Ionotropic Drugs: Limitations in Heart Failure Flashcards

1
Q

What does digoxin do?

A

decrease chronotropy/ increase ionotropy (weak)

  1. ^ baroreceptor activity > blocks NE > shuts off sympathetic system&raquo_space; decreased HR
  2. Blocks Na/ K ATPase > increase intracellular Na > less Ca exchanged out of cell&raquo_space; more Ca
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2
Q

How is digoxin excreted?

A

Renally

  • careful with patients with renal dysfxn
  • long half life - 7 days to steady state!
  • metabolism = P-glycoprotein
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3
Q

It’s important to monitor digoxin, what serum levels are desired (and don’t kill patient)?

A

.5 - 1 ng/ml

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4
Q

Who would you give digoxin to?

A
  • Patients with HFrEF, who aren’t responding well to treatment with ACEI/ ARBs, Beta blockers, diuretics
  • All patients with sever HF symptoms
  • No benefit in HFpEF!
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5
Q

When do you check digoxin serum levels?

A

7 - 14 days after starting therapy

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6
Q

What are the toxicities with digoxin?

A
  • Heart block, bradycardia, arrythmia
  • GI upset
  • seeing blue/ green halos
  • hyperkalemia
  • confusion
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7
Q

How does taking antiarrythmics affect your digoxin dosing?

A

They inhibit P-gp

-you should reduce digoxin dose by 50%

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8
Q

What other medications can adversely affect digoxin levels?

A
  • Azole antifungals
  • Calcium channel blockers (verapamil)
  • Macrolides
  • quinine

*inhibitors of P-gp
Induces: rifampin, St. John’s Wort

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9
Q

What effects do potassium, calcium, and magnesium have on digitoxin toxicity?

A

Toxicity from:

  • hypercalcemia
  • hypokalemia
  • hypomagnesemia
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10
Q

What medication can you give in the ER to someone who has digoxin toxicity?

A

Digoxin immune fab (ovine)

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11
Q

What happens if you stop digoxin treatment instantly?

A

Exercise intolerance

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12
Q

T/F: Digoxin reduces mortality

A

False- only reduces hospitalization

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13
Q

Name the two big inotrope medications

A

Dobutamine

Milrinone

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14
Q

What patients generally get inotropic medicine?

A

Class III - “cold and dry” (hypoperfusion)

Class IV - “cold and wet” (hypoperfusion and congestion)

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15
Q

Contrast the biochemical mechanism of action of milrinone and dobutamine?

A

Milrinone: inhibits PDE > accumulation of Ca
Dobutamine: B1 agonist to stimulate G proteins > increase Ca

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16
Q

With each of the following, does milrinone or dobutamine have a stronger effect?

1) vasodilation
2) enhanced inotropy
3) increased heart rate
4) tacchyarrythmia

A

Dobutamine:
enhanced inotropy
increased HR
tacchyarrythmia

milrinone:
vasodilation

17
Q

Are inotropes for short-term or long-term use?

A

Short term

18
Q

Which inotrope has a shorter half life?

A

=Dobutamine: 2 minutes
-more rapid onset/ clearing

Milrinone: 1- 3 hours
-cleared by kidneys

19
Q

If you have a hypotensive patient, which inotrope would be better?

A

Dobutamine

*milrinone has more moderate vasodilation

20
Q

If your patient is taking beta blockers, which inotrope would you use?

A

Milrinone

*dobutamine is a beta agonist

21
Q

According to the Heart Failure Society of America, when should you consider giving inotropes?

A
  • Patients with advanced HF and low output syndrome
  • patients have marginal BP ( to relieve symptoms and improve end-organ function
  • *NOT LONG TERM
  • *MAKES THEM FEEL BETTER, BUT NO BETTER OUTCOMES
22
Q

Side effects of both?

A

Milrinone: HYPOTENSION, thrombocytopenia, tachycardia, arrythmia

Dobutamine: Angina, tachyarrythmia

23
Q

Alright Dopamine is also an inotrope, but we didn’t talk about it much. How does it work?

A

Norepinephrine precursor > stimulates adrenergic receptors

24
Q

Dopamine has dose dependent effects. Explain the effects at low, moderate, and high doses?

A

RIP:
Renal - low dose > dopaminergic
Inotrope - moderate dose > beta receptors
Pressor - high dose > alpha receptor