secondary hypertension - dr. britt

8/10/2019 Secondary Hypertension - Dr. Britt

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Secondary Hypertension:

A Real World Approach

Evan Brittain, MD

December 7, 2012Kingston, Jamaica

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Disclosures

• None

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Real World Causes

• Renovascular Hypertension

• Endocrine

•

Obstructive Sleep Apnea• “Pseudosecondary” Hypertension

– Pseudo-resistant HTN

–

Drug-induced

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Index of Suspicion

Historical

• Recent onset (early or late)

• Loss of control

• Resistant/accelerating

Signs and Symptoms

• Tachycardia/blanching

• Evidence of PVD

(bruit, differential BP)

• Specific drug intolerance

(e.g. ACEI)

• Unprovoked hypokalemia

• Daytime sleepiness

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Age-Based Approach

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AgePercent with

Underlying Cause Most Common Etiologies



Age-Based Approach

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AgePercent with


≤ 18 years 10-15• Coarctation

• Renal parenchymal



Age-Based Approach

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AgePercent with




19-39 years 5

• Fibromuscular Dysplasia

• Thyroid disease• Renal Parenchymal



Age-Based Approach

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AgePercent with




19-39 years 5



40-64 years 8-12

• Hormone-induced Aldosteronism

Cushing’s

Pheo Thyroid

• Obstructive Sleep Apnea



Age-Based Approach

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AgePercent with




19-39 years 5



40-64 years 8-12

• Hormone-induced Aldosteronism

Cushing’s

Pheo

Thyroid• Obstructive Sleep Apnea

65+ years 17• Renal Artery Stenosis

• Renal Failure



Coarctation of the Aorta

• Diagnosed by HTN and murmur

• Bilateral brachial or

brachial/femoral BP differential

•

MRI preferred imaging method

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Coarctation of the AortaDiagnostic Strategies

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Real World Causes


• Endocrine

•



–

Drug-induced

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Renovascular HTNClinical Features

• Atherosclerotic RAS

– Older men

– Ostial or proximal 1/3 of vessel

– Stenosis ≠ HTN

• Suspected when:

– New HTN < 30 or > 55 years old

– Unexplained renal dysfunction

– Rapid decline in renal function after

starting ACEI/ARB – Recurrent “flash” pulmonary edema

• Atrophic kidney

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ACC/AHA 2011 Peripheral Arterial Disease Guidelines

J Am Coll Cardiol Intv 2009;2:161 –74



Renovascular HTNPathophysiology

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Anaesthesia and Intensive Care Medicine. Vol. 7: 8, 298 –302



Renovascular HTN:Diagnostic Strategies

Screening and Diagnosis: – Duplex ultrasound

– CT angiography

– MR angiography

Angiography still goldstandard

– High suspicion remains

– Suspected FMD

–

Contrast dose

May want to sample renalvein renin activity

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Renovascular HTN:Diagnostic Contrast Use

Radiocontrast (CT)- Higher risk in Cr > 1.5mg/dL and DM (Very low risk with normal GFR)

- Use non-ionic low osmolal agents

- Avoid volume depletion, pre-hydrate if CKD

- Onset 12-24hrs, usually transient

Gadolinium (MRI)- Nephrogenic Systemic Fibrosis

- Moderate to severe renal failure

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Kidney International (2007) 72, 260 –264;



Renovascular HTN:Management

Goals:

- Improvement in BP, preservation of renal function, decrease CV

morbidity

Unilateral:

- HTN control: ACEI/ARB ± others

- May cause decline in GFR and mild rise in Cr

- Revascularization

Bilateral:

- HTN control: ACEI/ARB ± thiazide diuretic- Revascularization

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Renovascular HTN:Fibromuscular Dysplasia

Clinical Features- Young women

- usually distal 2/3 of vessel

HTN control:- ACEI/ARB, then thiazide

- May drop GFR and increase Cr (usually mild)

Angioplasty:- Indications: young, intolerant/resistant HTN

- Duplex US after 6 months, then yearly

- Surgery reserved for unamenable lesions or failed

PTA

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J Am Coll Cardiol Intv 2009;2:161 –74



Real World Causes


• Endocrine

•



–

Drug-induced

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Hormone-Related Hypertension

• Hyperaldosteronism

• Thyroid

•

Cushing’s • Pheochromocytoma

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Primary Hyperaldosteronism:Clinical Features

Two common forms:

– Bilateral idiopathic hyperaldosteronism

– Aldosterone-producing adenoma

Diagnostic Clues – HTN

– Unprovoked or inappropriate

hypokalemia

– Hypernatremia = volume expansion

– Low k + low Na = volume depletion and

secondary aldosteronism

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cvphysiology.com



Primary Hyperaldosteronism:Diagnostic Strategies

Serum aldosterone/renin ratio(ARR)

- If > 20 and aldosterone > 15ng/dL salt suppression test

- False positive: Beta-blockers,clonidine

- False negative: diuretics, DHPCCBs, ACEI/ARBs

Localization: Adrenal CT

- Bilateral or large unilateral

- Small, hypodense

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HyperaldosteronismManagement

Goal: normalization of aldosterone

receptor blockade

Unilateral hypersecretion

- Adrenalectomy

Bilateral adrenal hyperplasia

- Aldosterone antagonist

(spironolactone, eplerenone)

- Monitor K, Cr, and BP frequently in

first 4-6 weeks

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Growth Hormone & IGF Research. Vol 13; 2003: S102 –S108



Real World Causes


• Endocrine

•



–

Drug-induced

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Obstructive Sleep ApneaClinical Features

Symptoms

• Daytime sleepiness

• Snoring

• Witnessed apneas

• Poor concentration

Signs

• Obesity

• Large Neck

• Systemic HTN

• Arrhythmias

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N Engl J Med 2000;342:1378-84



Obstructive Sleep ApneaDiagnostic Strategies

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http://www.mysleepapneatest.com/diagnosing-osa.aspx



Obstructive Sleep ApneaManagement

Continuous positive airway

pressure (CPAP)

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Circulation. 2003;107:68-73.



Real World Causes


• Endocrine

•



–

Drug-induced

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“Pseudo-resistant” HTN

Improper measurement

- Cuff size

- White-coat effect

Patient compliance- Lack of understanding/education

- Mistrust

- Poor adherence

- Cost

Physician causes

- Inadequate doses, inappropriate combinations

- Inertia

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Drug-Induced Hypertension

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Drug Class Common Examples

Estrogen Oral contraceptives

Herbal remedies Ephedra, gensing, ma huang,

licoriceIllicit Cocaine, amphetamines

NSAIDs COX-2 inhibitors, naproxen

Psychiatric Buspirone, lithium, TCAs

Steroid Prednisone, methylprednisolone

Sympathomemetic Decongestants, diet pills



Thank you for your attention

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secondary hypertension - dr. britt

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