HYPERTENSIVE EMERGENCIES

Trevor Langhan PGY-2

September 2, 2004

CASE

67 y male Known small cell lung CA, prev CVA, DM,

COPD, chronic steroids. Admitted to CCU one month ago with ACS Today was at TBCC getting CT scan for

malignancy staging Brought directly by wife after acute c/o

SOB and mild chest pain

CASE

BP 190/100, HR 140, RR 33, sats 81% r/a

Working hard to breathe, mottled skin, diaphoretic

Doesn’t want to lay down for EKG, IV pokes

Swollen legs R > L

Portable CXR RUL consolidation ?collapse Increased vascular markings bilaterally

CASE

Further Hx: Received 2 units PRBC 3 days prior Chemotherapy yesterday with large volume load Volume of fluid IV with contrast for CT Known LV dysfunction from prev echo Documented LEVEL II care in chart (NO intub) Clinical exam:

accessory muscle use elevated JVP inspiratory/expiratory wheezes bilat minimal air entry

CASE (our management)

Unable to get IV access

Couple/three NTG SL sprays

ABG - 7.09/61/98/30

Move to code room

Femoral langhan – i mean line

CASE (our management)

Started on BIPAPMedications: IV NTG

5 ug/min to maximum 100 ug/min (we went to 200 ug/min and he improved)

Mechanism: venous and mild arteriolar dilator IV Lasix

40 mg x 2 Any better than oral?

CASE (our management)

We chose venous and arteriolar vasodilatation + lasix

labetalol – decrease cardiac contractility COPD Known previous bronchospasm

Hydralazine – increase cardiac work, causes alpha blockade

Pulmonary edema

Pts with CHF usually have increased PVRAcute elevations in their BP may be secondary to hypoxia and subsequent catecholamine releaseAggressive treatment of the pulmonary edema will help decrease the BP Nitrates Morphine Lasix Oxygen

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

Hypertensive Emergency

Severely elevated blood pressure with signs of acute damage to target organs

Brain, eyes, heart, kidneys

Hypertensive Emergency

Conditions defined by Rosen’s as HE: Malignant hypertension

Hypertensive encephalopathy Microangiopathic hemolytic anemia Acute renal failure

Aortic dissection Eclampsia/preeclampsia Severe HTN in setting of:

MI Left ventricular failure Bleeding Thrombolytic therapy

Hypertensive Urgency

Situation where 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

Brief 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 failsElevated BP disrupts vasc endothelium, causing narrowing

Brief 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 2

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 2

PMHx: ? HTN, was on a “water pill” many years ago. No DM, no CAD, generally healthy

Labs normal, except Creat: 150

DDx? Mgnt?

Case 2

Goal of therapy is to reduce MAP by 25% in the first hourKeeping DBP > 110 mmHgReduction to pt’s relative normal BP by 4-6 hours is more long term goalWhat agents? Nitroprusside - 0.25-0.5 ug/kg/min, up to 10

ug/kg/min, titratable, easy off, potential toxicity labetalol – infusion 0.5-2 mg/min, or bolus 20 mg then

20-80 mg q 10 minutes (up to 300mg), alpha and beta blocker

Hypertensive Encephalopathy

Cerebral edema by breakthrough hyper-perfusion from severe and sudden increase BP

BP has exceeded the capacity of autoregulation

Elevated BP in vessels that can’t accommodate the pressure – leakage and edema

Autoregulation must be considered during treatment I.e. Hypertrophied vessels can’t vasodilate, so caution with

lowering blood pressure to avoid a relative hypoperfusion and resultant ischemia

Hypertensive Encephalopathy

HE is a 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

Case 3

67 y female known CAD, DM, smoker, atrial fib.Presents with c/o weakness left sideBP 160/100, HR 94, RR 14, sats 99%O/E left facial droop, markedly weak left upper/lower extremityEKG a fib, nil acuteChest exam unremarkable

Case 3

Management?

How do you treat her elevated BP?

Stroke syndromes

Most patients with this presentation are ischemic strokes (85%) not hemorrhagicLikely don’t have acutely elevated BP***caution*** with lowering BP as Watershed area sensitive to hypoperfusionLowering BP may worsen ischemic brain injury

Stroke syndromes

Rarely may see stoke with grossly elevated DBP > 140Pts receiving reperfusion therapy may require BP reduction, as BP > 185/110 is contraindication to tPAWhat do you think about nitroprusside here?Titrate labetalol diligently in 5 mg increments to achieve slow decrease in MAP by a max of 20%

Case 4

32 y female awaiting “sweatgland” surgery from plastics for hyperhydrosis, c/o H/A, palpitationsBP 170/90, HR 150 sinus, RR 18Otherwise healthyTreatment: 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

25 y G2P1, LMP 6 months agoWhen do you treat HTN in pregnancy? DBP > 110 SBP > 160 Treat to goal of 140-155 and 90-105

What agents? Hydralazine (older agent of choice) Labetalol (preferred modality now)

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

Give MONAYou order IV metoprolol to be hungBefore the Beta blocker, any concerns? 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

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)

Anything that’s contraindicated? Hydralazine – reflex tachycardia Nitroprusside – reflex tachycardia

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

drug dose onset duration indication Contra-indication

nitroprusside 0.3-10 ug/kg/min

1-2 min

1-2 min Any hypertensive emergency

Pregnancy

Prolong use

Renal failure

nitroglycerin 10-100 ug/kg/min

2-5 min

3-5 min AMI, CHF

hydralazine 5 mg

5-10mg q20min

10-20 min

3-8 h pregnancy AMI, aortic dissection

esmolol 500ug/kg then 50-300 ug/kg/min

1-2 min

10-20 min CAD, aortic dissection

CHF, heart block, asthma, catecholamine excess

labetalol 20mg then 20-80 q10 min to max 300 OR 1-2 mg/min

2-10 min

2-4 h CAD, aortic dissection, eclampsia, hypertensive crisis

CHF, heart block, asthma, catecholamine excess

phentolamine 5 mg q 1-2 min

1-2 min

10-30 min Catecholamine excess

AMI

Drug choices

Key concepts

Presence of acute target organ damage determines HTN crisisAll pts with persistent elevation of BP should be investigated of EODER doc should be familiar with indications and contraindications of meds to treat HTN crisisGoal of treat is relative decrease in MAP of 25% in first hour, DBP should not fall <110 mmHgPts without EOD rarely require urgent management of HTN and should be referred for outpt pharmacotherapy adjustments