2. 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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3. 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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4. 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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6. 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, 2005
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7. 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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8. 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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9. 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
11. 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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12. 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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13. 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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15. 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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16. 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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17. 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.
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18. 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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19. 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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20. 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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25. 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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26. 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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28. 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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29. 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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30. 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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32. What to choose?
First Line
PO
Isradipine
Nifedipine
IV
Nicardipine
Nitroprusside
Labetalol
Second Line
PO
Clonidine
IV
Hydralazine
Enalaprilat
Fenoldopam
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34. 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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35. 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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36. 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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37. 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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39. 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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40. 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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41. 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.
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42. 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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43. 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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44. 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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45. Complications
Retinopathy 27%
Encephalopathy 25%
LVH 13%
Facial palsy 12%
Visual changes 9%
Hemiplegia 8%
Deal, et al. Arch Dis Child, 1992
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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%.
