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Pharmacology - Exam 3 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

4 CHF pathophysiology changes or phenomena

A

1) reduced CO
2) with reduced ejection fraction (HFrEF)
3) with preserved ejection fraction (HFpEF)
4) Adverse remodeling: chronic stress signals stretching, Angiotensin II, catecholamines–> hypertrophy–> less contractility

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2
Q

HFrEF is associated with

A

volume overload (systolic dysfunction) stroke volume goes down, LV End Diastolic Volume (LVEDV) goes up

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3
Q

HFpEF is associated with

A

pressure overload: diastolic dysfunction

both SV and LVEDV go down

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4
Q

Adverse remodeling also includes

A

a-MHC to B-MHC so heart is less able to contract from hypertrophy

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5
Q

Compensatory Mechanism in CHF

A

increase CO, so increase preload to increase EDV, and EDPressure

But this is useless, and makes it worse from chronic B1 receptor and Ang. II stimulation. It’s a positive feedback cycle–>increased problem

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6
Q

Tx of systolic CHF

A

1) Reduce cardiac workload (loose weight, lower activity level, smoking cessation)
2) decrease preload (decrease Na+ intake)
3) Reduce BP, pre- and after-load (ARNI, ACEI, ARB)
4) Once stable (on RAAS agent) reduce myocardial contractility (low dose B-Blocker then work upwards)
5) Decrease pre-load with diuretic
6) For low EF, give aldosterone antagonist to protect against fibrosis

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7
Q

what was that again? (simplified tx of systolic CHF)

A 
1) lifestyle changes
(salt, weight smoking)
2) ARNI, ACI, ARB
3) B-blocker
4) Diuretic
5) Alodsterone antagonist
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8
Q

what is contraindicated in systolic CHF

A

Calcium Channel Blockers

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9
Q

Tx of Diastolic CHF

A

1) Rate control with carvedilol or metoprolol (beta blockers) to improve filling during diastole.
2) CCB can decrease contractility and let the ventricle fill better, and slow the rate down through the AV node as well.

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10
Q

Nelprilysin

A
  • seen in ARNI

- degrades ANP and BNP by reducing renin secretion, and increasing NA excretion and vasodilation.

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11
Q

Aldosterone antagonists

A

Spiralactone*

Eplerenone

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12
Q

Spironolactone’s MOA

A

blocks aldosterone receptor, so increases Na (less Na reabsorption).

  • decreases excretion of K (K-sparing)
  • inhibits P-glycoprotein
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13
Q

MOA of Eplerenone

A

same as Spironolactone but more selective for aldosterone receptors.

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14
Q

effect of concentration of aldosterone antagonist

A

low concentrations are protective against fibrosis

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15
Q

Contraindications for Spironolactone

A

renal insufficiency

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16
Q

adverse effects of spironolactone

A

hyperkalemia (esp with ACEI)

  • gynecomastia (block progesterone/ androgen receptors) (may be a good side-effect for trans women)
  • sexual dysfunction
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17
Q

Indications for Spironolactone

A

CHF, low doses protective against myocardial fibrosis

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18
Q

name 2 ACE Inhibitors

A

Captopril

Enalapril

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19
Q

MOA of ACEI

A

blocks conversion of Ang I–> Ang II

  • decreases vasoconstriction and after load
  • decreases aldosterone secretion so less Na reabsorption, so less water/preload
  • Protective against adverse remodeling
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20
Q

what do you have to do with ACEI

A

monitor K, BUN, creatine because they have renal effects

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21
Q

contraindications for ACEI

A

pregnancy, renal artery stenosis

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22
Q

adverse effects for ACEI

A 
dry cough (increases bradykinin)
hyperkalmeia
angioedema
renal insufficiency (decreased GFR)
hypotension in AA
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23
Q

what are the two ACEI again?

A

Captopril and

Enalapril

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24
Q

Indications for “Cap’t Prill” and “Ina La’Prill”

A

Those ACEI nicknames sound SO EUROPEAN right?= memory tool for not to use with AA patients due to worse outcomes

CHF, HTN, Post-MI
DM nephropathy

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25
Q

“-prils”

A

ACE Inhibitors

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26
Q

ARBs

A

Angiotensin II receptor blockers include:
Candesartan
Valsartan
all the “-artan”s

Shworak showed the Irish Gravedigger with the artan ARBs accent

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27
Q

MOA for ARBs

A

blocks Angiotensin II from binding to Arg I receptor
- decreased vasoconstriction in smooth muscle of artery (decreases afterload)
-decreases aldosterone secretion: so decreases preload (less Na reabsorption)
_also protective against adverse remodeling

28
Q

contraindications for ARBs

A

pregnancy, BL renal artery stenosis (same as ACEI)

29
Q

adverse effects of ARBs

A

1) hyperkalemia,
2) renal insufficiency (decreased GFR)
3) hypotension
(note 1,2&3 same as ACEI) 4) reflex tachycardia
5) headaches

30
Q

indication for ARBs

A

almost exactly the same as ACEI
CHF, HTN, DM nephropahty
(post-MI not listed)

31
Q

what is an ARNI?

A

Sacubitril and Valsartan combo

32
Q

MOA of ARNI

A

blocks both neprilysin and angiotensin I receptors enhancing ARB effects

decrease: BP, sympathetic tone, aldosterone secretion, fibrosis, hypertrophy.
increases: natriuresis and diuresis.

33
Q

with ARNIs

A

have to check K+, BUN, creatine

34
Q

indication for ARNI

A

better morbidity and mortality than ACEI for CHF

35
Q

contraindications for ARNI

A

pregnancy, ACEI use, hepatic disease/imparement

36
Q

adverse effects of ARNI

A 
hypotension (more than ACEI)
angioedema (esp. with ACEI)
hyperkalemia (less than with ACEI)
cough (less than with ACEI)
renal insufficiency (less than ACEI)
37
Q

2 popular Betablockers

A

metoprolol

carvedilol

38
Q

MOA for Carvedilol

A 
nonselective B1/B2, a1
decreases renin/AngII, 
vasoconstriction and after load down
decreased BP from CNS effect
SA node: decrease HR, decreased conduction velocity at AV node
myocardium: decreased contractility
blocks adrenergic adverse remodeling
39
Q

MOA for metorpolol

A

cardioselective B1

40
Q

BetaBlockers contraindicated for..

A

asthma, COPD

Pts with poor heart function (decompensated CHF, sick sinus syndrome, 2nd and 3rd degree heart block)

41
Q

Bad side effects for Beta Blockers

A

bronchospasm
bradycardia
hypotension
severe angina with abrupt withdrawal

42
Q

B. Blockers indicated for

A

CHF, given with ACEI, diuretic +/- digitoxin

HTN, post MI

43
Q

Funny channel blocker

A

Funny cuz “Eva dines in her bra…”

Ivabradine

44
Q

MOA of Ivabradine

A

inhibits pacemaker cell funny current to reduce SA node rate…
no effect on contractility/conduction

45
Q

contraindications for funny channel blocker ivabradine

A

bradycardia
sick sinus syndrome
3rd degree heart block
liver impairment

46
Q

Contraindications for ivabradine

A

A. fib

bradyarrhythmias

47
Q

Indications for ivabradine

A

stable sympathetic CHF with poor LVEF maxed on B lockers and HR>70
no decrease in mortality

48
Q

Vasodilator

A

Isosorbide dinitrate

49
Q

MOA of isosorbide dinitrate

A 
releases NO (it's a prodrug)
NO increases cGMP to decrease phosphylation of MLC so vasodilation: and decreased preload from veins opening more, and decrease after load from arteries opening more
50
Q

contraindications of isosorbide dinitrate

A

Viagra could kill them with this drug combo

51
Q

side effects for isosorbide dinitrate

A

hypotension,

headaches

52
Q

indications for isosorbide dinitrate

A

CHF

angina

53
Q

vasodilator combination

A

isosorbide denitrate & hydralazine (BiDil)

54
Q

MOA for isosorbide denitrate and hydralazine (ISDN-Hydro

A

unclear but dilates arterioles so decreases afterload

55
Q

ISDN-Hydralazine contraindication

A

CAD,
enhases Betablocker
SE (Brady cardia, fatigue, broncho spasm)

56
Q

side effects of combo vasodilator

A

agina, edema, palpitations, tachycardia, N/V/D for GI effects

57
Q

indications for combo vasodilator

A

CHF refractory ACEI/ARB
Essential or pregnancy HTN
BiDil for AA with CHF
*improves mortality and morbidity

58
Q

Phosphodiesterase inhibitor

A

milrinone

59
Q

MOA of milrinone

A

blocks cAMP destruction so increases cAMP in heart.
increased calcium so more contractility and cardiac output
increases cAMP in artery sec so increases vasodilation and decreases afterload

60
Q

contraindications fo milrinone

A

hypersensitivity reactions

61
Q

bad side effects of milrinone

A

hypotension,
SVT,
v.arrhythmias

62
Q

indications of milrinone

A

acute decompensated HF (short term <2 days)

63
Q

cardio glycoside

A

Digoxin= digitox= fox glove= digitoxin

64
Q

MOA of digoxin

A

inhibits Na/K/ATPase so more extracellular Na.
Increases Ca intracellularly so increases contractility and cardiac output
decreases intracellular K so increases automaticity f ventricular pacemakers and increases arrhythmias.
Increases baroreceptor reflex (icncreases vagal tone), decreasing HR via SA node, and conduction velocity (AV node)
Also improves CO by decreasing sympathetic and RAA tone.

65
Q

contraindications for digoxin

A 
V-fib,
older than 65
acute MI
partial AV block
sick sinus syndrome
renal failure
66
Q

bad side effects of digoxin

A

low Ti, hyperkalemia, AV-block hypotension, bradycardia, arrhythmias, N/V/D
increases Abx availability, spirnonolactore toxicity
diuretics have K effects

67
Q

Digoxin indicated for

A

CHF, symptomatic relief and reduces hospitalizations,

a fib

Pharmacology - Exam 3 (12 decks)

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