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Nursing Pharmacology > CHF + Lipids > Flashcards

CHF + Lipids Flashcards

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1
Q

What drug is the first line for CHF?

A

ACE inhibitors

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2
Q

What are the signs of toxicity for ACE inhibitors?

A

Kidney dysfunction
Volume ~ diuresis
Potassium levels

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3
Q

When would you use an ARB? Do ARBs have potential of causing angioedema?

A

ARB when patient cannot tolerate ACE/cough. Be careful of angioedema with ARB.

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4
Q

How does Beta Blocker work for CHF?

A

Blocks norephineprine
Slows HR for increased diastole filling
Negative inotrope - worsening sx so monitor closely and go slow on dosage

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5
Q

What is spironolactone MOA in CHF?

A

Aldosterone inhibitor = decreases volume

Monitor potassium

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6
Q

Does isosobride and hydralazine need to be a combo for CHF? Why or why not?

A

Yes they need to be together to affect both preload and afterload
Together they replicate a ACE inhibitor

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7
Q

What group of drugs decreases mortality in CHF?

A

Ace inhibitors, beta blockers, spironolactone, isosorbide/hydralazine

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8
Q

If patient has no HR problems with CHF what is the first line of pharmacological treatment?

A

ACE inhibitor first

If HR is 100, beta blocker first then add ACE inhibitor

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9
Q

What loop diuretic is the standard in treating CHF?

A

Furosemide/lasix

Lasix has poor availability so higher dose necessary 20-280mg PO

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10
Q

What should you monitor while on furosemide?

A

Potassium - furosemide may deplete potassium
BP
Renal function

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11
Q

What could be contributing to diuretic resistance?

A

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

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12
Q

What are adverse effects of ACE inhibitors?

A

Hyperkalemia
Renal insufficiency - monitor for increased serum creatinine
Cough
Angioedema
Anemia
Neutropenia - rare
Contraindicated in 2nd and 3rd trimester of pregnancy

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13
Q

What decreases efficacy of ACE?

A

Antacids and tetracyclines - bind to ACE
NSAIDS - sodium retention and renal insufficiency
High sodium load

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14
Q

What increases efficacy of ACE?

A

Phenothiazine, probenecid - prolongs effects of ACE

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15
Q

Do ACE inhibitors increase lithium and digoxin levels?

A

Yes - check levels

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16
Q

What dosage would you start an ACE inhibitor?

A

5mg lisinopril

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17
Q

Should diltiazem or verapamil be used in L SIDE CHF?

A

No

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18
Q

Beta blockers MOA in CHF?

A

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

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19
Q

Titration of beta blockers

A

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

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20
Q

MOA aldosterone

A

Stimulated in response to ACE

Increases sodium retention, sympathetic activation, promotes cardiac remodeling

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21
Q

What drug blocks aldosterone?

A

Spironolactone

22
Q

What dosage do you start spironolactone?

A

12.5mg

Adverse effects: gynecomastia, hyperkalemia

23
Q

When do you prescribe Eplerenone?

A

When patient has gynecomastia from spironolactone

24
Q

What is eplerenone?

A

Aldosterone blocker that selectively blocks mineralcorticoid receptors

25
Q

When are ARBs not a good alternative to ACE inhibitors?

A

Ace inhibitor related angioedema
Ace inhibitor related hyperkalemia
Ace inhibitor related renal insufficiency

26
Q

Neprilysin inhibitor MOA

A

Degrades vasoactive peptides such as natriuretic peptides and bradykinins
Bradykinins vasodilate
Natriuretic peptides help urinate

27
Q

Would you or a cardiologist prescribe entresto/valsartan?

A

Cardio

In primary care you would start ACE inhibitor

28
Q

Digoxin

A

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

29
Q

What does digoxin toxicity look like?

A

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

30
Q

Who is at risk for digoxin toxicity?

A

Dig is renally eliminated

Elderly
Hypokalemia
Renal insufficiency

31
Q

Digoxin drug interactions

A

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

32
Q

What is the therapeutic digoxin level for CHF?

A

<1

33
Q

Vasodilator: Hydralazine

A

Arterial vasodilator

Decreases afterload

34
Q

Vasodilator: isosorbide

A

Venous vasodilator

Decreases preload

35
Q

What is BIDIL

A

Fixed combo of hydralazine + isosorbide
Very expensive

Approved for tx of CHF in African American patients vs ACE inhibitors

36
Q

What is Diastolic CHF?

A

Normal EF
diastolic filling dysfunction
Heart pumps a lot but too much for blood to get into heart because of poor diastole = decreased CO

37
Q

Pharmacological tx for diastolic CHF

A

Improve diastolic function (decrease HR)
Beta blocker
Non-dihydropyridine
Use caution with diuretics

Nothing proven to improve mortality

38
Q

Who receives primary prevention for cholesterol/LDL

A

Patients without disease, goal is prevent the first event

Primary prevention consists of moderate intensity statins

39
Q

Who receives secondary prevention for cholesterol and LDL

A

Patients with CV disease and less than 75 yrs old

Secondary prevention consists of high intensity statins

40
Q

What is the most common pharmacologic tx for secondary prevention and high intensity statin?

A

Atorvastatin 40-80mg

41
Q

What is the most common pharmacologic tx for moderate intensity and primary prevention?

A

Atorvastatin 10-20mg
Rosuvastatin 5-10mg
Simvastatin 20-40mg

42
Q

Clinical signs/sx of hepatotoxicity

A

Prolonged flu like sx
Fatigue, anorexia, wt loss, fever, dark urine, jaundice
elevated LFT and T Bili

43
Q

How often do you draw LFT to monitor the liver?

A

First baseline LFT before tx
Get one 4-8 wks
Monitor for hepatotoxicity for vague flu like sx

Do not do serial LFTs

44
Q

Is isolated increase in LFT ok?

A

Yes
Expect LFT to rise because statins are metabolized and work in the liver
If also increased t bili then liver could be damaged

45
Q

LFT parameters with statin therapy

A

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

46
Q

Do you monitor for CPK?

A

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

47
Q

What are clinical signs/sx of myositis?

A

Fever, muscle aches, cramps, stomach pain, hematuria, reduction in urination, dark urine

48
Q

What are factors that increase risk of myositis/rhabdomyolysis?

A 
DI that increase levels of statins 
Renal insufficiency 
Hepatic insufficiency 
Combination of fibrates/niacin 
Elderly 
Etoh abuse 
Hypothyroidism 
DM
Muscle disorders
49
Q

What do statins lower?

A

Statins lower LDL

triglycerides

50
Q

What is the most common statin?

A

Atorvastatin

Moderate risk of DI
Bioavailability of 14% - need higher dose with lower bioavailability

Nursing Pharmacology (2 decks)

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