Hypertensive Emergencies Jason R. Frank MD MA(Ed) FRCPC Dept of Emergency Medicine

Case 1

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

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

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

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

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

MCC Objectives

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

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

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

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)

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

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

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

Coarctation of the Aorta Rare but early surgical intervention can improve prognosis Clinical triad: 1)upper extremity HTN 2)systolic murmur over back 3)delayed femoral pulses

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

Thinking About HTN: 1.Chronic HTN 2.Transient HTN 3.“White coat HTN” 4.Hypertensive “Urgencies” 5.Hypertensive “Emergencies”

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

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

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

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

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

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

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

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

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!

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

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

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

Other End-Organ Effects

Cardiovascular End-Organ Damage Pulmonary Edema Aortic Dissection ACS

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

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

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

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

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

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

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)

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 mcg/min, titrate up Special cases: Eclampsia, pre-eclampsia MgSO 4 (for seizures) 4-6gm/1 hr Hydralazine 10 mg IV

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

Hypertensive Emergencies Questions? Jason R. Frank MD MA(Ed) FRCPC Dept of Emergency Medicine