Define hypertensive urgency (HU) & emergency (HE)

Discuss the pathophysiology of hypertensive

urgency/emergency

Identify signs and symptoms associated with hypertensive urgency/emergency

Choose appropriate pharmacologic agents to treat

hypertensive urgency/emergency

Develop treatment goals for specific disease states related to

or caused by hypertensive urgency/emergency

Recognize possible adverse complications of

antihypertensive medications in certain hypertensive

emergencies

75 million adults in US affected by HTN

32% of the US population is diagnosed with HTN.

1 in 3 American adults has prehypertension.

54% of those diagnosed with HTN are adequately controlled.

High blood pressure costs the US about $48.6 billion each year

www.CDC.gov

Occurs in 1-2% patients with HTN

If untreated, carries a 70-90% 1-year

mortality and 100% 5-year mortality rate

Laragh J. Am J hypertens 2001.

Terminology for hypertensive

urgency/emergency is not consistent,

making data variable in published studies.

Billing codes make it difficult.

› Accelerated HTN

› Hypertensive crisis

› Malignant HTN

› HU/HE down-code to Essential HTN

Severe Hypertension is defined as:

BP ≥180/≥120 mmHg

Asymptomatic

Hypertensive Urgency is defined as:

BP ≥180/≥120 mmHg

Largely asymptomatic

Hypertensive Emergency is defined as:

Acute/rapidly evolving end-organ damage

(EOD)

BP ≥220/≥140 mmHg

Exact BP can vary

Bob is a 50-year-old man who comes to the ER complaining of a

headache. He has “no medical history” but also tells you he

hasn’t seen a doctor for over 20 years. Exam reveals BP 210/120

in the R arm and 216/118 in the L arm. ECG shows NSR 80 with

LVH. No other abnormal PE or diagnostic findings.

What does he have?

A. Severe hypertension

B. Hypertensive crisis

C. Hypertensive urgency

D. Hypertensive emergency

Blood volume

Cardiac Factors

•Heart rate

•Contractility

Humoral Factors

Constrictors Dilators

•Angiotensin II Prostaglandins

•Catecholamines

•Thromboxane

•Leukotrienes

•Endothelin

BP = Cardiac output x TPR

Neural Factors

Constrictors Dilators

α –Adrenergic β-Adrenergic

Sodium & H2O Retention

Potassium Excretion

Aldosterone

Volume Peripheral

vasoconstriction

Angiotensin II

Angiotensin I

AngiotensinogenRenin

ACE

Failure of the normal autoregulatory function

Increase in systemic vascular resistance

Endovascular injury and fibrinoid necrosis of arterioles

Cycle of ischemia & platelet deposition release vasoactive substances

The exact BP at which EOD begins is

different for everyone.

Patients who chronically have poorly

controlled BP have more compensatory

mechanisms to protect against EOD.

Treatment is guided by EOD.

SBP(mmHg)

220

200

180

160

140

120

100

Hyperperfusion

Perfusion

Hypoperfusion

Average SBP

Upward Shift of

Autoregulatory Mechanism

Prevailing BP

▪Normal Physiology

▪HTN Emergency

Perfusion

Hypoperfusion

Abrupt stop in prescribed BP meds

Elicit drugs

Secondary HTN causes

Neurologic insult

Undiagnosed HTN + OTC medication

Previous dx of HTN

Current medications/changes

Compliance

Risk factors

Elicit or OTC medications

Salt, alcohol intake

Other comorbidities

› CAD, CVA, DM, CKD

FH

Eyes› Blurred vision, papilledema, hemorrhages, venous

tapering, exudates

Heart› Chest pain, palpitations, dyspnea, displaced apical

pulse, S3/S4, JVD

Lungs› Dyspnea, crackles

Brain› Headache, stroke sx, ALOC

Kidney› Renal artery bruit, pulsatile abdominal mass

BMP: elevated BUN/creat

UA: protein

CXR: cardiomegaly, pulmonary edema

ECG: LVH, T-wave inversion, ACS

CT Head: small vessel ischemic changes,

hemorrhage

CT Chest: aortic dissection

Acute coronary syndrome

Acute heart failure

Aortic dissection

Hypertensive encephalopathy

Intracerebral hemorrhage

Ischemic stroke

Hemorrhagic stroke

Head trauma

Acute kidney injury

Acute increase in sympathetic activity

Eclampsia

“First Do No Harm”

No EOD, asymptomatic

BP ≥180/≥120 mmHg

Per ACC/AHA & JNC: Treat as Stage II

BP should be reduced over hours to days to

avoid ischemic events.

BP goal <160/<100 mmHg

MAP should not be lowered more than 25-

30% in first few hours to days.

Rapid control of HTN w/o symptoms =

increased adverse outcomes

Treat patients, not numbers!

Accurate BP readings

Reactive HTN?

“Without presence of acute EOD, no literature

demonstrated that patients receiving

pharmacologic interventions had better

outcomes than patients referred for BP

monitoring/close follow-up.”

Annals Emergency Medicine, March 2006

Can be treated as outpatient or

observation admission

PO medications in low doses with titration

preferred.

› Clonidine

› Captopril

› Furosemide

Ideal medication will lower BP without

adverse side effects.

Bob is a 50-year-old man who comes to the ER complaining of a headache. He has “no medical history,” but also tells you he hasn’t seen a doctor for over 20 years. Exam reveals BP 210/120 in the R arm and 216/118 in the L arm. ECG shows NSR 80 with LVH. No other abnormal PE or diagnostic findings.

What is your treatment plan?

A. Administer SL nifedipine

B. Dismiss to F/U w/PCP in 2 days on PO meds

C. Administer PO labetalol and admit to obs

D. Administer IV nitroprusside and admit to ICU

“Short-acting nifedipine should be used in

great caution (if at all), especially at higher

doses, in the treatment of hypertension.”

National Heart, Lung, & Blood Institute, ad hoc panel, 1995

ICU admission

Arterial line for BP monitoring

IV medications

Initiate goal-directed treatment even

before work-up is complete

Goal is to preserve kidney, brain, and

cardiac function

Severe acute HTN can cause ischemia/MI or may be the result

BP reduction is combined with reperfusion/antithrombotic therapies.

Beta-blockers (Labetalol) in conjunction with nitroglycerin preferred agents

Goals of therapy: treat until symptoms subside or DBP 100 mmHg

Can cause both systolic & diastolic HF

Reduction of afterload & preload with Nitroglycerin or Nitroprusside

Adjuncts include loop diuretic, morphine, and oxygen

ACE-I also 1st line agents for CHF

Goals of therapy: reduce sympathetic tone and filling pressures

Nitroprusside end product is thiocyanate

› Precursor to cyanide!

Extreme caution in patients with renal

insufficiency

Cyanide toxicity can be fatal.

Beta-blockers and calcium channel

blockers are NOT recommended in acute

decompensated heart failure.

› Further reduce SV and CO

Most rapidly fatal of HTN emergencies

Risk factors › Untreated HTN, advanced age, disease of aortic

wall

Type A surgical management.

Type B medical management.

Labetalol followed by Nitroprussidepreferred agents

SBP goal <100-120 mmHg within 20 minutes

Goal of therapy: reduce shearing forces caused by BP & tachycardia

Occurs from hyperperfusion of brain

Labetalol, Nicardipine, and Fenoldopamrecommended agents

If neurologic function worsens, suspend treatment.

Goals of therapy: reduce MAP no more than 10-20% in the first hour of treatment and no more than 25% at 24 hours

A 76-year-old male presents to the ED with

acute onset aphasia and R-sided weakness

upon awakening this AM. Serial blood

pressures are 180-195/95-105, HR 90s. He is

not a candidate for thrombolytics.

Would you treat this BP?

If so, what agent would you use?

HTN is single most identifiable risk factor for

acute stroke.

Management of HTN in acute stroke

remains controversial.

Long-term control of HTN for secondary

prevention of stroke confirmed literature

› HOPE, CAMELOT, PROGRESS trials

www.strokecenter.org

AHA recommends treatment of SBP > 220 mmHg or DBP >120 mmHg in patients not receiving thrombolytics.

Preferred agents are Labetalol (first-line) and Nicardipine (second-line)

Nitroprusside can be used to augment BP control.

Cautious reduction of BP by 15% in first 24 hours for those who require treatment.

Stead et al performed meta-analysis of 65

trials (11,500 patients) involving acute stroke

and HTN treatment within 1 week (2004).

› Results: insufficient evidence to evaluate effect

of altering BP on outcomes after stroke

ENOS trial showed higher rates of death or

disability in patients who continued blood

pressure treatment within 48 hours of stroke

(2015).

A cause or result of acute severe HTN?

HTN is the single most important risk factor for

cerebral bleed.

In ICH, use Esmolol or Labetalol.

In SAH, use Nimodipine (prevention of

vasospasm).

Goals of therapy: MAP 110 mmHg, BP 160/90

mmHg and adjust for patient mental status

If ↑ ICP is suspected, consider ICP monitoring.

To keep CPP adequate MAP must

exceed ICP.

CPP = MAP – ICP

Lowering BP even in ICH may cause

hypoperfusion of brain.

Goal CPP is 50-70 mmHg.

Cause and result of acute HTN

Fenoldopam preferred agent due to

increased renal perfusion while lowering BP

Goal of therapy: prevent further renal

damage

Pheochromocytoma, autonomic

dysfunction, sympathomimetic drug use,

and MAO-I use + tyramine ingestion

Recommended agents are Nitroprusside

and Phentolamine

Avoid beta-blocker alone d/t unopposed

alpha-adrenergic vasoconstriction.

Due to preeclampsia or exacerbation of

preexisting HTN

Preferred agents are Hydralazine and

Labetalol

Acute Disease State BP Goal Treatment

HTN Encephalopathy 10-20% reduction* Labetalol, Nicardipine, Fenoldopam

ACS 10-20% reduction* Labetalol, NTG

AKI 10-20% reduction* Fenoldopam

ICH/SAH MAP 110mmHg Labetalol, Esmolol,

Nimodipine (SAH)

Aortic Dissection

(Type B)

SBP <100-120mmHg in 20 min

Labetalol, Nitroprusside

Acute Ischemic Stroke Do not treat unless

SBP >220mmHg

Nicardipine, Labetalol

Acute Heart Failure 10-20% reduction* NTG, Nitroprusside, diuretic, ACE, Morphine

*In 1st hour, then additional 5-15% over next 24 hours.

Which of the following best classifies a

blood pressure of 148/92 mmHg?

A. Normal blood pressure

B. Prehypertension

C. Stage 1 hypertension

D. Stage 2 hypertension

E. Hypertensive urgency

In a patient with hypertensive emergency, in general, which of the following is the most appropriate blood pressure reduction goal within the first few hours?

A. 0-5%

B. 10-20%

C. 30-50%

D. 60-75%

E. 80-90%

Which of the following pharmacologic agents is preferred for the treatment of aortic dissection?

A. Furosemide

B. Labetalol

C. Lisinopril

D. Nicardipine

E. Nitroglycerine

HTN urgency BP ≥180/≥120 mmHg and NO end organ damage

HTN emergency = EOD

In most HE, no more than 10-20% reduction in BP in 1st hour

Treatment of HE directed by type of EOD

Treat BP in acute stroke only if >220 mmHg (DBP > 120 mmHg)

Treat the patient, not the numbers, when

it comes to severe hypertension.

Choose the appropriate drug for the

hypertensive condition you are treating.

Choose the appropriate level of care

when treating a hypertensive patient.

amber.brooks-gumbert@nau.edu

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