cardiovascular pharm mod 5 Flashcards
pharm angina goals
Goal: Relieve \_\_chest pain\_\_\_\_\_ Nitrates Beta Blockers Calcium Channel blockers Ranolazine
Goal: Reduce ___hyperlipidemia_________
Lipid lowering drug - statin
Aspirin or clopidogrel (Plavix) - blood thinner/anti-platelet
Goal: Improve morbidity & mortality
ACE Inhibitor or ARB
stable angina pharm
Nitrates & Ranolazine `
Beta Blockers, Calcium Channel Blockers, Statins and Aspirin
organic nitrates:
Nitroglycerin
rapid:
sublingual - Nitrostat - acute angina
short:
skin patch - Transderm-Nitro
Ointment - nitro-bid
Long:
sublingual or oral - Isosorbide
*prevention
first anti-angina med
MOA
Dilates veins
Decreases preload
Adverse effects
Related to vasodilation: H/A, hypotension, reflex tachycardia
Tolerance
Interactions:
Severe hypotension when taken with:
sindenafil/Viagra, antihypertensives, and ETOH
nursing implications NITRATES
No relief in 5 min – call 911
Ok to take a second SL tab in 5 min and a third in
5 more min – do not exceed 3 doses
- Monitor for headache
- –Mild analgesic
- —Most h/a subside in 20 min - Apply nitro patches in the morning and remove in the evening
- –Apply to hairless site and rotate sites - Pt Ed: Treatment of acute chest pain
–Take only as many SL tablets as needed -
TOLERANCE
—-Use SL form – do not swallow
—-Fall Precautions –dizziness/hypotension
—-No relief in 5 min – call 911
—-Ok to take a second SL tab in 5 min and a third in
5 more min – do not exceed 3 doses - IV form
- –Glass bottle with special tubing
- –Monitor for severe h/a, h/a, and tachycardia - Long acting forms - taper when d/c to prevent increased chest pain from vasospasm
call 911 if?
IMPORTANT: If chest pain has not improved or it has worsened 5 minutes after taking the first nitro, the patient
anti-anginas
ranolazine (Ranexa)
MOA:
Unknown
Possibly helps the myocardium use energy more efficiently
Warnings
Prolong the QT interval
Acute renal failure (existing renal disease)
Liver cirrhosis
Adverse reactions
Headache, dizziness
Nausea and constipation
CYP340 inhibitor– avoid grapefruit juice and other medications that are CYP inhibitors
Pharmacological Treatment of HF
ACE inhibitors or ARBs, ARNI Beta blockers Mineralocorticoid Receptor Antagonist (MRAs) SLGT2 Inhibitors Diuretics Digitalis Nitrates
ARNI:
Angiotensin Receptor-Neprilysin Inhibitor
SACUBITRIL/VALSARTAN
Survival benefit?
Decrease in mortality with decreased EF
MOA: Decreases preload & afterload, suppresses aldosterone, favorably impact cardiac remodeling
Use highest dose possible
Which one is favored and why?
+/-
ARBs might be tolerated better
ARNI is currently thought to be best– but newer and more expensive
Adverse effects
Hypotension, hyperkalemia, cough (ACEI)
beta blockers for heart failure
carvedilol (Coreg)
Beta and alpha blockade
MOA: Protects against SNS activation and dysrhythmias, reverses cardiac remodeling
Adverse effects: Fluid retention or worsening HF Fatigue Hypotension Bradycardia
SLG2 Inhibitors and HF
dapaglifozin
Diabetes medications
MOA in HF not well understood
Thought to help with ventricular unloading through natriuresis/osmotic diuresis without actually depleting volume like traditional diuretics
May affect cardiac metabolism/bioenergetics
Either way decreases readmissions, mortality and morbidity
diuretics
furosemide (Lasix)
First-line therapy: loop diuretics
Volume overload
Oral or IV
Adverse effects
Hypokalemia
Hypotension
Digoxin toxicity
Survival benefit?
Symptom relief
Inotropic Drugs
Cardiac glycosides: digitalis
Considered a second line drug because of increased risk for dysrhythmias
Sympathomimetics: dopamine and dobutamine
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 cardiac output.
Inotropic agent:
digitalis/Digoxin
Class: Cardiac glycoside: digitalis
MOA: Inhibits sodium-potassium ATP pump causing calcium to collect within the cells of the heart helping to increase myocardial contractility.
Increases blood flow to the kidney helping with excretion of sodium and water
Decreases sympathetic action and increases parasympathetic action= Decreased HR
Adverse Effects:
Cardiac dysrhythmias
Digitalis toxicity
digitalis toxicity
Who is at highest risk?
Age - older
Women
Combination drugs (digoxin and diuretic therapy)
Preventing Toxicity
Reduced dose
Serum Digitalis levels: Periodic monitoring of levels
Supplemental potassium
s/s digitalis toxicity
Bradycardia Headache Dizziness Confusion Nausea Visual disturbances- blurry/yellow vision
rn implications digitalis
Take apical pulse for a FULL minute prior to administering digoxin Hold if pulse below 60 bpm Monitor cardiac rhythm ANTIDOTE for digitalis toxicity Digoxin immune Fab (Digibind) given IV Pt education very important Taking own pulse
digitalis and monitoring
Monitor serum potassium levels Digitalis + hypokalemia digitalis toxicity cardiac dysfunction serious dysrhythmias
antidote digitalis toxicity
Digoxin immune Fab (Digibind) given IV
rate and rhythm control
Beta-blockers Calcium Channel Blockers Amiodarone Adenosine Atropine Dofetilide
amiodarone
MOA: prolongs the action potential duration and the effective refractory period in all cardiac tissues; blocks alpha- and beta-adrenergic receptors in the SNS
IV or PO
One of the most effective antidysrhythmic for PSVT and ventricular dysrhythmias; used also for afib with RVR
LOTS of adverse effects (75% have adverse effects); thyroid alterations, corneal microdeposits
Pulmonary toxicity= fatal in 10% of patients
Black box warning: pulmonary toxicity, hepatotoxicity, and pro-arhythmic effects
amiodarone has significant interactions with which two drugs?
2 significant drug interactions: digoxin and warfarin
Increase digoxin levels by 50%
And increase INR by 50-100%
amiodarone s/e
2 significant drug interactions: digoxin and warfarin
Increase digoxin levels by 50%
And increase INR by 50-100%
EXTREMELY long half-life– last in system many days
If someone has adverse effects, may take 2-3 months for them to fully go away
Contraindicated in people with severe bradycardia, or heart blocks (type of rhythm)
Class: Anticholinergic/Antimuscarinic
sinus brady
atropine
MOA: Poisons the vagus nerve; inhibits postganglionic acetylcholine receptors and direct vagolytic action
Given IV push ONLY for bradycardia; 1mg every 3-5 minutes, 3mg MAX
Only works for 28% of cases of bradycardia
Adverse effects: xerostomia, blurry vision, photophobia, tachycardia, flushing, hot skin
Nursing implications: Need to be on cardiac monitoring, if doesn’t work quickly, give a second dose
adenosine - SVT
MOA: slows the conduction time through the AV node
VERY SHORT HALF LIFE– may need multiple doses
Commonly causes a short burst of asystole until sinus rhythm returns
SE: other than implications above, very few
ONLY GIVEN IV
6mg IVP, if have not converted give 12mg IVP, can give a 3rd time 12 mg IVP
Always follow with rapid normal saline flush or 2 saline flushes
Class: antidysrhythmic
dofetilide (Tikosyn)
Indications: conversion from afib/aflutter to NSR
MOA: selectively blocking the rapid cardiac ion channel carrying potassium currents
Side effects: TORSADES, SVT, headache, dizziness, chest pain
Nursing Implications: started in-hospital with ECG monitoring due to risk of Torsades (black box warning); don’t give to patients with long QT intervals or other drugs that may prolong QT interval
