stroke
hemorrhagic, ischemic
coronary heart disease
angina, myocardial infarction, CHF
retinopathy
retinal infarcts, hemorrhages
nephropathy
chronic kidney disease
BP classification
systolic <120
diastolic <80
BP classification
systolic 120-129
diastolic <80
BP classification
systolic 130-139
diastolic 80-89
lifestyle modification
70.2% of american adults are overweight/obese
reduces BP
decreases total CHD risk
should be pursued in combination with drug therapy
lifestyle modification
excessive chronic intake can cause resistance to drug therapy
limit intake to
1 oz ethanol/day (2 drinks) in men
0.5 oz ethanol/day (1 drink) in women
lifestyle modification
regular aerobic exercise effective in lowering BP
enhances weight loss and overall health
lifestyle modification
largest benefit in black/elderly pts
optimal goal in <1500 mg/day
at least 1000 mg/day reduction
first line agent
initially lower BP through diuresis
chronically decrease peripheral vascular resistance
often used in combination w/ other antihypertensive drugs
adds second MOA
offsets sodium retention caused by other agents
nausea/diarrhea
erectile dysfunction
sun sensitivity
metabolic
hypokalemia
hyperglycemia
hyperlipidemia
won’t see at small dosages
most ADRs are dose related
limit dose to 25 mg/day
first line agent
-pril drugs
blocks the conversion of ANG I to ANG II
ANG II is potent vasoconstrictor
causes decreased aldosterone secretion
blocks degradation of bradykinin (natural vasodilators)
broken down by ACE, but blocked
specific advantages
HF
chronic kidney disease
first line agent
-sartan drugs
angiotensin II receptor antagonist
do not affect bradykinin levels (no cough)
cheaper, more used than ACE inhibitors
pregnancy warning
orthostasis
much less angioedema than ACEi (maybe none)
first line agent
dihydropyridine & non-dihydropyridine
both equally effective for HTN
blocks influx of calcium across cell membrane
causes coronary/peripheral vasodilation
negative inotropic effects
decreased contractile strength of heart
only affects pts who alr have CV problems
dizziness
flushing
headache
peripheral edema
anorexia & nausea
peripheral edema (less than DHP CCBs)
constipation (verapamil)
may have worse side effects than first line agents
still used but don’t have long term data
aliskiren (Tekturna)
blocks renin’s activity to convert angiotensinogen to angiotensin I
otherwise similar to ACE inhibitors
pregnancy warning
orthostasis
angioedema
alternative agent
alternative agent
cardioselective, non-selective, intrinsic sympathomimetic activity
does not have general better evidence of reducing morbidity/mortality; ARBs have better evidence
many physiologic effects documented, but uncertain what causes decreased BP effect
type of beta-blocker
greater affinity for B1 receptors (in heart/kidney) than B2 receptors (in lungs, liver, pancreas, arteriolar smooth muscle)
in general, more preferred for HTN
type of beta blocker
partial beta-receptor agonists (kind of stimulates receptors)
do not reduce CV events as well as other beta-blockers
basically never used for most people
bradycardia
dizziness/drowsiness
bronchoconstriction in COPD/asthma pts
abrupt discontinuation can result in rebound HTN or increased HR (taper dose 1-2 weeks)
alternative agent
selective alpha-1 receptor antagonists in the peripheral vasculature
results in vasodilation and lowered BP
reserved for pts with treatment resistant HTN
first dose effect
dizziness, faintness, syncope within 1-2 hours of first dose
take first dew doses before bedtime
can also occur with changes in dose/non-adherence
sustained orthostatic hypotension
esp elderly
CNS effects
lassitude (mental/physical fatigue)
vivid dreams
depression
priapism (erection >4 hours)
alternative agent
reduces sympathetic outflow from vasomotor center in the brain
decreases HR, CO, and BP
reserved for pts with treatment resistant hypertension
sodium/water retention, often used with diuretic
depression
high incidence of orthostatic hypotension (elderly)
anticholinergic effects (sedation, dry mouth, urinary retention)
abrupt cessation results in rebound hypertension
tend to have HTN at younger age and absolute pressures often higher
greater risk for HTN complications
most effective treatment are thiazides & calcium channel blockers
less effective as monotherapy (one drug) and less positive CVD outcomes
beta-blockers, ACEi, ARBs
chronic hypertension (already hypertensive before pregnancy)
preeclampsia/eclampsia
gestational hypertension (hypertensive from pregnancy)
preferred:
labetalol, long-acting nifedipine, methyldopa
good safety history
alternatives:
other beta-blockers and calcium channel blockers
contraindicated:
ACEi, ARB, direct renin inhibitors
often present with isolated systolic hypertension
no agents more effective, follow general drug selection guidelines
due to risk of orthostatis, generally avoid
central alpha agonists
peripheral alpha-blockers
start other drugs at lower doses
HTN more common in obese children
lifestyle modifications important
secondary hypertension more common
evidence supports use of
ACEi
ARB
beta-blocker
calcium channel blockers
thiazides
tend to not use ACEis, ARBs in adolescent girls due to pregnancy risk