Management of Hypertension and Hypotension in the Emergency Department

1
Management of Hypertension and Hypotension in the
Emergency Department
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
  

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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.

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Examples of Target Organ Dysfunction

• Acute MI/ Unstable Angina
• CVA
• ICH / Subarachnoid Hemorrhage
• CHF
• Aortic Dissection
• Acute Renal Failure
• Hypertensive Encephalopathy

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• How do we determine if
• Target Organ Dysfunction
• is present?
  

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Evaluation for Target Organ Dysfunction

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

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• Diagnosis and Management
• of
• Hypertensive Emergency

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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

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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

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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

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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

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• Management of Ischemic
• CVA

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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)

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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.

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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.

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• Management of
• Hemorrhagic CVA

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Causes of Hemorrhagic CVA

• Hypertensive Vascular Disease
• Arteriovenous Anomalies (AVM)
• Arterial Aneurysms
• Tumors
• Trauma

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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

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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)

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• Management of CHF/
• Pulmonary Edema

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Congestive Heart Failure / Pulmonary Edema

• Pathophysiology
• Increased Afterload with decreased Cardiac
  Output

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CHF / Pulmonary Edema

• Symptoms
• Shortness of Breath, Cough, Chest Pain
• Lower Extremity Swelling
• Signs
• Jugular Venous Distension, Rales, S3 Gallop
• Hepatomegaly, Pedal Edema

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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

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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

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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)

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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

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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)

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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)

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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.

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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

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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.

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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

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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

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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

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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)

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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

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• 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)

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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

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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

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• What is an Acute
• Hypertensive Episode?

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Acute Hypertensive Episode

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

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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??

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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

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• SWITCHING GEARS

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• Hypotension/Shock
• Management in the ED

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Hypotension/Shock

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

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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

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Management of Hypotension/Shock

• 2. Evaluate Signs and Symptoms
• - Tachycardia
• - Decreased Urine Output
• - Cool, Mottled Skin
• - Cyanosis
• - Confusion

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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)

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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

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Rapid Fluid Administration

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

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Goal of Fluid Resusciation

• Stabilization of pts mentation
• Improvement in Blood Pressure
• Reduction of Pulse Rate
• Improved Skin Perfusion
• Urine Output gt 30ml per hour

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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.

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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)

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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)

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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 ???