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

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) • 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)

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