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Cardiology > Inotropes > Flashcards

Inotropes Flashcards

1
Q

What is digoxin?

A

Cardiac glycoside that competes with K+ and blocks Na+/K+ pump leaving more Na+ in the cell to pump out in exchange for Ca2+ on Na/Ca exchanger

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2
Q

Does digoxin inc HR?

A

No, inc inotropy w/o inc in HR

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3
Q

List some pharmacological properties of digoxin

A
  • long half-life
  • oral
  • Quick onset
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4
Q

How is digoxin eliminated?

A

Renal

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5
Q

What does digoxin do to the CO?

A

Inc

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6
Q

What does digoxin do to the LVEF?

A

inc

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7
Q

What does digoxin do to the LVEDP?

A

Decrease (ie preload)

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8
Q

What does digoxin do to exercise tolerance?

A

Inc

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9
Q

What does digoxin do to natriuresis?

A

Inc (Excretion of Na and H2O from kidney)

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10
Q

What does digoxin do to the neurohormonal activation?

A

Dec

-Hrt works better, body doesn’t need as many hormones

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11
Q

What does digoxin do to the levels of plasma norpei

A

Dec

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12
Q

What does digoxin do to the peripheral NS activation?

A

dec

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13
Q

What does digoxin do to the RAAS activity?

A

Dec

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14
Q

What does digoxin do to vagal tone?

A

Increases, helps with HR control and normalizes arterial baroreceptors (were desensitized before administration of drug–>drug dec preload)

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15
Q

What is digoxin’s effects on the Atrial and AV node?

A

Decreases “automaticity” via increase in vagal tone and decrease in sympathetic activity (i.e. dec how quickly cells can cycle and fire again)

Increases refractory period of AV node in toxicity (high levels) and can lead to bradycardia and heart block

–>i.e. increase in PR invterval

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16
Q

What are digoxin’s effects on the ventricles?

A

Increases isotropy at therapeutic doses

At toxic doses, can inc sympathetic tone and directly inc automaticity leading to increased risk of ventricular tachycardia and fibrillation

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17
Q

What are inotropes?

A

Agents that increase cardiac contractility for our purposes by increasing intracellular Ca2+ and cAMP

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18
Q

Why are inotropes helpful in HF?

A

In HF, there is a reduction in the rate and extent of Ca2+ delivery to myofilaments, resulting in reduced contractility

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19
Q

What do inotropes do to the frank-starling curve?

A

Shifts them upward and left (greater end diastolic volume/preload and greater SV)

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20
Q

What are the clinical uses of Digoxin?

A
  • A fib with rapid ventricular response (increase AV nodal refractory period, more effective at rest than with exercise)
  • CHF symptoms despite medical therapy (don’t give an asymptomatic person the drug because you’ll only get the negative effects without the pos dec in symptoms)
  • Can be combined with other drugs
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21
Q

What are the negative long term effects of digoxin?

A

Increased MIs

More serious arrhythmias–vent tacky or fib

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22
Q

What are the positive long term effects of digoxin?

A

Fewer hx admissions for heart failure

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23
Q

What factors predispose people to digoxin toxicity?

A

Hypokalemia, hypomg, hypothyroidism, hypoxia

Drug interactions are common!

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24
Q

What are the contraindications for digoxin?

A
  • Advanced AV block without a pacemaker (will cause complete heart block)
  • Bradycardia or sick sinus syndrome without a pacemaker
  • Ventricular arrhythmias
  • Marked hypokalemia
  • Wolf-Parkinson-White with atria fibrillation (increases conduction through the bypass tract)
25
Q

What are the cardiac consequences of digoxin toxicity?

A

Arrhythmias:

  • Ventricular–>PVCs, tachycardia, fib
  • Supravent–>premature atrial contractions and supraventricular tachycarida

Blocks:
-SA and/or AV

Heart Failure Exacerbation
-Typically due to heart block/bradycardia

26
Q

What are the extra cardiac consequences of digoxin?

A

GI: nausea, vomiting, diarrhea

Nervous: depression, disorientation, paresthesias

Visual: blurred vision, scotomas, yellow-green vision

Hyperestrogenism: Gynecomastia, galactorrhea

27
Q

How do you treat digoxin toxicity?

A
  • Antibody rapidly reverses inhibition of myocardial sodium pump
  • Avoid hypo or hyperkalemia
28
Q

Where are the catecholamine effects on peripheral excitatory action on smooth muscle?

A
  • BVs of skin and mucous membranes

- Salivary and sweat glands

29
Q

Where do catecholamines have peripheral inhibitory action?

A

Gut, bronchial tree, BVs in skeletal muscle

30
Q

Catecholamine actions on metabolic activity

A
  • inc glycogenolysis in liver and muscle

- liberation of free fatty acids from adipose

31
Q

Catecholamine actions on endocrine activity

A

Modulation of insulin, renin, pituitary actions

32
Q

Catecholamine actions on CNS

A

Resp stim, inc wakefulness, dec appetite

33
Q

Where is beta 1 located?

A

Myocardium, SA node, AV node

34
Q

Where is beta 2 located?

A

Arterioles, lungs

35
Q

Where is alpha located?

A

Peripheral arterioles

36
Q

What neurohormone usually stimulates SNS?

A

Norepi

37
Q

What triggers eli and norepi release?

A

Stress causes release from adrenal medulla

38
Q

Where does dopamine have its effects?

A

CNS and periphery

39
Q

What are the dose-dependent responses of dopamine?

A
  • DA1 receptor: low dose, post-synaptic–>vasodilation of renal, mesenteric, coronary and cerebral
  • DA2 receptor: medium dose, pre-synaptic–>inhibits re-uptake of norepi allowing for indirect beta stimulation
  • Beta1 and Alpha receptors stimulated directly at high dose
40
Q

What is the half life of dopamine?

A

Very short!

41
Q

Dopamine side effects

A
  • Tachycardia (as dose inc)
  • Hypertension
  • Nausea/vomiting
  • Infiltration of IV site can lead to necrosis of skin or gangrene of fingers/toes (large vasoconstriction if dopamine binds)
42
Q

What is dobutamine?

A

A synthetic catecholamine

43
Q

How does dobutamine work?

A

Decreases afterload while increasing inotropy, esp at low doses and has beta and alpha adrenergic activity- (more isotropy than vasodilation)

44
Q

Side effects of dobutamine

A
  • Arrhythmias
  • Ischemia/angina
  • Hypotension
  • Tachycardia
  • Rapid vent response to a fib due to inc in A-V conduction
  • Nausea, headache, palpitations
45
Q

How can dobutamine be used as a diagnostic agent?

A

You can take advantage of the ischemic potential of dobutamine to diagnose coronary disease. It’s like pharma stimulating exercise. See what parts of the heart are not being perfused when it squeezes harder

46
Q

When do we use epinephrine?

A

After cardiopulmonary bypass or in resuscitations. Useful in denervated post-transplanted heart to stimulate rhythm

47
Q

How long is the epinephrine half life?

A

Very short!

48
Q

What are the side effects of epinephrine?

A

Tachycardia, ischemia, platelet agg and infarction, anxiety, fear, restlessness

49
Q

What does norepi do.?

A

Powerful vasoconstrictor, but only modest inotrope

50
Q

What is isoproterenol?

A

Non-selective beta agonist with powerful chronotropic effect

51
Q

When is isoproterenol used?

A

After heart transplant to drive HR and decrease pul vasc resistance

52
Q

What are phosphodiesterase inhibitors?

A

Type III: associated with the sarcoplasmic reticulum, increasing contractility without an increase in HR, esp at low dose. Act independently of beta receptors

They are potent vasodilators and therefore decrease preload

53
Q

Why don’t we use amrinone often?

A

Can cause significant thrombocytopenia

54
Q

How is milrinone eliminated?

A

Kidneys!

55
Q

What was the disappointment with PDE inhibitors?

A

they increase mortality

56
Q

What is vesnarinone?

A

PDE inhibitor inotrope and type III atriarrhythmic

57
Q

What is a problem with vesnarinone?

A

Improves quality of life, but inc morality and risks of arrhythmias

58
Q

Why use beta-adrenergic inotropic therapy in HF?

A

Increase contractility

59
Q

Why not use beta-adrenergic inotropic therapy in HF?

A
  • Weak vasodilator
  • Worsens diastolic fxn
  • Proarrythmic potential
  • Tachycardia
  • Desensitization/tachyphylaxis

Cardiology (16 decks)

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