Heart failure drugs Flashcards

1
Q

What is furosemides MOA?

A

inhibit Loop Na-K-2Cl transporter which will decrease preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is MOA of thiazides?

A

inhibit DCT NaCl transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the MOA for ACE inhibitors?

A

They block the ANG I from becoming ANG II

This allows for vasodilation which will decrease preload and afterload which allows the heart to work less and require less oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the MOA for ARBs?

A

Same as ACE basically but this time they block ANGII from binding to any of its sites. so they also decrease preload and afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do Neprilysin inhibitors work? (entresto)

A

Well with heart failure BNP is released which actually helps the heart but we have an enzyme that breaks it down. So Entresto which is Sacubitril and valsartan works by using Sacubitril to block the enzyme from breaking down BNP and Valsartan which is an ARB will block all ANGII receptors

BNP- widens blood vessels to help with ciculation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MOA of beta blockers?

A

Well B1 is stimulated by the SNS on the heart. If it is blocked the heart rate goes down. Heart goes down less stress on heart and less demand for O2.

In heart failure SNS will be stimulated because perfusion will be low so heart thinks it needs to pump more.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Between carvedilol, metoprolol and bisoprolol which one is non-selective?

A

carvedilol, this acts on alpha 1, beta 1, and beta 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Between carvedilol, metoprolol and bisoprolol which one is more specific for beta 1 receptor?

A

bisoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the MOA for hydralazine?

A

They open the arterial K+ channel which allows for vasodilation and decreases afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the MOA for isosorbide dinitrate?

A

the increase cGMP levels in veins causing vasodilation and decreasing preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the MOA for digoxin

A

It blocks the Na/K+ pump. This allows Ca+ to stay in the cell longer increasing contractility

Also stimulates PNS which decreases HR

also desensitizes BR responses decreasing the SNS response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Would you give someone a beta blocker who is in decompensated HF

A

No absolutely not it can make it worse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the MOA for dobutamine?

A

it increases contractility by acting as a beta 1 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the MOA for milrinone?

A

this is a PDE-3 inhibitor which increases cAMP levels which increases contractility and is also a vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What type of agents are dobutamine, milrinone, and digoxin

A

they are inotropic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the MOA for nitroprusside?

A

this converts NO in arterioles and veins which causes vasodilation and decreases preload and afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the MOA for nitroglycerin?

A

this works by increasing cGMP levels in veins causing venodilation which decreases preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What drugs decrease preload and afterload?

A
  1. ARBs
  2. Nitroprusside
  3. ACE inhibitors

Could be more but from his guide these one specifically say they decrease both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which of the two has a greater effect for blocking ANGII actions? The ACEi or ARB

A

The ARB does

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Would you use a beta blocker as a first line choice in Hf?

A

no, first you would get them stable on an ACEi and then add if need be a beta blocker starting at a low dose and titrate up slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which do you think digoxin would work better on. systolic heart failure or diastolic heart failure?

A

its systolic because it helps with contraction so the pumping out of blood

22
Q

When would you think about adding on a vasodilator like hydralazine or isosorbide dinitrate?

A

pretty far down the road. When pts who are on an ACEi and beta blocker but still suffer from HF symptoms seems to be more indicated in african americans

23
Q

Is dobutamine a drug you would use for any joe schmo who has heart failure?

A

No, it is generally used for pts who are in shock from severe decompensated HF. To help get these guys pumping some more blood “cold patient”

24
Q

If a pt has Afib and HF can digoxin be used as a first line agent?

A

Yes, but it is usually added on to those with systolic HF and symptoms persist on standard Tx

25
Q

If your rich and have HF what med would you want?

A

Entresto, this is a good med but its expensive

26
Q

Why would you put someone on an ARB?

A

primarily if they can not tolerate the ACEi

27
Q

If someone describes an acute DHF patient as warm and wet, what med should come to mind for you to use?

A

Nitroprusside along with a loop to get the water off them

Can also work for Cold and Wet with systolic pressure >90 mmhg

28
Q

If you had to use a diuretic for a heart failure pt which one would be the best choice?

A

loop diuretics, thiazides are generally insufficient

29
Q

Would aldosterone antagonists be used early or added on. If used as an add on when would you add it on?

A

They are usually added to tx if mod-severe symptoms still occur while a patient is taking an ACEi and Beta-blocker

30
Q

What is the one med every HF patient should be started on?

A

an ACEi, only ACEi increase bradykinin levels

31
Q

Adverse effects of furosemide?

A
  1. Hypokalemia
  2. increased gout risk
  3. decreased Mg, Ca levels
  4. ototoxicity w/ ethacrynic acid
32
Q

adverse effects of thiazides?

A
  1. Hypokalemia
  2. increased gout risk
  3. sulfa allergy
  4. Hyperglycemia and hyperlipidemia
33
Q

Adverse effects of aldosterone antagonists?

A
  1. Hyperkalemia ( to decrease chance of this, pt should have GFR >30)
  2. if they are on an ACEI or ARB and you want to add it they should have a K+ level < 5
  3. Gynecomastia
34
Q

Adverse effect of ACEI

A
  1. Cough
  2. Angioedema
  3. Hyperkalemia
  4. contraindicated for preggos
35
Q

Adverse reactions of ARBs

A
  1. Hyperkalemia
  2. no go for preggos

but no cough or angioedema

36
Q

adverse effect of Enresto?

A
  1. dizziness
  2. hypotension
  3. cough
  4. hyperkalemia
37
Q

Adverse effect of beta blokers?

A
  1. They can precipitate acute heart failure
  2. make asthma worse (bronchiospasm)
  3. may increase blood lipids and mask hypoglycemia
  4. sedation
  5. sleep disturbance
38
Q

Adverse effects of digoxin?

A
  1. N/V, anorexia, diarrhea are common
  2. Bradycardia
  3. Tachyarrhythmias (PVC’s and V Tach) increased risk if hypokalemia or epi use.
39
Q

OD treatment of digoxin?

A

So say someone digoxin levels where to high and then they went into V Tach, you would give them lidocaine

40
Q

For suicidal OD from digoxin what can you do?

A

Give digoxin antiboodies?

41
Q

Adverse effects of hydralazine?

A
  1. orthostatic Hypotension
  2. reflex tachy
  3. edema
42
Q

adverse effects of isosorbide dinitrate?

A
  1. Flushing
  2. Dizziness
  3. Reflex tachy
43
Q

Adverse effect of Milrinone?

A

ventricular-supraventricular arrhythmias

44
Q

How is hydralazine and isosorbide dinitrate taken?

A

As a combo drug TID

45
Q

How are metoprolol and carvedilol metabolized?

A

Hepatic- high 1st pass effect

Carvedilol is IR and taken BID

46
Q

How is entresto taken and metabolized?

A
  1. Taken orally BID

2. Metabolized to active metabolite

47
Q

How are ARBs taken and metabolized?

A
  1. Taken PO QD

2. metabolized to active metabolite

48
Q

How is digoxin eliminated?

A
  1. primarily renal elimination

2. T 1/2 life is 36-48 hrs (dependent on age, renal and cardiac function)

49
Q

Does the bioavailability of lasix decrease in HF

A

yep

50
Q

how is lisinopril taken and eliminated for HF pts

A

taken orally QD and renal excretion as unchanged drug