Doctor, Michael Jay Bresler, M.D The Patient’s Blood Pressure is Elevated! Page 1..

• 64 year old female you’ve diagnosed with acute bronchitis Hypertension in • Initial BP = 250/130 • On no meds Emergency Medicine • No history of hypertension • Feels fine except for cough MICHAEL JAY BRESLER, MD, FACEP • Ready for discharge: BP = 210/110

Clinical Professor Division of Emergency Medicine “Hey Doc, whadya want to give her?” Stanford University School of Medicine

• 64 year old female you’ve diagnosed • 64 year old male complaining of severe with acute bronchitis chest pain for 3 hours • Initial BP = 250/130 • Initial BP = 230/120 • On no meds • EKG normal • No history of hypertension • Widened mediastinum on CXR • Feels fine except for cough • Repeat BP = 170/90 • Ready for discharge: BP = 250/140 • “Doc, they’re ready in CT.”

“Hey Doc, whadya want to give her?” “Hey Doc, whadya want to give him?”

Agenda for Our Discussion Questions to be addressed • General Considerations In the Emergency Department • Blood Pressure Readings in the ED • When should HBP be treated ? • Pathophysiology • When should HBP not be treated ? • Pharmacologic Treatment Modalities • When should outpatient therapy be • Specific Emergencies Requiring BP started? Reduction in the ED • What agents should we use? • Post ED Therapy • For what conditions? • Summary - Hypertension in the ED

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• I will use primarily generic names • But I will also include on the slides the brand names since these are most commonly used in the real world - I have no financial relationship where we practice • When there are several brand names I with any drug company will try to include them all • I have no idea which companies make which drugs

What is Normal Blood Pressure ??

Prehypertension General 130-139/80-90 Considerations • Compared with normal BP – Double the risk for developing hypertension. • Lifestyle & diet intervention warranted Joint National Committee on Hypertension,2003

Incidence of Hypertension in U.S.A. Scope of the Problem

• > 140/90 (HTN) • Normotensive people at age 55 have a – 27% of adults 90% lifetime risk of developing HTN (Ref: Vasan) • > 130/90 (pre HTN + HTN) • Between age 40-70, the risk of – 60% of adults! cardiovascular disease doubles for every – 88% > 60 years old (independent variables) – 40% ages 18-39 !! – 20 mm Hg systolic above 115 Wang Arch Intern Med 2004 – 10 mm Hg diastolic above 70 »Lewington Lancet 2002

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Should BP Rise with Age? BP and Gender

• Estrogens protect NO !! • After menopause, women catch up with men and eventually surpass In societies with natural diet, less salt, and less obesity, more exercise the men – BP does not rise with age (in blood pressure that is….) • Diet is a particular problem - – We love our unhealthy diet!

BP and Ethnicity High Blood Pressure Readings in • Incidence of HTN – 1.5 - 2 x more common in Blacks the Emergency Department • 1 in 3 African Americans • 1 in 4-5 Caucasian and Hispanic Americans • ? Asians • African Americans – HTN begins earlier – More end organ damage –ACEI’s & ARB’s less effective

Is that reading real? Question • Asymptomatic E.D. patients with BP >140/90 – BP at home bid – > 1/2 continued >140/90 – Most of rest continued at pre-hypertensive level Are ED BP readings – Independent of pain or anxiety in E.D. accurate & reliable for » Tanabe Ann Emerg Med 2008 screening asymptomatic • E.D. patients with BP >140/90 followed in clinic patients for HTN? – 54% continued >140/90 » Cline Acad Emerg Med 2000

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ACEP Clinical Policy Question

• Level B Recommendation –If SBP persistently > 140 or Do asymptomatic –If DPB persistently > 90 patients with elevated BP Refer for follow up of possible HTN benefit from rapid and BP management lowering of their BP? Ann Emerg Med. 2006;47:237-249

ACEP Clinical Policy

• Level B Recommendation HBP in the ED – Initiating Tx in the ED is not necessary if F/U is available • Most useful terminology – Rapid lowering of BP is not necessary – Hypertensive Emergency and may be harmful – Hypertensive Urgency – When Tx is initiated, BP should be – Elevated Blood Pressure lowered gradually and should not be expected to be normalized during the ED visit Why is this the most useful classification?

Ann Emerg Med. 2006;47:237-249

HBP in the ED Hypertensive Emergency

• Hypertensive Emergency • By definition – Treated in ED with IV meds – Evidence of acute end organ damage • Hypertensive Urgency – Usually brain, heart, or kidney – May be treated in ED - oral meds OK • Definition implies that organ dysfunction – Usually give prescription is caused by acute HPB, rather than • Elevated Blood Pressure vice versa – Not treated in ED • Systolic usually > 220 – May or may not give prescription – We should refer for further evaluation • Diastolic usually > 130

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Hypertensive “Urgency” Hypertensive Urgency

• Major elevation of BP • Treatment may be administered in the (roughly in range of >220/>120) but ED if BP remains very elevated – Without evidence of acute organ – Controversial failure – Trend toward not treating in the ED – No acute symptoms directly • Outpatient treatment should generally attributable to elevated BP be initiated, however • Basic studies may be indicated

Diagnostic Studies in the ED • Incidental finding of moderate HBP – ED workup not necessarily indicated -> refer • If initiating outpatient treatment Pathophysiology – Basic studies in ED may be considered – CBC, lytes, renal, glucose, UA, EKG of Hypertension • If ED treatment required – Basic studies usually indicated • If hypertensive emergency - basic plus – Studies specific to disorder (CT, etc.)

Regulation of Blood Pressure Inherent stiffness of arterial wall

A Balance Between Cardiovascular risk factors lead to: • Replacement of elastin in arterial walls by collagen and fibrous tissue-> • Inherent stiffness of the arterial wall – Decreased compliance • Vasodilation – Increased resistance • Vasoconstriction • Endothelial dysfunction

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Pathophysiology Acute Regulation of BP  BP --> Endothelial wall stretch/stress • Vasodilation – Beta-2 adrenergic innervation Endothelial Dysfunction – Nitric oxide  c-AMP

• Vasoconstriction Capillary permeability – Alpha-1 adrenergic innervation Depletion of NO – Circulating catecholamines Inflammation – Angiotensin II

Renin-Angiotensin-Aldosterone Renin-Angiotensin-Aldosterone Angiotensin II

Angiotensinogen • Powerful vasoconstrictor Renin • Release of aldosterone Angiotensin I • Inflammatory response • Hypertrophy of smooth muscle cells ACE • Decreased nitric oxide -> Angiotensin II further vasoconstriction

Autoregulation and Hypertensive Crisis

Organ-specific autoregulation Auto-Regulation and • Normally maintains capillary pressure Hypertensive Crisis & flow within an acceptable range – Increased systemic BP -> vasoconstriction – Decreased systemic BP -> vasodilation

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Autoregulation of Cerebral Blood Flow Cerebral Autoregulation, Hypertension, and Excessive Correction

• Cerebral arterial resistance varies directly Hypertensive with BP to maintain cerebral perfusion within Person acceptable limits • “Set point” rises with chronic HBP • Rapid ED reduction of BP may drop CPF below adequate level Normotensive • Lower BP gently, Person • And usually never < 110 diastolic – Except • with aortic dissection Mean Arterial Pressure

Adapted from Elliott:Crit Care Clin 2001;17:435

Autoregulation and Hypertensive Crisis Pharmacologic Treatment Hypertensive crisis Modalities Autoregulation fails -> Endothelial dysfunction • Capillary permeability & edema • Inflammatory response • Prothrombotic response • Decreased nitric oxide Cell necrosis • Release of vasoconstrictors

Pharmacologic Treatment Modalities

• Parenteral Vasodilators • Beta Blockers • Calcium Channel Blockers • Angiotensin Converting Enzyme Parenteral Inhibitors • Angiotensin II Receptor Blockers Vasodilators • Direct Renin Inhibitors • Diuretics • Others

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Parenteral Vasodilators Parenteral Vasodilators

Nitroprusside (Nipride™, Nitropress™) Nitroprusside • Arterial > venodilator • Potential problems • Advantages – Unstable to UV light-must be wrapped – Most commonly used agent in EM – Orthostatic hypotension - keep supine – Metabolized to cyanide/thiocyanate – Extremely effective – Toxic at higher dose – Very short half-life • Potentially toxic to fetus • Are there better agents ?? – Tissue necrosis if extravasation – Increases intracranial pressure

Parenteral Vasodilators Parenteral Vasodilators

• Fenoldopam (Corlopam™) Nitroglycerin • Newer IV alternative to nitroprusside – Peripheral dopamine (DA-1) receptor agonist • Venodilation > arterial dilation – Rapid onset & offset of action – Good for CHF & angina – Improves renal function ? – Not a good drug for hypertensive crisis – Less chance of overshoot vs. nitroprusside – No thiocyanate toxicity or light sensitivity

Beta blockers

•ß1 blockade Beta – Lusitropic • (decreased cardiac contractility) Blockers – Decrease renin – Decrease norepinephrine

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Beta blockers Beta blockers • Most useful for Emergency Medicine • Advantages – Labetalol (IV, also alpha blocker) – Metoprolol (PO & IV) – Especially good with CAD – Esmolol • Decreased myocardial oxygen • (short acting cardioselective IV agent) demand • Among many other preparations available – Good with anxiety – Propranolol – Long acting preparations best for PO – Atenolol – Nadolol – Carvedilol (also alpha blocker)

Calcium Channel Blockers

• Decrease heart rate & contractility Calcium • Dilate peripheral vasculature Channel • 2 classes Blockers • Dihydropyridines • Nondihydropyridines

Calcium Channel Blockers Calcium Channel Blockers

• Nondihydropyridines Most useful for Emergency Medicine – Cardiac effect > vascular • In the ED (for blood pressure control) • verapamil, diltiazem – Nicardipine (Cardene™) IV – Clevidipine (Cleviprex™) IV • Dihydropyridines • Outpatient Rx – Vascular effect > cardiac – Long acting formulations of • nifedipine, amlodipine, nicardipine (DynaCyrc™, Cardene™) • felodipine, nicardipine nifedipine (Procardia™, Adalat™) • Dihyropyridines thus best for HBP – Do not use short acting dihydropyridines

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Calcium Blockers vs. Nitroprusside Advantages of IV calcium blockers Angiotensin (nicardipine, clevidipine) Converting • As effectifve as nitroprusside • No cyanide/thiocyanate toxicity Enzyme • Not light sensitive; no need for foil wrap • Less need for rate adjustment (1/3 as often) (ACE) • No need for arterial line Inhibitors • No intracerebral vasodilation causing edema

Regulation of BP ACE Inhibitors Renin-Angiotensin-Aldosterone Regulation of BP Renin-Angiotensin-Aldosterone Angiotensin II Angiotensinogen • Powerful vasoconstrictor Renin • Release of aldosterone Angiotensin I • Inflammatory response X ACE • Hypertrophy of smooth muscle cells • Decreased nitric oxide -> Angiotensin II further vasoconstriction ACEI’s block these effects

ACE Inhibitors ACE Inhibitors

• Also block metabolism of bradykinin • Especially beneficial with • Bradykinin is a strong vasodilator – Diabetes • However, bradykinin may cause the – Renal failure principal potential side effects of ACEI’s – Heart failure • Potential side effects - – Cough bradykinin mediated – Angioedema – Cough (1/10) – Angioedema (1/2,000)

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ACE Inhibitors

Most useful for Emergency Medicine • In the ED Angiotensin II – Enalaprilat IV (Vasotec™) • Outpatient Rx examples Receptor – Captopril (Capoten™) Blockers – Benazepril (Lotensin™) – Enalapril/enalaprilat (Vasotec™) – Lisinopril (Prininvil™, Zestril™) – Quinapril (Accupril™)

ACE Inhibitors Angiotensin II receptor blockers Regulation of BP Renin-Angiotensin-Aldosterone • Similar therapeutic effect as ACEI’s Angiotensinogen • Fewer side effects because unlike ACEI’s, they do not block bradykinin Renin breakdown. Therefore: Angiotensin I – No bradykinin mediated cough ACE – Extremely rare angioedema Angiotensin II • Rx examples: losartin (Cozaar™), valsartin (Diovan™), irbesartan X (Avapro™)

ACE Inhibitors Regulation of BP Renin-Angiotensin-Aldosterone Direct Angiotensinogen Renin X Renin Angiotensin I Inhibitors ACE Angiotensin II

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Direct Renin Inhibitor

• Similar therapeutic effect as ACEI’s • Fewer side effects because unlike ACEI’s, they do not block bradykinin breakdown. Therefore: Diuretics – No bradykinin mediated cough – Extremely rare angioedema • Rx examples: aliskiren (Tekturna™)

Diuretics Diuretics

• Reduce blood volume • Advantages of thiazide diuretics • Dilate vessels – Inexpensive – Chronic Tx: at least as effective as newer • 3 types drugs (ACEI & Ca blockers) in: – Loop (furosemide) - best for diuresis • Lowering BP – Thiazide (hydrochlorothiazide) - best • Preventing CV complications of HBP (Ref: ALLHAT, 2002) for lowering blood pressure – Most patients will require additional meds –K+ sparing (spironolactone) – (Ref: Joint National Committee on Hypertension, 2003)

Diuretics

Value for treating HBP in Emergency Medicine Other • In the ED Antihypertensive – None • Outpatient Rx Agents – Hydrochlorothiazide – Chlorthalidone

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Alpha Adrenergic Agents Alpha Adrenergic Agents Blockers & Agonists Blockers & Agonists

Alpha-1 receptors • Alpha-1 receptors – Vasoconstriction – Vasoconstriction • Alpha-1 blockers --> lower BP • Alpha-1 blockers --> lower BP •Phentolamine IV and • Alpha-2 receptors •Phenoxybenzamine PO – Inhibition of – Pheochromocytoma (with ß-blocker) – MAOI toxicity sympathetic (adrenergic) NS • Alpha-2 agonists --> lower BP

Alpha Adrenergic Agents Blockers & Agonists Rarely used older agents Alpha-2 receptors • Ganglionic blockers – Inhibition of – Trimethophan (Arfonad™) sympathetic (adrenergic) NS • Central sympatholytics • Alpha-2 agonists --> lower BP – Reserpine Most useful in Emergency Medicine – Alpha methyldopa (Aldomet™) – Clonidine (Catapres™) • Direct vasodilators – Hydralazine (Apresoline™) Pre-/Eclampsia? • PO for hypertensive urgency – Minoxidil (Lonitin™)

Specific Emergencies Your Patient Requiring Blood Pressure Reduction in the ED • 72 year old male • Gradual onset headache past 2 days • Nausea & vomiting • Blurred vision • No motor weakness • BP = 260/140

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Your Patient Hypertensive Encephalopathy

• Acute HTN overwhelms cerebral • 72 year old male autoregulation -> • Awakens not moving right side – arteriolar spasm – cerebral ischemia • Mild headache and nausea – vascular permeability • BP = 180/110 – edema • CT = early infarct signs – hemorrhage • What drug to lower his BP ?

Ischemic Stroke Ischemic Stroke

Acutely elevated BP on ED presentation • If BP remains very high, gentle – Common response to the stroke reduction may be reasonable – Probably beneficial – 10-15% reduction of MAP • May increase CBF to ischemic region – To diastolic no lower than 110 – Usually transient • May lower to 180/110 in ischemic stroke ’ •Dont treat! to meet t-PA criteria – Unless stays very high – Danger of cerebral hypoperfusion

Your Patient Ischemic Stroke

• “The level of blood pressure that would • 67 year old female mandate such treatment is not known, but • Sudden onset of severe headache consensus exists that medications should be withheld unless the systolic blood pressure is and vomiting >220 mm Hg or the diastolic blood pressure is • Not moving left side >120 mm Hg” – Class I, Level of Evidence C • BP = 230/130 Adams: American College of Neurology Circulation 2007 • CT = intracranial hemorrhage

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Hemorrhagic Stroke Hemorrhagic Stroke

• Recent evidence that size of • “In patients presenting with a systolic hemorrhage may be lessened – with no BP of 150 to 220 mm Hg, acute deleterious effect on perihematomal lowering of systolic BP to 140 mm Hg is edema - if systolic BP is lowered to the probably safe” 140’s • Class IIa; Level of Evidence: B • Preliminary studies • New recommendation

Arima, Hypertension 2010 Morgenstern, AHA/ASA Guidelines 2010 Anderson, Stroke 2010

Acute Brain Syndromes Acute Brain Syndromes

• Hypertensive Encephaopathy • Nitroprusside may not be best agent • Ischemic Stroke –Increases ICP • Hemorrhagic Stroke –Impairs cerebrovascular reactivity to PCO2 changes • What Agents Should We Use?? –Exacerbates drop in CPP in response to a given decrease in peripheral BP (Ref: Adams)

Acute Brain Syndromes Acute Brain Syndromes Labetalol Both alpha & beta adrenergic blocker Treatment – Theoretically • Controlled reduction of BP over 1 hour • Alpha blockade shifts cerebral • Never < 110 diastolic autoregulation “set point” to lower – Labetalol level (Ref: Adams) – Nicardipine – increasingly used by –Preserves CO2 reactivity stroke neurologists –Preserves CBF at lower BP level – Clevidipine and Fenoldopam may be alternatives

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Your Patient Acute Aortic Dissection

• 65 year old male with hx of HBP • Goals • Sudden onset of excruciating chest – Rapid reduction of BP to nearly pain radiating to the back hypotensive level • Systolic 100 - 120 • EKG = LVH • Within 20 minutes • CXR = ? Widened mediastinum –The only time a rapid drop is indicated - or safe • BP = 180/110 – Prevention of reflex tachycardia

Your Patient Acute Aortic Dissection • 55 year old female • BP Reduction: Vasodilator – Nitroprusside (most rapid) • Chest pain for 1 hour – Alternatives: fenoldopam, nicardipine • Dyspnea increasing x 2 days, • Tachycardia prevention: Beta blocker severe x 2 hours – Metoprolol or esmolol • Rales throughout chest • Alternatively • CXR = acute pulmonary edema – Labetalol alone -> • BP = 170/110 • alpha + beta blockade

Acute Coronary Syndromes & Your Patient Pulmonary Edema • 35 year old pregnant female • Nitroglycerin • If BP stays high, cause is usually • Headache & blurred vision insufficient nitroglycerin or analgesia • Nausea & vomiting – Increase nitroglycerin infusion rate • Hyper-reflexic • Nitroprusside is rarely needed • Pre-tibeal edema – An indication that acute HTN may be • Proteinuria the cause of the acute cardiac problem rather than vice versa • BP = 150/90

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Your Patient Eclampsia/Pre-eclampsia • 22 year old male Treatment • Classically • Partying with friends – IV hydralazine • (Not your son….) • Better allternatives • Chest pain and dyspnea – Labetalol, nicardipine • Freaked out – Nitroprusside falling out of favor • Jittery • concern re fetal cyanide • BP = 220/140

Your Patient Cocaine & Amphetamine Toxicity • 33 year old female • Benzodiazepines • Diabetic – Usually effective & sufficient • Increasing creatinine over past month • Creatinine 8.0 • BETA BLOCKERS CONTRAINDICATED • Lungs with slight basilar crackles – Unopposed alpha adrenergic effect • Cannot dialyze till morning • BP = 220/120

Your Patient Acute Renal Failure • 55 year old male • Nitroprusside has been traditional Tx • Sprained ankle – Slowly metabolized by kidney • No other symptoms – Danger of cyanide toxicity in ARF • No medical history • Probably safer • Reading sports page – Fenoldopam • Ready for discharge – Nicardipine, clavidipine • BP = 240/130

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Hypertensive Urgency Post ED Therapy • Sustained BP in range of >220/>120 without Guidelines for Writing evidence of acute organ dysfunction • Growing trend NOT to treat in the ED Prescriptions • If treated, JNC-7 recommends • Oral clonidine • 0.1 - 0.2 mg PO to start • then 0.1 mg/hr • Goal: 20% reduction of MAP or to 110 diastolic

Post ED Therapy – Post ED Therapy ALLHAT recommendations

• If BP stays high, Rx from ED may be • Diuretics are the bedrock of therapy indicated, especially in patients with • Probably all patients should be on a – Consistently > 100 diastolic diuretic (usually a thiazide), with additional meds added as needed – Chronic CHF • Additional meds eventually will be – Coronary artery disease needed in most patients – Chronic renal failure • But start with thiazides – Diabetes ALLHAT JAMA 2002 Moser J Hypertens 2007

Diuretics are the Bedrock of Post ED Therapy – Outpatient Therapy ALLHAT recommendations • If not on HBP medication – Start hydrochlorothiazde (HCTZ) • low dose • 12.5 - 25 mg per day • If taking other HBP medication(s), – Add HCTZ • 6.25 - 12.5 mg per day

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Post ED Therapy Post ED Therapy

• If already taking a diuretic, additional • Regardless of the ALLHAT drug may be tailored to other conditions recommendations, may physicians – CAD - Beta blocker begin with an ACI, ARB, or beta – CHF - ACEI or ARB blocker, and then add a diuretic if needed – Renal failure - ACEI or ARB • This alternative is acceptable for – Diabetes - ACEI or ARB beginning treatment from the ED – Isolated systolic hypertension • Long acting CCB or ACEI/ARB

Post ED Therapy - Summary Combined Preparations • Many new products now with varying Hypertension in the combinations of 2 or even 3 classes of Emergency Department anti-hypertensive agents • Also comibinations with lipid-lowering statins • Disadvantage - cost • Advantage - convenience and therefore compliance

Summary Summary - Hypertensive Emergencies

• High BP readings in the ED –Usually decline before discharge –Rarely require treatment • Hypertensive emergencies with acute organ damage require IV • in the ED treatment in the emergency –Often do reflect real HTN department –Sometimes warrant writing a prescription

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Summary - Hypertensive Emergencies Summary - Hypertensive Emergencies

• Encephalopathy • In general • Stroke – if treated – Reduce MAP about 20% gradually – Labetalol over at least 1 hour – Nicardipine • Aortic dissection -> over 20 minutes – Alternatives – Not lower than 110 diastolic • Clevidipine, Fenoldopam • As low as 100 systolic with dissection OK

Summary - Hypertensive Emergencies Summary - Hypertensive Emergencies • Aortic dissection • Acute coronary syndromes – Nitroprusside, fenoldopam, or – Nitroglycerin, analgesic nicardipine PLUS – beta-blockers, ?ACEI – Beta-blocker: metoprolol or esmolol • Acute CHF OR – Nitroglycerin, diuretic (?) – Labetalol alone – ? ACEI

Summary - Hypertensive Emergencies Summary - Hypertensive Emergencies

• Pre-/Eclampsia/Eclampsia • Cocaine/amphetamine toxicity – Labetalol or nicardipine – Benzodiazepine – ? Hydralazine • Pheochromocytoma • Acute renal failure – Nitroprusside IV or phentolamine – Nicardipine • PLUS beta-blocker – Alternatives: Fenoldopam, clevidipine

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Summary - Hypertensive Emergencies Summary - Outpatient Rx

Start with diuretic or add diuretic • Hypertensive URGENCY If already on diuretic: –Clonidine PO (if treated) • CAD - beta-blocker • CHF - ACEI or ARB • CRF - ACEI or ARB • Not as a prescription, however • DM - ACEI or ARB • Isolated systolic HTN - long acting CCB – Often eventually need ACE or ARB

• 64 year old female you’ve diagnosed • 64 year old female you’ve diagnosed with acute bronchitis with acute bronchitis • Initial BP = 250/130 • Initial BP = 250/130 • On no meds • On no meds • No history of hypertension • No history of hypertension • Feels fine except for cough • Feels fine except for cough • Ready for discharge: BP = 210/110 • Ready for discharge: BP = 250/140

“Hey Doc, whadya want to give her?” “Hey Doc, whadya want to give her?”

• 64 year old male complaining of severe chest pain for 3 hours Hypertension in • Initial BP = 230/120 Emergency Medicine • EKG normal • Widened mediastinum on CXR

• Repeat BP = 170/90 MICHAEL JAY BRESLER, MD, FACEP • “Doc, they’re ready in CT.” Clinical Professor Division of Emergency Medicine “Hey Doc, whadya want to give him?” Stanford University School of Medicine

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