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Cardiology > Myocardial Inotropic Agents I and II > Flashcards

Myocardial Inotropic Agents I and II Flashcards

1
Q

By what mechanism do all FDA approved inotropes act?

A

by increasing intracellular calcium and cAMP

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2
Q

How does beta receptor modulation affect calcium levels in myocytes?

A

agonist activity at beta receptor can increase cAMP which increases calcium via PKA-mediated phosphorylation of phospholamban

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3
Q

How does PDE modulation affect calcium levels in myocytes?

A

PDE-3 inhibitors block degradation of cAMP to AMP allowing for greater PKA-mediated phosphorylation of phospholamban to increase calcium stores

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4
Q

What does addition of an inotrope do the starling curve (stroke volume vs. EDV/preload)?

A

moves curve up and to the left (improves contractility)

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5
Q

What does addition of a vasodilator do the starling curve (stroke volume vs. EDV/preload)?

A

moves curve up and to the left (improves contractility by reducing afterload)

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6
Q

What does addition of a vasodilator and inotrope do the starling curve (stroke volume vs. EDV/preload)?

A

moves curve up and to the left b/c of synergistic contractility improving effects of both drugs

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7
Q

What does addition of a diuretic do the starling curve (stroke volume vs. EDV/preload)?

A

shift along curve to left b/c reducing volume

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8
Q

What is the most commonly prescribed heart failure medicine and how does it work?

A

digoxin –> binds to Na/K atpase –> increases intracellular Na –> increased action by Na/Ca exchanger –> increased intracellular calcium causing increased inotropy without increasing HR

*upward and left shift of starling curve)

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9
Q

What do normal levels of extracellular potassium do to efficacy of digoxin?

A

reduces –> competitively decreases digoxin binding and may be protective in digoxin toxicity

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10
Q

What does hypokalemia do to efficacy of digoxin?

A

unlike at higher levels/normal potassium which is protective, hypokalemia may increase both effect and toxicity of digoxin

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11
Q

What is the concern with desensitization/tolerance of digoxin?

A

none –> it’s pretty unique in that you don’t get desensitized

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12
Q

How do low doses of digoxin affect mortality risk?

A

does not at LOW doses

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13
Q

How is digoxin administered and how is it cleared?

A

oral administration, renal elimination

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14
Q

What is the therapeutic level of digoxin?

A

.5-1 (some textbooks say up to 2 but that is dangerous) –> keep levels low!

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15
Q

Hemodynamic effects of digoxin

A

increased cardiac output, increased LV ejection fraction, increased exercise tolerance, increased natriuresis

decreased LVEDP/preload, decreased neurohormonal activation (reduce norepi, RAAS activity, increased vagal tone/normalization of baroreceptors)

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16
Q

Adverse effects of digoxin

A
  1. increased vagal tone reducing AV node automatcity leading to bradycardia and heart block
  2. at toxic doses, increase sympathetic tone and directly increase automaticity and delayed after polarizations leading to ventricular tachycardia and fibrillation
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17
Q

What was the main lesson from the dig trial?

A

you have to control digoxin dose for body surface area or you end up with lots of toxic side effects

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18
Q

Clinical uses of digoxin

A

a-fib with rapid ventricular response, CHF symptoms despite medical therapy

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19
Q

Why must we exercise caution when using digoxin with a beta blocker?

A

risk of bradycardia and heart block

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20
Q

Does the factor predispose or protect against digoxin toxicity? hypokalemia

A

predispose

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20
Q

Does the factor predispose or protect against digoxin toxicity? hypokalemia

A

predispose

21
Q

Does the factor predispose or protect against digoxin toxicity? hyperkalemia

A

predispose

21
Q

Does the factor predispose or protect against digoxin toxicity? hypomagnesia

A

predispose

22
Q

Does the factor predispose or protect against digoxin toxicity? hyperkalemia

A

protect

22
Q

Contraindications to digoxin use

A
  1. toxicity

without pacemakers:

  1. advanced av block
  2. bradcardia or sick sinus syndrome
  3. ventricular arrhythmias
  4. marked hypokalemia
  5. wolf-parkinson-white w/ afib
23
Q

Classic rhythm of digoxin toxcity

A

atrial tachycardia w/ av block

23
Q

Tx of digoxin toxicity

A

antibody to digoxin, increase potassium

24
Q

Does the factor predispose or protect against digoxin toxicity? hypoxia and acidosis

A

predispose

24
Q

Does the factor predispose or protect against digoxin toxicity? hypoxia and acidosis

A

predispose

25
Q

Contraindications to digoxin use

A
  1. toxicity

without pacemakers:

  1. advanced av block
  2. bradcardia or sick sinus syndrome
  3. ventricular arrhythmias
  4. marked hypokalemia
  5. wolf-parkinson-white w/ afib
26
Q

Classic rhythm of digoxin toxcity

A

atrial tachycardia w/ av block

27
Q

Tx of digoxin toxicity

A

antibody to digoxin, increase potassium

33
Q

Side effects of dopamine

A

dose dependent tachycardia, htn, nausea, iv site necrosis/gangrene due to alpha vasoconstriction

34
Q

Dopamine antidote

A

phentolamine

35
Q

What is the problem with continuous administration of dopamine or dobutamine?

A

desensitization

36
Q

How do beta blockers interact with dobutamine and dopamine?

A

beta blockers inhibit these drugs –> need higher doses of dobutamine/dopamine to overcome effect but also increase side effect risk

37
Q

Are dobutamine/dopamine short/long half life? is this good or bad?

A

short half life –> advantage b/c allows for real time monitoring/modulation

38
Q

Side effects of dobutamine

A

arrhythmia, ischemia/angina, hypOtension, tachycardia, rapid ventricular response in afib due to increase in AV conduction, nausea, headache

39
Q

Why is epinephrine not commonly used in heart failure therapy?

A

it is non selective and can lead to tachyphylaxis

40
Q

How does PDE3I differ in peripheral arterial system and in myocytes?

A

in myocytes–> upregulates cAMP to increase contractility but in peripheral arterial system cAMP reduces contractility/increases vasodilation

41
Q

How is the parameter affected by PDE3I? cardiac index

A

increased

42
Q

How is the parameter affected by PDE3I? SVR/MAP

A

decreased

43
Q

How is the parameter affected by PDE3I? PAWP/LVEDP

A

decreased

44
Q

How is the parameter affected by PDE3I? heart rate

A

not much change

45
Q

How is the parameter affected by PDE3I? ventricular dP/dT/performance

A

increased

46
Q

Side effects of PDE3I

A

hypotension if filling pressures are not elevated due to venodilator properties of inhibitors which drop pre/afterload simultaneously

47
Q

Main risk associated with amrinone

A

causes thrombocytopenia in pts with advanced heart failure

48
Q

Administration of milrinone

A

bolus + infusion but risk of bolus is acute hypotension

49
Q

Elimination of milrinone

A

kidney –> bad renal clearance in heart failure patients can reduce infusion rate

50
Q

How do oral PDE3I affect mortality?

A

increase mortality despite great hemodynamic effects in hospital

Cardiology (41 decks)

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