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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

Hypertensive Emergencies

Herb Russell D.O.

September 28, 2006

why this is a difficult topic
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
why this is a difficult topic3
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
jnc 7
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
  • 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.
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

ed evaluation

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
ed evaluation8
ED Evaluation
  • 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

diagnostic studies
Diagnostic Studies
  • CBC-hemolytic anemia
  • BUN/Cr-azotemia, ARF
  • Urine-proteinuria, RBC cast
  • CXR-Pulmonary edema, aortic dissection
  • ECG-ischemia, infarction pattern
  • Head CT-hemorrhage, infarction
what precipitates an emergency
What precipitates an emergency?
  • 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
our job
Our Job
  • 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.
general management goals
General Management Goals
  • 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
general management goals17
General Management Goals
  • Exceptions: aortic dissection and eclampsia
  • In aortic dissection and eclampsia, BP should be lowered to normal levels
  • Search for secondary causes
pharmacology nitroprusside
  • 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
pharmacology nitroprusside19
  • 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.)
pharmacology labetalol
  • 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.
pharmacology labetalol21
  • 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
pharmacology esmolol
  • 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
pharmacology esmolol23
  • 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
pharmacology nitroglycerin
  • 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
pharmacology nitroglycerin25
  • Onset: Immediate
  • Half-life: 4 mins
  • Metabolism: Hepatic
  • Adverse Effects: HA, tachycardia, hypotension
  • Contraindications:
    • Other cyclic GMP inhibitors (i.e. sildenafil, etc.)
pharmacology hydralazine
  • 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
pharmacology hydralazine27
  • 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
pharmacology enalaprilat
  • 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
pharmacology enalaprilat29
  • Excreted: Urine
  • Adverse Effects:
    • Angioedema
    • Cough
    • Worsening renal function
    • Hyperkalemia
pharmacology others
  • 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
categories of hypertensive emergencies
Categories of Hypertensive Emergencies
  • Hypertensive encephalopathy
  • Stroke syndromes
    • Embolic
    • Hemorrhagic
    • Subarachnoid hemorrhage
categories of hypertensive emergencies32
Categories of Hypertensive Emergencies
  • Cardiovascular
    • Acute LV failure (“Flash” pulmonary edema)
    • Acute coronary syndrome
    • Aortic dissection
  • Pregnancy related hypertension
    • Pre-eclampsia
    • Eclampsia
    • HELLP syndrome
  • Catecholamine excess
    • Pheochromocytoma
    • MAOI + tyramine
    • Cocaine/amphetamines/OTCs
    • Clonidine withdrawal
  • Other
    • Renal failure
    • Epistaxis
    • Childhood hypertension
hypertensive encephalopathy
Hypertensive Encephalopathy
  • 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
  • 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
  • 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.
  • 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)
  • Loss of autoregulation leads to:
    • Cerebral hyper-perfusion
    • Vascular permeability
    • Cerebral edema
    • Vasospasm
    • Ischemia
    • Punctuate hemorrhages
  • 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
  • Nitroprusside
    • 1st line, 0.3 – 10 mcg/kg/minute
  • Labetalol
  • Enalaprilat
  • Fenoldopam
thrombo embolic cva
Thrombo-Embolic CVA
  • 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
embolic cva dilemma
Embolic CVA - Dilemma
  • 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)
embolic cva when to treat htn
Embolic CVA – When to treat HTN
  • 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!
embolic cva when to treat htn46
Embolic CVA – When to treat HTN
  • 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
embolic cva when to treat
Embolic CVA – When to treat
  • If complicated by:
    • Aortic dissection
    • Hypertensive encephalopathy
    • AMI
    • Renal failure
embolic cva how to treat htn
Embolic CVA – How to treat HTN
  • Goal is to reduce MAP 10-20% in uncomplicated embolic CVA with markedly elevated pressures
  • Labetalol: 5mg doses
  • Nitroglycerin IV or nitroprusside
why not treat everybody
Why not treat everybody?
  • 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.
hemorrhagic cva
Hemorrhagic CVA
  • 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
hemorrhagic cva when to rx
Hemorrhagic CVA – When to Rx
  • 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.
hemorrhagic cva rx
Hemorrhagic CVA - Rx
  • 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
subarachnoid hemorrhage
Subarachnoid Hemorrhage
  • 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
  • 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
signs and symptoms
Signs and Symptoms
  • Abrupt and severe dyspnea, tachypnea, and diaphoresis
  • Rales, wheezes, distant breath sounds, frothy sputum, and gallop rhythm
goals of therapy
Goals of therapy
  • 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.
  • 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
acute coronary syndrome
Acute Coronary Syndrome
  • Elevated BP significantly increases LV wall tension
  • Wall tension is one of main determinants of myocardial oxygen demand.
acs therapy goals
ACS therapy goals
  • 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.
Stanford A

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

risk factors



Chest Trauma


CV Surgery



MDMA (ecstasy)

-1 antitrypsin def.

Age >60

Risk Factors
  • 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
  • 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)
  • 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
  • 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
signs and symptoms68
Signs and Symptoms
  • 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
  • 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
  • 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!!
  • 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
  • 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
pregnancy and hypertension
Pregnancy and Hypertension
  • Complicates 5% of pregnancies
  • Risk factors:
    • Nulliparity
    • Age >40
    • African American
    • Chronic renal failure
    • Diabetes mellitus
    • Multiple gestations
pregnancy and hypertension75
Pregnancy and Hypertension
  • 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
pregnancy and hypertension76


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
  • 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
signs and symptoms78
Signs and symptoms
  • Restlessness and hyper-reflexia early
  • Headache
  • Visual disturbance
  • Peripheral edema
  • Abdominal pain
  • 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!
  • 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
catecholamine excess
Catecholamine excess
  • Pheochromocytoma
  • Monoamine oxidase inhibitor + tyramine
  • Cocaine/amphetamines/OTC herbals (PPA, ephedra, trytophan)
  • Clonidine withdrawal
  • Is a tumor of adrenergic cells
  • Most common site is adrenal medulla
  • Increased risk in patients with

von Recklinhausen’s disease (aka neurofibromatosis)

signs and symptoms84
Signs and symptoms
  • 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
  • Commonly mislabeled as panic attacks or anxiety disorder
  • Diagnosed by detecting elevated levels of catecholamines and their by-products in the urine
clonidine withdrawal
Clonidine withdrawal
  • 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
maoi tyramine
MAOI + tyramine
  • 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
foods containing tyramine


Aged cheeses




Chicken liver

Pickled herring

Broad beans (dopamine)


Citrus fruits


Foods containing tyramine
maois and medications
Some pharmaceuticals can also cause severe hypertension when taken with MAOIs








MAOIs and medications
  • 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
  • Over-the counter medications
    • Ephedra – weight loss supplements
    • PPA – (Phenylpropanolamine ) decongestants and weight loss supplements
    • Tryptophan – supplement for depression, insomnia, migraines
treatment goals
Treatment goals
  • Typically the goal is to reduce MAP by ~25% over several hours
treatment for catecholamine excess
Treatment for catecholamine excess
  • 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
treatment for catecholamine excess94
Treatment for catecholamine excess
  • 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
treatment of hypertensive urgencies
Goal: Gradual reduction of blood pressure over 24 hours


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
treatment of hypertensive episode
Treatment of Hypertensive Episode
  • 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
why not treat all elevated bp in the ed
Why not treat all elevated BP in the ED?
  • 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?
from journal of emergency medicine 2000 pp 339 45
From Journal 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
Case 1
  • 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
Case 2
  • 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
case 2101
Case 2
  • 2 hours later in the ED, complained of severe vision loss
  • BP 160/85
  • Ophthalmology consult confirmed retinal ischemia
  • Only partial recovery of vision
starting anti htn therapy in the ed
Starting anti-HTN therapy in the ED
  • 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!
summary neurologic emergencies
Hypertensive encephalopathy

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
summary cardiovascular emergency
Aortic dissection

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
summary other emergencies
Eclampsia and HELLP

Catecholamine excess

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

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

Summary – Other emergencies
summary hypertensive urgency
Summary – Hypertensive Urgency
  • 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