1. Richard Dionne MD CCFP-EM Assistant Professor Emergency Medicine – University of Ottawa Associate Medical Director – Regional Paramedic Program for Eastern Ontario Special Thanks : Dr Jason Frank April 1 st, 2010

2. Goals & Objectives  Differentiate malignant hypertension from secondary causes  Understand the principles of managing hypertension and the risks associated  Differentiate and identify the target-organ damage causes by hypertension emergencies

3. Definition  Essential hypertension  > 140 systolic / > 90 diastolic  BP = CO X PVR  Blood Pressure = Cardiac Output X Vascular Resistance  Autoregulation phenomenon overwhelmed  Rapid rate rise in MAP : Mean Arterial Pressure MAP = 1/3 Systolic + 2/3 Diastolic  Vascular endothelial stress injury pattern

4. Causes  Severe uncontrolled Hypertension :  > 180 systolic / > 120 diastolic  Hypertensive Emergency (Malignant):  Acute target organ damage / effect  Hypertensive Urgencies:  At risk of short term end organ effect

5. Differential Diagnosis  Primary Hypertension  Long standing, uncontrolled, drug withdrawal  Secondary Hypertension A- Increased cardiac output  Renal failure with fluid overload  Acute renal disease  Hyperaldosteronism B-Increased vascular resistance  Renovascular hypertension  Pheochromocytoma  Drugs (sympathomimetics, MOA,etc.)  Cerebrovascular (CVA, ICH, SAH)

6. Renin-Angiotensin-Aldosterone  Renin produced by the kidneys stimulates the formation of angiotensin II, a potent vasoconstrictor.  DDX: Renal Artery Stenosis  In turn promotes aldosterone release and consequently the retention of Na+ & water.  Both increase in vascular resistance and intravascular volume will increase blood pressure.

7. Hyperaldosteronism  Na+ retention, water retention, increased CO  Hypernatremia & Hypokalemia typical  Primary:  Adrenal adenoma / hyperplasia  Secondary:  Cushing’s, exogenous mineralocorticoids

8. Pheochromocytoma  Tumour in the adrenal gland (medulla)  Increase in catecholamines (epi, norepi)  Paroxysmal : HTN, HA, palpitations, diaphoresis, anxiety... Not panic attacks!  Dx: urine metanephrines & vandillymandelic acid

9. Break Down  Malignant Hypertension & Emergencies  Hypertensive Urgencies  Severe Uncontrolled Hypertension

10. Malignant Hypertension  1% of patient with primary hypertension will go on to have an accelerated malignant phase Severe Hypertension + End-organ damage  Denotes an elevated blood pressure with the presence of papilledema on fundoscopy  Grade 3: vascular injury with possible hemorrhages, cotton-wool spots, arterio-venous “nicking”

11. End-organ damage  CNS:  Hypertensive encephalopathy / CVA  CVS:  Cardiac ischemia / Pulmonary edema / Aortic dissection  Renal: ARF  Heme: microangiopathic hemolytic anemia

12. End-Organ Effects

14. Clinical Evaluation  Focus on “End-organ compromise”:  Headache, Chest pain, Dyspnea,Visual disturbance, Change in mental status / confusion.  Potential drug interactions, compliance to RX, etc.  Examination: BP both arms with appropriate size cuff, fundoscopy, cardiac & neurological.  Work-up: CBC, Lytes, renal function, ECG, urine & CXR.  May need CT-head / urine tox screen, etc.

15. Regulation Brain Vasculature  Normal individual:  Adapts with cerebral vasoconstriction if BP rises, and vasodilation if BP drops...  Adaptation to a wide range of MAP changes  Chronic Hypertensive:  Cannot adapt as well, so a rapid drop in BP will cause drop in cerebral perfusion pressure, therefore a risk of cerebral ischemia...  Caution with lowering the BP too fast !!!

16. Management Goal 1- Decrease MAP 15-20% within 1 hour 2- Further reduction towards 160/100 mmHg within the following 6 hours 3- Gradual reduction to normal range over the next 24 hrs if the patient is stable

17. Treatment  Vasodilators:  Nitroprusside:  0,25 – 10 ug/kg/min perfusion IV  Vasodilator: decrease in MAP, afterload, preload & renal blood flow.  Adrenergic inhibitors:  Labetolol:  20 – 80 mg IV q 10 min, then infusion prn  Beta-blocker with an alpha blocking property, reduces PVR with no reflex tachycardia...

18. Hypertensive Urgencies  Severe elevation in blood pressure that is not causing end-organ damage... Goal  Control within 24hrs  Consider if Diastolic BP > 115 – 130  Oral regiment may be all that is needed  Captopril : 6.25 – 25 mg q 6h  Clonidine: 0,1 – 0,2 mg q 12 – 24 h  Labetolol : 100 – 200 mg q 12 h

19. Severe Uncontrolled Hypertension Classification Stage 1: SBP 120-139 / DBP 80-89  “prehypertension” Stage 2: > 160 / 100  Categorize according to risk profile... Treatment regiment:  Diuretics: older patients & African Americans  ACE inhibitors: comorbidity, diabetes, etc.  Beta-Blockers: cardiovascular disease, Hx: MI & angina

20. Follow-up  Hypertensive Emergency & Malignant crisis:  Admission & IV start of treatment required  Needs ICU & monitoring  Hypertensive urgencies & Uncontrolled severe hypertension:  Oral treament started in ER vs early outpatient, but mandatory close follow-up with primary care MD

21. Conclusion  Measure blood pressure appropriately  Most patient do not require emergent treatment for their hypertension in the ED  Severe hypertension = evaluate for end-organ effects  Rapid recognition & lowering of BP in hypertensive emergencies  Careful of over treating & risk of cerebral ischemia

22. Question?