HTN drugs Flashcards
SE of loop diuretics
e- imbalances hypotension dehydration postural hypotension ototoxicity increased risk of digoxin toxicity increased uric acid-- gout pts
loop diuretics and lithium
lithium acts like a salt! it can cause a lithium toxicity if these are used together
thiazide diuretics onset
2 hrs, peaks in 4-6, lasts for 12
what is the most widely used diuretics
thiazides!
SE of thiazides
e- imbalances dehydration hypovolemia hyperglycemia (DM patients!) increase uric acid digoxin and Li toxicity
K sparing SE
hyperkalemia, watch for added K in diet
K sparing and ACE + ARBs
have d-d interactions related to potassium, with k sparing diuretics
typical order for K sparing
with another diuretic!
nursing considerations for diuretics
Hypokalemia (thiazide + loop)
hyperkalemia (k-sparing)
hydration status (daily weights, admin early in day)
NOT safe for pregnancy
Alpha 1 Adrenergic antagonists MOA
blocks the SNS action on arterioles and veins resulting in vasodilation
Alpha 1 is….
BLOOD VESSELS
SE of alpha 1 adrenergic antagonists
ortho hypo, 1st dose phenomena (don’t get up for 3 hours), reflex tachy (baroreceptor tachy), nasal congestion, inhibits ejaculation
alpha 2 agonist MOA
works on central nervous system in sympathetic OUTFLOW
alpha 2 is PREsynaptic.
causes norepi to accumulate in synapse. body recognizes it has enough and decreases synthesis of norepi.
results in vasodilation, decreased bp and decreased co
SE of alpha-2 agonist
dry mouth, sedation (will get better over time), rebound hypertension (if stopped abruptly)
BB types
beta 1– cardioselective
beta 2– cardio non selective
BB MOA
decreases HR, slows conduction through myocardium, decreases force of contraction
decreases peripheral vascular resistance over time
blocks beta1 on juxtaglomerular cells that release renin
BB SE
brady and AV heartblock, decrease CO (watch for falls), rebound cardiac excitation. may mask s/s of hypoglycemia in DM
common SE of bb
fatigue, drowsyness, dizzy, headache, sexual dysfunction
NSG considerations for BB
check BP and pulse, hold if less than 60
teach pt to wean off, not sudden
teach DM pts to monitor glucose more closely
s/s of HF
Alpha-beta blockers MOA
blocks alpha 1, beta 1&2
alpha blockade: dilation of arteriole and vein
beta blockade: decrease HR, contractility and conduction
SE of alpha-beta blockers
brady, heart block, bronchocontriction, postural hypotension
CCB MOA
works by inhibiting the influx of Ca, preventing muscular contraction. also vasodilation occurs
CCB action on the heart (1)
normal Ca entry into the heart is positive ionotropic and has strong contraction.
CCB blocks Ca which decreases the contraction
CCB action on the heart (2)
Normal Ca regulates the pace of the heart. BLOCKING Ca decreases the heart rate.
CCB action on the heart (3)
AV node – excitability is controlled by the Ca influx. BLOCKING Ca decreases the conduction.
CCB and BB
have the SAME effect on the heart. NO pts on them both at the same time! but nifedipine is ok!
CCB dipines MOA
work primarily on b.v., vasodilation of arterioles and arteries, decreases BP
SE of CCB dipines
flushing, dizziness, peripheral edema, postural hypo, rash, gingival hypertrophy reflex tachy (give BB to decrease this!)
CCB non dipines effects
decrease contract, HR, and conduction
vasodilates, and increases coronary perfusion
why is there no reflex tachy with nondipines?
the effects on the heart and the BV counterbalance one another!
SE of CCBs nondip
constipation, dizziness, facial flushing, edema
can cause brady and heart blockand
SE of CCBs nondip
constipation, dizziness, facial flushing, edema
can cause brady and heart block and heart failure
NSG considerations for CCB
check pulse and BP
watch for reflex tachy
IV admin– tachy and hypo
no grapefruit juice
what does aldersterone do in the body
promotes cardiac remodeling
initiates SNS activity
vascular fibrosis
disrupts baroreceptor activity
what does angie do in the body
triggers release of Al from the adrenal cortex (hold on to water and sodium)
increases inflammation in the arteries
prothrombotic
increases insulin resistance at the tissues (hyperglycemia)
causes cardiac hypertrophy and vascular remodeling
overview of benefits of ACE
treats HTN, post MI, HF, diabetes, prevents diabetic nephropathy, stroke and MI prevention
ACE MOA for diabetic kidneys
decreases AT, vasodilation of the efferent arteriole, pressure in the glomerulus falls, slows the progression in CKD.
what is recommended for DM pts as far as ACE goes
recommend all diabetics to be on an ACE even if BP is normal to protect the kidney from nephropathy
ACE MOA
blocks the conversion of angie 1 to 2, resulting in vasodilation and decreased fluid volume
blocks aldosterone
increased bradykinin
SE of ACE
dry cough, angioedema, 1st dose hypotension, and increased potassium
ARBs MOA
angie gets made but blocked at receptors
potent vasodilator
prevents bad effects from AT2
blocks Al (but not as well)
SE of ARB
decreased risk of cough
Direct Renin inhibitors MOA
blocks the entire RAAS process
SE of direct renin inhibitors
angioedema, cough, diarrhea
direct vasodilators MOA (hydralazine)
causes direct relaxation of arteriolar smooth muscle
SE of direct vasodilator (hydra)
reflex tachy (give BB), increases blood volume, SLE syndrome
Direct vasodilator MOA nitro
causes venous and arteriolar dilation
characteristics of nitroprusside
drug of choice for HTN emergencies, given continous IV, effects in seconds! don’t use for longer than 72 hours (toxic accumulation of thiocyanate)
what do you give if blood volume increases while on nitroprusside?
lasix baby!
