CHF + Lipids Flashcards
What drug is the first line for CHF?
ACE inhibitors
What are the signs of toxicity for ACE inhibitors?
Kidney dysfunction
Volume ~ diuresis
Potassium levels
When would you use an ARB? Do ARBs have potential of causing angioedema?
ARB when patient cannot tolerate ACE/cough. Be careful of angioedema with ARB.
How does Beta Blocker work for CHF?
Blocks norephineprine
Slows HR for increased diastole filling
Negative inotrope - worsening sx so monitor closely and go slow on dosage
What is spironolactone MOA in CHF?
Aldosterone inhibitor = decreases volume
Monitor potassium
Does isosobride and hydralazine need to be a combo for CHF? Why or why not?
Yes they need to be together to affect both preload and afterload
Together they replicate a ACE inhibitor
What group of drugs decreases mortality in CHF?
Ace inhibitors, beta blockers, spironolactone, isosorbide/hydralazine
If patient has no HR problems with CHF what is the first line of pharmacological treatment?
ACE inhibitor first
If HR is 100, beta blocker first then add ACE inhibitor
What loop diuretic is the standard in treating CHF?
Furosemide/lasix
Lasix has poor availability so higher dose necessary 20-280mg PO
What should you monitor while on furosemide?
Potassium - furosemide may deplete potassium
BP
Renal function
What could be contributing to diuretic resistance?
Inadequate dose
Increased sodium intake
Decreased GI absorption (ascites)
Decreases delivery to nephron (renal insufficiency)
Add metolazone - more effective when compared to other thiazides
Continuous infusion - vs frequent PO doses
Loops are reinforcement for other medications - try adjusting ACE, BB, spironolactone to improve clinical status
What are adverse effects of ACE inhibitors?
Hyperkalemia
Renal insufficiency - monitor for increased serum creatinine
Cough
Angioedema
Anemia
Neutropenia - rare
Contraindicated in 2nd and 3rd trimester of pregnancy
What decreases efficacy of ACE?
Antacids and tetracyclines - bind to ACE
NSAIDS - sodium retention and renal insufficiency
High sodium load
What increases efficacy of ACE?
Phenothiazine, probenecid - prolongs effects of ACE
Do ACE inhibitors increase lithium and digoxin levels?
Yes - check levels
What dosage would you start an ACE inhibitor?
5mg lisinopril
Should diltiazem or verapamil be used in L SIDE CHF?
No
Beta blockers MOA in CHF?
Blocks norepinephrine
Reduce myocardial oxygen consumption by decreasing HR
Increases diastole filling period (coronary myocardium perfuses in diastole)
Prevention of ventricular dysrhythmia
Negative inotrope decreases contractility
Titration of beta blockers
Initial sx: sob, edema
Start with lowest dose
Assess pt weight
Titrate to HR <70 or as tolerated
Monitor for sob, BP, hr, worsening of CHF
MOA aldosterone
Stimulated in response to ACE
Increases sodium retention, sympathetic activation, promotes cardiac remodeling
What drug blocks aldosterone?
Spironolactone
What dosage do you start spironolactone?
12.5mg
Adverse effects: gynecomastia, hyperkalemia
When do you prescribe Eplerenone?
When patient has gynecomastia from spironolactone
What is eplerenone?
Aldosterone blocker that selectively blocks mineralcorticoid receptors
When are ARBs not a good alternative to ACE inhibitors?
Ace inhibitor related angioedema
Ace inhibitor related hyperkalemia
Ace inhibitor related renal insufficiency
Neprilysin inhibitor MOA
Degrades vasoactive peptides such as natriuretic peptides and bradykinins
Bradykinins vasodilate
Natriuretic peptides help urinate
Would you or a cardiologist prescribe entresto/valsartan?
Cardio
In primary care you would start ACE inhibitor
Digoxin
No reduction in mortality
Withdrawal dig if:
-increased risk of worsening CHF
-reduction of exercise tolerance and worsening of NYHA class
-lower ejection fraction and quality of life
Positive inotrope
Increases cardiac contractility
Would benefit CHF in patients with COPD, asthma
What does digoxin toxicity look like?
Digoxin binds to sodium/potassium pump-if potassium is low, there is more risk for dig toxicity
Arrhythmia
2nd and 3rd degree heart block
N/V, anorexia, abdominal pain
Fatigue, weakness, dizziness, headache, confusion, visual halos, photophobia
Who is at risk for digoxin toxicity?
Dig is renally eliminated
Elderly
Hypokalemia
Renal insufficiency
Digoxin drug interactions
Increase dig levels: verapamil, diltiazem, quinidine, amiodarone, anticholinergic (decrease GI motility), indomethacin
Antibiotics may decrease GI flora responsible for metabolizing digoxin
Decrease digoxin levels: antacids, kaolin, cholestyramine, colestipol, metoclopramide
What is the therapeutic digoxin level for CHF?
<1
Vasodilator: Hydralazine
Arterial vasodilator
Decreases afterload
Vasodilator: isosorbide
Venous vasodilator
Decreases preload
What is BIDIL
Fixed combo of hydralazine + isosorbide
Very expensive
Approved for tx of CHF in African American patients vs ACE inhibitors
What is Diastolic CHF?
Normal EF
diastolic filling dysfunction
Heart pumps a lot but too much for blood to get into heart because of poor diastole = decreased CO
Pharmacological tx for diastolic CHF
Improve diastolic function (decrease HR)
Beta blocker
Non-dihydropyridine
Use caution with diuretics
Nothing proven to improve mortality
Who receives primary prevention for cholesterol/LDL
Patients without disease, goal is prevent the first event
Primary prevention consists of moderate intensity statins
Who receives secondary prevention for cholesterol and LDL
Patients with CV disease and less than 75 yrs old
Secondary prevention consists of high intensity statins
What is the most common pharmacologic tx for secondary prevention and high intensity statin?
Atorvastatin 40-80mg
What is the most common pharmacologic tx for moderate intensity and primary prevention?
Atorvastatin 10-20mg
Rosuvastatin 5-10mg
Simvastatin 20-40mg
Clinical signs/sx of hepatotoxicity
Prolonged flu like sx
Fatigue, anorexia, wt loss, fever, dark urine, jaundice
elevated LFT and T Bili
How often do you draw LFT to monitor the liver?
First baseline LFT before tx
Get one 4-8 wks
Monitor for hepatotoxicity for vague flu like sx
Do not do serial LFTs
Is isolated increase in LFT ok?
Yes
Expect LFT to rise because statins are metabolized and work in the liver
If also increased t bili then liver could be damaged
LFT parameters with statin therapy
If LFT increase <3 times normal continue tx and f/u monitoring in 2-4 wks
If LFT increases 3-5 times normal continue and f/u monitoring in 1-2 wks
If LFT increases >5 times normal reduce dose or D.C. And f/u I. 1 wk
Do you monitor for CPK?
Do not obtain baseline cpk
If patient on statin therapy presents with achy muscles then check cpk - if increased then patient could be at risk for rhabdo
What are clinical signs/sx of myositis?
Fever, muscle aches, cramps, stomach pain, hematuria, reduction in urination, dark urine
What are factors that increase risk of myositis/rhabdomyolysis?
DI that increase levels of statins Renal insufficiency Hepatic insufficiency Combination of fibrates/niacin Elderly Etoh abuse Hypothyroidism DM Muscle disorders
What do statins lower?
Statins lower LDL
triglycerides
What is the most common statin?
Atorvastatin
Moderate risk of DI
Bioavailability of 14% - need higher dose with lower bioavailability
