Hypertensive Emergency Deborah DeWaay MD

Objectives Knowledge. Residents should be able to: Define hypertensive emergency and describe the signs and symptoms of conditions associated with it Describe the epidemiology of hypertensive emergency Describe the prognosis of hypertensive emergency untreated and treated Describe the uses of the drugs commonly used to treat hypertensive emergencies.

Objectives Skills –Understand which physical exam maneuvers and labs are important to diagnosing HTN emergency Attitude –Residents should understand and appreciate that hypertensive emergency is a serious illness that carries a significant morbidity and mortality

Key Messages 1-2% of patients with systemic hypertension will develop hypertensive emergency HTN emergency needs to be treated with IV drips, not IV push HTN emergency should be treated in the ICU

The Old Malignant hypertension is not a term that is used any more It was used to mean elevated BP + encephalopathy or AKI

Hypertensive Emergency Elevated blood pressure with symptoms –Shortness of breath (29%) –Chest pain (26%) –Headache (23%) –Altered mental status (20%) –Focal neurologic deficit (11%) –Microangiopathic hemolysis (27%) There is no absolute BP cut off The rate of increase is as important as the absolute BP

Hypertensive Urgency Elevated blood pressure without symptoms JNC 7 does not specifically define a BP number for HTN urgency –Stage 2 hypertension is SBP≥160 mmHg, DBP≥100 mmHg –Hypertensive crisis is SBP≥179 mmHg, DBP≥109 mmHg

Epidemiology Systemic hypertension affections 1 billion people world wide and 65 million Americans 1-2% of patients with systemic hypertension will develop hypertensive emergency Men are affected 2x more than women More common in the elderly and African- Americans Essential HTN accounts for 20-30% of HTN emergency in whites, but over 80% in African- Americans

Prognosis Per one study in 1939, untreated malignant hypertension has a 79% 1 year mortality with a median survival of 10.5 months Mortality has decreased in recent years –One study showed that the 5 year survival was 32% prior to 1977, but between 1977 – 2006 it increased to 91% Per Studying the Treatment of Acute Hypertension (STAT) registry: in hospital mortality for HTN emergency was 6.7%, 90 day mortality of 11%

History Medication history –Anti- HTN meds –OTC meds –Illegal drugs: especially cocaine, amphetamines, phencyclidine HTN? –History of control –Compliance

Physical Exam Blood pressures in both arms and orthostatics Pt should be seated with the back supported and legs uncrossed If the cuff is too small, the BP will be falsely elevated Per American Heart Association –Arm circumference cm, small adult cuff, 12x22 cm –Arm circumference cm, adult cuff, 16x30 cm –Arm circumference cm, large adult cuff, 16x36 cm –Arm circumference cm, adult thigh cuff, 16x42 cm

Physical Exam Neuro exam Cardiac exam Pulmonary exam Ocular exam: only happens in 13% of pts Extremity exam [they are critically ill so need a full exam]

Labs to consider BMP CBC with peripheral smear, LDH UA EKG CXR CT head Echocardiogram

Pathophysiology The DD genotype of the angiotensin- converting enzyme (ACE) gene has been found to be associated with increased risk of HTN emergency Overall cause is poorly understood One theory is that there is a triggering factor that causes the release of humoral vasoconstrictors leading to an increased in systemic vascular resistance (SVR)

Pathophysiology SVR eventually ↓organs ability to autoregulate blood flow mechanical wall stress & endothelial injury Pressure naturesis triggers coagulation cascade RAS fibrin disposition Vasoconstriction fibrinoid necrosis of arterioles Ischemia

The Effects Brain: –CVA: ischemic, hemorrhagic –Hypertensive Encephalopathy Heart: –Myocardial infarction –Heart failure: systolic, diastolic Aorta: –Aortic dissection Kidney: –Acute kidney injury Blood vessels –Microangiopathic hemolytic anemia –Retinal hemorrhages, exudates and papilledema

Pathophysiology

Hypertensive Encephalopathy Clinical presentation: acute or subacute lethargy, confusion, headache, visual disturbance or seizures More common in patients with SLE, HUS, cryoglobulinemia, on cyclosporin or cisplatin –Diseases with underlying vascular disturbances

Hypertensive Encephalopathy Typically symmetrical white matter edema in the posterior cerebral hemispheres PRES: Posterior reversible encephalopathy syndrome

Normally CBF is unchanged between a MAP of As MAP increases  autoregulation stops  cerebral vasodilation  edema As endothelial damage occurs  capillary leakage  breakdown of blood brain barrier  edema

Chronically hypertensive patients lose normal autoregulation in their brain. They require a higher BP to maintain CBF Therefore the BP HTN emergency happens at is dependent on the patients baseline BP

Goals of Tx: Hypertensive Urgency –Use oral medications –BP should be lowered gradually over 1-2 days –Rapid correction below autoregulatory range  hypoperfusion  ischemia and infarction

Goals of Tx: Hypertensive Emergency Altered auto-regulation is present End-organ damage is already present Excessive correction can worsen damage Use IV infusion of a short acting, titratable medication Use intra-arterial BP monitoring if severe clinical manifestations or labile BP Goal: ↓DBP 15-20% or to about 110mmHg over 1-2hr –If dissection: this should be done in 5-10 minutes

Other Important Points ***Admit to ICU*** –Per STAT registry: only 15% of pts were admitted 1 st line Once BP is stable, PO should be started as gtt is titrated off Do not use sublingual nifedipine or IV hydralazine because they lower BP too quickly

Other Important Points Don’t use nitroprusside (except with aortic dissection) because is will decrease BP to quickly, causes a decrease in cerebral blood flow and increases intracranial pressure Many patients are volume depleted from pressure naturesis so use caution with diuretics  BP will drop too quickly

The Drugs Nicardipine: –2 nd generation dihydropyridine Ca ++ channel blocker –Selective for the peripheral vasculature –Cerebral vasodilatation –Coronary vasodilatation Clevidipine –3 rd generation dihydropyridine Ca++ channel blocker –Decreases SVR via relaxing smooth muscles of small arteries, increases CO and SV –Metabolized by plasma esterases so independent of liver and kidney function

The Drugs Labetalol: –Alpha 1 and non-selective Beta blocker (1:7 ratio) –Metabolized by liver –Maintains cardiac output, decreases SVR  maintains peripheral blood flow Esmolol –Ultra-short acting cardioselective beta blocker –Metabolized by RBC esterases, independent of liver and kidney function

PELabDrug ACSNew S4EKG, Troponins labetalol or esmolol + nitroglycerin Sys CHF + Pulmonary Edema Crackles, JVD, LE edema CXR, EKG, BNP nicardipine or clevidipine + nitro + loop diuretic Dia CHF + Pulmonary Edema Crackles, JVD, LE edema CXR, EKG, BNP esmolol or labetalol or metoprolol or verapamil + nitro + loop diuretic Aortic Dissection Unequal pulses & BP Wide mediastinum on CXR; CT chest with contrast labetalol or nicardipine + esmolol or nitroprusside + esmolol

PELabDrug Acute Kidney Injury Edema, ocular exam – retinopathy elevated Cr, hematuria on UA nicardipine, clevidipine, fenoldopam HTN Encephalopathy Altered level of consciousness CT head; MRI nicardipine, clevidipine, labetalol CVAFocal neurologic deficits CT head with angiography Same as encephalop athy Hemolytic anemia CBC, haptoglobin, LDH, smear, LFTs Anemia, schistocytes, low plts nicardipine, clevidipine, fenoldopam Pregnancy related end organ damage: pre-eclampsia, eclampsia, HELLP syndrome will not be addressed in this lecture.

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