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HYPERTENSION

OVERVIEW

Definitions
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Based on average of 2 office visits after an initial screen
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Normal BP <120 and <80
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Pre-HTN 120-130 or 80-89
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HTN

Stage 1 140-159 or 90-99

Stage 2 160 or 100


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In clinical practice, pts taking anti-hypertensive meds are defined as having HTN regardless of observed BP
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Definitions not specifically addressed by JNC-8 but did adopt thresholds for Tx of BP
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Isolated systolic HTN when BP is 140/<90
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Isolated diastolic HTN when BP is <140/90
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Pts w/ BP 140/90 have mixed systolic/diastolic HTN
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Prognostic significance of BP as CV RF:

Age dependent

>50-60y/o SBP is greatest predictor of risk

<50y/o DBP is better predictor of mortality than SBP


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Definitions based on ambulatory and home readings:

24h average of 130/80

Daytime (awake) average of 135/85

Nighttime (asleep) average of 120/70


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White coat HTN BP thats consistently elevated by office readings but doesnt meet diagnostic criteria for HTN based on out-ofoffice readings
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Masked HTN BP thats consistently elevated by out-of-office measurements but doesnt meet criteria for HTN based on office
readings
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Moderate-severe hypertensive retinopathy (aka malignant HTN)

Corresponds to grade III and IV hypertensive retinopathy

Refers to specific pathophysiological changes that can be associated w/ marked HTN

Includes retinal hemorrhages, exudates of papilledema

May be associated w/ hypertensive encephalopathy and acute hypertensive nephrosclerosis (aka malignant
nephrosclerosis)

Malignant HTN usually associated w/ DBP >120, but can occur at DBP as low as 100 in previously normotensive pts w/ acute
HTN d/t preeclampsia or acute GLN
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Hypertensive emergency

Severe HTN (usually DBP >120) w/ evidence of acute end-organ damage

Can be life-threatening and requires immediate Tx usually w/ parenteral meds in a monitored setting
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Hypertensive urgency

Severe HTN (usually DBP >120) in A-Sx pts

No proven benefit of rapid reduction in BP in A-Sx pts w/ no evidence of acute end-organ damage and theyre at little shortterm risk
1o (essential) HTN
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Maintenance of arterial BP necessary for organ perfusion

Arterial BP determined by:

BP = CO x SVR

Main factors determining the BP are:

Symp NS

RAAS

Plasma volume
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RFs for 1o HTN:

Age advancing age associated w/ increased BP, esp SBP, and thus an increased incidence of HTN

Obesity and wt gain are major RFs for HTN and are also determinants of the rise in BP seen w/ aging

F-Hx HTN approx. 2x as common in pts w/ 1 or 2 hypertensive parents

Genetic factors account for approx. 30% of variation in BP in various populations

Race HTN is more common, more severe, occurs earlier in life and is associated w/ greater target organ damage in blacks

Reduced nephron number reduced adult nephron mass can predispose to HTN

Can be related to genetic factors, intra-uterine developmental disturbance (eg hypoxia, drugs, nutritional
deficiency), premature birth and post-natal environment (eg malnutrition, infxns)

High Na diet XS Na intake (eg >3g/day) increases risk for HTN

Na restriction lowers BP

XS alcohol consumption associated w/ development of HTN

Physical inactivity increases risk for HTN

Exercise is an effective means of lowering BP

Diabetes and dyslipidemia presence of these other CV RFs is associated w/ increased risk of developing HTN

Personality traits and depression HTN may be more common in those w/ personality traits like hostility or impatience as
well as in those w/ depression

Hypovitaminosis D vit-D deficiency increasingly appears to be associated w/ increased risk of HTN in some populations
2o (contributing causes) HTN
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Many common/uncommon medical conditions can increase BP and lead to 2 o HTN
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They can coexist w/ RFs for 1o HTN and are barriers to achieving adequate BP control
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Major causes of 2o HTN include:

Rx or OTC meds

OCs esp those w/ higher doses of estrogen, can raise BP w/in normal range but also induce overt HTN

NSAIDs esp w/ chronic use

Antidepressants including TCAs and SSRIs

Glucocorticoids

Decongestants (eg pseudoephedrine)

Wt loss meds

EPO

Cyclosporine

Stimulants (eg methylphenidate and amphetamines)

Illicit drug use eg methamphetamines and cocaine

1o renal disease both acute and chronic kidney disease, esp w/ glomerular or vascular disorders, can lead to HTN

1o aldosteronism presence of 1o mineralocorticoid XS (mainly aldosterone) should be suspected in pts w/ triad of HTN,
unexplained hypokalemia and metabolic alkalosis

Some pts can have normal plasma [K]

Should also be considered in pts w/ resistant HTN

Renovascular HTN relatively common

More often d/t fibromuscular dysplasia in younger pts and atherosclerosis in older pts

OSA disordered breathing during sleep apnea is an independent RF for systemic HTN

Pheochromocytoma a rare cause of 2o HTN

Approx. of pts w/ pheochromocytoma have paroxysmal HTN, the rest have 1 o HTN

Cushings syndrome a rare cause of 2o HTN

HTN is a major cause of morbidity and death in these pts

Other endocrine disorders hypothyroidism, hyperthyroidism and hyperparathyroidism can also induce HTN

Coarctation of the aorta 1 of the major causes of 2o HTN in young children, but can also be Dxd in adulthood
Complications of HTN
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Associated w/ some serious adverse effects and likelihood of developing these is increased w/ higher BPs
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Increase in risk begins as BP rises >115/75 in all age groups
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HTN is quantitatively the major modifiable RF for premature CV disease and is more common than smoking, dyslipidemia or diabetes
which are the other major RFs

In older pts, SBP and pulse pressure are more powerful determinants of risk than DBP

Also, the increase in CV risk associated w/ HTN is affected by presence/absence of other RFs
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Each of the following complications is closely associated w/ presence of HTN:

LVH a common and early finding in pts w/ HTN

Associated w/ a higher incidence of subsequent HF, MI, sudden death and stroke

Risk of HF both systolic (reduced EF) and diastolic (preserved EF) increases w/ degree of BP elevation

Pathogenesis of HF in pts w/ HTN is both ischemic and non-ischemic


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Ischemic stroke HTN is most common and most important RF

Incidence can be markedly reduced by effective antihypertensive therapy


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Intracerebral hemorrhage HTN is most important RF
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IHD HTN is a leading RF for IHD including MI and coronary interventions
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CKD and ESRD HTN is a RF and can both directly cause kidney disease (called hypertensive nephrosclerosis) and accelerate
progression of other renal diseases

Relationship b/w BP and renal disease is stronger among AAs


Dx of HTN
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USPSTF recommend screening Q2years for pts w/ SBP and DBP <120/80

Recommend yearly screening for pts w/ SBP 120-139 or DBP 80-89


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In absence of end-organ damage, Dx of mild HTN shouldnt be made until BP has been measured on at least 3 visits, spaced over a
period of wks-mths

Also, BP should be measured in both arms

SBP in L&R arms should be approx. equivalent

Discrepancy of >15mmHg may indicate subclavian stenosis and thus PAD

And esp in older pts or those w/ potential orthostatic Sx, postural measurements should be taken

Postural htn is defined as a 20mmHg fall in SBP upon rising from supine to unassisted upright position
Evaluation
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Once determined that pt has persistent HTN, should evaluate for the following information:

Determine extent of target-organ damage and/or established CV disease

Assess other CV RFs

ID lifestyle factors that could be contributing

ID interfering substances (eg chronic use of NSAIDs, OCs) and potentially curable causes of 2 o HTN
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Labs

Electrolytes and SCr (to calculate estimated GFR)

Fasting glucose

U/A

Lipid profile

EKG

Other tests may be indicated:

Increased albuminuria is increasingly recognized as independent RF for CV disease

Echo a more sensitive way to ID LVH than EKG


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Indicated in pts w/ clinically evident HF or if LV dysfunction or CAD is suspected
Tx
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Antihypertensive therapy almost 50% RR reduction in incidence of HF, a 30-40% RR reduction in stroke and 20-25% RR reduction in
MI
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All hypertensive pts should undergo appropriate non-pharmacologic (lifestyle) modification

Dietary salt restriction moderate Na reduction can lead to fall in BP

Weight loss in overweight/obese pts can lead to significant fall in BP (even w/o dietary Na restriction)

DASH diet veg, fruits, low-fat dairy, whole grains, poultry, fish, nuts

Exercise

Limited alcohol intake

Pt education
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When antihypertensive drugs are used we can use the following general approach:

Begin antihypertensive meds if SBP is persistently 140 (in pts <60y/o) or 150 (in pts 60+y/o) and/or DBP is persistently
90 despite attempted non-pharmacologic therapy

Starting w/ 2 drugs should be considered in pts w/ baseline BP >160/100

May reach target BP in more reasonable time but use cautiously in pts w/ increased risk for orthostatic htn (eg
diabetes and elderly)
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Initial monotherapy in uncomplicated HTN

4 main classes recommended in absence of a specific indication:

Thiazide diuretics

Long-acting CCBs (most often a dihydropyridine like amlodipine)

ACE-Is

ARBs

Thiazide or long-acting CCB should be used as initial monotherapy in black pts

ACE-I or ARB should be used as initial monotherapy in pts w/ diabetic nephropathy or non-diabetic CKD complicated by
proteinuria

Beta-blockers no longer recommended as initial monotherapu in absence of specific indication like IHD or HFrEF
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Combination therapy

In most cases, single-agent therapy wont adequately control BP (esp in those whose BP is >20/10 above goal)

So combination therapy w/ drugs from different classes has substantially greater BP-lowering effect than doubling dose of a
single agent

Can use ACE-I or ARB w/ long-acting CCB


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Can use a thiazide instead of CCB but less beneficial
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Dont use ACE-I and ARB together
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Goal BP

After antihypertensive therapy initiated, pts should be reevaluated and therapy increased Q2-4wks until adequate BP control
achieved

Once achieved, pts can be reevaluated Q3-4mths to ensure maintenance of control

Goal BP <140/90 for general hypertensive population <60y/o

Also for pts of all ages w/ diabetes of CKD who dont have proteinuria

Goal BP <150/90 for general hypertensive population 80y/o

Goal BP <150/90 for most of general population 60-79y/o

<140/90 may be appropriate for some pts depending on general health, comorbid conditions, postural BP changes,
number of meds needed to reach goal, and individual preferences

For hypertensive pts >65y/o with isolated systolic HTN (eg DBP <90mmHg) caution is needed not to reduce DBP too
aggressively (<55-60) as low achieved diastolic pressures associated w/ increased risk of MI and stroke
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Resistant HTN

BP not controlled despite adherence to an appropriate 3-drug regimen (including a diuretic) in which all drugs are dosed at
50% of max recommended antihypertensive dose

Or BP that requires at least 4 meds to achieve control

Many pts who appear to have resistant HTN have pseudoresistance resulting from:

Inaccurate BP measurement (eg inappropriately small cuff)

Poor adherence to BP meds

Poor adherence to lifestyle and dietary approaches to lower BP

Suboptimal antihypertensive therapy (inadequate doses of or exclusion of diuretic from regimen)

White coat resistance

1 or more of the following issues may contribute to true resistant HTN:

EC vol expansion

Increased sympathetic activation

Ingestion of substances that can elevate BP (eg NSAIDs or stimulants)

2o or contributing causes of HTN


Discontinuing Tx
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Some pts w/ stage 1 HTN are well controlled, often on a single medication
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After d/c Tx 5-55% of pts remain normotensive for at least 1-2yrs

A larger fraction of pts do well w/ a decrease in number and/or dose of meds


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More gradual tapering of drug dose is indicated in well-controlled pts taking multiple drugs
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Abrupt cessation of therapy w/ short-acting BB or short actin alpha-agonist (eg clonidine) can lead to potentially fatal withdrawal
syndrome

Prevent w/ gradual d/c these agents over weeks