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Cardiology > Inotropic agents > Flashcards

Inotropic agents Flashcards

1
Q

definition of contractility

A

-intrinsic property of cardiac muscle that determines the strength of contraction -independent of external loading, valve loading, valve function or filling pressure -cardiac performance is the entity which considers all of these parameters

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2
Q

All of the approved inotropes act by ________.

A

-increasing intracellular Ca (and cAMP) -the mechanisms by which additional Ca is released by SR varies with drugs and it is these mechanisms that determine potency and side effects

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3
Q

Famous example of cardiac glycoside

A

-digitalis aka digoxin

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4
Q

Digoxin, a cardiac glycoside inotrope, binds to what?

A

-binds to Na/K ATPase and blocks it; this causes Na to build up within the cell and turn on the Na/Ca exchanger. This exchanges Na with Ca, thus raising intracellular Ca which can increase contractility

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5
Q

Digoxin: effect on starling curve, inotropy, tolerance, mortality

A

-upward and left shift of starling -no desensitization/tolerance -increases inotropy WITHOUT increased HR - no increase in mortality at low doses

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6
Q

Digoxin structure

A

-lactone ring, steroid nucleus, sugar residues

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7
Q

Oral absorption, protein binding, half life, elimination, onset, max effect, duration, therapeutic level of digoxin

A

-60-75%; 25% protein bound -36 hr half life -RENAL elimination -5-30min onset via IV or 30-90 oral; max effect in 2-4 hrs IV and 3-6 oral -duration:2-6 days -Tx level 0.5-2 but really 0.5 to 1.0

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8
Q

Should you increase or decrease digoxin doses in pts with kidney disease?

A

-decreases!! it is renally excreted!

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9
Q

Digoxin hemodynamic effects

A

-increase CO -Increase LVEF -decrease LVEDP -increase exercise tolerance -inc natriuresis -decrease neurohormonal activation

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10
Q

Why are physicians not too worried about the increase in CO due to digoxin as further stressing an already failing heart?

A

-the increase in CO reduces the HR and PVR which offsets the increased myocardial demance for oxygen the increased contractility might create

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11
Q

Digoxin neurohormonal effects (5)

A

-decrease plasma NE: dec HR -decrease peripheral nervous system activity -decrease RAAS activity -increase VAGAL tone -normalizes arterial baroR

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12
Q

Digoxin EP properties

A

-affects atrial and ventricular muscle and pacemaker/conduction fibers differently due to direct effect of digoxin with neural effects -level of digoxin impacts which effects supercede

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13
Q

Digoxin effects on Atrial and AV node and ventricles

A

-atrial and AV: decreases automaticity via increase in vagal tone and decrease in sympathetic activity; increase refractory period of AV node (block/bradycardia issue in high doses) -ventricular tx doses increases inotropy while toxic doses can increase sympathetic tone and directly increase automaticity leading to risk of v. fib

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14
Q

Patients with CHF who had digoxin removed from their treatments did worse prognosis wise. Yet what was the overall mortality seen of digoxin in the DIG trial?

A

-no increase or decrease in mortality of pts vs placebo -survival similar to placebo, but have few hospitalizations for heart failure, more serious arrythmias (VT and V fib) and more MIs

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15
Q

Digoxin clinica uses

A

-A-fib with rapid ventricular response since it slows conduction in AV node; rate control; works better at rest than exercise -CHF symptoms despite medical therapy–NEED TO BE SYMPTOMATIC since it is beneficial in relieving symptoms -can be combined with other drugs

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16
Q

Goal levels of digoxin

A

-0.5- 1.0 to achieve benefit and avoid mortality

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17
Q

Factors predisposing to digoxin toxicity

A

-hypoK, hypoMg, hypothryoid, hypoxia -being on other drugs since drug interactions are VERY common!

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18
Q

Absolute and relative contraindications of digoxin

A

-absolute: digoxin toxicity -relative: advanced AV block without pacemaker, bradycardia or sick sinus without pacemaker, ventricular arrythmias or tachycardias, marked hypokalemia, Wolf-parkinson-white syndrome with a-fib since it will increase conduction through bypass tract which increases odds of ventricular arrhythmia

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19
Q

Digoxin toxicity locations

A

-cardiac: other card -GI: nausea, vomiting, diarrhea -CNS: depression, disorientation, paresthesias -Visual: blurred vision, scotomas, yellow-green vision -Hyperestrogenism: gynecomastia, galactorrhea

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20
Q

Digoxin cardiac toxicity

A
  1. arrhthmias: ventricular (PVCs, V Tach, V fib) or supraventricular: PAC, SVT 2. Blocks: SA and/or AV node blocks–MORE COMMONLY SEE THESE!! 3. Heart failure exacerbation: usually due to heart block/bradycardia
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21
Q

Treatment for digoxin toxicity

A

-specific antibody: Fab fragment directed against digoxin which rapidly reverses inhibiton of myocardial sodium pump -bound fragments excreted in urine -increase K to normal range to decrease digoxin binding to R but be careful not to overshoot

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22
Q

Stimulation of the SNS usually is mediated by what NT?

A

-NE

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23
Q

6 adrenergic agents and if used clinically

A
  1. dobutamine: yes 2. Dopamine: yes 3. Epinephrine: occassional 4. Isoproterenol: rarely 5. NE: occassional 6. Phenylephrine: yes(pressor!)
24
Q

What allows dopamine to be especially handy?

A

-it has an incredible short half life so it is easy to make changes to its dosing

25
Q

Affects of DA dosing

A

-at low doses: DA1R post synaptic leading to renal vasodilation and coronary and cerebral as well: renal dose dopamine -intermediate dose: DA2R (presynaptic) that inhibits NE reuptake (indirect B1 stimulation): inotrope!! -B1 and a receptors stimulated directly by high dose: pressor!!!

26
Q

Dopamine side effects

A

-tachycardia (as dose increases) -HTN -nausea/vomiting -infiltration of IV site can lead to necrosis of skin or gangrene of fingers/toes due to vasoconstriction

27
Q

Antidote for DA injection site skin necrosis

A

-Phentolamine

28
Q

Dobutamine effects at low doses

A

-decreases afterload while increasing inotrophy -racemic mixture of isomers

29
Q

Dobutamine dosing

A

-start at 2-3 ug/kg/min and titrate up to 20 max -continuous infusions causes desensitization -inhibited by B blockers so need higher doses here

30
Q

Dobutamine half life

A

short acting; T1/2= 2 min -works quickly, usually without much hypotension

31
Q

Dobutamine side effects

A

-arrythmias -ischemia/angina (can be used for stress test dx) -hypotension but less common than milrinone -tachycardia as dose increases -rapid ventricular response in a fib due to increase in AV conduction -nausea, headache, palpitations

32
Q

Dobutamine as diagnostic agent

A

-take advantage of ischemic potential of it to dx coronary disease -pharm. stimulate exercise–useful in pts who cannot walk or ride a bike

33
Q

T/F: Epinepherine is commonly used to treat CHF

A

false; used most commonly after cardiopulmonary bypass or in resuscitations -useful in denervated post-transplant heart

34
Q

Half life and dosing of Epi

A

-very short half life -0.05 to 0.5 ug/kg/min

35
Q

Side effects of epinepherine

A

-tachycardia -ischemia -platelet aggregation and infarction -anxiety, fear, restlessness

36
Q

Function of NE

A

-powerful vasoconstrictor but only modest inotrope (sepsis and cardiogenic shock) -0.5-12 u/min

37
Q

Does NE or Epi have more cardiac effects?

A

-Epi; NE basically is only a vasoconstrictor

38
Q

Isoproterenol function and clinical use

A

-non-selective B-agonist with powerful chronotropic effect -used almost exclusively after heart transplant to drive HR and decrease PVR -dose; 0.005 to 0.05 u/kg/min

39
Q

Phosphodiesterase type _____ is associated with the SR. Specific PDE inhibitors can increase ______ without an increase in _______.

A

-3 -contractility without increase in HR, esp at low doses

40
Q

How can PDE III Inhibitors not increase HR?

A

-they act independently of B receptors

41
Q

In addition to being inotropes and not chronotropes, what else are PDEI-3s?

A
  • potent vasodilators including the venous capacitance vessels and pulmonary vascular bed -increase SV and decrease afterload!
  • inotropic vasodilators
42
Q

PDEIs in decompensated heart failure

A
  • pharm effects should be beneficial in advanced HF
  • improved systolic and diastolic function
  • improved exercise tolerance
  • excellent venodilator and pulmonary vasodilator
  • inhibits platelet aggregation
  • may inhibit proinflammatory cytokine formation
43
Q

PDEI cautions

A

-can cause significant hypotension if filling pressures are not elevated due to the venodilator properties of PDEIs dropping preload

44
Q

Currently available PDEIs

A
  • amrinone
  • milrinone
  • both IV but oral PDEIs can be given now!
45
Q

Why is amrinone rarely used?

A
  • can cause significant thrombocytopenia especially in pts with advanced heart failure
  • less potent than milrinone
46
Q

Milrinone

A
  • more potent selective PDE III Inhibitor
  • long half life of 2.3 hours
  • recommended to give bolus loading dose followed by maintenance infusion but rarely do this at Penn bc of hypotension risks
47
Q

Milrinone elimination and implications

A

-80% eliminated by kidney (recall digoxin was too) so in renal failure patients, decrease in infusion rate by about 50%

48
Q

Vesnarinone

A
  • related to quinolinones
  • oral med!!
  • both PDEI inotrope and type III antiarrhthmic
  • does not increase HR!!–advantage!
  • increased risk of arrythmias including torsade de pointes–disadvantage
  • improved quality of life but increased mortality
49
Q

List 2 pros and cons of vesnarinone

A
  • oral PDEI
  • good: no increase in HR, improved QOL
  • bad: increased risk of arrhthmia including torsade de pointes, increased mortality
50
Q

Enoximone utility

A
  • low dose is safe in advanced heart failure but does not produce sufficient efficacy
  • therefore, not approved!
51
Q

Pros and Cons of B-adrenergic therapy in HF

A
  • pro: increased contractility
  • con: weak vasodilator properties, worsens diastolic function, proarrythmic potential, tachycardia, desensitization
52
Q

PDEI inotropic therapy pros and cons in decompensated HF

A
  • pro: increased contractility, improved diastolic function, veno/vasodilator (systemic and pulm), no tachyphylaxis, effective in setting of B blocker therapy
  • con: proarrhythmic potential, tachycardia, hypotenion, thrombocytopenia
53
Q

Not only have oral inotropes been associated with excess mortality, but acute and chronic IV injections of both ____ and ______ have been associated with excess mortality.

A
  • dobutamine
  • milrinone
54
Q

IV inotropic therapy patient selection

A
  • acute: decompensated with V overload and impaired perfusion, V overload with diuretic resistance and/or organ hypoperfusion–including low CO states
  • chronic: transplant listed recipients as a bridge; refractory HF sxs after maximal medical therapy as palliation
55
Q

3 classes of inotropic agents

A
  1. cardiac glycosides
  2. B-agonists
  3. PDEIs

Cardiology (27 decks)

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