Hypertensive Emergency

Deborah DeWaay MD

ObjectivesKnowledge. 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 22 - 26 cm, small adult cuff, 12x22 cm– Arm circumference 27 - 34 cm, adult cuff, 16x30 cm– Arm circumference 35 - 44 cm, large adult cuff, 16x36 cm– Arm circumference 45 - 52 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)

PathophysiologySVR 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

http://www.cardeneiv.com/a3_cardeneiv_ah_py.shtml

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

www.wikipedia.org

PRES: Posterior reversible encephalopathy syndrome

http://jap.physiology.org/content/91/5/1986/F1.large.jpg

• Normally CBF is unchanged between a MAP of 60-120• 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 1st 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:

– 2nd generation dihydropyridine Ca ++ channel blocker – Selective for the peripheral vasculature– Cerebral vasodilatation– Coronary vasodilatation

• Clevidipine– 3rd 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

PE Lab DrugACS New S4 EKG,

Troponinslabetalol 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

PE Lab DrugAcute 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

CVA Focal neurologic deficits

CT head with angiography

Same as encephalopathy

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.

References1. Marik P, Rivera R. Hypertensive emergencies: an update. Current Opinion in

Critical Care 2011; 17:569-5802. Deshmukh A, Kumar G, Kumar N, Nanchal R, Gobal F, Sakhuja A, Mehta J.

Effect of Joint National Committee VII report on hospitalization for hypertensive emergencies in the United States. American Journal of Cardiology 2011; 108:1277-1282

3. Franklin S, Neutel J. Initial combination therapy for rapid and effective control of moderate and severe hypertension. Journal of Human Hypertension 2009; 23: 4-11

4. Aronson S, Dyke C, Stierer K, Levy J, Cheung A, Lumb P, Kereiakes D, Newman M. The ECLIPSE Trials: comparative studies of Clevidipine to Nitroglycerin, Sodium Nitroprusside, and Nicardipine for acute hypertension treatment in cardiac surgery patients. Anesth Analg 2008; 107:1110-21

5. Varon J. Treatment of Acute Severe Hypertension. Drugs 2008; 68(3): 283-297

6. Vaughan C, Norman D. Hypertensive Emergencies. Lancet 2000; 356: 411-17