Lecture 4 - Heart Failure Drugs 2 Flashcards

(40 cards)

1
Q

List examples of B-blockers

A

Metoprolol, carvedilol

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2
Q

How are B-blockers usually administered to HF patients?

A

Low doses (0.1 x) gradually increased over weeks cause some but little hemodynamic depression

  • reduces heart rate and oxygen consumption
  • cardiac output is increased after several months

*chance of irregular heart beat reduced

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3
Q

When are B-blockers most effecting in HF patients?

A

post-MI

**Mortality reduced post-MI

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4
Q

Benefits of B-blockers?

A
  • decrease adverse effects of high catecholamine levels on the heart
  • decreased cardiomyocyte apoptosis (cell death)
  • decreased cardiac remodeling (decreased mitogenic activity)

*mechanism is not completely understood but clinical benefits are clear!

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5
Q

How does Carvedilol (B blocker) work?

A
  • blocks B and alpha receptors
  • alpha blockage helps to relax (dilate) arteries
  • the heart does not have to work as hard to eject blood
  • decreases afterload
  • B adrenergic receptor blockade slows the heart and decreases force of contraction
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6
Q

How does Metoprolol (B blocker) work?

A
  • similar benefits to carvedilol

- selectively blocks B1 adrenergic receptors

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7
Q

____ is a B1 selective B blocker

A

Metoprolol

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8
Q

In what kinds of patients should you avoid/caution B blockers with?

A

-asthma, COPD, peripheral vascular disease, insulin dependent diabetes, the very physically active

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9
Q

B blockers are good if what certain other diseases are present (i.e. they will treat both the HF and the other condition)

A
  • hypertension
  • glaucoma
  • certain arrhythmia
  • myocardial infarction
  • angina
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10
Q

Carvedilol interacts with _____ and will worsen breathing problems due to narrowing of airways

A

ventolin

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11
Q

Carvedilol and Metoprolol - interact with _____ (anti-hypertensive) and may cause irregular heartbeat

A

verapamil

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12
Q

B blockers and ____ medications could cause arrhythmia

A

antiretroviral

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13
Q

B blockers and ____ are dangerous since it is has additive effects of lowering blood pressure

A

alcohol

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14
Q

What are inotropes?

A

Agents which alter the force of contraction of the heart

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15
Q

Do we want positive or negative inotropes to treat HF?

A

positive

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16
Q

List 2 positive inotropes used in HF

A

digoxin

dobutamine

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17
Q

What effects do digoxin and dobutamine have?

A
  • increase contractility of the heart
  • symptomatic relief - long-term benefit unclear
  • chronic use associated with increased mortality
18
Q

Why don’t you want to use positive inotropes (digoxin, dobutamine) long term?

A

Positive inotropes increase strain on the heart, which is unfavourable. We want to reduce strain on the heart. Don’t want to use these long-term because of the increased strain on the heart.

19
Q

Dobutamine must be given by ____

20
Q

What does dobutamine do?

A

stimulates B1-adrenergic receptors in the heart to increase heart rate and more importantly, contractility

21
Q

Why must you carefully monitor dobutamine?

A
  • it may increase HR, myocardial oxygen, consumption and blood pressure
  • may aggravate ischema (inadequate blood supply to an organ) and provoke arrhythmias
22
Q

What does digoxin do?

A
  • increases heart contractility (increases calcium in myocardial cells)
  • blocks Na/K ATPase (intracellular calcium levels stay high)
23
Q

Why must you carefully monitor digoxin?

A
  • may increase HR, myocardial O2 consumption, BP

- may aggravate ischemia and provoke arrhythmias

24
Q

Digoxin provides symptomatic improvement: describe this

A
  • improved exercise capacity

- decreased hospitalization for heart failure

25
Digoxin does not improve _____
mortality
26
Digoxin does improve ____
QOL (quality of life)
27
Mechanism of action for Digoxin ?
increases calcium release for each beat
28
When on digoxin, must monitor _____ levels
potassium
29
____ increases digoxin toxicity
hypokalemia | *both inhibit the Na/K ATPase
30
____ use may produce hypokalemia and increase digoxin toxicity
diuretic
31
ACEi and ARBs or B blockers may _____ K+ levels
increase
32
What kind of diuretics do not cause hypokalemia??
potassium sparing diuretics (spironolactone) *not as good at increasing sodium excretion though
33
What type of drug interactions with digoxin can dangerously increase blood levels of digoxin and result in cardiac arrhythmias?
- common antibiotics such as amoxicillin and erythromycin | - the anti-arrhythmic agent amiodarone
34
Diuretics are discussed in this lecture, but i've already made flashcards on diuretics so go see those fam
alrighty
35
Describe the treatment of heart failure
1) Manage conditions that contribute to heart failure - identify and treat risk factors (hypertension, diabetes, lipids, etc) - diet, physical activity and lifestyle changes 2) Start with ACEi or B-blocker - lower BP and reduce stress on heart * if ACEi not tolerated, may switch to ARB 3) Diuretic - in patients with edema - Remove excess fluid and sodium from body 4) Extreme failure - add inotrope - Increase contractility to alleviate heart failure symptoms
36
How do you treat Stage A (High risk with no symptoms)?
Risk-factor reduction | Patient Education
37
How do you treat Stage B (Structural heart disease, no symptoms)?
ACEi or ARBs in all patients B blockers in selected patients
38
How do you treat Stage C (Structural heart disease, previous or current symptoms)?
ACEi and B blockers in all patients
39
Describe the sequence for a "typical" patient
1) Loop diuretic - act to rapidly control symptoms of volume overload (edema) - more important in overt heart failure - may not need early 2) ACEi - once diuretic therapy optimized if needed - start at low dose 3) B blocker - once patient is stable on ACEi - start at low dose 4) Inotropes - in those that have symptoms of HF in spite of above regimen
40
Read case studies at end of lecture
ok