Hypertensive Emergencies Trevor Langhan PGY-3 November 10, 2005

Hypertensive Emergencies

Trevor Langhan PGY-3November 10, 2005

Objectives

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

alpha-receptor Vasoconstriction iris dilation intestinal relaxation intestinal sphincter

contraction bladder sphincter

contraction

beta-receptor vasodilation (b2) cardioacceleration

(b1) intestinal relaxation

(b2) uterus relaxation(b2) bronchodilation (b2)

quiz

Nitroprusside

PRO Vasodilator Direct effect on smooth

muscle Dose related BP

reduction Drug of choice for most

HTN emergencies Rapid onset Short duration

CON Increase ICP Metabolized to thiocyanate

by KD cyanide can build up ARF and prolonged use Avoid in pregnancy

Must be IV Unstable in UV light Must be wrapped

Supine to prevent orthostasis

S/E due to decreased BP and vasodilation

Fenoldopam

PRO Peripheral dopamine

agonist Improves renal function Rapid action Does not cross blood

brain barrier Hypotension less often

CON Tachycardia, flushing and

h/a may occur

nitroglycerin

PRO Vasodilating agent

venous Decreases LVEDP Reduces BP by

decreasing preload and CO

Sublingual or IV

CON Limit to pts with cardiac

ischemia or pulmonary edema

Hypotension with pts who have RV dysfunction

hydralazine

PRO Direct arterial vasodilator Historically used ++ in

PIH and eclampsia

CON Reflex tachycardia May provoke angina Flushing, n/v, h/a Chronic use results in

lupus like syndrome

Beta-blockers - labetalol

PRO Selective alpha1 and

non-selective 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 IV use has deep

orthostasis Supine post admin x 2-3

hours No effect on renal or

cerebral blood flow Contraindicated:

Heart block CHF Asthma pheo

Beta-blockers - esmolol

PRO Ultra short acting Selective beta1 Little BP effects Good for reflex tachy

CON Thrombophlebitis Tissue necrosis Contraindicated:

Heart block CHF Asthma Pheo cocaine

alpha-blockers - phentolamine

PRO Alpha-blocker Use in catecholamine

HTN crisis: Pheo MAOI crisis cocaine

CON Reflex tachycardia

nicardipine

PRO IV CCB Titratable Less negative inotropy Less tachycardia Mostly vasodilator Safe in pregnancy

CON Caution in poor LV fxn Liver metabolism H/a, flushing, tachycardia

Enalaprilat/enalipril

PRO IV ace-I Infrequent hypotension Increasing evidence for

use in cardiac Remodeling

CON Not dose related May precipitate ischemia

if MAP drop too steep Angioedema Cough ARF Toxic in 1st 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

EtOH, 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

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

<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

Rosen’s states: True medical emergencies 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 mmHg

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 tPA 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

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

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

Standard treatment of CHF: Morphine Oxygen Nitrates (nitroprusside better than NTG) 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 G2P1, 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

Ecclampsia Dx: Elevated BP in late 2nd or 3rd trimester

SBP > 140, DBP >90 Elevated urine proteins 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

24-48 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 V1-V3 Nurse asks “what do you want to give?”

Case 6

Beta blocker contraindicated Beta antagonism will decrease heart rate,

but will also block B2 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 mmHg

Pts without EOD rarely require urgent management of HTN