21-31 - Heart Failure Flashcards

1
Q

bowditch phenomenon

A

icnreases in heart rate cause an increase in contractility ( saves CO - filling time issues)

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2
Q

frank-starling mechanism

A

increases in preload increase the contractility

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3
Q

Anrep =

A

if you increase the afterload, contractility will increase

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4
Q

in the excited state ____- preload is needed to increase SV because of changes in contractility

A

smaller preload to get same increase in SV

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5
Q

main cause CHF

A

cardiac remodeling

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6
Q

high risk for developing HF

A

stage A

  • HTN
  • CAD
  • DM
  • family hx
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7
Q

asymptomatic HF

A

stage B

  • previous MI
  • LV systolic dysfunction
  • asymptomatic valvular disease
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8
Q

symptomatic HF

A

stage C

  • known structural heart disease
  • SOB and fatigue
  • reduced exercise tolerance
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9
Q

refractory end-stage HF

A

stage D

  • marked symptoms at rest despite maximal medical therapy
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10
Q

drug at all stages of HF

A

ACEi or ARB

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11
Q

drug starting at stage B of HF

A

b- blocker

added to ACEi or ARB

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12
Q

drug starting at stage C of HF

A

lots, notably Diuretics and Digoxin added to ACEi or ARB

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13
Q

symptomatic HF, african-american race

A

hydralazine and nitrates and ACEi and B blocker

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14
Q

symptomatic HF with afib

A

digoxin
ACEi
b-blocker

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15
Q

drug that is bridge to transplantation or end of life

A

positive ionotropes

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16
Q

4 practical approaches to increase intrinsic myocardial contractility

A
  1. increase cytosolic Ca2+
  2. increase myocardial cAMP
  3. agonism of B1 receptors
  4. increase B1 receptor density
17
Q

what drugs increase B1 receptor density?

A

b1 adrenergic antagonists

18
Q

example b adrenergic agonists

A

dobutamin, epinepthrin, NE, dopamine

19
Q

what drugs increase myocardial cAMP

A

phosphodiesterase inhibitors

amrinone, milrinone

20
Q

what drugs increase cytosolic Ca2+

A

cardiac glycosides

digoxin

21
Q

MOA digoxin

A

blocks Na/K ATPase to increase intracellular sodium and extracellular Ca2+

22
Q

positive ionotropic effects of digoxin

A

decrease EDV and ESV

decrease systemic and pulmonary venous pressure

decrease SANS

23
Q

digoxin has a ____ vagal effect

A

direct –> increases vagal tone

24
Q

how does digoxin affect coronary flow

A

increases it (by decrease hypertrophy)

25
Q

adverse effect of digoxin

A

proarrhythmic

need to watch K levels

26
Q

pharmacokinetics of digoxin

A

7 days to reach steady state

excreted by kidney

27
Q

what inactivates digoxin

A

eubacterium lentum

and cimetidine

28
Q

early sign of difitalis intoxication

A

anorexia, nausea, vomiting, visual change

you will see arrhythmia later

monitor K values!

29
Q

does digoxin improve mortality?

A

no

30
Q

I gave the pt too much digoxin - help!

A

cholestyaramin or digoxin immune Fab

31
Q

MOA phsophodiesterase 3 inhibitors

A

block type III phosphodiesterase activity leading to an incrrease in caMP and –> vasodiltation, positive ionotropic and lusitropic effects

32
Q

phosphodiesterase 3 inhibitors work downstream of what drug

A

b agonsits

33
Q

what are the two phosphodiesterase 3 inhibitors?

A

inamrinone

milrinone

34
Q

how do inamrinone and milrinone increase CO?

A
  • directly stimualte myocardial contractility
  • accelerate relaxation
  • balance arterial and venous dialtion to decrease filling pressure
35
Q

indication for inamrinone and milrinone

A

short term circulation support in advanced CHF