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

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

13. Diagnosis and Managementof
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 Shortness of Breath, Cough, Chest Pain
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 )
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 )

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 mmHg 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: Signs:
- 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 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 (inadequate circulating volume) - Cardiogenic
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 ???