Management of

Hypertension and
Hypotension in the
Emergency Department

Hypertension
How do we manage
Hypertension in the
ER??

Hypertension
Management in the ED

Annual Census = 78,000 patients

Approximately 215 patients per day
40 to 50% have elevated BP
readings upon admission to the ED
That is roughly 39,000 patients/yr
with elevated blood pressure
readings in the ER.

First Step:
Categorize Types of
Hypertension

Four Categories of
Hypertension
- Hypertensive Emergency
- Hypertensive Urgency
- Acute Hypertensive Episode
- Transient Hypertension

What is a
Hypertensive
Emergency?

Hypertensive
Emergency
- A relative increase in blood pressure
from baseline combined with Target
Organ Dysfunction (TOD)
- No Defined Pressure Measurement
- Target Organ Damage is evident
- Also known as Hypertensive Crisis or
Malignant Hypertension
- The MOST Serious form of hypertension

How do we define
Target Organ
Dysfunction

???

Target Organ
Dysfunction
Evidence of Damage or
Injury to Target Organs
such as the Heart, Brain,
Lungs, Kidneys, or Aorta.

Examples of Target
Organ Dysfunction

Acute MI/ Unstable Angina

CVA
ICH / Subarachnoid Hemorrhage
CHF
Aortic Dissection
Acute Renal Failure
Hypertensive Encephalopathy

How do we determine if
Target Organ Dysfunction
is present?

Evaluation for Target

Organ Dysfunction
1.

EKG: (Evaluation for ST elevation or depression, new T-wave

inversions, LVH, or new Left BBB)

2.

CXR: (CHF/pulmonary edema, cardiomegaly, widened mediastinum)

3.

UA or urine dip: (looking for proteinuria, red cells, or red cell casts)

4.

Chem 8: (elevated BUN/CR indicating acute renal insufficiency or

failure, look for other etiologies causing mental status changes, like
hypoglycemia)

5.

Neurological Exam: (Evaluate for lateralizing signs and

symptoms)

6.

Funduscopic Exam: (looking for papilledema or hemorrhages)

7.

CT Head: (only if neurological findings are suspicious for acute CVA)

Diagnosis and
Management
of
Hypertensive
Emergency

Hypertensive
Encephalopathy
Pathophysiology:
- Loss of Cerebral Autoregulation of blood flow
resulting in hyperperfusion of the brain, loss
of integrity of the blood brain barrier, and
vascular necrosis.
- Loss of Autoregulation occurs at a constant
cerebral blood flow of above MAP 150 to 160
mmHg.
- Acute Onset
- Reversible

Hypertensive
Encephalopathy
Symptoms:
Headache, Nausea/Vomiting, Lethargy,
Confusion, Lateralizing neurological symptoms
that are not often in an anatomical distribution.
Signs:
Papilledema, Retinal Hemorrhages
Decreased level of consciousness, Coma
Focal neurological findings

Management of
Hypertensive
Encephalopathy

Reduce Mean Arterial Pressure (MAP) by 20

to 25% (T.397) and do not exceed this within
first 30 to 60 min.
Rosen recommends reduction of 30 to 40%
(R.1759)
MAP= 1/3(SBP-DBP) + DBP
Treatment Reduces vasospasm that occurs at
these high pressures
Avoid excessive BP reduction to prevent
hypoperfusion of the brain and further
cerebral ischemia

Management of
Hypertensive
Encephalopathy
- Nitroprusside is the agent of
choice (T.397) and (R.1759)
- Nitroglycerin and Labetalol have
been used successfully, but
have not replaced Nitroprusside

Management of
Ischemic
CVA

Ischemic CVA
Pathophysiology:
Elevated Blood Pressure can be the
cause of the central nervous
system event, OR, it may be a
normal physiologic response
(Cushings Reflex)

Ischemic CVA
Management

Elevated blood pressure is usually a

physiologic response to the stroke itself
and NOT the immediate cause
This elevation of blood pressure maintains
cerebral perfusion to viable but edematous
tissue surrounding the ischemic area.
Most embolic or thrombotic strokes do
NOT have substantial BP elevations and
do not need aggressive therapy

Ischemic CVA
Management
Management: VERY CONTROVERSIAL!
Recent Trends leans towards NOT
treating hypertension in the presence
of a Cerebrovascular Accident
(thrombotic or embolic) unless
Diastolic Blood Pressure exceeds
140mmHg.

Ischemic CVA
Management
Tintinelli: Favors lowering MAP
(mean arterial pressure) by 20%.
Recommends IV Labetalol in small
doses of 5mg increments IF
Diastolic Blood Pressure is higher
than 140 mmHg.
(T. 398)

Ischemic CVA
Managment
Rosen: In most cases, recommends
no treatment of Hypertension in CVA
patients.
(p. 1760).
- However, the author does
recommend treating HTN if diastolic
blood pressure is greater than 140
mmHg.

Management of
Hemorrhagic CVA

Causes of Hemorrhagic
CVA
Hypertensive

Vascular Disease
Arteriovenous Anomalies (AVM)
Arterial Aneurysms
Tumors
Trauma

Hemorrhagic CVA
Management
Hypertension

associated
with hemorrhagic stroke is
usually transitory and the
result of increased
intracranial pressure and
irritation of the Autonomic
Nervous System

Hemorrhagic CVA
Management

Hemorrhagic CVAs commonly results in

a profound reactive rise in blood
pressure
Management is CONTROVERSIAL.
Subarachnoid Hemorrhage: oral
nimodipine (nimotop) 60mg po q 4
hours to reverse vasospasm. (T.398)
Nicardipine: 2mg IV boluses followed by
an IV infusion of 4 to 15 mg/hr is used
by some to treat Subarachnoid
Hemorrhage. (T.398)

Management of
CHF/
Pulmonary Edema

Congestive Heart
Failure / Pulmonary
Edema
Pathophysiology:

Increased Afterload with

decreased Cardiac
Output

CHF / Pulmonary
Edema
Symptoms:
Shortness of Breath, Cough, Chest Pain
Lower Extremity Swelling

Signs:
Jugular Venous Distension, Rales, S3
Gallop
Hepatomegaly, Pedal Edema

CHF / Pulmonary
Edema Management in
the ED
-

Nitroprusside or IV Nitroglycerin (T. 398)

Rosen: May start with Nitroglycerin, but
Nitroprusside is agent of choice if
Pulmonary Edema is present. (R. 1760)
Attempt treatment of CHF initially with
standard agents (Lasix,sublingual NTG,
morphine), as these often lower blood
pressure, but resort to Nitroprusside if
necessary (R. 1761)

Management of
Acute
Coronary Syndrome/
Acute MI

Acute Coronary
Syndrome /
Acute MI
Pathophysiology:
- Increased afterload,
cardiac
workload, and
myocardial oxygen demand
- Decreased coronary
artery blood flow

Acute Coronary
Syndrome /
Acute
Symptoms: MI

Chest Pain, Nausea / Vomiting, Diaphoresis,

Shortness of Breath

Signs:
Congestive Heart Failure Signs,
S4 Gallop
(due to decreased ventricular compliance)
Few physical findings in many patients
Clinical History is very Important

Acute Coronary
Syndrome/
Acute MI
-

Immediate Blood Pressure

reduction is indicated to prevent
Myocardial Damage
No specific Defined BP target
Tailor treatment to symptom relief
(T. 398)

Acute Coronary
Syndrome /
Acute MI
Management:
Nitroglycerin IV or Sublingual (T. 398)
Nitroprusside (T. 398)
Beta Blockers (Esmolol,Lopressor) (T.
356-357)
Nitroglycerin is Drug of Choice (R.
1761)

Dissection of
Thoracic Aorta

Dissection of Thoracic
Aorta
Pathophysiology:
- Atherosclerotic Vascular Disease,
Chronic Hypertension, increased
shearing force on the thoracic aorta,
leading to intimal tear.
- 50% begin in ascending aorta
- 30% at aortic arch
- 20% in descending aorta (R.1762-3)

Dissection of Thoracic
Aorta
Symptoms:
-

Chest pain radiating to the back (classic presentation)

Neurological Symptoms (carotid artery dissection)
Angina (coronary artery dissection)
Shortness of breath (aortic insufficiency, cardiac
tamponade)

Signs:

- Differential Blood Pressure (in UE)

Bruit (interscapular)
Neurological Deficits
Acute Cardiac Tamponade (rare)

Dissection of Thoracic
Aorta
Management:
-

Medications with negative inotropic

effects (beta-blockers) MUST be given
FIRST. (reduces shearing force)

Vasodilators (nitroprusside) may be

added for further antihypertensive
treatment after administration of a
negative inotropic agent.

Dissection of Thoracic
Aorta
Optimal Blood Pressure in these
patients is undefined and
must be tailored for each
patient, however,
SBP of 120-130mmHg may be a
intial starting point. (T.408)

Acute Renal
Failure

Acute Renal Failure

Pathophysiology:
-

Hypertensive Glomerulonephropathy,
Acute Tubular Necrosis (ATN)

- Worsening renal function in the setting

of severe hypertension with elevation of
BUN/CR, proteinuria, or the presence of
red cells and red cell casts in the urine.

Acute Renal Failure

Symptoms:

- Many times there are few actual

symptoms
- Facial or Peripheral Edema due to fluid
overload or proteinuria may be present,
shortness of breath

Signs:
-

Few findings unless edematous

Pulmonary Edema

Acute Renal Failure

Management:
-

Nitroprusside is agent of choice (T.398)

Dialysis (as needed)
Rosen: Lasix to enhance Sodium
excretion; Also recommends
Nitroprusside or Nifedipine (R.1761)
Nitroglycerin is also a good agent in this
setting since it is hepatically metabolized
and gastrointestinally excreted.

Pheochromocyto
ma

Pheochromocytoma
Pathophysiology:
- Alpha and Beta stimulation of the
cardiovascular system due to
adrenergic excess states

Pheochromocytoma
Symptoms:
Episodic Headaches, flushing, tremor,
diaphoresis, diarrhea, hyperactivity,
and palpitations
Signs:
Tachycardia, tachypnea, tremor,
hyperdynamic state (high output CHF)

Pheochromocytoma
Management:
-

Alpha Blocker FIRST, followed by a

Beta Blocker
Phentolamine (alpha) + Esmolol
(beta)
Labetalol IV (combined alpha and
beta blockade)

Toxemia of Pregnancy
Eclampsia/PreEclampsia

Toxemia of Pregnancy
Pathophysiology:
-

Systemic arterial vasoconstriction

(including placental, leading to
decreased uterine blood flow).
Defined as SBP = 140/90 mmHg or
greater, OR a 20 mmHg rise in SBP or
10 mmHg rise in DBP from baseline
and evidence of HELLP Syndrome

Toxemia of Pregnancy
Symptoms:
Lower extremity swelling, headache,
confusion, seizures, coma
Signs:
Edema, hyperreflexia, elevation of blood
pressure related to baseline BP prior to
pregnancy (elevation may be mild
125/75)

Toxemia of Pregnancy
Management:
-

IV Magnesium Sulfate, Hydralazine.

May also use nifedipine or labetalol
(R.1762)
Delivery of Fetus is definitive
treatment of pre-eclampsia

Summary of Medications
used for Hypertensive
Emergencies
- Intravenous Nitroglycerin:
Start at 0.2 to 0.4 mcg/kg/min (10 to 30 mcg/min) and
rapidly increase in 5 to10 mcg/min increments. Titrate to BP
and symptomatic improvement. (T.369)
- Nitroprusside:
Start 0.3 mcg/kg/min and titrate up every 5 to 10 minutes
based on BP and clinical response. (T.369)
- Esmolol: 500 mcg/kg initial bolus over 1 minute, then start
infusion at 50 to 150 mcg/kg/min (T.408)
- Metoprolol (Lopressor): 5mg IV every 2 minutes for a total of
3 doses, then start infusion at 2 to 5 mg/hr. (T.408)

Summary of Medications
used for Hypertensive
Emergencies
- Labetalol: 20mg IV initial dose, with repeat doses of
40mg to 80mg every 10 minutes to reach desired
effect or max dose 300mg. (T. 408)
-

Nicardipine: 2mg IV boluses followed by an IV infusion

of 4 to 15 mg/hr

Magnesium Sulfate IV: 4 to 6 grams over 15 minutes,

followed by IV infusion of 1 to 2 grams/hour

Hydralazine: 10 to 20mg IV

What is a
Hypertensive
Urgency??

Hypertensive
Urgency
- A relative increase in blood

pressure from baseline WITHOUT

current evidence of TOD, but
potential of progression to TOD is
HIGH.
- Increased likelihood when preexisting conditions are present
(renal insufficiency, CAD, CHF)

Hypertensive Urgency
-

Current recommendation is the gradual

reduction of blood pressure within 24 to 48
hours by using oral antihypertensive
agents
Non-compliance is a common cause,
therefore, restarting a current regimen of
blood pressure medication is appropriate
Making needed changes to current blood
pressure medication regimens is also
appropriate
Follow-up within 24 hours should be
arranged with Primary Care Physician

Oral Regimens for

Treatment of
Hypertensive
(Tintinelli pg. 402)
Urgency in the ED
-

Clonidine: 0.1 to 0.2mg PO, repeat

0.1mg q hour to desired BP reduction
or max of 0.7mg.
Labetalol: 200 to 400mg PO, repeat
every 2 to 3 hours
Captopril: 25mg PO
Losartan: 50mg PO

What is an Acute
Hypertensive Episode?

Acute Hypertensive
Episode
Elevation of Blood Pressure
relative to baseline, but
WITHOUT evidence of acute OR
impending Target Organ
Dysfunction (TOD)

Management of Acute
Hypertensive Episode
-

Paucity of evidence that acute intervention in ED

is warranted for Hypertensive Episode
Complications can occur in acute treatment of
patients with chronically elevated blood pressure
If HTN is newly diagnosed in the ER, patients
should be referred to Primary Care physician for
evaluation and initiation of therapy within 24 to
48 hours
Again, restarting prior blood pressure medication
regimens or adjusting doses is appropriate for
patients with previously diagnosed hypertension.

What is Transient
Hypertension??

Treatment of Transient
Hypertension
-

Transient HTN occurs in association with

other conditions like anxiety, alcohol
withdrawal syndromes, toxicological
substances, and sudden cessation of
medications)
Treatment is aimed at underlying cause
White-Coat Hypertension
Single encounter in ED does not warrant
diagnosis of HTN or treatment of HTN
Follow-up with Primary Care Physician

SWITCHING
GEARS

Hypotension/Shock
Management in the ED

Hypotension/Shock
Types of Shock:

- Hypovolemic
(inadequate circulating volume)
- Cardiogenic
(inadequate pump function)
- Distributive
(peripheral vasodilitation)
- Obstructive
(extra-cardiac obstruction of blood
flow)

Hypotension/Shock
Goals of Management

1. Determine Cause:
- Usually very apparent
- Can be subtle
- No single Vital Sign that is
diagnostic of
Shock
- Initial Therapy guided by clinical
findings

Management of
Hypotension/Shock

2. Evaluate Signs and

Symptoms:
- Tachycardia
- Decreased Urine Output
- Cool, Mottled Skin
- Cyanosis
- Confusion

Hypotension/Shock
Goals of Resuscitation
ABCs:
A- Secure Airway (intubate if needed)
B- Insure oxygenation and ventillation
C- Provide Hemodynamic
Stabilization (correction of
hypotension based on etiology)

Resuscitation
Initiate Fluid Therapy:
0.25 to 0.5 Liters of Normal
Saline (NS) or similar
isotonic crystalloid should
be administered every 5 to
10 minutes as needed for
correction of hypotension

Rapid Fluid
Administration
It is not unusual for a
patient to require 4 to 6
Liters of fluid in the initial
phase of resuscitation.

Goal of Fluid
Resusciation
-

Stabilization of pts mentation

Improvement in Blood Pressure
Reduction of Pulse Rate
Improved Skin Perfusion
Urine Output > 30ml per hour

Inotropic Support
If NO response to initial fluid
infusion of 3 to 4 L is noted, OR if
there are signs of fluid overload
(pulmonary edema), Inotropic
agents should be started.

Inotropic Agents
-

Dopamine: Start infusion at 5

mcg/kg/min and titrate up to 20
mcg/kg/min in order to achieve
desired BP
Indicated for reversing hypotension
related to AMI, trauma, sepsis, heart
failure, and renal failure when fluid
resuscitation is unsuccessful or not
appropriate (T. 212)

Inotropic Agents
-

Dobutamine: Dosage range is 2 to 20

mcg/kg/min, however, most patients can
be maintained at a rate of 10 mcg/kg/min
Indicated for cardiovascular
decompensation due to ventricular
dysfunction or low-output heart failure
Agent of choice for management of
Cardiogenic Shock
Less effect on Heart Rate than Dopamine
(T. 212)

Inotropic Agents
-

Norepinephrine (Levophed): start infusion at 2

mcg/min and titrate to achieve desired blood
pressure.
Used when there is inadequate response to
other pressors.
Lowest dosage that maintains BP should be
used in order to minimize the complications of
vasoconstriction
Increased survival rates of up to 40% in septic
shock have been reported in the literature
(T. 246)

End Point of
Resuscitation
-

Normalization of blood pressure,

heart rate, and urine output

Goal is to maximize survival and

minimize morbidity using objective
hemodynamic and physiologic
values to guide therapy

Questions ???