HYPERTENSIONHypertensive Emergencies

Mohammad Ilyas, M.D.

Assistant Clinical Professor

University of Florida / Health Sciences Center

Jacksonville, Florida USA

6/24/2014

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Outline

1. Definition, Regulation and Pathophysiology

2. Measurement of Blood Pressure, Staging of Hypertension and Ambulatory

Blood Pressure Monitoring

3. Evaluation of Primary Versus Secondary

4. Sequel of Hypertension and Hypertension Emergencies

5. Management of Hypertension (Non-Pharmacology versus Drug Therapy)

6. The Relation Between Hypertension: Obesity, Drugs, Stress and Sleep

Disorders.

7. Hypertension in Renal diseases and Pregnancies

8. Pediatric, Neonatal and Genetic Hypertension

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Clinical Quiz

1. A 56 y/o M with no significant PMH

presents to the ER with headache,

found to have BP 210/110mmHg

and papilledema.

2. 5 y/o boy with rash, abd. pain, joint pain, tea colored urine and BP 117/81

3. 16 y/o athletic boy in clinic for sports PE BP 132/84

HTN Treat

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Clinical Quiz

4. A 76 y/o female is brought to the ER by the family due to altered mental status. BP is 240/110 mmHg with no focal neuro findings.

5. An 62 y/o male with h/o HTN, chronic renal insufficiency presents for a routine physical, found to have BP of 210/110mmHg.

HTN Treat

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Discussion

Categories

Etiology/pathophysiology

History/Physical

Workup

Treatment

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Urgency vs. Emergency

Urgency – severely elevated BP with no current evidence of secondary organ damage, although if left untreated, target organ injury may result imminently

→ Decrease BP Soon Emergency – severely elevated BP with evidence of

target organ injury

→ Decrease BP Immediately Target organs – CNS, heart, kidney, eye

Constantine and Linakis, Pediatric Emergency Care, 20056/24/2014

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Severe Hypertension

“Hypertension that represents a threat to life or to the function of

vital organs”

OR

Severe hypertension is when your blood pressure goes up too!

Adelman, et al. Pediatric Nephrology, 2000

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Etiology (Adult)

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

TTP

Idiopathic hypertension

Post-op hypertension

Coarctation of aorta

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Etiology (Children)

Newborn Pre School

(Infant - 6 yr)

School Age

(6 - 12 yr)

Adolescence

•Renal vein

thrombosis

•Coarctation

•Renal artery

stenosis

•Congenital

renal anomalies

•Renal

parenchymal

disease

•Renovascular

disease

•Coarctation

•Renal

parenchymal

disease

•Renovascular

disease

•Essential

hypertension

•Essential

hypertension

•Renal

parenchymal

disease

•Renovascular

disease

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Constantine and Linakis, Pediatric Emergency Care, 2005

Miscellaneous Causes

Endocrine

Hyperthyroid

Pheochromocytoma

Elevated ICP/CNS disease

Drug use (cocaine, ecstasy)

Medication (abrupt withdrawal)

Exercise

Traction

Hypovolemia6/24/2014

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Pathophysiology

NORMAL AUTOREGULATION

RISE IN BP

ARTERIAL AND ARTERIOLAR

CONSTRICTION

Normal flow.(flow=P/r)

RISE IN BP

FAILURE OF

VASOCONSTRICTION

ENDOTHELIAL DAMAGE

(due to shear stress on the wall)

AUTOREGULATION FAILURE

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Pathophysiology

BP = PVR x CO(SV x HR) Rate at which MAP rises more important than absolute rise.

Acute rise in BP Failure of vasoconstriction Endothelial

by autoregulation damage

FIBRINOID Activates coagulation Depsn. Of proteins and

NECROSIS and inflammation fibrinogen in vessel wall

Note: RAAS plays an important role in initiating and perpetuating BP rise by causing

vasoconstriction and fluid retention.6/24/2014

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CENTRAL NERVOUS SYSTEM

1. The CNS is affected as the elevated BP overwhelms the normal cerebral auto regulation.

2. Under normal circumstances, with an increase in BP, cerebral arterioles vasoconstrict and cerebral blood flow (CBF) remains constant.

3. During a hypertensive emergency, the elevated BP overwhelms arteriolar control over vasoconstriction and autoregulation of CBF.

4. This results in transudate leak across capillaries and continued arteriolar damage.

5. Subsequent fibrinoid necrosis causes normal autoregulatory mechanisms to fail, leading to clinically apparent papilledema, the sine qua non of malignant hypertension.

6. The end result of loss of autoregulation is hypertensive encephalopathy.

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EYE

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CARDIOVASCULAR SYSTEM

The cardiovascular system is affected as increased

cardiac workload leads to cardiac failure; this is

accompanied by pulmonary edema, myocardial

ischemia, or myocardial infarction.

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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.

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Epidemiology

In the US: More than 60 million Americans, about 25-30% of the population, have hypertension. Of these individuals, 70% have mild disease, 20% moderate, and 10% severe hypertension (diastolic BP [DBP] >110 mm Hg). Approximately 1-2% develop a hypertensive emergency with end-organ damage.

Mortality/Morbidity: Morbidity and mortality depend on the extent of end-organ damage on presentation and the degree to which BP is controlled subsequently. BP control may prevent progression to end-organ impairment. 1 yr mortality in untreated pts. >90%. 5 yr survival of all presentations is 74%.

Race: African Americans have a higher incidence of hypertensive emergencies than Caucasians.

Sex: Males are at greater risk of hypertensive emergencies than females.

Age: Most commonly in middle-aged people. Peak age:40-50yrs.6/24/2014

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History

Focus on circumstances surrounding hypertension & etiology :

-Medications: esp. hypertensive drugs/their compliance, illicit drugs

-Duration of hypertension

-Duration of current symptoms

-Date of LMP

-Other medical problems: prior hypertension, thyrotoxicosis, Cushing’s,

SLE, renal

Focus on complications :

-CNS: headaches, blurred vision, wt. loss, nausea, vomiting, weakness,

fatigue, confusion and mental status changes.

-CVS: symptoms of CHF, angina, dissection & SOB

-Renal: hematuria, oliguria. 6/24/2014

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Physical

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: JVD, lung auscultation for crackles, peripheral

edema, extra heart sounds, equal and symmetric BP

and pulses bilaterally.

-Check for abdominal masses and bruits.

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Clinical Signs of Malignant HTN

Eyes

Retinal hemorrhages, exudates and papilledema

Malignant Nephrosclerosis

ARF, Hematuria, Proteinuria

Hypertensive Encephalopathy

Headache, nausea, vomiting

Restlessness, confusion seizures, coma MRI (T2-weighted images) ;

Edema of the white matter of the parieto-occipital regions: posterior leukoencephalopathy

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Eyes

Papilledema, blurred optic disk, hemorrhages 6/24/2014

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Hypertensive Encephalopathy

Failure of auto regulation

Flynn, Ped Neph 2009; 24, 1101-1112

Shifted

baseline

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Hypertensive Encephalopathy

Headache, nausea, vomiting

Restlessness, confusion → seizures, coma

Posterior leukoencephalopathy

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Posterior Leukoencephalopathy

T1 weighted images –

normal appearing

T2 weighted images –

occipital hyper intensity

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Treatment Goals

1. Prevent adverse events

2. Reduce BP in controlled manner

3. Preserve target organ function

4. Minimize complications of therapy

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Severe Hypertension

Treatment Risks

Rapid reduction of BP can lead to

complications

Risk of hypo perfusion (ischemia) secondary to

auto regulation

Medication side effects may have adverse effects

depending on cause of hypertension (e.g. ACEi)

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How Much?

Just Enough

Depends on Acute vs. Chronic6/24/2014

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How Much?

Reduce by 25% of the planned reduction over 8-12 hrs

Another 25% over the next 8-12 hrs

Final 50% over the next 24 hrs

Planned reduction – goal is to the 95-99% for age and height

If Unsure, slower is safer

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What to do first ?

Monitor, Monitor, Monitor

Need cardiopulmonary monitoring

Need continual BP monitoring (frequently

cycling cuff vs. arterial line)

Decide oral vs. IV

Oral OK if asymptomatic

IV necessary if acute target organ damage is present

or imminent

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Oral vs. IV

IV Medication

Rapid Action

Titratable

Easy to adjust the dose

Requires IV access

PO Medication

Don’t need an IV

Harder to control effects

Absorption variable

Slower kinetics can make

titrating more difficult

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What to choose?

First Line

PO

Isradipine

Nifedipine

IV

Nicardipine

Nitroprusside

Labetalol

Second Line

PO

Clonidine

IV

Hydralazine

Enalaprilat

Fenoldopam

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Work-up

CBC, Chemistry (Na, K, Cl, HCO3, BUN, Cr, Glucose, Ca)

Urinalysis: hematuria, proteinuria, RBCs, RBC casts.

Toxicology, pregnancy, endocrine causes.

Imaging: Chest X-ray, Head CT, Chest CT, aortic

angiogram

EKG, cardiac enzymes

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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."

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Treatment

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.

Consider the context of the elevated BP (eg, severe pain)

Screen for end-organ damage- Patients with end-organ damage usually require admission and rapid lowering of BP using iv meds. Suggested meds depend on the end-organ system damaged.

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Treatment

Patients without evidence of end-organ effects may be discharged with follow–up. It is a misconception that a patient should not be discharged from the ER with elevated BP.

Giving oral meds such as Nifedipine to rapidly lower BP may be dangerous as the BP may have been elevated for sometime and there may be organ hypo perfusion.

Acute control has not improved long term mortality and morbidity rates.

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DRUGS

Once the diagnosis of hypertension is made and end-

organ damage confirmed, the BP should be lowered by

about 25% of the mean arterial pressure.

There are 2 main classes of drugs:

-Vasodilators

-Adrenergic inhibitors

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VASODILATORS

DRUG DOSAGE ONSET/DUR ADV.EFFE

Nitroprusside 0.25-

10mcg/kg/min

Instant/1-2min. Thiocyanate,cyani

de poisoning

Nitroglycerine 5-100mcg/min 1-5min/3-5min Flushing,headach

e,methemoglobin

Nicardipine 5-15mg/hr 5-10min/1-4hr Tachycardia,flushing

.avoid-heart failure

Hydralazine 10-20mg 5-15min/3-8hr Flushing,tachy,avoid

-A.diss,MI

Enalapril 10-40mg IM,1.25-

5MG1Vq6hr

20-30min/6hr Hypotension,renal

failure,hyperkalemia

Fenoldopam 0.1-

0.3mcg/kg/min

5min/10-15min Flushing,headache,t

achy

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ADRENERGIC INHIBITORS

DRUG DOSAGE ONSET/DUR ADV.EFF

Labetalol

(a+b blocker)

20-80mgiv bolus

every 10

min,2mg.min iv

infusion

5-10min/3-6hrs Heart block, ortho.

hypotension.

Avoid in heart

failure, asthma

Esmolol

(b-1 selective

blocker)

200-500

mcg/kg/min for

4min,then 150-

300mcg/kg/min

1-2min/10-20min Hypotension ,avoid-

heart failure, asthma

Phentolamine

(a1 blocker)

5-15mg iv 1-2min/3-10min Tachycardia,

flushing, headache

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ORAL DRUGS

DRUG DOSAGE ONSET/

DURATION

ADVERSE EFFECTS

CAPTOPRIL

(ACE inhibitor)

6.25-25MG q 6hrs. 15-30min/6 hrs. Hypotension in high renin states

CLONIDINE

(a2 agonist-

centrally acting)

0.1-0.2 mg hrly,

Upto max 0.8mg in

24hrs.

30-60min/6-12hrs. Sedation, bradycardia, dry mouth

LABETALOL 100-200mg q 12hrs 30-120min/8-12hrs Heart failure, heart block,

bronchospasm

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Specific Treatment

Hypertensive Encephalopathy: Goal is to reduce MAP

by not >25% or DBP to100mmHg in the first hour.

Nitroprusside (widely used in past)is a powerful arteriolar dilator, so a rise in ICP may occur.

Labetalol, fenoldopam used more now.

Intracerebral Hemorrhage: CPP=MAP-ICP. As ICP rises,

MAP must rise for perfusion but this raises risk of bleeding from small

arteries and arterioles.

A prosp. Obs. study in 1997 did not confirm these concerns but it

was obscured by early use of anti-hypertensives.

Cerebral auto regulation curve in chronic hypertensive may be

altered, making them less likely to tolerate aggressive lowering of

BP. MAP guidelines: decrease when MAP>130 or SBP>220.

Labetalol, esmolol agents of choice.6/24/2014

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Specific Treatment

Acute Ischemic Stroke: High BP can cause hemorrhagic

transformation of infarct and cerebral edema.

If CPP is low, ischemic penumbra may occur. CPP beyond obstruction is low. Distal vessels become dilated with, loss of auto

regulation.

A decline to pre-stroke values in 4 days has been documented

often.

AHA guidelines: 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.

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Specific Treatment

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 perfusion. BP reduction should

proceed with reduction in force of LV contraction.

Labetalol or nitroprusside+b-blocker like propranolol agents of choice.

MI: NTG, b-blockers, ACE inhibitors.

Acute LVF: usually associated with pulm. edema and diastolic/systolic

dysfunction. IV nitroprusside, NTG agents of choice. Titrate until BP

controlled and signs of heart failure alleviated.

Renal insufficiency: is a cause and effect of high BP. Goal is to prevent

further renal damage by maintaining adequate blood flow.

Nitroprusside effective.6/24/2014

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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.

1. For systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm BP within 2 months.

2. For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg, evaluate within a month.

3. For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg, evaluate within a week.

4. For systolic BP >210 mm Hg/diastolic >120 mm Hg, evaluate immediately.

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Complications

Retinopathy 27%

Encephalopathy 25%

LVH 13%

Facial palsy 12%

Visual changes 9%

Hemiplegia 8%

Deal, et al. Arch Dis Child, 19926/24/2014

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PROGNOSIS: Median survival duration is 144 months for all patients

presenting to ED with hypertensive emergency. 5 yr. survival rate is 74%.