1. Management of
Hypertension and
Hypotension in the
Emergency Department
Dr.Shahid Bashir Chaudhary

2. Hypertension
How do we manage
Hypertension in the ER??

3. 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.

4. First Step:
Categorize Types of
Hypertension

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

6. What is a Hypertensive
Emergency?

7. 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

8. How do we define
Target Organ Dysfunction
???

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

10. Examples of Target Organ
Dysfunction
 Acute MI/ Unstable Angina
 CVA
 ICH / Subarachnoid Hemorrhage
 CHF
 Aortic Dissection
 Acute Renal Failure
 Hypertensive Encephalopathy

11. How do we determine if
Target Organ Dysfunction
is present?

12. Evaluation for Target
Organ Dysfunction
1. EKG: (Evaluation for ST elevation or depression, new T-wave inversions,
LVH, or new Left BBB)
4. CXR: (CHF/pulmonary edema, cardiomegaly, widened mediastinum)
6. UA or urine dip: (looking for proteinuria, red cells, or red cell casts)
8. Chem 8: (elevated BUN/CR indicating acute renal insufficiency or failure,
look for other etiologies causing mental status changes, like hypoglycemia)
10. Neurological Exam: (Evaluate for lateralizing signs and symptoms)
12. Funduscopic Exam: (looking for papilledema or hemorrhages)
7. CT Head: (only if neurological findings are suspicious for acute CVA)

13. Diagnosis and Management
of
Hypertensive Emergency

14. 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

15. 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

16. 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

17. 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

18. Management of Ischemic
CVA

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

20. 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

21. 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.

22. 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)

23. 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.

24. Management of
Hemorrhagic CVA

25. Causes of Hemorrhagic
CVA
 Hypertensive Vascular Disease
 Arteriovenous Anomalies
(AVM)
 Arterial Aneurysms
 Tumors
 Trauma

26. 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

27. Hemorrhagic CVA
Management
 Hemorrhagic CVA’s 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)

28. Management of CHF/
Pulmonary Edema

29. Congestive Heart
Failure / Pulmonary
Edema
Pathophysiology:
Increased Afterload with
decreased Cardiac Output

30. CHF / Pulmonary Edema
Symptoms:
Shortness of Breath, Cough, Chest Pain
Lower Extremity Swelling
Signs:
Jugular Venous Distension, Rales, S3 Gallop
Hepatomegaly, Pedal Edema

31. 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)

32. Management of Acute
Coronary Syndrome/
Acute MI

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

34. Acute Coronary Syndrome /
Acute MI
Symptoms:
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

35. 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)

36. 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)

37. Dissection of
Thoracic Aorta

38. 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)

39. 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)

40. 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.

41. 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)

42. Acute Renal Failure

43. 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.

44. 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

45. 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.

46. Pheochromocytoma

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

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

49. Pheochromocytoma
Management:
- Alpha Blocker FIRST, followed by a
Beta Blocker
- Phentolamine (alpha) + Esmolol (beta)
- Labetalol IV (combined alpha and beta
blockade)

50. Toxemia of Pregnancy
Eclampsia/Pre-Eclampsia

51. 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

52. 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)

53. 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

54. 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)

55. 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

56. What is a Hypertensive
Urgency??

57. 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 pre-
existing conditions are present
(renal insufficiency, CAD, CHF)

58. 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

59. Oral Regimens for
Treatment of Hypertensive
Urgency in the ED
(Tintinelli pg. 402)
- 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

60. What is an Acute
Hypertensive Episode?

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

62. 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.

63. What is Transient
Hypertension??

64. 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

65. SWITCHING GEARS

66. Hypotension/Shock
Management in the ED

67. Hypotension/Shock
Types of Shock:
- Hypovolemic
(inadequate circulating volume)
- Cardiogenic
(inadequate pump function)
- Distributive
(peripheral vasodilitation)
- Obstructive
(extra-cardiac obstruction of blood
flow)

68. 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

69. Management of
Hypotension/Shock
2. Evaluate Signs and
Symptoms:
- Tachycardia
- Decreased Urine Output
- Cool, Mottled Skin
- Cyanosis
- Confusion

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

71. 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

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

73. Goal of Fluid Resusciation
- Stabilization of pt’s mentation
- Improvement in Blood
Pressure
- Reduction of Pulse Rate
- Improved Skin Perfusion
- Urine Output > 30ml per hour

74. 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.

75. 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)

76. 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)

77. 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)

78. 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

79. Questions ???