stroke syndromes § § What if on CT it is an ICH? Little data about acute BP lowering in ICH Many centers lower MAP 20% § May be a negative thing to do § CPP depends on BP in setting of increased ICP § Most ICHs have elevations of ICP If lowering is done, use an agent that dose not vasodilate § Avoid nitrates § Labetolol is best (ACE-I have some benefit)

Case 3 n n n n 55 year male known LV dysfunction (EF 30%) Chronic HTN On low dose lasix and daily asa, metoprolol Was off his low Na+ diet over all-inclusive vacation to Mexico Weighs 8 pounds more than usual Legs swollen HR 95, BP 190/120, sats 89%, RR 25

Case 3 n n Chronic pulmonary edema results in increased PVR and HTN Acute decompensation in setting of CHF can have marked increase in BP due to catecholamines

Case 3 n n n Standard treatment of CHF: n Morphine n Oxygen n Nitrates (nitroprusside better than NTG) n lasix Improving evidence for use of ACE-I in setting of acute LV dysfunction and CHF Be on lookout for stroke syndrome as result of acutely lowered BP in someone chronically HTN

§Case 4 § § 32 y female awaiting “sweatgland” surgery from plastics for hyperhydrosis, c/o H/A, palpitations BP 170/90, HR 150 sinus, RR 18 Otherwise healthy Treatment: § Nitroprusside if emergency § Phentolamine – 1 -5 mg IV boluses (alpha-block) § Followed by beta-blockade

§Case 4 § § § Pheochromocytoma Rare tumor – 0. 2% of pts with essential HTN Episodic H/A, tachycardia, sweating, HTN Tumor secreting norepinephrine and epinephrine Diagnosis: § Radiographic § measurement of urinary and plasma levels of catecholamines and metabolites

§Case 5 Hypertension in pregnancy § § § 25 y G 2 P 1, LMP 6 months ago When do you treat HTN in pregnancy? § SBP > 160 § Treat to goal of 140 -155 § 5 -10% of all pregnancies Any acute DBP elevation >100 is a true HTN emergency Eclampsia and preeclampsia may occur without extreme elevation of BP Treatment: § Prevention and control of seizures § Early obs consult

n n n Ecclampsia Dx: nd or 3 rd trimester n Elevated BP in late 2 n SBP > 140, DBP >90 n Elevated urine proteins n Pedal edema No mortality benefit treating SBP 140 -170 Expert consensus that SBP > 160 need treatment Methyldopa, CCB, acute episodes with lobetolol or hydralazine Eclampsia seizure risk peaks during delivery and 2448 hours after – prevention of seizures with prophylaxis recommended

§Case 6 § § § 33 year male stock broker. Snorted a “couple of rails” of cocaine ½ hour ago. Presents with crushing retrosternal chest pain, diaphoresis and H/A BP 190/100, HR 130, RR 28, sats 96% EKG ST segment elevation V 1 -V 3 Nurse asks “what do you want to give? ”

§Case 6 § Beta blocker contraindicated § Beta antagonism will decrease heart rate, but will also block B 2 receptors § Will have unopposed alpha agonism by cocaine toxicity – dangerous HTN crisis § Need alpha blockade first § Like pheo can use phentolamine, some sources say hydralazine § benzo dosing to decrease BP, HR and battle sympathetic tone of cocaine

§Case 7 § § § 55 year male smoker, HTN, DM, unstable angina getting worse. Shoveling snow and developed left RSCP that radiated to his jaw. HR 120, BP 190/90, RR 19, sats 99% EKG obvious ant/lateral infarct How do you treat his pressure?

§Case 7 § § Agents of choice in HTN during ACS § Immediate lowering of BP indicated to prevent myocardial damage § Also lower BP if pt to undergo reperfusion tx § NTG agent of choice § Beta block § ACE-I (shown improvement in mortality) § CCB (if BB is contraindicated) Contraindicated agents include: § Hydralazine – reflex tachycardia § Nitroprusside – reflex tachycardia

§Key concepts § § § Presence of acute target organ damage determines HTN crisis All pts with persistent elevation of BP should be investigated for EOD ER doc should be familiar with indications and contraindications of meds to treat HTN crisis Goal of treat is relative decrease in MAP of 25% in first hour, DBP should not fall <110 mm. Hg Pts without EOD rarely require urgent management of HTN