CHF + Lipids Flashcards

(50 cards)

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
When are ARBs not a good alternative to ACE inhibitors?
Ace inhibitor related angioedema Ace inhibitor related hyperkalemia Ace inhibitor related renal insufficiency
26
Neprilysin inhibitor MOA
Degrades vasoactive peptides such as natriuretic peptides and bradykinins Bradykinins vasodilate Natriuretic peptides help urinate
27
Would you or a cardiologist prescribe entresto/valsartan?
Cardio | In primary care you would start ACE inhibitor
28
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
29
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
30
Who is at risk for digoxin toxicity?
Dig is renally eliminated Elderly Hypokalemia Renal insufficiency
31
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
32
What is the therapeutic digoxin level for CHF?
<1
33
Vasodilator: Hydralazine
Arterial vasodilator | Decreases afterload
34
Vasodilator: isosorbide
Venous vasodilator | Decreases preload
35
What is BIDIL
Fixed combo of hydralazine + isosorbide Very expensive Approved for tx of CHF in African American patients vs ACE inhibitors
36
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
37
Pharmacological tx for diastolic CHF
Improve diastolic function (decrease HR) Beta blocker Non-dihydropyridine Use caution with diuretics Nothing proven to improve mortality
38
Who receives primary prevention for cholesterol/LDL
Patients without disease, goal is prevent the first event | Primary prevention consists of moderate intensity statins
39
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
40
What is the most common pharmacologic tx for secondary prevention and high intensity statin?
Atorvastatin 40-80mg
41
What is the most common pharmacologic tx for moderate intensity and primary prevention?
Atorvastatin 10-20mg Rosuvastatin 5-10mg Simvastatin 20-40mg
42
Clinical signs/sx of hepatotoxicity
Prolonged flu like sx Fatigue, anorexia, wt loss, fever, dark urine, jaundice elevated LFT and T Bili
43
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
44
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
45
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
46
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
47
What are clinical signs/sx of myositis?
Fever, muscle aches, cramps, stomach pain, hematuria, reduction in urination, dark urine
48
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 ```
49
What do statins lower?
Statins lower LDL | triglycerides
50
What is the most common statin?
Atorvastatin Moderate risk of DI Bioavailability of 14% - need higher dose with lower bioavailability