cardio pharm

Question 1

pharm for PVD

Answer 1

antiplt (aspirin, clopidogrel)
anticoags (apixaban, warfarin)
thrombolytics
lipid lowering agents (antilipemics - statins)
antihtn
agents that increase blood supply to extremities

Question 2

cilostazol

Answer 2

moa: Plt inhibitor, vasodilation
I: Intermittent claudication (arterial disease)

Question 3

cilostazol: SE

Answer 3

HA, dizzy, d, abn stools, palpitations, peripheral edema Metabolized by P450 – interactions with other drugs

Question 4

pentoxifylline

Answer 4

vasoactive agent
moa: Relieve leg pain by increasing blood flow and oxygen through the blood vessels, helps to increase walking distance and duration
I: intermittent claudication
SE: n/v, dizzy
PO TID

Question 5

anti anginals

Answer 5

treat stable angina
relieve chest pain - nitrates, BB, CCB, ranolazine
reduce hld - lipid lowering drugs (statins), aspirin and clopidogrel (decrease risk of making plaques larger)
improve morbidity and mortality - ACEi and ARB

Question 6

nitrates

Answer 6

dilate veins which decreases preload and takes P off heart - decrease demand

Question 7

beta blockers

Answer 7

decrease HR and contractility

Question 8

calcium channel blockers

Answer 8

dilate arterioles which decreases afterload
decrease HR and contractility

Question 9

ranolazine

Answer 9

helps myocardium generate energy more efficiently

Question 10

pharm treatment of stable angina

Answer 10

1st line: BB/CCB + nitrate

Question 11

Nitroglycerin (prototype)

Answer 11

Organic nitrates
moa: Dilate veins (works on all but primarily venous)
decrease preload
Prophylactic for chest pain

Question 12

nitroglycerin - nitrostat

Answer 12

Rapid
Sublingual
for active angina (q5 min x3)

Question 13

nitroglcerin - transderm nitro and nitrobid

Answer 13

Short
skin patch – transderm nitro
ointment – nitro-bid 2%
chest or thigh daily, no hair, rotate area, on in the morning, off at night

Question 14

nitroglycerin - isosorbide

Answer 14

Long
sublingual or oral
for prevention of anginal attacks, tolerance builds up, prevention

Question 15

nitroglycerin: SE

Answer 15

Related to vasodilation: HA, hypoT, reflex tachy
Tolerance
Interactions: severe hypoT when taken with sildenafil, antihypertensives, and ETOH

Question 16

nitroglycerin: nc

Answer 16

Monitor for HA – mild analgesic, most subside in 20 min
Pt ed: take only as many SL tablets as needed (tolerance), don’t swallow, fall precautions (dizzy, hypoT), call 911 if no relief in 5 min (don’t exceed 3 doses)
IV: glass bottle with special tubing, monitor for severe HA and tachy
Taper long acting forms to prevent increased chest pain from vasospasm

Question 17

ranolazine

Answer 17

moa: Unknown, possibly helps myocardium use energy more efficiently
SE: Prolonged QT interval
Acute renal failure (existing renal disease)
Liver cirrhosis
HA, dizzy, n, c
PO only
Cyp 340 inhibitor – avoid grapefruit juice and other inhibitors

Question 18

HF pharm

Answer 18

ACEi or ARB, ARNI
BB
mineralcorticoid receptor antagonist (MRAs) - k sparing diuretics
SLGT2 I
diuretics
digoxin
nitrates

Question 19

RAAS inhibitors in HF

Answer 19

ACEi, ARB, ARNI
on one, not all 3
ARBs tolerated better but ARNI though to be best (but expesive)
use highest dose possible
SE: hypoT, hyperK, cough (ACEi)

Question 20

diuretics in HF

Answer 20

1st line: loop - furosemide
for FVE
oral or IV
SE: hypoK, hypoT, digoxin (can precipitate)
no survival benefit - just S relief

Question 21

inotropic drugs

Answer 21

cardiac glycosides: digitalis
sympathomimetics: dopamine and dobutamine
increase contractility of heart muscle -> increase force of contraction -> increase CO

Question 22

digoxin tox

Answer 22

rf: OA, F, combo drugs (digoxin and diuretic)
prevent: reduced dose, serum digitalis levels - periodic monitoring; supplemental K

Question 23

Digoxin/digitalis

Answer 23

Inotropic drugs
Cardiac glycosides
moa: Inhibit Na/K ATP pump causing Ca to collect in cells of heart to increase myocardial contractility
Increase BF to kidney helping with excretion of Na and H2O
Decrease sympathetic action and increase parasympathetic action = decreased HR
I: 2nd line bc increased risk of dysrhythmias

Question 24

digoxin/digitalis: SE and NC

Answer 24

Cardiac dysrhythmias – go into other rhythm issues
digitalis tox: brady, HA, dizzy, confusion, n, blurry/yellow vision
Made from foxglove plant
Monitor K – hypoK = serious dysR, cardiac dysF, digitalis tox
Take apical rate for full min before admin (hold <60)
Monitor cardiac rhythm
Antidote = digibind/digoxin immune fab (IV)
Pt ed: take pulse, monitor K, supplements

Question 25

Sacubitril/valsartan

Answer 25

ARNI = angiotensin receptor neprilysin inhibitor
moa: Decreases preload and afterload, suppress aldosterone, favorably impact cardiac remodeling (protect from all chm mediator release)
I: Decrease mortality in those with decreased EF
use highest dose possible

Question 26

Carvedilol

Answer 26

beta blocker
moa: Beta and alpha blockade
Protect against SNS activation (neurohormonal activation) and dysrhythmias, reverse cardiac remodeling
SE: Fluid retention or worsening HF, fatigue, hypoT, brady

Question 27

spironolactone

Answer 27

Mineralcorticoid receptor antagonist
K sparing
moa: Suppress Na/water retention to help with offloading the LV
I: HF and htn
SE: Watch for hyperK and worsening renal fail

Question 28

dapagliflozin

Answer 28

SLG2I
moa: Not well understood in HF – help with ventricular offloading through natriuresis/osmotic diuresis without actually depleting volume like traditional diuretics, may affect cardiac metabolism/bioenergetics
I: DM and HF

Question 29

rate and rhythm control

Answer 29

BB, CCB, amiodarone, adenosine, atropine, dofetilide
goal of HR <100 and normal rhythm

Question 30

amiodarone

Answer 30

moa: Prolongs action potential duration and the effective refractory period in all cardiac tissues; blocks alpha and beta adrenergic receptors in SNS
I: A Fib, ventricular dysR
One of most effective antidysrhythmic for PSVT and ventricular dysR; also used for afib with RVR

Question 31

amiodarone: SE

Answer 31

SE: LOTS
Thyroid alterations (iodine), corneal microdeposits – light sensitivity, dry, halos
Pulm tox = fatal in 10% of pts
BB: pulm tox ([] in lungs, 10% fatal), hepatotox, pro-arhythmic effects (can elicit new arrhythmia)
More common with higher and sustained doses

Question 32

amiodarone: nc

Answer 32

IV or PO
Lipophilic drug (fat loving) – [] in adipose tissues
Interactions: increase digoxin and INR (warfarin)
V long ½ life – can take 2-3 mo for SE to go away fully
CI: severe brady or heart blocks (type of rhythm)

Question 33

atropine

Answer 33

Anticholinergic/antimuscarinic
moa: Poisons vagus nerve, inhibits postganglionic acetylcholine receptors and direct vagolytic action
I: Sinus brady – symptomatic
Only if vagal induced! Not induction issue

Question 34

atropine: SE and nc

Answer 34

SE: Xerostomia, blurry vision, photophobia, tachy, flush, hot skin
NC: IV push only for brady; 1 mg q3-5 min, 3mg MAX
Only works ~28% of cases
Need to be on cardiac monitoring, if doesn’t work quickly, give 2nd dose

Question 35

adenosine

Answer 35

moa: Slow conduction time through AV node
I: PSVT, sinus tachy

Question 36

adenosine: SE and nc

Answer 36

SE: Commonly causes short burst of asystole (flatline) until sinus rhythm returns
Very few
nc: V short ½ life – need multiple doses
Only IV – 6mg IVP if not corrected give 12mg IVP, can give 3rd time 12 mg IVP – always follow with rapid NS flush or 2
3 way stopcock
Usually have shock pads on them

Question 37

dofetilide

Answer 37

Antidysrhythmic
moa: Selectively block rapid cardiac ion channel carrying K currents
I: Conversion from afib/aflutter to NSR and stay there – can take at home