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12. Pharmacology > Inotropic drugs > Flashcards

Inotropic drugs Flashcards

1
Q

Inotropic drugs: broad categories

A

B agonists
Digitalis compound
PDEi
Ca2+ sensitizers

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2
Q

B agonist MOA

A
  • Sympathomimetic drug: bind B-R in cardiac nodal, conducting system and myocytes
    o ↑Ca2+ availability via cAMP
  • Limited efficacy in B-R downregulation: 24-72h
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3
Q

Natural B-R ligands

A

NE from ∑ nerves or in systemic circulation

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4
Q

B-R types

A

o B1-R = heart muscle
o B2-R = vascular and bronchial SM
o B3-R = endothelial

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5
Q

B1-R effects

A

 Heart: positive inotrope, dromotrope, chronotrope and lusitrope
 Kidneys: renin release → Ang II + aldosterone release

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6
Q

B2-R effects

A

 Bronchodilation
 ↑ blood glucose
* Hepatic glycogenolysis
* Pancreatic release of glucagon

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7
Q

B agonist drugs

A

Epinephrine
NE
Dopamine
Dobutamine
Isoproterenol

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8
Q

Epinephrine: which R action

A

o Beta selective: B1 = B2 > α1 = α2

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9
Q

Epinephrine: effect depend on

A

dose
 Low dose → cardiac stimulation and vasodilation
 High dose → vasoconstriction
* α = β selectivity

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10
Q

Epinephrine: indication

A

anaphylactic, cardiogenic shock, cardiac arrest

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11
Q

NE: which R action

A

o R-1 selective: B1 = α1 > β2 = α2

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12
Q

NE: side effects

A

o Reflex bradycardia → mask direct effects on SA node

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13
Q

NE: indications

A

septic shock, severe hypotension

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14
Q

Dopamine: dose

A

2-8mcg/kg/min

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15
Q

Dopamine: which R action

A

o Beta selective: B1 = B2 > α1

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16
Q

Dopamine: MOA

A

o Biosynthetic precursor of NE → stimulate NE release

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17
Q

Dopamine: effect depend on

A

o Effect depend on dose
 Low dose (<5mcg/kg/min): ↑ contractility and ↓ SVR
* Selective vasodilation from peripheral dopamine R: renal (D1-R), mesenteric, coronary, cerebral vascular beds → improve blood flow
 High dose: vasoconstriction
* Will bind to lower affinity α-R

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18
Q

Dopamine: indications

A

acute CHF, cardiogenic shock

19
Q

Dobutamine: dose

A

5-15mcg/kg/min

20
Q

Dobutamine: which R action

A

o B-1 selective: B1 > B2 > α1

21
Q

Dobutamine: net effect

A

cardiac stimulation, modest vasodilation, little change in HR or afterload

22
Q

Dobutamine: indications

A

CHF, cardiogenic shock

23
Q

Isoproterenol: net effect

A

cardiac stimulation, vasodilation with little change in pressure

24
Q

Isoproterenol: indications

A

bradycardia, AVB

25
Q

PharmacoK B agonists

A
  • Dobutamine/dopamine: synthetic catecholamines
    o Short ½ life → short term IV use
26
Q

Digitalis compound MOA

A
  • Inhibit Na+/K+ ATPase on sarcolemma of myocytes
    o Bind site where K+ attach
    o Activate Na+/Ca2+ exchanger → ↑ intracell [Ca2+] + ↑ Ca2+ release from SR
     ↑ Ca2+ available to bind Troponin C → ↑ contractility

o Depolarization → SM contraction → vasoconstriction

  • ↑ vagal afferent activity = p∑ activation:
    o ↓ SA node firing rate → negative chronotrope
    o ↓ AV node conduction velocity and prolong refractoriness → negative dromotrope
27
Q

Normal action of Na+/K+ ATPase

A

normally move K+ in, Na+ out → maintain resting membrane potential
* Inhibition leads to ↑[Na+] intracell

28
Q

Normal action of Na+/Ca2+ exch

A

normally move Ca2+ out and Na+ in
* Intracell [Na+] compete for intracell [Ca2+]
* As [Na+] ↑ → ↓ concentration gradient driving Na+ into cell
o ↓ activity of exchanger → ↑[Ca2+]

29
Q

Inotrope effect of digitalis vs B agonist

A
  • Positive inotrope effect is 1/3 of effect seen w B agonists
30
Q

1/2 life digitalis

A

Long → necessitate constant dosing to reach therapeutic plasma levels
o Digoxin: 40h
o Digitoxin: 160h
o Ouabain: 20h
o Digitalization: loading doses to ↑ plasma levels rapidly

31
Q

Digitalis: toxicity dose

A
  • Toxicity >2.0ng/ml
    o Narrow therapeutic safety window: 0.5-1.5ng/ml

o Can take days for levels to ↓

32
Q

Digitalis: what can potentiate toxicity

A

o HypoK+: potentiate toxicity
 Compete for binding sites
 ↑ # of sites available

33
Q

C/s digitalis

A

 GI dysfunction: anorexia, vomiting
* Effects on chemoR in area postrema in medulla

 Neurologic signs: depression, disorientation, delirium

 Myocardial toxicity: arrhythmias
* Slow conduction + alter refractory period of myocardial cells
o ↑ risk for re-entrant arrhythmias
* High doses → ↑∑ activity to heart → ↑ normal automaticity
* Promote abnormal automaticity in myocardial cells
* DADs from Ca2+ overload
o Especially in myocardium w structural changes (stretch)
o HypoK+ environment
* Bradyarrhythmias: AVB, sinus brady, sinus arrest

34
Q

Treatment digitalis tox

A

 Digibind (Immune Fab): ↓ plasma digoxin levels
 K+ supplementation: reverse toxic effects related to hypoK+

35
Q

Oral bioavailability digitalis

A

 Digoxin:75%, 27% bound to albumin
 Digitoxin: >90%
 Ouabain: 0%

36
Q

Elimination digitalis

A

 Digoxin: renal
 Digitoxin: hepatic
 Ouabain: renal

37
Q

Drug interactions digitalis

A
  • Class IA anti arrhythmic: Quinidine
    o Compete w digoxin binding site
  • ↓ Renal clearance → can lead to toxicity (↓ dose by 50%)
  • Ca2+ channel blockers = similar mechanism
  • NSAIDs = similar mechanism
  • Amiodarone
  • Beta blockers
  • Diuretics: indirect interaction
    o Potential to ↓ K+ levels → ↑ digoxin binding to Na+/K+ ATPase pump
    o ↑ therapeutic/toxic effects
  • Hyper Ca2+ → ↑ intracell Ca2+ → Ca2+ overload → ↑ susceptibility to arrhythmias
38
Q

PDE3i: drugs

A

Pimobendan, milrinone, amrinone

39
Q

PDE3i MOA and effect

A

inhibit PDE3 enzyme
o Responsible for breaking down cAMP
o Effect: ↑ cAMP levels
 ↑ inotropy, chronotropy, dromotropy
 Vasodilation

40
Q

PDE5i drugs

A

Sildenafil, tadalafil

41
Q

PDE5i: MOA and effect

A
  • Mechanism: inhibit PDE5 enzyme
    o Responsible for breaking down cGMP
    o Effect: ↑ cGMP levels → ↑ NO and ↓[Ca2+]
     SM relaxation → vasodilation
42
Q

Ca2+ sensitizers drugs

A

Pimobendan, levosimendan

43
Q

Ca2+ sensitizers effect

A
  • ↑ sensitivity of Troponin-C to Ca2+ → ↑ contractility

12. Pharmacology (10 decks)

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