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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
Age dependent
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
Can be life-threatening and requires immediate Tx usually w/ parenteral meds in a monitored setting
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Hypertensive urgency
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
BP = CO x SVR
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
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)
Na restriction lowers 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
Glucocorticoids
Wt loss meds
EPO
Cyclosporine
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
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
Approx. of pts w/ pheochromocytoma have paroxysmal HTN, the rest have 1 o HTN
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:
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
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:
ID interfering substances (eg chronic use of NSAIDs, OCs) and potentially curable causes of 2 o HTN
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Labs
Fasting glucose
U/A
Lipid profile
EKG
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
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
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
Thiazide diuretics
ACE-Is
ARBs
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
After antihypertensive therapy initiated, pts should be reevaluated and therapy increased Q2-4wks until adequate BP control
achieved
Also for pts of all ages w/ diabetes of CKD who dont have proteinuria
<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
Many pts who appear to have resistant HTN have pseudoresistance resulting from:
EC vol expansion