Hypertensive Crises

1. Hypertensive Crises Nadim J Lalani 08.03.2007 Thanks to Dr Sarah McPherson Dr Trevor Langhan [who usually presents this talk]

2. Famous Last words? “I have a terrific headache” April 12 1945

3. Clues: • Survived Assassination Feb 1933 • “we have nothing to fear but fear itself” • President during Pearl Harbor

4. FDR • Arguably the greatest US President of all time • Only US President to be elected to 4 terms • “New Deal” brought the US back from the Great Depression  Social Security • Suffered from complications of GBS and was a paraplegic • Started the “March of Dimes”  is on the dime • Dies April 12 1945 of ICH from Hypertension

5. West J Med. 2001 August; 175(2): 119–124.

6. Objectives • Definitions • Pathophys [briefly] • Cases • Q/A format:

7. Definitions? • Normal BP? • sys BP < 120 mm Hg • dias BP < 80 mm Hg • Hypertension? • sBP > 140 mm Hg • dBP > 90 mm Hg • In Between = “prehypertension” • Hypertension acc to Rosen: • SBP > 160 • DBP > 95

8. Definitions? • Hypertensive Crisis? • Hypertensive Urgency? • Hypertensive emergency? • Malignant Hypertension? • Severe Hypertension?

9. Definitions

10. Malignant/Severe Hypertension Malignant: • Older term [no longer used]  but often asked for it by attendings • Essentially Hypertensive Emergency  with the end organ effects Severe: • Sys BP > 180 • Dias BP > 120 • No end organ effects

11. What Counts as “End organ Damage”? H E A D T O T O E

12. Hypertensive “syndromes” • Encephalopathy • Stroke • Pulmonary edema • ACS • Aortic dissection • Pregnant • Renal failure • Other end-organ [retinal findings, hemolysis]

14. BP Measurement

15. BP Measurement If no extinguishment • NB Cuff Size • 10 minutes in between • Pt supine/ lights off &c.

16. Increased BP in the ED • Things that cause “reactive” HTN in the ED? • Anxiety • Pain • Drugs (illicit - cocaine, amphetamines, LSD, PCP & OTC’s) • ETOH withdrawal • BP cuff too small • Machine vs sphygmomanometer

17. Hypertension • Classified into: • Primary = Essential Hypertension [95%] • Secondary [5%] • Secondary more likely to cause severe HTn

18. Essential hypertension • Cause not entirely understood • Theories…. • Alterations in contractile properties of vascular smooth muscle • Change in vascular smooth muscle from chronic elevated BP from primary failure of normal autoregulation • Change in RAAS p-way

19. Secondary Hypertension

20. Specific 20 causes 1)Renal Disease: [most prevalent] • Renal artery stenosis  high renin state • Fibromuscular dysplasia of the renal artery • Young white women • Flank bruits  Primary renal disease (e.g chronic pyelo) ? From local ischemia  Renin secreting tumors

21. 2) Arterial disease: • large artery abN can lead to HTn • Coarctation of the aorta TRIAD? • Upper extremity hypertension • Possible delayed femoral pulses • Systolic murmur heard over the back • Loss of elasticity of the arteries with age

22. 3) Glucocorticoids: • Iatrogenic • Cushing’s • 10 Pituitary tumor  ACTH • ACTH – secreting tumor [>50% lung] • Adrenal tumors • Primary hyperaldosteronism [Conn’s] • hypokalemia

23. 4)Pheochromocytoma: • Catecholamine-secreting tumors • Also w/ Neurofibro & MEN type ii • Clinically • Paroxysms of HTN • Tachycardia • Fatigue • Malaise • Sweating • Apprehension • Elevated urine catecholamines and metanephrines • Nb any incidental adrenaloma  screen for pheo

24. 4) Drugs  Sympathomimetics &c.  MAOI and tyramine  Withdrawal • B and a blockers • ETOH, benzos -

25. ED Presentation • Four general ways: • Hypertensive emergencies • Requires BP reduction in 1h • Hypertensive urgency • Mild-moderate hypertension • Transient hypertension

26. Approach • ABC’s • Assess whether the reading is correct • Hx &P/E: • Pulmonary Oedema? • CHF / Ischemia/ dissection? • High ICP/ SAH/ Neuro deficits? • Diagnostix • Lytes, Urine +/ - TNT, EKG, CXR, +/- CT head • Is this a Hypertensive Emergency?

27. Fundoscopy

28. Fundoscopy

29. Case 1 • 84 yo F presents to the ED c/o HA feeling unwell for 1 week • Hx HTn • O/e: BP 190/130, HR 80, rest of exam N • Approach?

30. Hypertensive Urgency • No benefit to treating in the ED • Real risk of harm even with appropriate MAP reduction • Most will have lower BP on f/u exams • Bottom Line : DON’T TREAT  but refer

32. Recommendations

33. Case 2 • 53-year-old M presents To ED w/ increased SOB, headache, N/V and visual changes, worsening for several days. • O/e: Confused, BP 253/140 mm Hg. • Approach?

34. Hypertensive encephalopathy • Pathophys: • Acute increase in BP [ MAP usually > 160] • Overwhelms cerebral autoregulation [resistance vessels can’t cope] • Eventually leads to vasospasm & ischemia. • Ischemia leads to leaky capillaries and edema • Clinically • Acute and reversible • Headache, vomiting, drowsiness, confusion, seizures, focal neuro deficits blurred vision • Normal CT head and bloodwork, elevated opening pressure on LP

35. Management: • Sodium Nitroprusside or Labetalol • Goal: decrease MAP by 25% in 1 hour • Keep DBP > 110 • Admit

36. Case 3 • 40 y female family hx HTN, CVA • Presents w/ L sided weakness • BP 190/120, HR 94, RR 14, sats 99% • O/E left facial droop, L dense hemi-plegia • Considerations?

37. Hypertensive Emergency- Stroke • Most (85%) are ischemic not hemorrhagic strokes • Elevated BP usually result of the stroke itself • May have mild to moderate BP elevation • NB!! • Lowering BP may worsen ischemic brain injury • watershed areas sensitive to hypoperfusion • Do not treat [exception is stroke 20 Ao Dissection]

38. Hypertensive Stroke - lytics • BP >185/110 is a contraindication to tPA • Lower BP 1st

39. Hypertensive stroke • Management: • Labetalol agent of choice • Titrate slowly to goal reduction in MAP by a max of 20%

40. Hypertension + hemarrhagic Stroke • No data on acute BP lowering in ICH • ICH causes inc ICP • So May be inadvertently lowering CPP if you lower BP • My bottom line: treat only in concert with ICU/Nsx • If lowering is done, use an agent that dose not vasodilate • Avoid nitrates • Labetolol is best (ACE-I have some benefit)

41. Case 4 • 50 yo M at a “rave” comes into ED with ALOC [Pmhx: takes phenelzine] • O/E: HR 100, BP 190/130, diaphoretic, GCS 9 and rigid extremeties • Approach?

42. MAOI – drug interactions • sympathetic surge • Avoid B-blockers • Management: • ABCDEF’s of tox • Phentolamine 5mg IV over 1min repeat Q5-10min • Sodium nitroprusside 0.3 mcg/kg/min

43. Case 5 • 55 year male known LV dysfunction (EF 30%), Chronic HTN , smoker • Has not been able to buy meds • Presents to ED w/ incr SOB, leg swelling • HR 95, BP 190/120, sats 89%, RR 25, Rales • Approach?

44. Hypertension – Pulmonary edema • Pts w/ CHF have incr PVR  so have HTn • Poor control  LVH  LV failure • Management: • Standard therapy for CHF • NTG / nitroprusside • Low dose ACE-i

45. Case 6 • 32 y female presents to ED c/o H/A, palpitations and feeling uneasy • BP 170/90, HR 150 sinus, RR 18, diaphoretic, pupils 6mm • Approach? • Patient leaves AMA

46. Case 7 • Same lady comes back the next day with SOB, Palpitations after doing cocaine • O/E: BP 190/100, HR 130, RR 28, sats 96% • EKG ST segment elevation V1-V3 • Considerations?

47. Pheochromocytoma/Cocaine • Treatment: • Avoid Beta blockade  unopposed alpha • Nitroprusside if emergency • Phentolamine – 1-5 mg IV boluses (alpha-block) • With cocaine can use benzos to counteract sympathetic drive

48. Case 8 • 55 year male smoker, HTN, DM, • c/o left RSCP that radiated to his jaw after 1st training run for his 10k this summer. • HR 120, BP 190/90, RR 19, sats 99%

49. EKG • Approach?

50. HTn + ACS • Management: • Immediate lowering of BP indicated to prevent myocardial damage • NTG agent of choice • Beta block [labetalol] • CCB (if BB is contraindicated)