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Kaplan Pharm: Cardiac and Renal > Drugs for Heart Failure > Flashcards

Drugs for Heart Failure Flashcards

1
Q

What are currently the drugs of chronic management for CHF? What are the primary drugs?

A

ACEIs and ARBs

ACEIs, ARBs, beta blockers, diuretics loop or thiazide or spironolactone or eplerenone, hydralazine + isosorbide dinitrate

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2
Q

Why may hydralazine and isosorbide dinitrate be used as a therapy for CHF?

A

preferred for chronic therapy in patients who cannot tolerate an ACEI or ARB

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3
Q

What major factor can be linked to stopping cardiac remodeling?

A

stopping secretion of aldosterone

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4
Q

Does digoxin improve survival of a patient with CHF?

A

no

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5
Q

Describe chronotropy, dromotropy, and inotropy of digoxin.

A

+ inotropy (FOC)
- dromotropy (conduction velocity)
-chronotropy (HR) (SA node)

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6
Q

What are the direct effects of digoxin?

A

inhibition of cardiac Na+/K+ ATPase

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7
Q

What are the direct effects (MOA) of digoxin?

A

Inhibition of Na+ -K+ ATPase
inc. intracellular Na+
Dec Na+/Ca2+ exchange
Inc intracellular Ca 2+
Increases Ca2+ release from sarcoplasmic reticulum
Inc. actin-myosin interaction
Inc. contractile force

Indirect effect: inhibition of neuronal Na+/K+ ATPase (results in inc. vagal activity)

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8
Q

Describe 1/2 life of Digoxin.

A

long 1/2 life

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9
Q

Which groups of people should you use digoxin in with caution?

A

in those with renal impairment

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10
Q

Describe Vd of Digoxin?

A

large Vd

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11
Q

Uses of digoxin.

A

CHF
supra ventricular tachycardias, except Wolff-Parkinson-White syndrome

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12
Q

What are the S/E of using Digoxin?

A

early signs include anorexia, nausea, ECG changes

later signs include disorientation, visual effects (yellow-green color disturbances, blurry vision)

in toxic doses, any cardiac arrythmias

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13
Q

How do you manage Digoxin toxicity?

A

use Fab antibodies towards digoxin; supportive therapy (electrolytes and antiarrhythmics class 1B)

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14
Q

Some drug interactions to be on the lookout for when using with Digoxin?

A

dec. K+, dec Mg2+, inc. Ca2+

quinidine and verapamil

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15
Q

CHF that is caused by diastolic dysfunction (CHF with preserved ejection fraction) is best treated with what drugs?

A

beta blockers and diuretics

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16
Q

What are the phosphodiesterase inhibitors discussed that treat CHF?

A

inamrinone and milrinone

17
Q

What do inamrinone and Milrinone treat?

A

acute CHF only

18
Q

Do phosphdiesterase inhibitors increase cAMP or decrease it?

A

increase it

19
Q

How does increased cAMP affect the heart and smooth muscles?

A

increase inotropy
decreased TPR (respectively)

20
Q

MOA of Dobutamine.

A

Stim. B1 which inc. contractility of the heart

also stim B2 receptors but more effect on B1

B1> B2

21
Q

Uses of Dobutamine and Dopamine?

A

acute CHF only

22
Q

What is a S/E of Dobutamine and Dopamine?

A

can lead to tachyphylaxis which is rapid tolerance w/i one day

23
Q

Compare tachyphylaxis to true tolerance.

A

True tolerance takes days or weeks

24
Q

MOA of Sacubitril.

A

ARNI angiotensin receptor neprolysin inhibitor that inhibits breakdown of these peptides >inc. ANP and BNP which are 2 BP lowering peptides

25
Q

What is Sacubitril usu. given in combo with?

A

valsartan

26
Q

MOA of Ivabridine

A

heart rate lowering by blocking funny Na+ channels which causes SA nodes that controls the spontaneous depolarization in the sinoatrial (SA) node and hence regulates the heart rate.

This SA node activity is unregulated in CHF patients

27
Q

S/E of Ivabridine.

A

bradycardia
blurred vision

28
Q

What is a benefit of using Ivabridine?

A

can slow HR without dir. effects on contractility

29
Q

Why should you limit doses of B blockers in CHF?

A

can depress contractility

30
Q

What are methods of management of Wolff-Parkinson-White Syndrome? What should you and what should you not do?

A

Do block accessory pathway with IA or III
Do not slow AV conduction (avoid digoxin, B-blocker, Ca2+ channel blocker, adenosine)

Kaplan Pharm: Cardiac and Renal (6 decks)

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