Management of Hypertensive Emergencies

Dr. Abdulkareem Alsuwiada, FRCPC, MSc

Learning Objectives

To identify and triage severe hypertensive states accurately

To effectively manage hypertensive crises with drug therapy

Hypertensive Urgency

“Severe elevation of blood pressure” Generally DBP >115-130 No progressive end organ damage

Hypertensive Emergency

Hypertensive Emergency: Severe elevation in blood pressure in the Severe elevation in blood pressure in the presence of acute or ongoing end-organ presence of acute or ongoing end-organ damage.damage.

“Recognition of hypertensive emergency depends on the clinical state of the patient, not on the absolute level of blood pressure”

Target Organs

Hypertensive Emergency Key Points

Cardiac Emergencies• Acute CHF• Acute coronary insufficiency• Aortic dissection

Hypertensive Emergency Key Points

CNS Emergencies Hypertensive encephalopathy Intracerebral or

subarachnoidal hemorrhage Thrombotic brain infarction

with severe HTN

Hypertensive Emergency Key Points

Renal EmergenciesRenal Emergencies Rapidly progressive renal Rapidly progressive renal

failure failure

Fundoscopy/ Neuro

• Hemorrhages• Exudates• Papillodema

Urgency vs. Emergency

Distinguishing between hypertensive emergency and urgency is a crucial step in appropriate management

Urgency vs. Emergency

Urgency No need to acutely lower blood pressure May be harmful to rapidly lower blood

pressure Death not imminent

Emergency Immediate control of BP essentialImmediate control of BP essential Irreversible end organ damage or death Irreversible end organ damage or death

within hourswithin hours

Approach to PatientsApproach to Patients

Approach to patients

Recheck blood pressure! Appropriate size cuff Cuff not over clothing Check in all limbs

History Prior crises Renal disease Medications

Compliance Recreational drugs

Approach to patients

Physical Exam Signs of end organ damage?

Neuro

Hypertensive encephalopathy Severe Headache Nausea/Vomiting Papilledema Visual Changes Seizures

Focal Neurological Deficits Ischemic vs hemorrhagic CVA

Fundoscopy/ Neuro

Cardiac

Cardiac ischemia Chest pain EKG for ischemic changes

Acute left ventricular failure Pulmonary edema Hypoxia EKG for left ventricular strain pattern CXR

Renal

Electrolytes BUN/Cr

Chronic failure/insufficiency vs acute failure

Cause vs effect UA with micro

Protein Blood Casts

Major Causes of Hypertensive Emergencies and Urgencies

Untreated essential hypertension Withdrawal / non-adherence to

antihypertensive drug therapy Development of secondary

hypertension

Major Causes of Hypertensive Emergencies and Urgencies

Renal Disease Renal artery stenosis Pregnancy Endorine

Pheochromocytoma Primary aldosteronism Glucocorticoid excess Renin-secreting tumors

Pathogenesis for Hypertension Arterial and arteriolar vasoconstriction

Prevents the increase in pressure from being transmitted to the smaller, more distal vessels

With increasingly severe hypertension Autoregulation failure Vascular endothelial injury Plasma constituents (including fibrinoid material)

to enter the vascular wall narrowing or obliterating the vascular lumen.

Tissue edema and activation of endothelial vasoactive system

Goals of TreatmentGoals of Treatment

Goals of Treatment

Prevent end organ damage NOT normalize BP

Exceptions??

HTN Urgencies: Goals of Therapy

No proven benefit of rapid BP reduction in asymptomatic patients

Goal BP <160/110 mm Hg over several hours, oral therapy

Initial BP fall less than 25% in first six hours can be managed using oral antihypertensive

agents in an outpatient or same-day observational setting

Ensure follow-up: Long-term management

HTN Urgencies: Therapy Captopril , 25-mg oral dose initially, followed by

incremental doses of 50 to 100 mg 90 to 120 min later

The calcium channel blocker nicardipine, 30 mg, q 8 hours until the target BP

Labetolol, the starting dose is 200 mg orally, which can be repeated every 3 to 4 hours

Clonidine is a central sympatholytic a 0.1 to 0.2 mg loading dose followed by 0.05 to 0.1 mg every hour until target BP is achieved (Max 0.7 mg).

Hypertensive Emergency

ICU with close monitoring IV and Short acting medications

Avoid sublingual or IM Arterial line

Goals of Treatment

Within 1-2 hrs Lower MAP 20-25%

CONTROLLED IV titratable meds

Complications for rapid BP Reduction in Severe Hypertension

Widening Neurologic Deficits Retinal ischemia and Blindness Acute MI Deteriorating renal function

Goals of Treatment

WHY ?WHY ?

Cerebral Autoregulation

Strandgaard, et al. BMJ: 1973C

ereb

ral b

lood

flo

w

MAP

60mmHg

160mmHg

120mmHg

Adapted from: Chest, 2000; 118:214-227

PharmacotherapyPharmacotherapy

Given by continuous infusion Sodium nitroprusside Nitroglycerin Nicardipine Labetalol Esmolol Fenoldapam

Antihypertensive Drugs for Hypertensive Crisis

Specific TreatmentSpecific Treatment

Hypertensive Encephalopathy

Nitroprusside• Fenoldopam

Nicardipine Labetolol

Symptoms of encephalopathy should improve with treatment

CVA

Nicardipine Labetolol Fenoldopam

Decrease DBP no more than 20% in 24hrs

Cardiac Ischemia

Nitroglycerine Nitroprusside

• Fenoldopam

Nifedipine Reflex tachy Increases myocardial O2 demand May aggravate ischemia

Acute LVF

Nitroprusside Afterload reduction

Fenoldopam

Nitroglycerine If ischemia is suspected

Furosemide Loop diuretic

Opioids

Acute Aortic Dissection

Nitroprusside• Nicardipine, Fenoldopam Afterload reduction Increases ventricular contraction velocity Requires blockade Esmolol, metoprolol

Labetolol Goal: SBP ~100 mmHg Monitor patient closely

Acute Aortic Dissection

ββ-block FIRST!-block FIRST! Esmolol Metoprolol

Sympathetic Crisis

Nicardipine Nitroprusside Phentolamine

Acute Renal Failure

Nicardipine Nitroprusside

“Use with caution” toxic metabolites...

Thiocyanate excreted via kidneys

Fenoldopam Labetolol

Eclampsia

Hydralazine Used historically Arterial vasodilator Maintains placental blood flow

Nicardipine Labetolol

Magnesium

The Discharged PatientThe Discharged Patient

The discharged patient

JNC-VII Recommendations Stage 2

Combination tx Thiazide + ACEI, ARB, BB, CCB

“Compelling Indications”...

The discharged patient

JNC-VII Recommendations “Compelling Indications”

URGENCY: ALL PATIENTS WITH HTN URGENCY BEING

DISCHARGED HOME SHOULD BE PLACED ON COMBINATION THERAPY AND HAVE RAPID FOLLOW UP.

THIAZIDE ACEI / ARB / BB / CCB

Follow up...

Stage I: 140-159 / or 90-99

Stage II: >160 / or ≥100

“Higher”: ≥180 / ≥110

The discharged patient

Follow-up

2 Months

< 1 week

1 Months

Goals of therapy in JNC7 & Euro Guidelines

Maximum reduction in long-term total risk of cardiovascular morbidity and mortality: Smoking Life style modification Lipid Diabetes Blood pressure

< 140/90 If DM or renal disease

<130/80

The following 5 patients in ER

Patient A is a 65-year-old man with nausea, vomiting, and confusion.

Patient B is a 73-year-old woman with sudden shortness of breath, pink sputum, and heavy chest pain.

Patient C is a 56-year-old man with sharp, tearing chest and back pain.

Patient D is a 64-year-old woman with a 6-hour history of right-sided weakness.

Patient E is a 51-year-old woman with a mild headache, concerned about her history of hypertension.

all 5 patients arrive with identical vital signs: BP of 209/105 mm Hg

Which of the 5 patients require emergent hypertension treatment?

Patient A is a 65-year-old man with nausea, vomiting, and confusion.

Hypertensive encephalopathy Pure vasodilators like nitroprusside

have risks of intracranial shunting, which could increase intracranial pressure.

Drug of choice: Intravenous labetalol, bolus or infusion.

Target: Reduce MAP by 20% to 25% over 2 to 8 hours.

Patient B: 73-year-old woman with sudden shortness of breath, pink sputum, and heavy chest pain.

Physical examination reveals bilateral crackles in her lungs, an elevated JVP, and no heart murmurs.

Acute pulmonary edema often presents with extreme hypertension, which overloads cardiac reserve.

Drug of choice: Nitroglycerin infusion; IV enalaprilat or sublingual captopril.

Target: Reduce MAP by 20% to 25% and symptomatic improvement.

Patient C: 56-year-old man with sharp, tearing chest and back pain.

Physical examination reveals differential BPs and evidence of a new aortic insufficiency murmur.

Aortic dissection is largely a disease of hypertension.

Drug of choice: Nitroprusside or esmolol infusion;labetalol boluses or infusion.

Target: Rapidly reduce systolic BP to 110 mm Hg if there is no evidence of hypoperfusion.

Patient D: 64-year-old woman with a 6-hour history of right-sided weakness.

Marked right-sided hemiplegia is noted. a higher MAP is essential to

maintaining adequate cerebral blood flow and not extending the affected stroke territory.

BP should not be lowered in the acute period except in extreme situations BP > 220/120 mm Hg in embolic CVA > 180/100 in hemorrhagic CVA

Patient D: 64-year-old woman with a 6-hour history of right-sided weakness.

Drug of choice: Labetalol; nicardipine; hydralazine.

Target: If no thrombolytic is given, reduce BP only if

it is greater than 220/120 mm Hg (embolic) or greater than 180/100 mm Hg (hemorrhagic)

If a thrombolytic is given, reduce BP to 180/100 mm Hg.

Patient E: 51-year-old woman with a mild headache, concerned about her history of hypertension.

These patients require gradual BP reduction over time on an outpatient basis

Summary

Accurate history and timeline of onset

Evaluate Target organ injury Set the time frame for intervention Appropriate “pace” of therapy

Initial reduction Stabilization

Follow-up care/ Diagnostic studies

Questions...

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