Hypertensive Emergencies

1. Jason R. FrankMD MA(Ed) FRCPC Dept of Emergency Medicine Hypertensive Emergencies

2. Case 1

3. Case 1 • 82 yo female • CC: acute onset severe headache, n/v • Noted by family to be confused • Denies trauma • PMHx: HTN, elevated cholesterol

4. Your Assessment • VS: HR-110, BP-230/150 RR 32, O2 96% RA • GCS 14 (speech confused) • No focal neurological signs • No signs of trauma • CVS/Resp: bilateral crackles

5. What now? • What concerns you about this pt? • Differential diagnosis? • Investigations? • Immediate management?

6. Concerning Features • VS: HR-110, BP-230/150 RR 32, O2 96% RA • GCS 14 (speech confused) • No focal neurological signs • No signs of trauma • CVS/Resp: bilateral crackles

7. Differential Diagnosis 62 yo with headache, confusion, HTN • CVA • ICH: spontaneous, traumatic • CNS Infection: meningitis, encephalitis, abscess • CNS neoplasm: primary or mets • Migraine HA • Metabolic or toxic encephalopathy • Hypertensive encephalopathy

8. MCC Objectives

9. MCC OBJECTIVES – HTN EM KEY objectives: • Differentiate “malignant” HTN from secondary conditions • Conduct initial HTN lowering treatment OBJECTIVES: • Differentiate non-localizing neurologic symptoms • Determine presence of other hypertensive emergencies • Interpret clinical & lab findings • Conduct an effective management plan, including specific Rx

10. HYPERTENSION Standard Definition • Based on 3 measurements, each 1 wk apart > 140 systolic > 90 diastolic • Most important # acutely: Diastolic • MAP = 1/3 Systolic, 2/3 Diastolic

11. Primary or Secondary • Majority (90-95%) essential HTN • Of Secondary: ½ have a potentially curable cause

12. Secondary HTN Increased CO: • RF with fluid overload • Acute renal disease • Hyperaldosteronism • Cushing’s syndrome • Coarctation of the Aorta Increased vascular resistance: • Renal Artery Stenosis • Pheochromocytoma • Drugs • Cerebrovascular (CVA, ICH, SAH)

13. Renal Artery Stenosis • most common treatable cause (1-5%) • compromised renal perfusion => activation of RAA • 2 pt groups: • Elderly with atherosclerotic disease • Young females with fibromuscular dysplasia • Clinical: abdo bruit (40-80%), retinopathy, HTN resistant to Rx, hypoK

14. Aldosteronism • Uncommon but treatable • Na retention, volume expansion, increased CO • Hypernatremia & Hypokalemia typical • Primary: Adrenal adenoma, hyperplasia • Secondary: Cushing’s, CAH, exogenous mineralcorticoids

15. Pheochromocytoma • Tumour, usually in adrenal medulla • Produces xs catecholamines (epi, NE) • Paroxysmal HTN…difficult to recognize • Episodic HTN, HA, palpitations, diaphoresis, anxiety…not a panic attack! • Easy to diagnose: elevated urinary catecholamines, metanephrines, vandillylmandelic acid

16. Coarctation of the Aorta • Rare but early surgical intervention can improve prognosis • Clinical triad: • upper extremity HTN • systolic murmur over back • delayed femoral pulses

17. Drugs • Cocaine, amphetamines • ETOH withdrawal • Withdrawal from clonidine, beta blocker • MAOI + tyramine containing foods or certain Rx (meperidine, TCA, ephedrine) • Tyramine causes release of NE • Usually rapidly destroyed by MAO

18. Thinking About HTN: • Chronic HTN • Transient HTN • “White coat HTN” • Hypertensive “Urgencies” • Hypertensive “Emergencies”

19. Hypertensive “Urgencies” • Elevated BP WITHOUT evidence of acute end-organ damage • BP arbitrary levels • In past, treated with SL nifedipine • Demonstrated adverse outcomes (stroke, MI) • “rarely requires therapy” • Consider initiating chronic Rx

20. Malignant Hypertension Severe HTN & Evidence of acute end-organ damage • Diastolic BP usually > 130 mm Hg or MAP > 160 • Relative rise much more important than # • Affects 1% of hypertensive patients

21. End-Organ Damage • CNS: Hypertensive encephalopathy • CVS: Cardiac Ischemia Pulmonary Edema Aortic Dissection • Renal: ARF • Heme: microangiopathic hemolytic anemia • Eclampsia/Pre-eclampsia

22. Case 1 • 62 yo female • CC: acute onset severe headache, n/v • Noted by family to be confused • Denies trauma • PMHx: HTN, elevated cholesterol

23. Your Assessment • VS: HR 110, BP 230/150, RR 32, O2 96% RA • GCS 14 • No focal neurological signs • No signs of trauma • CVS/Resp: bilateral crackles

24. Case 1 • What is your initial management for this pt? • What is causing her symptoms?

25. Cerebral Perfusion • Autoregulation: cerebral blood flow maintained through normal range of BP by afferent arterioles • N: autoregulation for MAP > 60 • Chronic HTN: level of autoregulation in elevated

26. Hypertensive Encephalopathy Abrupt, sustained raised in BP (DBP > 140) => exceeds capacity of autoregulation uncontrolled cerebral blood flow vasospasm, ischemia, punctate hemorrhages, increased vascular permeability => ischemia, cerebral edema

27. Hypertensive Encephalopathy: Clinical • Acute in onset & reversible • Severe HA, N/V, drowsiness, confusion • +/- seizures, coma, focal neurological deficits, blindness • Papilledema usually present • EMERGENCY….untreated pts may die within hrs!

28. How to Differentiate? • Focal deficits do not usually follow a singular anatomic pattern • Onset: usually hours to days • Can be associated with hemorrhage • CT usually N • EEG non-specific • CSF: clear, increased opening pressure

29. Management ABC’s Control BP! • Goal reduce MAP by 25% or diastolic to minimum of 110 mm Hg over 1 hr • IV Nitroglycerine • IV Nitroprusside • Labetolol: selective alpha & non-selective beta blocker

30. Physical Exam in HTN • Eye: • Acute: papilledema, retinal hemorrhages, vasospasm • Chronic: AV nicking, cotton wool spots, silver wiring • CVS: • Pulm edema: S3, rales JVD, peripheral edema • LVH: displaced apex • Coarctation murmur • Renal • Bruit • Fluid overload

31. Other End-Organ Effects

33. Cardiovascular End-Organ Damage • Pulmonary Edema • Aortic Dissection • ACS

34. Pulmonary Edema • Long standing HTN  myocardial hypertrophy • Eventually leads to LVF & dilatation • Stress of pulmonary edema  to xs catecholamines leading to HTN • Standard treatment causes fall in levels & BP returns to normal

35. Pulmonary Edema • In some, sudden, severe HTN precipitates acute LVF, causing pulmonary edema • BP must be lowered to reverse the process

36. Management of Pulmonary Edema • Standard Therapy: nitrates, O2, Furosemide, ACEI Focused antihypertensive Rx: • Nitroglycerin IV • Nitroprusside IV • ACEI as an adjunct

37. Cardiac Ischemia • If severe HTN associated with angina, lower BP to prevent myocardial damage • Nitroglycerin SL, IV • Beta-blockers (careful in setting of poor LVF) • ACEI • Nitroprusside NOT used as may cause reflex tachycardia

38. Aortic Dissection • Classic: acute onset ‘tearing” chest pain radiating to back • Widened mediastinum on CXR • CT angio modality of choice • Immediate control of BP to limit extent of dissection • Type A: involve ascending Ao, Tx: OR • Type B: treated medically

39. Management Aortic Dissection • Goal to reduce BP to sys 100-120 mm Hg • Reduce ejection force of heart • Rx • Vasodilator (e.g. nitroprusside, fendolopam) PLUS Beta blocker • Or monotherapy with Labetolol (alpha/beta blocker)

40. Acute Renal Failure • Urine dip: protein, RBC • Labs: BUN, Cr, electrolytes • Management • Nitroprusside IV, Labetolol IV • ACE-I, although takes a few hours • CCB IV (nicardipine)

41. Specific Therapies in Acute Hypertensive Emergencies • Labetolol • 20mg IV, may incrementally increase dose (40mg, 80mg) q20 min, max 300mg/24 hr • Nitroprusside: 0.3 mcg/kg/min, titrate up to 10 mcg/kg/min • Nitroglycerin: start at 10-20 mcg/min, titrate up • Special cases: Eclampsia, pre-eclampsia • MgSO4(for seizures) 4-6gm/1 hr • Hydralazine 10 mg IV

42. Acute Hypertension: Overview • Most pts do NOT require emergent treatment for their HTN (do no harm) • With severe HTN, evaluate immediately for end-organ effects • Appropriate BP measurement • Rapid recognition & appropriate reduction in BP for hypertensive emergencies • Careful of over-treatment of HTN & risk of cerebral ischemia

43. Jason R. FrankMD MA(Ed) FRCPC Dept of Emergency Medicine Hypertensive EmergenciesQuestions?