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Cardiovascular Medicine > Heart Failure Pharm > Flashcards

Heart Failure Pharm Flashcards

1
Q

3 top causes of heart failure?

A

CAD/MI, HTN, and Diabetes

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2
Q

Systolic Heart failure is defined as what?

A

Can’t pump. EF usually less than 50%.

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3
Q

Diastolic heart failure is described as what?

A

Can’t fill, heart is too stiff.

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4
Q

What gender is Diastolic heart failure more common in?

A

Females

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5
Q

3 cardinal symptoms of HF?

A

Dyspnea, fatigue, and edema.

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6
Q

Briefly explain the viscous cycle of heart failure?

A

Chronic activation of sympathetic division and RAAS leading to cardiac remodeling, loss of myocytes, hypertrophy and fibrosis.

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7
Q

What 4 things are we looking to do with heart failure drugs?

A

Lower heart work/demand, get rid of edema, improve contractility of the heart, lower the rate of cardiac remodeling.

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8
Q

What are the three compensatory mechanisms of heart failure?

A

Increased sympathetic activity, RAAS, and hypertrophy

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9
Q

Explain what is happening with the increase in sympathetic activity and how, in the setting of HF, actually can be a problem?

A

Through beta receptors, you can increase HR and contractility to increase CO. Through adrenergic receptors, you can vasoconstrict to increase VR, which increases Preload which will increase SV and CO. In heart failure, this puts increased demand/work on the heart.

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10
Q

Explain whats going on with RAAS and how, in the setting of heart failure, its a problem?

A

Reduced blood flow to the kidney releases renin which leads to angiotensin 2 and aldosterone. We get vasoconstriction which leads to increased afterload and retention of sodium and water leading to increased BV. The increased afterload puts more demand/work. The heart is not strong enough to pump out the increase BV so we get lots of edema, especially pulmonary edema.

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11
Q

Explain the problem with hypertrophy?

A

At first it is great because it is providing a stronger contraction. Over time though it can stretch too much, become too stiff, or even fibrotic. This can lead to a systolic heart failure where the LV cant pump effective enough or a diastolic heart failure where it loses its ability to adequately fill.

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12
Q

What is the difference between compensated and de compensated heart failure?

A

Compensated is where the responses can restore CO and decompensated is when the response cannot restore CO.

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13
Q

What are the three drug families inhibiting the RAAS system?

A

ARBS and ACE inhibitors and aldosterone antagonist

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14
Q

What are the respective endings for ACEI and ARBS?

A

Prils and Sartans

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15
Q

What are the 3 major effects of ACEIs?

A

No a2, lots of bradykinin and no aldosterone

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16
Q

What are the 3 effects ACEIs have on the heart?

A

Because no A2, there is a drop in vascular resistance which means decreased after load and preload leading to increased CO.
Drop in aldosterone reduces the retention of more fluid.
Less bad heart remodeling.

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17
Q

What is the big time indication for ACEI?

A

Systolic heart failure or left sided heart failure.

18
Q

2 adverse effects of ace inhibitors?

A

Cough and angioedema

19
Q

MOA for ARBs, effects on the heart and when do we use them for patients?

A

Block angiotensin 2 receptor. Same effects as ACEI, they drop afterload and preload and increase CO. We use these in replace of ACEI if the patient has angioedema and cough.

20
Q

What is noteworthy to remember about losartan, valsartan, and candesartan?

A

High first pass effect. Not a pro drug. Irreversible binding.

21
Q

4 patients we probably shouldn’t use ACEI or ARBS in?

A

Pregnant, Hypotensive, hyperkalemia, and high serum creatinine

22
Q

What is the thought process behind using a beta blocker for heart failure?

A

Prevent the problems due to chronic activation of the sympathetic division

23
Q

4 positive effects on the heart due to a beta blocker?

A

Drops HR, drops oxygen consumption, reduces renin, and limits bad heart remodeling (hypertrophy and cell death).

24
Q

Why will diastolic heart failure patients benefit from a beta blocker?

A

They will benefit from the lower heart rate.

25
Q

Indication for a beta blocker?

A

All patients with chronic, stable heart failure.

26
Q

What patients get a beta blocker with their ACEI?

A

Patients with left ventricular systolic dysfunction caused by MI

27
Q

What specific indication is for eplerenone?

A

Post MI heart failure

28
Q

Besides reducing volume from blocking aldosterone, what 3 positive effects does spironolactone exert on the heart?

A

Lowers heart fibrosis, reduces early morning rise of HR, reduces mortality and morbidity

29
Q

What is the aldosterone antagonists indicated for but why aren’t they used?

A

Symptomatic HF with reduced systolic function but not used because of fear of hyperkalemia.

30
Q

What is the effect on heart failure of using a diuretic?

A

Clear up the edema. Drop blood volume which can drop preload and afterload.

31
Q

What is the most common family of diuretics used in heart failure?

A

Loop diuretics.

32
Q

What is the reasoning behind relieving congestion of the heart?

A

You are returning the muscle fibers back to optimal length.

33
Q

What is the order of diuretics to use for HF?

A

Loop, potassium sparing, and then thiazides

34
Q

Why are vasodilators used for HF?

A

They dilate out the venous side and lower preload so lower heart work.

35
Q

What two drugs are used in combo as a VD and why?

A

Iso dinitrate and hydralazine. Iso lowers preload by dilating out veins. Hydra dilates out arteries to decrease afterload.

36
Q

This combo drug is great for which race?

A

AA

37
Q

What are the there inotropic drug families he wants us to know and what is its MOA for the first one?

A

Digoxin and beta agonist and PDEI. It blocks the pump, so there is an increase in intracellular calcium because the sodium calcium exchanger ain’t working. leads to increased contractility.

38
Q

What is an added benefit to using digoxin?

A

It directly suppresses AV node conduction By increasing vagal tone, so it lowers HR and can help with Afib.

39
Q

What is a big time drug interactions with digoxin and why?

A

Diuretics causing low potassium because it leads to digoxin toxicity because it competes with potassium.

40
Q

2 beta agonist he wants us to know and in what clinical setting are they used and what is their MOA?

A

Dobutamine and dopamine. Rescue therapy in the ED. Increase cAMP leading to increased calcium and contractility.

41
Q

MOA of of PDE inhibitors?

A

Increase cAMP leading to increased calcium and contractility

42
Q

What 3 drug families to avoid in HF treatment?

A

Calcium channel blockers, NSAIDS and class 1 anti arr

Cardiovascular Medicine (25 decks)

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