Hypertension

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Hypertension

• Hasan Khamash
• Assistant Professor of Medicine KCOM

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KEY MESSAGES

• Hypertension (HTN) affects 50 million in U.S and
  one billion worldwide
• If normotensive at age 55 ?
• 90 lifetime risk for developing HTN
• BP and risk of CVD events is continuous,
  consistent, and independent of other risk factors
• Risk of CVD beginning at 115/75 mmHg doubles with
  each increment of 20/10

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KEY MESSAGES

• SBP is a more important CVD risk factor than DBP
  except in patients younger lt 50
• If BP is gt20/10 mmHg above goal, drug therapy
  should be initiated with two agents
• One usually should be a Thiazide-type diuretic
• Motivation improves compliance
• Motivation improves with trust in the clinician
• Empathy builds trust ? potent motivator

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BP MEASUREMENT

• Measurement of BP should be obtained
• In all adults (age gt18) at each visit
• gt 30 minutes after use of nicotine or caffeine
• After 5 minutes of rest with arm supported at
  heart level
• With appropriate sized cuff
• bladder should encircle 80 of the arm

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BP MEASUREMENT

• Measurement of BP should be obtained
• Twice, at least two minutes apart
• repeat if gt5 mm pressure difference
• With patient seated with feet flat on floor, back
  and arm supported, and arm at heart level
• Use manual mercury sphygmomanometer or recently
  calibrated aneroid manometer or validated
  automated device (JNCVI and VII)

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BP MEASUREMENT

• Ambulatory Blood Pressure Monitor (ABPM) is
  warranted for evaluation of white-coat HTN in
  the absence of target organ injury
• It is also helpful to assess patients with
• apparent drug resistance
• hypotensive symptoms with antihypertensives
• episodic HTN
• autonomic dysfunction
• Correlates better than office measurements with
  target organ injury
• BP should drop 10 to 20 during the night
• If not ? increased risk for CV events

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BP MEASUREMENT

• Self measurement of BP
• An avg BP more than 135/85 mmHg measured at home
  is generally considered to be hypertensive
• Wrist and finger manometers are not recommended

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Risk Factors

• HTN
• Smoking
• Dyslipidemia
• Diabetes mellitus
• Age (gt 55 for men, gt65 for women)
• FmHx of premature CAD
• (women lt 65 or men lt 55)
• Obesity (BMI gt30 kg/m2)
• Physical inactivity
• Microalbuminuria or estimated GFR lt60 mL/min
  (HOPE trial N Engl J Med. 2000)

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TARGET ORGAN DAMAGE

• Heart
• Left ventricular hypertrophy
• Angina or prior myocardial infarction
• Prior coronary revascularization
• Heart failure
• Brain
• Stroke or transient ischemic attack
• Chronic kidney disease
• Peripheral arterial disease
• Retinopathy

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CLINICAL EVALUATION

• Other historical factors that may affect
  treatment decisions
• Gout, sexual dysfunction, bronchospasm, migraine,
  heart block, pregnancy plans in female
• Physical Examination
• Goal is to assess for target organ damage and
  clues to secondary causes

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CLINICAL EVALUATION

• Laboratory and other testing
• Serum chemistries (fasting glucose, electrolytes,
  renal function)
• Blood counts, lipid panel, urine analysis, EKG
• Additional evaluations to consider include
  microalbuminuria, TSH, calcium, uric acid and
  echocardiography

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PREVENTION AND TREATMENT

• JNCVII
• Lifestyle Modifications
• Dietary Approaches to Stop Hypertension (DASH)
  diet N Engl J Med. 2001

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Lifestyle Modifications
SBP Reduction 520 mmHg/10 kg wt loss 814
mmHg 28 mmHg
Recommendation BMI 18.524.9 -diet rich in
fruits, vegetables, and lowfat dairy products
-reduced saturated and total fat No more than
2.4 g sodium/day

• Modification
• Weight reduction
• Adopt DASH eating plan
• Dietary sodium reduction

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Lifestyle Modifications
SBP Reduction 49 mmHg 28 mmHg
Recommendation Regular aerobic physical activity
gt 30 min/day, most days of the week No more
than 2 drinks/day in most men and No more than 1
drink/day in women.

• Modification
• Physical activity
• Moderation of alcohol consumption

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GOALS OF THERAPY

• Goal BP
• HTN lt140/90
• Diabetics lt130/80
• Renal failure lt130/80

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ANTIHYPERTENSIVE MEDICATIONS

• Uncomplicated HTN
• Thiazide diuretics
• Either alone or in combination with an ACE-I,
  ARB, ? -blocker, or CCB

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ANTIHYPERTENSIVE MEDICATIONS
JNCVII

• Compelling Indications
• Diabetes mellitus (type 1) with proteinuria
• Heart failure
• High coronary disease risk
• (stable angina/silent ischemia)

Diuretic, ? -blocker, ACE-I, ARB,
CCB Diuretic, ? -blocker, ACE-I, ARB, and aldo
antagonist Diuretic, ? -blocker, ACE-I, CCB
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ANTIHYPERTENSIVE MEDICATIONS
JNCVII

• Compelling Indications
• Post Myocardial infarction
• Chronic kidney disease
• Recurrent stroke prevention

? -blockers, ACE-I, aldo antagonist (w/
HF) ACE-I, ARB Diuretic, ACE-I
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ANTIHYPERTENSIVE MEDICATIONS

• Additional considerations
• Diuretics
• Compelling indications DM, HF, high CAD risk,
  recurrent stroke prevention
• May have favorable effects on osteoporosis
  (thiazides)
• May have unfavorable effects on DM
  (hyperglycemia at higher doses), dyslipidemia
  (high dose), gout (gt in men), hyponatremia (gt in
  women)

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ANTIHYPERTENSIVE MEDICATIONS

• Additional considerations
• ? -blockers
• Compelling indications DM, HF, post-MI, high
  CAD risk
• May have favorable effects on atrial tachycardia
  and a-fib, essential tremor, thyrotoxicosis,
  migraine, peri-operative hypertension
• May have unfavorable effects on asthma, 2nd or
  3rd degree heart block

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ANTIHYPERTENSIVE MEDICATIONS

• Additional considerations
• ACE-I
• Compelling indications DM, HF, post-MI, high
  risk CAD, chronic kidney disease, recurrent
  stroke prevention
• May have unfavorable effects on hyperkalemia
• Contraindicated in pregnancy

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ANTIHYPERTENSIVE MEDICATIONS

• Additional considerations
• ARB
• Compelling indications DM, HF, chronic kidney
  disease
• Contraindicated in pregnancy

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ANTIHYPERTENSIVE MEDICATIONS

• Additional considerations
• CCB
• Compelling indications DM, high CAD risk
• May have favorable effects on Raynauds syndrome
  and certain arrhythmias

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ANTIHYPERTENSIVE MEDICATIONS

• Additional considerations
• Aldosterone antagonist
• Compelling indications HF, Post-MI (w/ LV
  dysfunction)
• May have unfavorable effects on hyperkalemia

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SECONDARY HYPERTENSION

• Sleep apnea
• Chronic kidney disease
• Primary aldosteronism
• Renovascular disease
• Chronic steroid therapy and Cushings syndrome
• Pheochromocytoma
• Coarctation of the aorta
• Thyroid or parathyroid disease

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SECONDARY HYPERTENSION

• Drug-induced or related causes
• NSAIDs
• Cocaine, amphetamines, other illicit drugs
• Sympathomimetics, oral contraceptives, steroids
• Cyclosporine and tacrolimus
• Erythropoietin
• Selected OTC dietary supplements and medicines
  (e.g., ephedra, ma haung, bitter orange)

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Screening

• Testing can be expensive and requires clinical
  suspicion and knowledge of limitations of
  different tests
• General principles
• New onset HTN if before puberty or gt50 years of
  age
• HTN refractory to medical Rx (gt3-4 meds)
• Specific clinical/lab features typical for dz
• i.e., hypokalemia, epigastric bruits,
  differential BP in arms, episodic
  HTN/flushing/palp, flash pulmonary edema, end
  organ damage etc

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Causes of Secondary HTN

• Common
• Intrinsic Renal Disease
• Renovascular Dz
• Mineralocorticoid excess/ aldosteronism
• OSA

• Uncommon
• Pheochromocytoma
• Glucocorticoid excess/ Cushings dz
• Coarctation of Aorta
• Hyper/hypothyroidism

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Renovascular HTN

• Incidence 1-30
• Etiology
• Atherosclerosis 75-90
• Fibromuscular dysplasia 10-25
• Other
• Aortic/renal dissection
• Takayasus arteritis
• Thrombotic/cholesterol emboli
• Post transplantation stenosis
• Post radiation

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Renovascular HTN - Pathophysiology

• Decrease in renal perfusion pressure activates
  RAAS, renin release converts angiotensinogen? Ang
  I ACE converts Ang I? Ang II
• Ang II causes vasoconstriction (among other
  effects) which causes HTN and enhances adrenal
  release of aldosterone leads to sodium and fluid
  retention
• Contralateral kidney (if unilateral RAS)
  responds with diuresis/ Na, H2O excretion which
  can return plasma volume to normal
• with sustained HTN, plasma renin activity
  decreases (limited usefulness for dx)
• Bilateral RAS or solitary kidney RAS leads to
  rapid volume expansion and ultimate decline in
  renin secretion

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Renovascular HTN - Clinical

• History
• onset HTN age lt30 or gt55
• Sudden onset uncontrolled HTN in previously well
  controlled pt
• Accelerated/malignant HTN
• Intermittent pulm edema with nl LV fxn
• PE/Lab
• Epigastric bruit, particulary systolic/diastolic
• Azotemia induced by ACEI
• Unilateral small kidney

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Renovascular HTN - diagnosis

• Physical findings (bruit)
• Duplex U/S
• Captopril renography
• Magnetic Resonance Angiography with Gadolinium.
• CT Angiogram.
• Renal Angiography

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RAS screening/diagnostics
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Fibromuscular dysplasia

• 10-25 of all RAS
• Young female, age 15-40
• Medial disease 90, often involves distal RA
• 30 progressively worsen but total occlusion is
  rare
• Treatment PTRA
• Successful in 82-100 of patients
• Restenosis in 5-11
• Cure of HTN in 60

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Atherosclerotic RAS

• 75-90 of RAS
• Usually men, agegt55, other atherosclerotic dz
• Progression of stenosis 51 _at_ 5years, 3-16 to
  occlusion, with renal atrophy noted in 21 of RAS
  lesions gt60
• ESRD in 11 ( higher risk if gt60, baseline renal
  insufficiency, SBPgt160)
• Treatment
• PTRA success 60-80 with restenosis 10-47
• Stent success 94-100 with restenosis 11-23
  (1yr)
• Cure of RV HTN lt30

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Fibromuscular Dysplasia, before and after PTRA
Atherosclerotic RAS before and after stent
Safian Textor. NEJM 3446
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Renovascular HTN Medical Rx

• Aggressive risk factor modification (lipid,
  tobacco, etc)
• ACEI/ARB safe in unilateral RAS if careful
  titration and close monitoring contraindicated
  in bilat RAS or solitary kidney RAS.
• Usu if BP is controlled and kidney fxn stable we
  do not resort to intervention.

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Renovascular HTN - principles

• Not all RAS causes HTN or ischemic nephropathy
• Differing etiology of RAS has different outcomes
  in regards to treatment (FMD vs atherosclerosis)
• No current rationale for drive-by interventions
• Importance of medical rx
• No current consensus guidelines for
  screening/outcomes/treatment ( as opposed to
  carotid artery stenosis, AAA, etc)

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