Cardio Pharm Flashcards
goals of pharm with stable angina
–relieve CP
–reduce HLD
–improve morbidity and mortality
what pharm is used to relieve CP in stable angina?
–nitrates
–beta blockers
–calcium channel blockers
–ranolazine
what pharm is used to reduce HLD in stable angina?
–lipid lowering drugs (statins)
–aspirin or clopidogrel (antiplatelets)
what pharm is used to improve morbidity and mortality in stable angina?
ACE inhibitor or ARB
nitrate mechanism of pain relief for stable angina
dilates veins –> decreases preload
beta blocker mechanism of pain relief for stable angina
decreases HR and contractility
CCB mechanism of pain relief for stable angina
–dilates arterioles, which decreases afterload
–decrease HR and contractility
ranolazine mechanism of pain relief for stable angina
helps the myocardium generate energy more efficiently
first line meds for stable angina
BB or CCB + nitrates
secondary prevention for stable angina
–ACEi
–statin
–aspirin
organic nitrate example
nitroglycerin
MOA of nitro
–dilates veins
–decreases preload
adverse effects of nitro
–related to vasodilation: HA, hypotension, reflex tachycardia
–tolerance
route of nitrostat
sublingual
usage of nitrostat
–put underneath tongue
–repeat q 5 min x 3 as needed
when should nitrostat be used?
for active angina
route of transderm-nitro
skin patch
directions for transderm-nitro
–apply to chest or thigh area
–daily
–no hair
–change site with each use
route of Nitro-Bid
ointment
directions for Nitro-Bid
apply 1-2 inches to chest or thigh area
route for isosorbide
sublingual or oral
use of isosorbide
–long acting
–prevention of anginal attacks
–tolerance builds up over time
nursing implications with nitrates
–monitor for HA (most subside in 20 minutes)
–apply nitro patches in morning and remove in evening
–only take as many SL as needed
–don’t swallow
–risk for dizziness/hypotension
–no relief in 5 min = call 911
IV nitrate nursing considerations
–glass bottle with special tubing
–monitor for severe HA, HA, and tachycardia
long acting nitrate considerations
taper when d/c to prevent increased CP from vasospasm
interactions of nitrates
severe hypotension when taken with:
–sindenafil/Viagra
–antihypertensives
–ETOH
MOA of ranolazine
–unknown
–possible helps the myocardium use energy more efficiently
warnings with ranolazine
–prolongs QT interval
–acute renal failure
–liver cirrhosis
adverse reactions with ranolazine
–HA
–dizziness
–nausea
–constipation
nursing considerations for ranolazine
CYP340 inhibitor–avoid grapefruit juice and other meds that are CYP inhibitors
pharm treatment of HF
–ACEi or ARBs, ARNIs
–BB
–mineralocorticoid receptor antagonist (potassium-sparing diuretics)
–SLGT2 inhibitors
–diuretics
–digitalis
–nitrates
example of ARNI (angiotensin receptor-neprilysin inhibitor)
sacubitril/valsartan
survival benefit of RAAS inhibitors in HF
decrease mortality with decreased EF
RAAS inhibitors
ACEi
ARBs
ARNIs
MOA of RAAS inhibitors
–decreases preload and afterload
–suppresses aldosterone
–favorably impact cardiac remodeling
dose of RAAS with HF
highest dose possible
which RAAS inhibitor is favored in HF treatment?
–ARBs might be tolerated better
–ARNI is currently thought to be best–but newer and more expensive
adverse effects of RAAS inhibitors
–hypotension
–hyperkalemia
–cough (ACEi)
preferred BB in HF
carvedilol (beta and alpha blockade)
MOA of carvedilol
–protects against SNS activation and dysrhythmias
–reverses cardiac remodeling
adverse effects of carvedilol
–fluid retention or worsening HF
–fatigue
–hypotension
–bradycardia
use of spironolactone in HF
–used for suppression of sodium/water retention to help with offloading the LV
–decreased hospitalizations and cardiac death
–watch for hyperkalemia and worsening renal failure
SLG2 inhibitor example
dapaglifozin
role of dapaglifozin in HF
thought to help with ventricular unloading through natiuresis/osmotic diuresis without depleting volume
adverse effects of diuretics in HF
–hypokalemia
–hypotension
–Digoxin toxicity
examples of inotropic drugs
–cardiac glycosides (digitalis)
–sympathomimetics (dopamine and dobutamine)
cardiac glycoside example
digitalis
important info about digitalis
considered second line drug because of risk of dysrhythmias
role of sympathomimetics
helps the heart pump squeeze harder
what does positive inotropic effect mean?
if we can increase the contractility of the heart muscle, then we increase the force of contraction –> increasing the CO
what is digitalis made from?
foxglove plant
MOA of digitalis
–inhibits sodium-potassium ATP pump causing calcium to collect within the cells of the heart, helping to increase myocardial contractility
–increases blood flow to kidneys to help with excretion of sodium and water
–decreases sympathetic action and increases parasympathetic action = decreased HR
adverse effects of digitalis/digoxin
–cardiac dysrhythmias
–digitalis toxicity
who is at highest risk for digitalis toxicity?
–increased age
–women
–combination drugs (digoxin and diuretic therapy)
preventing digoxin toxicity
–reduced dose
–periodic monitoring of serum digitalis levels
–supplemental potassium
nursing implications when giving digoxin
–monitor serum potassium levels (hypokalemia)
–take apical pulse for full minute prior to admin
–hold if pulse < 60
–monitor cardiac rhythm
–digibind = antidote
–pt education = taking own pulse
s/s of digitalis toxicity
–bradycardia
–headache
–dizziness
–confusion
–nausea
–visual disturbances
meds used for rhythm and rate control
–BB
–CCB
–amiodarone
–adenosine
–atropine
–dofetilide
MOA of amiodarone
–prolongs action potential duration and the effective refractory period in all cardiac tissues
–blocks alpha and beta adrenergic receptors in SNS
route for amiodarone
IV or PO
uses for amiodarone
–one of the most effective antidysrhythmics for PSVT and ventricular dysrhythmias
–afib with RVR
adverse effects of amiodarone
–thyroid alterations
–corneal microdeposits
–pulmonary toxicity
black box warning for amiodarone
–pulmonary toxicity
–hepatotoxicity
–proarrythmic effects
drug interactions with amiodarone
–digoxin (increase levels by 50%)
–warfarin (increase INR by 50-100%)
half life of amiodarone and effects
–extremely long half-life
–adverse effects may take 2-3 months to fully go away
contraindications of amiodarone
–severe bradycardia
–heart blocks
class for atropine
anticholinergic/antimuscarinic
MOA for atropine
–poisons the vagus nerve
–inhibits postganglionic acetylcholine receptors and direct vagolytic action
route for atropine
IV push only for bradycardia
dose of atropine
1mg every 3-5 minutes, 3mg MAX
adverse effects of atropine
–xerostomia (dry mouth)
–blurry vision
–photophobia
–tachycardia
–flushing
–hot skin
nursing implications for atropine
–need to be on cardiac monitoring
–give second dose if doesn’t work quickly
MOA for adenosine
slows the conduction time through the AV node
half life for adenosine
very short; may need multiple doses
how does adenosine work?
causes a short burst of asystole until sinus rhythm returns
route for adenosine
only IV
dosing for adenosine
(1) 6mg
(2) 12 mg if not converted
(3) 12 mg
always follow with rapid NS flush or 2 saline flushes
class for dofetilide
antidysrhythmic
indications for dofetilide
conversion from afib/aflutter to NSR
MOA for dofetilide
selectively blocking the rapid cardiac ion channel carrying potassium currents
side effects of dofetilide
–TORSADES
–SVT
–HA
–dizziness
–chest pain
nursing implications of dofetilide
–start in hospital with ECG monitoring d/t risk of Torsades
–don’t give to patients with long QT intervals or other drugs that may prolong QT intervals
what should you do if your patient falls into Torsades?
immediately start CPR
what other medication should be monitored with dofetilide?
warfarin
