Hypertensive Emergencies

1
Hypertensive Emergencies

• Dr. Herb Russell
• Prepared by
• Anthony G. Hillier, D.O.
• September 2005

2
Why this is a difficult topic

• Hypertension is common (up to 25) 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

3
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

4
Definitions

• Hypertensive Emergency A relatively high blood
  pressure with evidence of target organ damage.
• Hypertensive Urgency Elevated BP with imminent
  risk of target organ damage

5
Definitions

• Acute Hypertensive Episode SBP gt180 or DBP gt110
  and no target organ damage
• Transient Hypertension Hypertension that occurs
  in association with
• Pain
• Withdrawal syndromes
• Some toxic substances

• Anxiety
• Cessation of medications

6
ED Evaluation

• History
• History of HTN
• Blood pressure trends
• Prescribed medications
• OTC medications
• Review of systems directed at
• CNS (HA, hemiparesis)
• Cardiac (CP, dyspnea)

• Compliance
• Past medical history
• Family history
• Illicit drug use
• Renal (hematuria)

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ED Evaluation

• Physical Exam
• Appropriate sized cuff
• Measure arms and legs
• Brachial difference lt20mm Hg
• Focus on areas of potential target-organ damage
• -CNS -Heart -Retina
• -Pulmonary -Pulses -Renal

8
Cotton wool spot (soft exudates)
9
Cotton wool spots
10
Hard exudates
11
Retinal Hemorrhage
12
Disk Edema
13
Diagnostic Studies

• CBC-hemolytic anemia
• Glucose-hypoglycemia
• Electrolytes-hyperkalemia
• BUN/Cr-azotemia, ARF
• Urine-proteinuria, RBC cast
• CXR-Pulmonary edema, aortic dissection
• ECG-ischemia, infarction pattern
• Head CT-hemorrhage, infarction

14
Schistocytes
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What precipitates an emergency?

1. Non-compliance with medications in a chronic
   hypertensive patient
2. Those with secondary hypertension (e.g.
   pheochromocytoma, reno-vascular hypertension,
   Cushings)
3. Hypertension during pregnancy is a major risk
   factor for women

16
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

17
General Management Goals

• Exceptions aortic dissection and eclampsia
• In aortic dissection and eclampsia, BP should be
  lowered to normal levels
• Search for secondary causes

18
Pharmacology-Nitroprusside

• Dose 0.3-10 mcg/kg/min
• Actions Equally rapid decrease of both preload
  and afterload
• Indications All hypertensive emergencies
  including post-partum eclamplsia
• Half-life 3-4 minutes
• Metabolism Liver

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Pharmacology-Nitroprusside

• Excretion Kidney
• Adverse Effects
• Cyanide toxicity with prolonged use (rare)
• Inhibits hypoxia induced pulmonary
  vasoconstriction
• Coronary steal syndrome
• Increased ICP
• Contraindications
• Other cyclic GMP inhibitors (i.e. sildenafil)

20
Pharmacology-Labetalol

• Dose Bolus of 20mg IV, double bolus up to 80 mg,
  or infusion of 2mg/min to maximum total of 300mg
• Actions Selective a1 and nonselective ßblocker
  4-8 times that of a-blockade.
• Indications Hypertensive emergencies, including
  those from catecholamine stimulation and PIH.
  Does not decrease cerebral or coronary blood flow.

21
Pharmacology-Labetalol

• 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

22
Pharmacology-Esmolol

• Dose Loading dose of 500mcg/kg over 1 min, the
  infusion of 50-300mcg/kg/min
• Actions Ultra-short acting ß1-selective
  adrenergic blocker
• Indications Used in conjunction with
  nitroprusside or phentolamine for hypertensive
  emergencies

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Pharmacology-Esmolol

• Onset Less than 5 mins
• Half-life 9mins
• Metabolism Erythrocytes
• Adverse Effects
• May induce bronchospasm
• Avoid as sole agent in catecholamine excess

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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

25
Pharmacology-Nitroglycerin

• Onset Immediate
• Half-life 4 mins
• Metabolism Hepatic
• Adverse Effects HA, tachycardia, hypotension
• Contraindications
• Other cyclic GMP inhibitors (i.e. sildenafil)

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Pharmacology-Hydralazine

• Dose 10-20 mg, repeated in 30 mins
• Actions Direct arteriolar dilator
• Indications PIH, pre-eclampsia
• Onset 10 mins
• Half-life 2-4 hrs
• Metabolism Liver acetylation
• Excreted Urine

27
Pharmacology-Hydralazine

• 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

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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

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Pharmacology-Enalaprilat

• Excreted Urine
• Adverse Effects
• Angioedema
• Cough
• Worsening renal function
• Hyperkalemia

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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

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Categories of Hypertensive Emergencies

• Hypertensive encephalopathy
• Stroke syndromes
• Embolic
• Hemorrhagic
• Subarachnoid hemorrhage

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Categories of Hypertensive Emergencies

• 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

• Catecholamine excess
• Pheochromocytoma
• MAOI tyramine
• Cocaine/amphetamines/OTCs
• Clonidine withdrawal
• Other
• Renal failure
• Epistaxis
• Childhood hypertension

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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

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Diagnostics

• 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

• A loss of cerebral autoregulation.
• Autoregulation is best studied in the brain but
  present in heart and kidneys as well
• Represents the bodys attempt to maintain
  constant FLOW of blood to perfuse the cells

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Autoregulation

• 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
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Pathophysiology

• Loss of autoregulation leads to
• Cerebral hyper-perfusion
• Vascular permeability
• Cerebral edema
• Vasospasm
• Ischemia
• Punctuate hemorrhages

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Therapy

• 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

• Nitroprusside
• 1st line, 0.3 10 mcg/kg/minute
• Labetalol
• Enalaprilat
• Fenoldopam

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Stroke Syndromes
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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

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Embolic CVA - Dilemma

• Inappropriate lowering of the BP may convert the
  potentially salvageable ischemic penumbra to true
  infarction.
• However, persistent BP gt185/110 is a
  contraindication to thrombolytic therapy (it
  significantly increases risk of intra-cranial
  bleeding)

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Embolic CVA When to Rx HTN

• For thrombolytic candidates, 1-2 doses of
  labetalol (5mg) or nitroglycerin paste may be
  used in attempt to get BP lt185/110
• If thrombolytics are given, then the BP MUST be
  aggressively kept below 185/110!

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Embolic CVA When to Rx HTN

• According to National Institutes of Neurologic
  Disorders and Stroke
• SBP lt220, no treatment
• DBP lt120, no treatment
• Tintinalli suggests not treating DBP lt140
• Others use MAP lt130

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Embolic CVA When to RX

• If complicated by
• Aortic dissection
• Hypertensive encephalopathy
• AMI
• Renal failure

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Embolic CVA How to Rx HTN

• Goal is to reduce MAP 10-20 in uncomplicated
  embolic CVA with markedly elevated pressures
• Labetalol 5mg doses
• Nitroglycerin paste

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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.

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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

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Hemorrhagic CVA When to Rx

• Evidence to support anti-hypertensive therapy in
  acute intracranial hemorrhage is lacking
• However, modest reductions of 20 MAP have not
  been show to adversely affect outcome

52
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

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Subarachnoid Hemorrhage

• A special subset of hemorrhagic CVA.
• Evidence suggests that there may be less
  vasospasm and less re-bleeding if SBP lt160 or MAP
  lt110
• 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
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Pathophysiology

• 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

• Abrupt and severe dyspnea, tachypnea, and
  diaphoresis
• Rales, wheezes, distant breath sounds, frothy
  sputum, and gallop rhythm

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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.

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Therapy

• Nitroglycerin
• Arterial (especially coronaries) and
  veno-dilator, reducing preload and afterload
• Lasix
• Initially a vasodilator, then diuretic
• Morphine
• Vasodilator and sympatholytic
• ACE inhibitor
• Interrupts the renin-angiotensin-aldosterone axis

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Acute Coronary Syndrome

• 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

• 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
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Classification

• Stanford A
• Involves ASCENDING aorta
• More common
• More often fatal
• REQUIRES surgery for survival
• Stanford B
• Involves DESCENDING aorta
• May be managed medically

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Pathophysiology

• Degeneration of the media
• Normal aging
• Pregnancy
• Marfans and Erhlers-Danlos syndromes
• Hypertension
• Bicuspid aortic valve
• Flexion of aorta with each heartbeat
• Atherosclerosis minor factor

64
Pathophysiology

• 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

• 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

• Retrograde Dissection
• Into AV acute regurgitation and CHF
• Into pericardium tamponade
• Into coronary arteries - AMI
• Anterograde Dissection
• Into carotid artery - CVA
• Into renal arteries ARF
• Into anterior spinal artery - paraplegia

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Signs and Symptoms

• Severe tearing chest pain, maximal at onset,
  radiates to back, may migrate as the dissection
  propagates
• Diaphoresis
• N/V
• Feeling of doom (angor animi) and anxiety

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Diagnostics

• CXR
• may be normal in up to 12 !!
• Wide mediastinum
• Calcium sign
• Deviation of trachea or NG tube

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Diagnostics - CXR
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Therapy

• 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

• 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

• 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

• Complicates 5 of pregnancies
• Risk factors
• Nulliparity
• Age gt40
• African American
• Chronic renal failure
• Diabetes mellitus
• Multiple gestations

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Pregnancy and Hypertension

• Accounts for 18 of maternal deaths
• Most common risk factor for placental abruption
• Defined as
• Greater than 140/90
• SBP increased gt20 from baseline
• DBP increased gt10 from baseline

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Pregnancy and Hypertension

• Pre-eclampsia
• Hypertension
• Proteinuria gt300mg per 24 hr.
• Peripheral edema or weight gain gt5 lbs in 1 week
• Presents gt20 weeks except in gestational
  trophoblastic disease

• Eclampsia
• Pre-eclampsia seizures This is an emergency
  !!!!
• HELLP syndrome
• Variant of pre-eclampsia
• Blood pressure lower
• Predilection for multigravid

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Pathophysiology

• 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

• Restlessness and hyper-reflexia early
• Headache
• Visual disturbance
• Peripheral edema
• Abdominal pain

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Therapy

• Any pregnant patient with BP gt140/90 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!

79
Therapy

• 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

80
Catecholamine excess

• Pheochromocytoma
• Monoamine oxidase inhibitor tyramine
• Cocaine/amphetamines/OTC herbals (PPA, ephedra,
  trytophan)
• Clonidine withdrawal

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Pheochromocytoma

• Is a tumor of adrenergic cells
• Most common site is adrenal medulla
• Increased risk in patients with von
  Recklinhausens disease (aka neurofibromatosis)

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Neurofibromas and café au lait spots
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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

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Diagnosis

• Commonly mislabeled as panic attacks or anxiety
  disorder
• Diagnosed by detecting elevated levels of
  catecholamines and their by-products in the urine

85
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

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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

87
Foods containing tyramine

• Beer
• Wine
• Aged cheeses
• Chocolate
• Coffee
• Cream

• Chicken liver
• Pickled herring
• Broad beans (dopamine)
• Yeast
• Citrus fruits
• Snails

88
MAOIs and medications

• Some pharmaceuticals can also cause severe
  hypertension when taken with MAOIs

• Meperidine
• Ephedrine
• TCAs
• Reserpine
• Dopamine
• Methyldopa
• Guanethidine

89
Ingestions

• 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

90
Ingestions

• Over-the counter medications
• Ephedra weight loss supplements
• PPA (Phenylpropanolamine ) decongestants and
  weight loss supplements
• Tryptophan supplement for depression, insomnia,
  migraines

91
Treatment goals

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

92
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

93
Treatment for catecholamine excess

• Labetalol
• Its use as monotherapy is controversial
• Recall that its alpha beta is 13 to 18
• Some texts recommend it other note the potential
  for worsening BP with it as monotherapy for the
  catecholamine excess conditions
• Probably best to use phentolamine 1st

94
Treatment of Hypertensive Urgencies

• Goal Gradual reduction of blood pressure over 24
  hours
• Treatment
• Restart prescribed anti-hypertensive medications
  for the non-compliant patient
• Clonidine
• Captopril
• Losartan
• Follow up within 24 hours

• Sublingual nitroglycerine
• Nifedipine (dont use)

95
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

96
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?

97
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.

98
Case

• 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.

99
Case

• 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

100
Case

• 2 hours later in the ED, complained of severe
  vision loss
• BP 160/85
• Ophthalmology consult confirmed retinal ischemia
• Only partial recovery of vision

101
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 likely education
  regarding the chronic nature of hypertension and
  need for follow up!

102
Summary Neurologic emergencies

• Hypertensive encephalopathy
• Embolic CVA
• Hemorrhagic CVA
• SAH

• Nitroprusside, goal 25 reduction
• Only if gt220/120 orgt185/110 for t-PA
• Labetalol for 10-20 reduction
• Nimodipine 60 mg Q4hrs x 21 days

103
Summary Cardiovascular emergency

• Aortic dissection
• Acute LV failure
• Acute coronary syndrome

• Nitroprusside Esmolol or Labetalol SBP 100
• NTG, Lasix, MS04 for symptoms and 10-15
  reduction
• NTG, MS04, beta-blocker to symptom improvement

104
Summary Other emergencies

• Eclampsia and HELLP
• Catecholamine excess

• Goal DBP 90 magnesium, hydralazine, labetalol,
  delivery!
• Phentolamine /-beta blocker for 25 reduction
  over several hours

105
Pre-Test Questions
106
1. In which of the following would a SBP of
100-120 be appropriate?

• A. Aortic dissection
• B. Thrombo-embolic CVA
• C. Hemorrhagic CVA
• D. Subarachnoid hemorrhage
• E. Hypertensive encephalopathy

107
A. Aortic dissection

• In all the other scenarios, such a precipitous
  drop in BP is likely to worsen outcome

108
2. Which emergency medication is LEAST
appropriate?

• A. Aortic dissection esmolol nipride
• B. Aortic dissection labetalol
• C. Eclampsia magnesium /- hydralazine
• D. Pheochromocytoma esmolol
• E. Acute LV failure - NTG

109
D. Pheochromocytoma - esmolol

• Although use of Labetalol is controversial and
  possibly indicated, a pure beta-blocker like
  esmolol is grossly inappropriate in emergencies
  caused by catecholamine excess.

110
3. All the following regarding CVAs are true
EXCEPT

• A. Persistent BP gt185/110 is a contraindication
  to thrombolytics
• B. Hemorrhagic CVAs tend to have higher BP than
  embolic
• C. Lowering the BP in the acute setting may
  worsen outcome
• D. If BP needs lowering in hemorrhagic CVA,
  Nipride is the agent of choice

111
D. If BP needs lowering in hemorrhagic CVA,
Nipride is the agent of choice

• Nipride and other vasodilators are relatively
  contraindicated in hemorrhagic CVA as they may
  worsen ICP.
• Labetalol is the agent of choice IF BP needs to
  be lowered

112
4. In HTN with pregnancy, all the following are
true EXCEPT

• A. At a BP of 130/85, a patient may experience a
  HTN emergency
• B. Definitive therapy for eclampsia is magnesium
• C. HELLP is a variant of pre-eclampsia, is
  treated as aggressively as eclampsia
• D. HTN is the most common risk factor for
  placental abruption

113
B. Definitive therapy for eclampsia is magnesium

• Definitive therapy for eclampsia is delivery of
  the fetus and placenta involve your consultant
  early!!

114
Questions and Comments