Severe Hypertension in the ED (Back to Basics 2010)

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 1st, 2010 Severe Hypertension in the ED(Back to Basics 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:microangiopathichemolyticanemia

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?