HYPERTENSION EMERGENCY Categories Etiology/pathophysiology History/Physical Workup Treatment Terminology & definition Urgency: Severe HTN + JNC 7 >180/100

0/100 Emergency: End organ damage - CHF - ACS/AMI - Renal failure - Stroke & ischemia - Encephalopathy - Aortic dissection - Pre eclampsia

HYPERTENSION (JNC-7 class) SBP DBP (mmHg) (mmHg) Normal <120 <80 PreHTN 120-139 80-89 Stage I 140-159 90-99 Stage II 160 100

Definition: 1. HYPERTENSIVE EMERGENCY: - also called Hypertensive Crisis, - severe hypertension with acute impairment of an organ system (e.g., central nervous system [CNS], cardiovascular, renal). - blood pressure should be lowered aggressively over minutes to hours. 2. Presence of papilledema indicates MALIGNANT HYPERTENSION. 3. HYPERTENSIVE URGENCY: the - BP is a potential risk but has not yet caused acute end-organ damage. - These patients require BP control over several days to weeks. 4. ACCELERATED HYPERTENSION: - recent significant increase over baseline blood pressure that is associated with target organ damage. - This is usually vascular damage on fundoscopic examination, such as flame-shaped hemorrhages or soft exudates, but without papilledema. Etiology Essential hypertension : Inadequate blood pressure control and noncompliance are common precipitants Renovascular Eclampsia/pre-eclampsia Acute glomerulonephritis Pheochromocytoma Anti-hypertensive withdrawal syndromes

Head injuries and CNS trauma Renin-secreting tumors Drug-induced hypertension Burns Vasculitis Idiopathic hypertension Post-op hypertension Coarctation of aorta

Pathophysiology Normal autoregulation Rise in BP arterial & arteriolar constriction Normal flow(flow= p/r) Failure of autoregulation failure of vc endothelial damage (dt shear stress on the wall) BP = PVR X CO (SV X HR) *rate at which MAP rises more important than absolute rise. 1. Acute rise in BP 2. Failure of vc by autoregulation 3. Endothelial damage 4. Deposition of protein/ fibrinogen in vessel wall 5. Activates coagulation & inflammation 6. FIBRINOID NECROSIS RAAS plays an important role in initiating & perpetuating BP rise by causing vc & fluid retention. Normal vessel wall: the endothelium actively modulates vascular tone aotucrine/paracrine function

Endogenous vd NO PGI2

Endogenous vc Catecholamines AT-II ET1 Aldosterone ADH (vasopressin)

Acute rises in BP can promote cellular adhesion molecule (CAM) expression. In HTN urgency acute changes in vascular resistance occur in response to excess vc or low endogenous vd. In HTN emergency endothelial control of vascular tone is overwhelmed end organ hyperperfusion, afteriolar fibrinoid necrosis Increased endothelial permeability / perivascular eodema. Loss of endothelial fibrinolytic activity + activation of coagulation & plt promotes DIC.

Clinical presentations 1. HTN urgencies - Arrhythmia - Epistaxis - Headache - Psychomotor agitation usually 1ry ED dx: HTN

2. HTN emergencies - Chest pain - Dypsnea - Neurologic deficit Usually 1ry ED dx: CVA, APE,HTN encephalopathy, acute heart failure

renal system: The renal system is impaired when high BP leads to arteriosclerosis, fibrinoid necrosis, and an overall impairment of renal protective autoregulation mechanisms. This may manifest as worsening renal function, hematuria, red blood cell (RBC) cast formation, and/or proteinuria.

History 1. circumstances surrounding hypertension & etiology - Medications:esp. hypertensive drugs/their compliance,illicit drugs - Duration of hypertension - Duration of current symptoms - Other medical problems:prior hypertension,thyrotoxicosis, cushishings,SLE,renal 2. Complications : - CNS:headaches,blurred vision, wt loss, nausea, vomiting, weakness, fatigue, confusion and mental status changes. - CVS:symptoms of CHF, angina, dissection - Renal:hematuria,oliguria. Physical examinations: Use an approach based on organ systems to identify signs of end-organ damage - CNS: focal neuro deficits, seizures, stupor, coma, papilledema, hemorrhages, exudates, or evidence of closed-angle glaucoma - CVS: JVP,lung auscultaion for crackles,peripheral edema,extra heart sounds, equal and symmetric BP and pulses bilaterally. - Check for abdominal masses and bruits. DDx: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Acute Coronary Syndrome Aortic dissection CHF,pulmonary edema Acute Coronary Syndrome Aneurysm, Abdominal Anxiety Congestive Heart Failure Pulmonary Edema Cushing Syndrome Delirium Tremens Encephalitis Glomerulonephritis

13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23.

Headache, Cluster Headache, Migraine Headache, Tension Hyperthyroidism, Thyroid Storm, Graves Disease Myocardial Infarction Pregnancy, Eclampsia Pregnancy, Preeclampsia Stroke, Hemorrhagic Stroke, Ischemic Subarachnoid Hemorrhage Systemic Lupus Erythematosus

Work up Lab Ix: CBC, Renal & liver function tests Electrolytes BGL lipid profile Others: ECG CXR PA view Echo Fundus examination

D-Dimer Cardiac biomarkers. Urinanalysis Urinary Metanephrines Toxicology

CT brain MSCT Triple rule out (i.e. Aortography, Coronary Angiography & pulmonary angiography)

Treatment: Weigh benefits of decreasing BP against risks of decreasing end-organ perfusion. Important steps include: Appropriately evaluating patients with an elevated BP Correctly classifying the hypertension Determining aggressiveness of therapy An important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number." Initial steps: Initial considerations: Place patient who is not in distress in a quiet room and reevaluate after an initial interview. In one study, 27% of patients with an initial DBP >130 mm Hg had their DBP fall below critical levels after relaxation without specific treatment. Treatment goals for HTN EMERGENCY 1. Prompt, but smooth reduction of BP - Reduce BP 25% during 1st minute to 1hour - If stable, reduce BP in next 2-6hours - Gradual reduction toward N BP over next 24-48hours - Exceptions requiring special care: Ischemic stroke Stroke eligible for thrombolytic agent Aortic dissection 2. Avoid excessive drops in BP - May cause renal, cerebral or coronary ischemia - Need careful and close monitoring - Use of an arterial catheter for monitoring BP routinely required 3. Choice of pharmacological agent should be tailored to patient - Based on risks, comorbidities and type of end organ damage

2 main groups of drug: 1. Vasodilators 2. Adrenergic inhibitors VASODILATORS DRUG Nitroprusside Nitroglycerine Nicardipine Hydralazine Enalapril Fenoldopam

DOSAGE 0.25-10mcg/kg/min 5-100mcg/min 5-15mg/hr 10-20mg 10-40mg IM,1.255MG1Vq6hr 0.1-0.3mcg/kg/min

ONSET/DUR Instant/1-2min. 1-5min/3-5min 5-10min/1-4hr 5-15min/3-8hr 20-30min/6hr 5min/10-15min

ADV.EFFE Thiocyanate,cyanide poisoning Flushing,headache,methemoglobin Tachycardia,flushing.avoid-heart failure Flushing,tachy,avoid-A.diss,MI Hypotension, renal failure, hyperkalemia Flushing, headache, tachycardia

ADRENERGIC INHIBITORS DRUG DOSAGE Labetalol 20-80mgiv bolus every 10 (a+b blocker) min,2mg.min iv infusion Esmolol (b-1 selective blocker) Phentolamine (a1 blocker) Oral drugs DRUG CAPTOPRIL (ACE inhibitor) CLONIDINE (a2 agonistcentrally acting) LABETALOL 200-500 mcg/kg/min for 4min,then 150300mcg/kg/min 5-15mg iv

ONSET/DUR 5-10min/3-6hrs

1-2min/10-20min

ADV.EFF Heart block,ortho hypotension.avoid-heart failure,asthma Hypotension,avoid-heart failure,asthma Tachycardia,flushing,headache

1-2min/3-10min

DOSAGE 6.25-25MG q 6hrs. 0.1-0.2 mg hrly, Upto max 0.8mg in 24hrs. 100-200mg q 12hrs

ONSET/DURATION 15-30min/6 hrs. 30-60min/6-12hrs.

ADV. EFF. Hypotension in high renin states Sedation,bradycardia,dry mouth

30-120min/8-12hrs

Heart failure,heart block,bronchospasm

Specific treatment 1. Hypertensive Encephalopathy: - Goal is to reduce MAP by not>25% or DBP to 100mmHg in the first hour. - Nitroprussi(widely used in past)is a powerful arteriloar dilator,so a rise in ICP may occur. - Labetalol,fenoldopam used more now. 2. Intracerebral Hemorrhage: - CPP=MAP-ICP.As ICP rises,MAP must rise for perfusion but this raises risk of bleeding from small arteries and arterioles.MAP guidelines:decrease when MAP>130 or SBP>220. - Labetalol,esmolol agents of choice.

3. Acute Ischemic Stroke: - High BP can cause hemorrhagic transformation of infarct ,cerebral edema.But,if CPP is low, ischemic penumbra may occur.CPP beyond obstn is low.Distal vessels become dilated with ,loss of autoregulation.A decilne to pre-stroke values in 4 days has been documented often. - BP be reduced only if SBP>220 or DBP>120mmHg.(unless end-organ damage is due to BP). - Labetalol,nitroprusside-agents of choice.For thrombolysis,BP <185/110. 4. Aortic dissection: - Immediate reduction in BP and mainly,shear stress(change in BP with change in time) is essential to limit the extension of damage as surgery is being considered. - Eliminate pain and reduce systolic BP to 100-120 or lowest level that permits perusion. - BP reduction should proceed with reduction in force of LV contraction. - Labetalol or nitroprusside+b-blocker like propranolol agents of choice. 5. MI: NTG,b-blockers,ACE inhibitors. 6. Acute LVF: - Usually associated with pulm edema and diastolic/systolic dysfx. - IV nitroprusside, NTG agents of choice. - Titrate until BP controlled and signs of heart failure alleviated. Follow up: The Joint National Committee on High Blood Pressure has published a series of recommendations for appropriate follow-up, assuming no end-organ damage. Systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm BP within 2 months. Systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg, evaluate within a month. Systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg, evaluate within a week. Systolic BP greater than 210 mm Hg/diastolic greater than 120 mm Hg, evaluate immediately.

Case scenario 1. A 56 yo male with no significant PMH presents to the ER with headache, found to have BP 210/110mmHg and papilledema. 2. An 82 yo male with h/o HTN, chronic renal insufficiency presents for a routine physical, found to have BP of 230/130mmHg. 3. A 76 yo female is brought to the ER by the family due to altered mental status. BP is 240/110 mmHg with no focal neurological findings.