Hypertensive emergencies
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Hypertensive Emergencies. Trevor Langhan PGY-3 November 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?. alpha-receptor Vasoconstriction iris dilation intestinal relaxation intestinal sphincter contraction

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Hypertensive Emergencies

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Hypertensive emergencies

Hypertensive Emergencies

Trevor Langhan PGY-3

November 10, 2005



  • 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



iris dilation

intestinal relaxation

intestinal sphinctercontraction

bladder sphincter contraction


vasodilation (b2)

cardioacceleration (b1)

intestinal relaxation (b2)

uterus relaxation(b2)

bronchodilation (b2)

Receptor sites

Hypertensive emergencies





Direct effect on smooth muscle

Dose related BP reduction

Drug of choice for most HTN emergencies

Rapid onset

Short duration


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




Peripheral dopamine agonist

Improves renal function

Rapid action

Does not cross blood brain barrier

Hypotension less often


Tachycardia, flushing and h/a may occur




Vasodilating agent


Decreases LVEDP

Reduces BP by decreasing preload and CO

Sublingual or IV


Limit to pts with cardiac ischemia or pulmonary edema

Hypotension with pts who have RV dysfunction




Direct arterial vasodilator

Historically used ++ in PIH and eclampsia


Reflex tachycardia

May provoke angina

Flushing, n/v, h/a

Chronic use results in lupus like syndrome


Beta blockers labetalol


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


IV use has deep orthostasis

Supine post admin x 2-3 hours

No effect on renal or cerebral blood flow


Heart block




Beta-blockers - labetalol

Beta blockers esmolol


Ultra short acting

Selective beta1

Little BP effects

Good for reflex tachy



Tissue necrosis


Heart block





Beta-blockers - esmolol

Alpha blockers phentolamine



Use in catecholamine HTN crisis:


MAOI crisis



Reflex tachycardia

alpha-blockers - phentolamine





Less negative inotropy

Less tachycardia

Mostly vasodilator

Safe in pregnancy


Caution in poor LV fxn

Liver metabolism

H/a, flushing, tachycardia


Enalaprilat enalipril


IV ace-I

Infrequent hypotension

Increasing evidence for use in cardiac



Not dose related

May precipitate ischemia if MAP drop too steep




Toxic in 1st trimester


Hypertensive emergencies

quiz - fin



  • What is normal BP?

    • SBP < 140

    • DBP < 90

  • What is hypertension?

    • SBP >160

    • DBP >100

  • Anything in between GRAY.

  • Hypertension1


    • 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



    • Endocrine causes for elevated BP:

      • Pheo

      • Excess steroids

        • Often iatrogenic

        • Cushings

          • Look for hypokalemia

          • Volume overload from Na retention



    • 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



    • 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

    • 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

    Hypertensive Emergency

    • Also called hypertensive crisis

    • Elevated blood pressure

      • signs of acute damage to target organs

        • Brain

        • Eyes

        • Heart

        • kidneys

    Hypertensive emergency1

    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

    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 emergency2

    Hypertensive Emergency

    • Rosen’s states:

      • True medical emergencies

      • Immediate reduction of BP in 1 hour



    • 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



    • 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

    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 11

    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 emergency3

    Hypertensive Emergency

    Hypertensive emergency4

    Hypertensive Emergency

    Hypertensive encephalopathy

    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 encephalopathy1

    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 encephalopathy2

    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 encephalopathy3

    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

    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 21

    Case 2

    • Management?

    • How do you treat her elevated BP?

    Stroke syndromes

    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 syndromes1

    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 syndromes2

    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

    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 31

    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 32

    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

    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 41

    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

    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

    Hypertensive emergencies

    • 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

    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 61

    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

    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 71

    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

    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

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