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Hypertensive Emergencies. Herb Russell D.O. September 28, 2006. Why this is a difficult topic. Hypertension is common (up to 25%, 50 million ) but emergencies are rare Failing to treat an emergency AND treating a non-emergency can have serious consequences for the patient

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Hypertensive emergencies l.jpg

Hypertensive Emergencies

Herb Russell D.O.

September 28, 2006

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Why this is a difficult topic

  • Hypertension is common (up to 25%, 50 million) but emergencies are rare

  • Failing to treat an emergency AND treating a non-emergency can have serious consequences for the patient

  • Blood pressure alone is a poor indicator of an emergency

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Why this is a difficult topic

  • The physical exam is often not helpful

  • Different emergencies have vastly different goals in BP reduction

  • The first line agent for one emergency may be contraindicated for another emergency

  • Lack of consensus regarding definitions, therapeutic goals, and 1st line medications

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JNC - 7

New classification scheme:

  • PreHTN SBP 120-139 DBP 80-89

  • Stage I SBP 140-159 DBP 90-99

  • Stage II SBP 160 DBP 100

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  • Hypertensive Emergency: A relatively high blood pressure with evidence of target organ damage (CNS, CV, renal).

    • Urgent lowering in minutes to hours.

  • Hypertensive Urgency: Severely elevated BP without target organ damage.

    • Lower in days to weeks.

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Acute Hypertensive Episode: SBP >180 or DBP >110 and no target organ damage

Transient Hypertension: Hypertension that occurs in association with


Withdrawal syndromes

Some toxic substances


Cessation of medications


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History target organ damage

History of HTN

Blood pressure trends

Prescribed medications

OTC medications

Review of systems directed at:

CNS (HA, hemiparesis)

Cardiac (CP, dyspnea)


Past medical history

Family history

Illicit drug use

Renal (hematuria)

ED Evaluation

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ED Evaluation target organ damage

  • Physical Exam

    • Appropriate sized cuff

    • Measure both arms and legs

    • Brachial difference <20mm Hg

    • Focus on areas of potential target-organ damage

      -CNS -Heart -Retina

      -Pulmonary -Pulses -Renal

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Hard exudates target organ damage

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Disk Edema target organ damage

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Diagnostic Studies target organ damage

  • CBC-hemolytic anemia

  • BUN/Cr-azotemia, ARF

  • Urine-proteinuria, RBC cast

  • CXR-Pulmonary edema, aortic dissection

  • ECG-ischemia, infarction pattern

  • Head CT-hemorrhage, infarction

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Schistocytes target organ damage

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What precipitates an emergency? target organ damage

  • Non-compliance with medications in a chronic hypertensive patient

  • Those with secondary hypertension (e.g. pheochromocytoma, reno-vascular hypertension, Cushing’s Reflex)

  • Hypertension during pregnancy is a major risk factor for women

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Our Job target organ damage

  • ED physician must:

    • 1. Appropriately evaluate patients with elevated BP.

    • 2. Correctly classify the HTN.

    • 3. Determine aggressiveness and timing of the therapeutic interventions.

    • 4. Make the correct disposition.

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General Management Goals target organ damage

  • Reduce BP so autoregulation can be re-established

  • Typically, this is a ~25% reduction in MAP

  • Or, reduce MAP to 110-115

  • Avoid

    • Lowering the BP too much or too fast.

    • Treating non-emergent hypertension

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General Management Goals target organ damage

  • Exceptions: aortic dissection and eclampsia

  • In aortic dissection and eclampsia, BP should be lowered to normal levels

  • Search for secondary causes

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Pharmacology-Nitroprusside target organ damage

  • Dose: 0.3-10 mcg/kg/min

  • Actions: Equally rapid decrease of both preload and afterload (arterialor and venous smooth muscle).

  • Indications: All hypertensive emergencies including post-partum eclamplsia

  • Half-life: 3-4 minutes

  • Metabolism: Liver

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Pharmacology-Nitroprusside target organ damage

  • Excretion: Kidney

  • Adverse Effects:

    • Cyanide toxicity with prolonged use (rare)

      • Prolonged use and >10g/min

    • Inhibits hypoxia induced pulmonary vasoconstriction

    • Coronary steal syndrome

    • Increased ICP

  • Contraindications:

    • Other cyclic GMP inhibitors (i.e. sildenafil, etc.)

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Pharmacology-Labetalol target organ damage

  • Dose: Bolus of 20mg IV, double bolus up to 80 mg, or infusion of 2mg/min to maximum total of 300mg

    • Peds: 0.4-1 mg/kg/hr

  • Actions: Selective α1 and nonselective β–blocker 4-8 times that of α-blockade.

  • Indications: Hypertensive emergencies, including those from catecholamine stimulation and PIH. Does not decrease cerebral or coronary blood flow.

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Pharmacology-Labetalol target organ damage

  • Onset: 5-10 min

  • Half-life: 5.5 hrs

  • Metabolism: Hepatic

  • Adverse Effects:

    • May exacerbate CHF and induce bronchospasm

    • In low doses, may have a paradoxical increase in BP when used in catecholamine excess

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Pharmacology-Esmolol target organ damage

  • Dose: Loading dose of 500mcg/kg over 1 min, then infusion of 50-300mcg/kg/min

  • Actions: Ultra-short acting β1-selective adrenergic blocker

  • Indications: Used in conjunction with nitroprusside or phentolamine for hypertensive emergencies

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Pharmacology-Esmolol target organ damage

  • Onset: Less than 5 mins

  • Half-life: 9mins

  • Metabolism: Erythrocytes

  • Adverse Effects:

    • May induce bronchospasm (rare)

    • Bradycardia and heart block

    • Avoid as sole agent in catecholamine excess

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Pharmacology-Nitroglycerin target organ damage

  • Dose: Infusion rate 5-10mcg/min, titrate up 10mcg every 5 mins

  • Actions: Greater preload reduction than afterload, until high rates, then equal

  • Indications: Agent of choice for moderate hypertension complicating unstable angina, MI or pulmonary edema

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Pharmacology-Nitroglycerin target organ damage

  • Onset: Immediate

  • Half-life: 4 mins

  • Metabolism: Hepatic

  • Adverse Effects: HA, tachycardia, hypotension

  • Contraindications:

    • Other cyclic GMP inhibitors (i.e. sildenafil, etc.)

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Pharmacology-Hydralazine target organ damage

  • Dose: 10-20 mg, repeated in 30 mins

    • Peds: 0.1 mg/kg

  • Actions: Direct arteriolar dilator

  • Indications: PIH, pre-eclampsia

  • Onset: 10 mins

  • Half-life: 2-4 hrs

  • Metabolism: Liver acetylation

  • Excreted: Urine

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Pharmacology-Hydralazine target organ damage

  • Adverse Effects:

    • Decrease dose in renal insufficiency

    • High incidence of hypotension in “slow acetylators”

    • Reflex tachycardia

    • Should not be used in aortic dissection and Coronary artery disease

    • Lethargy

    • Drug-induced Lupus

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Pharmacology-Enalaprilat target organ damage

  • Dose: 0.625-1.25mg IV bolus

  • Actions: Afterload reduction with lowered MAP, PCWP and increased coronary vasodilatation

  • Indications: Hypertensive emergencies

  • Onset: Within minutes

  • Metabolism: None

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Pharmacology-Enalaprilat target organ damage

  • Excreted: Urine

  • Adverse Effects:

    • Angioedema

    • Cough

    • Worsening renal function

    • Hyperkalemia

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Pharmacology-Others target organ damage

  • Trimethaphan-ganglionic blocking agent

  • Fenoldopam-dopaminergic receptor agonist

  • Nicardipine-dihydropyridine calcium channel blocker

  • Urapidil-peripheral a1-receptor blocker and a central 5-HT1A-receptor agonist

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Categories of Hypertensive Emergencies target organ damage

  • Hypertensive encephalopathy

  • Stroke syndromes

    • Embolic

    • Hemorrhagic

    • Subarachnoid hemorrhage

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Categories of Hypertensive Emergencies target organ damage

  • Cardiovascular

    • Acute LV failure (“Flash” pulmonary edema)

    • Acute coronary syndrome

    • Aortic dissection

  • Pregnancy related hypertension

    • Pre-eclampsia

    • Eclampsia

    • HELLP syndrome

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Categories target organ damage

  • Catecholamine excess

    • Pheochromocytoma

    • MAOI + tyramine

    • Cocaine/amphetamines/OTCs

    • Clonidine withdrawal

  • Other

    • Renal failure

    • Epistaxis

    • Childhood hypertension

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Hypertensive Encephalopathy target organ damage

  • Symptoms:

    • Mental status change – somnolence, confusion, lethargy, stupor, coma, seizure

    • Focal neurologic deficit

    • Headache – alone not sufficient to diagnose a hypertensive encephalopathy

    • Nausea and vomiting

  • Signs:

    • Papilledema, cotton wool exudates

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Diagnostics target organ damage

  • Hypertensive encephalopathy is a diagnosis of exclusion – thus, exclude the other possibilities!

  • Only definitive criteria is a favorable response to BP reduction. However clinical improvement may lag behind BP improvement by hours to days

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Pathophysiology target organ damage

  • A loss of cerebral autoregulation causing edema and microhemorrhages.

  • Autoregulation is best studied in the brain but present in heart and kidneys as well

  • Represents the body’s attempt to maintain constant FLOW of blood to perfuse the cells despite change in BP.

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Autoregulation target organ damage

  • In the uninjured, normotensive brain, autoregulation is effective over MAP ranging from about 50 – 150

  • In the chronic hypertensive, this range is increased (e.g. 80 – 180)

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Autoregulation target organ damage

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Pathophysiology target organ damage

  • Loss of autoregulation leads to:

    • Cerebral hyper-perfusion

    • Vascular permeability

    • Cerebral edema

    • Vasospasm

    • Ischemia

    • Punctuate hemorrhages

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Therapy target organ damage

  • Untreated, hypertensive encephalopathy leads to coma and death

  • Goal is to reduce MAP by 20-25% in the first hour

  • This will get MAP back into range where autoregulation is re-instituted

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Therapy target organ damage

  • Nitroprusside

    • 1st line, 0.3 – 10 mcg/kg/minute

  • Labetalol

  • Enalaprilat

  • Fenoldopam

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Stroke Syndromes target organ damage

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Thrombo-Embolic CVA target organ damage

  • Represent 85% of all strokes

  • BP elevations are generally mild-moderate and represent a physiologic response to maintain cerebral perfusion pressure to the penumbra, which has lost its ability to autoregulate

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Embolic CVA - Dilemma target organ damage

  • Inappropriate lowering of the BP may convert the potentially salvageable ischemic penumbra to true infarction.

  • However, persistent BP >185/110 is a contraindication to thrombolytic therapy (it significantly increases risk of intra-cranial bleeding)

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Embolic CVA – When to treat HTN target organ damage

  • For thrombolytic candidates, 1-2 doses of labetalol (5mg) or nitroglycerin paste may be used in attempt to get BP <185/110

  • If thrombolytics are given, then the BP MUST be aggressively kept below 185/110!

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Embolic CVA – When to treat HTN target organ damage

  • According to National Institutes of Neurologic Disorders and Stroke:

    • SBP <220, no treatment

    • DBP <120, no treatment

  • Tintinalli suggests not treating DBP <140

  • Others use MAP <130

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Embolic CVA – When to treat target organ damage

  • If complicated by:

    • Aortic dissection

    • Hypertensive encephalopathy

    • AMI

    • Renal failure

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Embolic CVA – How to treat HTN target organ damage

  • Goal is to reduce MAP 10-20% in uncomplicated embolic CVA with markedly elevated pressures

  • Labetalol: 5mg doses

  • Nitroglycerin IV or nitroprusside

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Why not treat everybody? target organ damage

  • Danger of being too aggressive in acute CVA is well documented.

  • Many studies show a worsening of neurologic outcome when the above guidelines are not followed.

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Hemorrhagic CVA target organ damage

  • Unlike embolic CVA, BP elevations in hemorrhagic CVA are profound

  • However, this again represents a physiologic response to increased intracranial pressure (and free blood irritating the autonomic nervous system)

  • Typically is transient

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Hemorrhagic CVA – When to Rx target organ damage

  • Evidence to support anti-hypertensive therapy in acute intracranial hemorrhage is lacking.

    • There is no evidence to suggest that HTN provokes further bleeding in ICH.

  • However, modest reductions of ~20% MAP have not been show to adversely affect outcome.

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Hemorrhagic CVA - Rx target organ damage

  • Labetalol is agent of choice

  • ACE inhibitor can be used but not as well studied.

  • Vasodilators such as nitroprusside and nitroglycerin are contraindicated because they may raise the ICP

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Subarachnoid Hemorrhage target organ damage

  • A special subset of hemorrhagic CVA.

  • Evidence suggests that there may be less vasospasm and less re-bleeding if SBP <160 or MAP <110

  • Agents:

    • Oral nimodipine 60mg q 4hr x 21 days

    • IV nicardipine 2mg bolus, then 4-15mg/hr

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Acute Left Ventricle Failure target organ damage

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Pathophysiology target organ damage

  • Abrupt, severe increase in afterload leads to systolic and diastolic dysfunction.

  • Vicious cycle ensues:

    • Heart failure causes poor coronary perfusion, LV ischemia and worsening failure

    • CHF leads to hypoxia and worsens LV ischemia

    • Renal hypoperfusion leads to renin release and this increases afterload

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Signs and Symptoms target organ damage

  • Abrupt and severe dyspnea, tachypnea, and diaphoresis

  • Rales, wheezes, distant breath sounds, frothy sputum, and gallop rhythm

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Goals of therapy target organ damage

  • 1. Reduce preload and afterload!

  • 2. Minimize coronary ischemia by increasing supply (blood to coronary arteries) and decrease demand (wall tension, tachycardia)

  • 3. Oxygenate, ventilate, clear pulmonary edema.

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Therapy target organ damage

  • Nitroglycerin

    • First Line in combination with ACE-I

    • Arterial (especially coronaries) and veno-dilator, reducing preload and afterload

  • ACE inhibitor

    • Interrupts the renin-angiotensin-aldosterone axis

  • Lasix

    • Initially a vasodilator, then diuretic

  • Morphine

    • Vasodilator and sympatholytic

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Acute Coronary Syndrome target organ damage

  • Elevated BP significantly increases LV wall tension

  • Wall tension is one of main determinants of myocardial oxygen demand.

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ACS therapy goals target organ damage

  • Goal is to decrease wall tension by decreasing preload and afterload.

  • Typical agents do this well: Nitroglycerin, beta-blockers, morphine

  • Avoid hydralazine and minoxidil, as they increase myocardial oxygen demand.

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Aortic Dissection target organ damage

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Stanford A target organ damage

Involves ASCENDING aorta

More common

More often fatal

REQUIRES surgery for survival

Stanford B

Involves DESCENDING aorta

May be managed medically

DeBakey (old)

1 – Ascending and Descending

2 – Ascending Only

3 – Descending Only

A – above diaphragm

B – below diaphragm


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Male target organ damage



Chest Trauma


CV Surgery



MDMA (ecstasy)

-1 antitrypsin def.

Age >60

Risk Factors

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Pathophysiology target organ damage

  • Degeneration of the media

    • Normal aging

    • Pregnancy

    • Marfan’s and Erhlers-Danlos syndromes

  • Hypertension

  • Bicuspid aortic valve

  • Flexion of aorta with each heartbeat

  • Atherosclerosis – minor factor

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Pathophysiology target organ damage

  • Hydrodynamic force of blood column tears the intima and dissects into the media, creating a false lumen.

  • Can extend proximal or distal, re-enter the aorta through the intima (rare), or dissect through the adventitia (fatal)

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Pathophysiology target organ damage

  • Worsening of the dissection dependent on:

    • 1. Level of elevated BP

    • 2. Slope of the pulse wave – dP/dt. This increases the “shear force” on the dissection. Increased shear force leads to propagation of the dissection

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Complications target organ damage

  • Retrograde Dissection

    • Into AV – acute regurgitation and CHF

    • Into pericardium – tamponade

    • Into coronary arteries - AMI

  • Anterograde Dissection

    • Into carotid artery – CVA

    • Into subclavian artery – Ischemic limb

    • Into renal arteries – ARF

    • Into anterior spinal artery - paraplegia

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Signs and Symptoms target organ damage

  • Severe tearing chest pain, maximal at onset, radiates to back, may migrate as the dissection propagates

  • Diaphoresis

  • N/V

  • Feeling of impending doom (angor animi) and anxiety

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Diagnostics target organ damage

  • CXR

    • may be normal in up to 12% !!

    • Wide mediastinum

    • Calcium sign

    • Deviation of trachea or NG tube to right

    • Left pleural effusion

    • Apical cap

    • Left Mainstem Bronchus shift

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Diagnostics - CXR target organ damage

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Therapy target organ damage

  • Goal is to reduce both the BP and the slope of the pulse wave!

  • BP goal is SBP of 100-120

  • If patient presents with normal BP, still need to decrease the shear forces!!

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Therapy target organ damage

  • Beta-blocker for decreasing the slope of the pulse wave (e.g. esmolol)

  • Nitroprusside for BP reduction (started after or with the beta-blocker to avoid reflex tachycardia)

  • Labetalol as monotherapy

  • Trimethaphan if beta-blocker contraindicated

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Doses target organ damage

  • Esmolol: 500mcg/kg bolus, then 50-300 mcg/kg/min

  • Nitroprusside: 0.3 – 10 mcg/kg/min

  • Labetalol: 20mg IV q5-10 minutes, increasing by 20mg up to 80mg per dose, total not to exceed 300mg.

  • Trimethaphan: 1 – 2mg/minute

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Pregnancy and Hypertension target organ damage

  • Complicates 5% of pregnancies

  • Risk factors:

    • Nulliparity

    • Age >40

    • African American

    • Chronic renal failure

    • Diabetes mellitus

    • Multiple gestations

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Pregnancy and Hypertension target organ damage

  • Accounts for 18% of maternal deaths

  • Most common risk factor for placental abruption

  • Defined as:

    • Greater than 140/90

    • SBP increased >20 from baseline

    • DBP increased >10 from baseline

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Pre-eclampsia target organ damage


Proteinuria >300mg per 24 hr.

Peripheral edema or weight gain >5 lbs in 1 week

Presents >20 weeks except in gestational trophoblastic disease


Pre-eclampsia + seizures – This is an emergency !!!!

HELLP syndrome

Variant of pre-eclampsia

Blood pressure lower

Predilection for multigravids

Pregnancy and Hypertension

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Pathophysiology target organ damage

  • Pre-eclampsia and eclampsia may occur up to 6 weeks post partum

  • Not well understood, but thought to be loss of normal vasodilatation:

    • Increased thromboxane

    • Increased endothelin

    • Increased sympathetic nerve activity

    • Decreased nitric oxide formation

    • Oxidative stress

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Signs and symptoms target organ damage

  • Restlessness and hyper-reflexia early

  • Headache

  • Visual disturbance

  • Peripheral edema

  • Abdominal pain

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Therapy target organ damage

  • Any pregnant patient with BP >140/90 and any symptoms should be hospitalized

  • Eclampsia and patients with pre-eclampsia + severe symptoms (HA, abdominal pain) but no seizures should be treated very aggressively!

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Therapy target organ damage

  • Definitive therapy is delivery of the fetus and placenta

  • Magnesium: 4-6gm over 15 minutes, drip 1-2gm per hour

  • Hydralazine: 5-10mg IV, drip 5-10mg per hour

  • Labetalol: 20mg IV, repeat prn q 10 minutes, drip 1-2mg per minute

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Catecholamine excess target organ damage

  • Pheochromocytoma

  • Monoamine oxidase inhibitor + tyramine

  • Cocaine/amphetamines/OTC herbals (PPA, ephedra, trytophan)

  • Clonidine withdrawal

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Pheochromocytoma target organ damage

  • Is a tumor of adrenergic cells

  • Most common site is adrenal medulla

  • Increased risk in patients with

    von Recklinhausen’s disease (aka neurofibromatosis)

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Signs and symptoms target organ damage

  • Chronically elevated BP with paroxysms of palpitations, diaphoresis, tachycardia, malaise, apprehension, HA, abdominal pain, and angina

  • Episodes precipitated by physical or emotion stress, eating, position, or micturation

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Diagnosis target organ damage

  • Commonly mislabeled as panic attacks or anxiety disorder

  • Diagnosed by detecting elevated levels of catecholamines and their by-products in the urine

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Clonidine withdrawal target organ damage

  • Occurs in patients on clonidine who abruptly discontinue therapy

  • Symptoms very similar to pheochromocytoma

  • Occur 16-48 hours after last dose

  • Treatment is to re-start clonidine

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MAOI + tyramine target organ damage

  • Tyramine is found in many foods, is a sympathomimetic like amphetamine, and causes a transient release of norepinephrine (NE) in all people when ingested

  • Patients on MAOIs (Nardil, Parnate, Marplan) experience an exaggerated response to tyramine, resulting in prolonged and severe hypertension

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Beer target organ damage


Aged cheeses




Chicken liver

Pickled herring

Broad beans (dopamine)


Citrus fruits


Foods containing tyramine

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Some pharmaceuticals can also cause severe hypertension when taken with MAOIs








MAOIs and medications

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Ingestions taken with MAOIs

  • Cocaine

    • blocks re-uptake of NE, dopamine, and serotonin

  • Amphetamines

    • Stimulate release of and block re-uptake of catecholamines

    • Also may directly stimulate catecholamine receptors

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Ingestions taken with MAOIs

  • Over-the counter medications

    • Ephedra – weight loss supplements

    • PPA – (Phenylpropanolamine ) decongestants and weight loss supplements

    • Tryptophan – supplement for depression, insomnia, migraines

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Treatment goals taken with MAOIs

  • Typically the goal is to reduce MAP by ~25% over several hours

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Treatment for catecholamine excess taken with MAOIs

  • Phentolamine

    • Alpha blocker; the mainstay of therapy

    • Dose: 1-5mg IV bolus or drip 5-10mcg/kg per minute

  • Beta-blocker

    • May be added to control tachycardia

  • Benzodiazepines

    • May be helpful in cocaine/amphetamine

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Treatment for catecholamine excess taken with MAOIs

  • Labetalol

    • Its use as monotherapy is controversial

    • Recall that its alpha : beta is 1:3 to 1:8

    • Some texts recommend it; others note the potential for worsening BP with it as monotherapy for the catecholamine excess conditions

    • Probably best to use phentolamine 1st

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Goal: Gradual reduction of blood pressure over 24 hours taken with MAOIs


Restart prescribed anti-hypertensive medications for the non-compliant patient




Follow up within 24 hours

Sublingual nitroglycerine

Nifedipine (don’t use)

Treatment of Hypertensive Urgencies

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Treatment of Hypertensive Episode taken with MAOIs

  • Treat cause of hypertensive episode (i.e. pain, anxiety)

  • Refer to a primary care physician and start anti-hypertensive medications only upon advice of referring physician

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Why not treat all elevated BP in the ED? taken with MAOIs

  • Association of overly aggressive BP reduction in setting of stroke with worse neurologic outcome widely shown

  • What about the person incidentally found to have elevated BP?

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From taken with MAOIsJournal of Emergency Medicine, 2000, pp 339-45.

  • “Stroke Precipitated by Moderate Blood Pressure Reduction”

  • 6 cases total; All presented to an ED. 2 with completely resolved TIAs and 4 with no neurological complaints at all.

  • All suffered CVAs and had permanent dysfunction or death.

Case 1 l.jpg
Case 1 taken with MAOIs

  • 60 year male with “malaise”

  • Initial BP 170/100, remainder of exam normal

  • Treated with 10mg nifedipine sublingual

  • Returned 3 hours later with BP 120/88 and left hemiparesis.

  • MRI showed infarct.

Case 2 l.jpg
Case 2 taken with MAOIs

  • 30 year female with “abdominal pain”

  • Known hypertensive, off meds for 2 weeks

  • BP 280/120 initially

  • All HTN meds restarted in ED: captopril, triamterene/HCTZ, nifedipine, and hydralazine

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Case 2 taken with MAOIs

  • 2 hours later in the ED, complained of severe vision loss

  • BP 160/85

  • Ophthalmology consult confirmed retinal ischemia

  • Only partial recovery of vision

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Starting anti-HTN therapy in the ED taken with MAOIs

  • May mislead the patient to believe that they are cured

  • May interfere with office assessment of the true nature of the HTN

  • Best treatment in the ED is education regarding the chronic nature of hypertension and need for follow up!

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Hypertensive encephalopathy taken with MAOIs

Embolic CVA

Hemorrhagic CVA


Nitroprusside, goal ~25 reduction

Only if >220/120 or>185/110 for t-PA

Labetalol for ~10-20% reduction

Nimodipine 60 mg Q4hrs x 21 days

Summary – Neurologic emergencies

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Aortic dissection taken with MAOIs

Acute LV failure

Acute coronary syndrome

Nitroprusside + Esmolol or Labetalol – SBP ~100

NTG, ACEI, Lasix for symptoms and ~10-15% reduction

NTG, MS04, beta-blocker for symptom improvement

Summary – Cardiovascular emergency

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Eclampsia and HELLP taken with MAOIs

Catecholamine excess

Goal DBP ~90; magnesium, hydralazine, labetalol, delivery!

Phentolamine +/-beta blocker for ~25% reduction over several hours

Summary – Other emergencies

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Summary – Hypertensive Urgency taken with MAOIs

  • Unnecessary to lower BP in the ED

    • May be harmful-First do no harm

  • No history of renal dysfunction?

    • Normal UA obviates need for lab tests

  • History of renal dysfunction?

    • UA and BMP

  • Symptoms of cardiac dysfunction or chest pain

    • CXR and ECG

  • Disposition

    • If above negative, refer for outpatient evaluation within 7 days

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Questions and Comments taken with MAOIs