Anti-HTN Flashcards
hydrochlorothiazide
thiazide diuretic for anti-HTN
blocks reuptake of Cl and Na from tubular fluid after filtration; appears to cause a decrease in TPR via unclear mechanisms; lowers BP by 10-15mm in monotherapy, more in combinations; Chlorthalidone may eventually replace HCTZ b/c it may be more effective.
F~70%, excreted unchanged in urine (causes increase in frequency of urination); short half life (hours); only available as oral formulation; onset 2hr, peak 5h, duration 10h
may cause K and Mg depletion, Na and Cl depletion, metabolic alkalosis, volume depletion, worsen hyperuricemia
additive effects with other anti-HTN
more side effects with geriatric patients; pregnancy class D; less effective in patients with reduced GFR
12.5 or 25mg po every morning;
monitor BP, weight, edema, K, Mg, BUN, creatinine
Lisinopril
ACE inhibitor for anti-HTN, treatment of CHF, preserving renal function, preserving LV function s/p MI, acute management of MI
inhibits conversion of AT1 to AT2 via ACE; attenuates AT2 induced vasoconstriction + aldosterone release
well absorbed, onset 1h, peak 6h, duration 24h; used once per day. excreted renal as unchanged drug
can cause orthostatic hypotension; caution in patients with impaired renal fxn or RAS (reduces GFR); careful use in patients on diuretics or with aortic stenosis; can cause angiodema in lips/throat/face (can be lethal); cough, acute renal failure
additive effects with other anti-HTN; nsaids may attenuate BP lowering effects; preserves K+, and can cause hyperkalemia if taken with KCl or others
D/C diuretics prior to beginning use to reduce hypotension; category C/D in pregnancy; can cause abnormal cartilage development
begin w/ 10mg per day, titrate upward to 40mg per day max
monitor BP, weight, edema, K, BUN, and creatinine (to assess renal fxn)
Losartan
angiotensin-1 receptor blocker (ARB) for anti-HTN, preserving renal fxn, treatment of CHF
blocks stimulation of AT1R by AT2, reducing AT2 induced vasoconstriction + aldosterone release
F ~30%, onset 6h, extensive first pass; active metabolite is 40x more potent with longer half-life
can cause dizziness, orthostatic hypotension, worsening of renal failure
additive effects with other anti-HTN
pregnancy class C/D, use care in patients on diuretics or with RAS; caution with mitral or aortic stenosis
25-100mg per day for HTN
Monitor BP, weight, edema, electrolytes, BUN, creatinine
Nitroprusside
vasodilator for acute anti-HTN, severe CHF, pulmonary HTN, and during surgery to produce controlled hypotension
metabolized to release CN- and NO; vascular smooth muscle dilatation in veins + arteries via activation of guanylate cyclase > increased cGMP > vasodilation > cGMP hydrolyzed to GMP by phosphodiesterase (PDE)
only administered via iv; rapid onset and cessation (allows minute to minute titration); CN- metabolite is converted to SCN in liver and excreted in urine
can cause excessive hypotension, accumulation of CN- and thiocyanate, headache, decreased blood flow to brain (syncope)
additive effect with other anti-HTN
only administered in ICU with arterial line; avoid high rate or prolonged infusion;
0.3-10mcg/kg/min IV infusion for HTN crisis
monitor BP, HR, metabolic acidosis
Hydralazine
peripheral vasodilator for anti-HTN, treatment of CHF, vasodilator
“direct” acting vasodilator, acts by inducing endothelium to produce NO > increased cGMP; minimal venodilating effect
given po, im, or iv; metabolized extensively in GI mucosa and liver, excreted in urine as metabolites; F ~40%; onset 30m po, 10m iv; persists 2-6h
dangerous in patients with renal dz, prior stroke, angina; watch for hypotension, edema, drug-induced lupus
additive effects with other anti-HTN
never use as chronic oral mono therapy for HTN since it causes edema and reflex tachycardia; cautious use in patients with CAD
10-50mg po tid
monitor BP, weight, edema, BUN, creatinine, symptoms of lupus or angina
Verapamil
calcium entry blocker for anti-HTN, anti-anginal, anti-arrythmic
reduces BP by inhibiting influx of calcium through “slow channels”, dilates peripheral arterioles; produces negative inotropic effect; reduces afterload (in angina) to lower oxygen consumption; inhibits spasm of coronary arteries in vasospastic angina; blocks reentry paths through AV nodes in paroxysmal SVT
absorbed rapidly, but F~30%; also available in SR tablets; cleared by liver and kidney (produces active metabolites); onset 2h po, 1-5m iv; half-life 6-12h, may be given po or iv
can cause hypotension, AV block, worsening of CHF, bradycardia
additive effects with other anti-HTN; additive toxic effects on heart when given with beta-blockers
reduce dose in patients with both renal and hepatic dz; short-acting nifedipine (other calcium entry blockers) can increase risk of MI for unclear reasons; pregnancy class C
80mg tid, or 240mg SR qd
monitor weight, edema, BP
clonidine
CNS alpha-2 agonist for anti-HTN, adjunct to Rx of opioid withdrawal, migraine prophylaxis
stimulates a-2 AR in the brainstem leading to a down-regulation of sympathetic outflow
onset 1h, duration 8h, F~85%; also available as skin patch
withdraw gradually to avoid rebound HTN; risk of bradycardia in sinus node dz; causes lethargy, fatigue, depression
additive effects with other anti-HTN; additive sedation with other CNS drugs
Pregnancy C; avoid in patients with renal insufficiency
begin w/ 0.1mg po bid, up to 1.2mg per day; transdermal begin with 0.1mg per 24h, 7 day patch
monitor BP, HR, fatigue
Trimethaphan
** this drug is not used in treatment of HTN; know mechanism only***
blocks ganglionic transmission for anti-HTN
blocks nicotinic transmission in both sympathetic and parasympathetic ganglia (all Nn receptors); produces vaso + veno dilation
useful only IV; produces BP fall w/in minutes; partly metabolized, partly excreted by kidneys
caution re sudden, severe drop in BP or HR; systemic reduction in all sympathetic or parasympathetic responses
additive effects w/ other anti-HTN
makes patients miserable, so only use during general anesthesia; tilt patients to help control BP
given by iv only, and only to treat HTN crisis, or for controlled hypotension during surgery
monitor minute to minute BP and HR changes
Reserpine
not used in long-term management of HTN; only know mechanism
Rauwolfia alkaloid for anti-HTN
binds to vesicles that contain NE or serotonin, preventing uptake, and ultimately depleting the neuron of NE or serotonin; this effect takes 203 weeks to develop, and including neurons and also the adrenal medulla
good oral bioavailability, but biological effects take 2-3 weeks
causes dizziness, orthostatic hypertension, depression
additive effects with most other anti-HTN
approved by the FDA in 1953; first anti-HTN ever approved
for HTN, 0.1-0.2mg every day
monitor BP, sympathetic tone, depression
Atenolol
B1-AR selective blocker for anti-HTN, antiarrhythmic, primary, secondary prevention of MI, anti-anginal
binds to b-AR with preferences for B1 over B2 (at higher doses, also binds to B2), leading to lower BP via several mechanisms (lower CO, less RAAS); less effective preventing strokes
available po or iv, variable oral F; onset 1-2h, duration 12-24h, given once daily, excreted renally
can cause excessive hypotension, bradycardia, heart block to worsen CHF (but it is indicated for mild/moderate CHF); worsens bronchospasm in asthmatics
additive effects with other anti-HTN, additive AV block with CEBs (calcium entry blockers)
may be useful in HTN patients with exertional angina, MI, a fib; do not withdraw abruptly, taper down slowly; may not be a first line drug any longer (not recommended for monotherapy)
for HTN, 25-100mg qd or bid
monitor BP, HR, exercise tolerance
Prazosin
a1-AR blocker for anti-HTN, treatment of BPH, Raynaud’s, kidney stones
blocks a1-AR on arterioles and veins, inhibits NE mediated vaso and venoconstriction
available po or transdermal; variable oral F (60%), onset 2h, duration 12-24h, extensive liver metabolization
can cause excessive hypotension with syncope, especially orthostatic hypotension; diuretics
additive effects with most other anti-HTN especially diuretics
start gradually, at bedtime, to avoid syncope; male patients with BPH(?)
as mono therapy being at 1mg did, advance to 20mg per day divided did
monitor BP, weight, edema
Labetalol
alpha & beta-AR blocker for anti-HTN, treatment of CHF
reduces BP by blocker NE receptors, thereby lowering BP by several mechanisms; patients differ in beta vs alpha blockade
excellent absorption but high first-pass effect, leading to F~25%; onset 1-2h after po, 2-5m iv; extensively metabolized in liver by IID6
avoid in patients with bradycardia, heart block, CHF, asthma, shock; use caution in patients with cardiomyopathy, pheochromocytoma; Pregnancy D
additive effects with most anti-HTN
use reduced doses in patients with impaired liver fxn; dizziness is most troubling early side effect, most often used for HTN crises (as with nitroprusside)
commonly given iv in small boluses of 20mg, followed by continuous infusion at 2mg/m; not usually given po for chronic treatment (80mg tid, or 240mgSR qd)
monitor BP and HR
