Drugs Used in Heart Failure I Flashcards

1
Q

heart failure

A

CO inadequate to proved O2 needed by body

CAD, MI, HTN, damaged valves, external pressure around heart, Vit B deficiency, cardiac muscle disease

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2
Q

decreased mortality in HF

A

ACE, ARBs, aldosterone antagonists, beta-blockers

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3
Q

Tx for symptoms of HF

A

volume overload - diuretics

myocardial dysfunction - positive inotropes

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4
Q

most efficacious for reducing volume overload

A

loop diuretics

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5
Q

loop diuretics

A

forusemide
bumetadine
ethacrynic acid (no sulfa)
torsemide

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6
Q

furosemide

A

loop diuretic
-inhibit Na, K, 2Cl cotransporter in thick ascending limb of loop of henle

decreased reabsorption of Ca and Mg

improve symptoms, NOT mortality

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7
Q

ethacrynic acid

A

loop diuretic - no sulfa allergy

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8
Q

adverse of loops

A
hypokalemia
alkalosis
hypocalcemia
hypomagnesemia
hyperuricemia
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9
Q

hypercalcemic state

A

loop diuretic

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10
Q

nagging cough and swollen tongue

A

ACE inhibitor

angioedema

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11
Q

combination with furosemide to control BP and edema in CHF patient

A

losartan

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12
Q

ACE and ARBs

A

reduce mortality for CHF***

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13
Q

ANG II

A

blocked by ACE and ARB

vasoconstrictor
Na/water retention
increased aldosterone
catecholamine release
arrhythmias
hypertrophy of cardiac
myocyte death
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14
Q

HF drug - symptoms first worse and then better

A

beta blocker

3-6 months

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15
Q

beta blocker

A

reduce symptoms AND improve mortality in HF patients

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16
Q

beta blockers in HF

A

increased CO initially

  • dowregulation of beta receptors
  • reduced responsive myocardium

low dose beta blockers***
-increased EF, slow HR, reduce symptoms and mortality

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17
Q

spironolactone

A

aldosterone antagonist

18
Q

eplerone

A

aldosterone antagonist

19
Q

hydralazine and nitrate

A

reduce mortality
-improves quality of life

in HF patients

useful, especially in AA patients who have persistance symptoms regardless of ACE and beta blocker therapy

20
Q

aldosterone antagonists

A

reduce mortality with CHF

monitor for normal plasma K levels

21
Q

drug that may cause paroxysmal atrial tachycardia with block at high concentrations

22
Q

digoxin

A

cardiac glycoside

inhibit Na/K ATPase and increase myocardial contractility

narrow therapeutic index

NO effect on mortality for HF
-only reduces symptoms

23
Q

mechanism of digoxin

A

block Na/K ATPase

  • decreased Na/Ca exchange
  • results in more Ca intracellular
  • stronger contraction
24
Q

effects of therapeutic digoxin

A

prolongation of AP with AP shortening
-increased intracellular calcium

-increased cardiac contractility

increased PS tone, decreased S tone

25
effects of toxic digoxin
shortened AP with depolarizing afterpotentials** - results in premature ectopic beats - tachycardia may deteriorate into fibrillation -toxic levels - sympathetic outflow increased
26
digoxin at SA node
decreased rate
27
digoxin on EKG
therapeutic - increased PR interval, decreased QT interval toxic - tachycardia, fib, arrest at very high doses
28
increased PR interval
seen with digoxin
29
digoxin at AV node
decreased conduction velocity and increased refractory period
30
potentiate toxic effects of digoxin
furosemide | -due to potassium levels
31
hyperkalemia
can reduce effects of digoxin - especially the toxic effects binds to competing site of Na/K ATPase
32
hypokalemia
can potentiate toxic effects of digoxin***
33
hypercalcemia and hypomagnesemia
increase risk of digoxin induced arrhythmia hypercalcemia - accelerates overloading of intracellular Ca stores
34
increase force of heart contraction and produce vasodilation
bipyridines
35
inamrinone
bipyridine
36
milrinone
bipyridine
37
bipyridine
selective inhibition of PDE3 phosphodiesterase PDE3 degrades cAMP increases concentrations of cAMP in heart - stimulate myocardial contractility and accelerate relaxation balance arterial and venous dilation
38
PDE3 phosphodiesterase
inhibited by bipyridines
39
short term support of circulation in advanced HF
bipyridines
40
cAMP in cardiac vs. smooth muscle cells
smooth m - increased vascular smooth m contraction