Cardiology (Pharmacotherapy Of Heart Failure)

Front 1

What is NOT a physiologic compensatory mechanism of chronic heart failure?

a. chronic activation of parasympathetic NS
b. inc RAAS to keep up BP
c. remodeling of cardiac tissue (ventricles become more spherical and less efficient as a pump)
d. none of the above

Back 1

A. it's the SYMPATHETIC NS that will be chronically activated

Front 2

what is the most common mode of death for chronic heart failure?

Back 2

sudden cardiac death

Front 3

Higher norepinephrine levels in plasma indicate:

a. better prognosis of CHF
b. poorer prognosis of CHF

Back 3

B. the more you have in the plasma, the more higher the mortality rate

Front 4

inotropic drugs are useful for:

a. acute HF
b. chronic HF

Back 4

A. to get the heart to do more

Front 5

what is the drug of choice for chronic heart failure?

a. diuretics
b. beta blockers
c. CCBs
d. ACE inhibitors

Back 5

B. to reduce the load on the heart

Front 6

what is the mechanism of digitalis/digoxin? (remember that digoxin is what is used nowadays)

Back 6

inhibits Na/K ATPase pump present in cardiac cell membranes. this keeps Na from exiting and the increase in Na also increases Ca conc within the cell--> positive inotropic effect (greater contractility)

Front 7

What do you have to monitor when placing a patient on both digixon (for HF) and diuretics (for HTN)?

Back 7

the hypokalemia that diuretics causes will increase digitalis/digoxin toxicity

Front 8

which of the following is digoxin/digitalis NOT useful for?

a. systolic heart failure
b. diastolic heart failure
c. supraventricular arrhythmias
d. ventricular arrhythmias
e. two of these (name 'em)

Back 8

B and D.

Front 9

side effects of digoxin/digitalis

Back 9

arrhythmias (so can't give to pt with VFIB), PVCs (can't give to pt with ventricular tachycardia), muscle weakness

Front 10

digitalis/digoxin has a WIDE/NARROW therapeutic window

Back 10

narrow (therfore, digitalis toxicity is very common)

Front 11

"-inone"

Back 11

phosphodiesterase type III inhibitors (ie. amrinone and milrinone)

Front 12

mechanism of amrinone

Back 12

amrinone- phosphodiesterase III inhibitor

inhibit PDE III and prevents breakdown of cAMP --> inc cAMP does two things: 1) inc intracellular cAMP in myocytes to increase contractility
2) inc cAMP in blood vessels to cause vasodilation

this is helpful in chf

Front 13

why are PDE III inhibitors rarely used (except in acute cases )

Back 13

it has high toxicities (GI, liver, thrombocytopenia) and increases mortality rate

Front 14

class & mechanism of dobutamine. how does it help CHF?

Back 14

class = mainly beta-1 agonist
mechanism = increases contractility and CO---> 1) decreases afterload (since CO improvement will lead to decreased sympathetic tone) & 2) reduce preload (by increasing LV emptying)

Front 15

Hydralazine are mainly:

a. arterial vasodilators
b. venous vasodilators

Back 15

A (as opposed to NTG which is venous vasodilator)

Front 16

name 2 vasodilators

Back 16

nitrates (venodilator) and hydralazine (direct arterial dilator)

Front 17

Which is NOT effective in CHF therapy?

a. digoxin
b. nitrates
c. thiazide-type diuretics
d. loop diuretics

Back 17

C.

Front 18

name a loop diuretic

Back 18

furosemide

Front 19

which of the following is NOT true about digoxin therapy in CHF pts?

a. it reduces hospitalizations in CHF pts
b. it decreases mortality
c. it may increase death rates in women more than men
d. it may reduce the occurrence of atrial fibrillation

Back 19

B

Front 20

what is the order of drugs you would give for systolic HF?

Back 20

BB would be used first, ACEI (or ARB…never both) next. When they are stable, then and only then, add aldosterone antagonist can be added cautiously.

Front 21

what drug given for CHF can cause lupus as a potential side effect?

Back 21

hydraLazine?

Front 22

T or F. CCBs are generally contraindicated for CHF.

Back 22

T

Front 23

what are the effects of beta-blockers on ACUTE vs. CHRONIC heart failure?

Back 23

acute = BBs can actually worsen CHF acutely (pt's will feel awful)

chronic = after a while, BBs can actually improve quality of life and increase survival (if you add alpha1 receptor blocker "carvedilol", the mortality decreases even more)

Front 24

why don't ARBs cause coughing as a side effect compared to ACE inhibitors?

Back 24

ACE inhibitors, in addition to inhibiting conversion of AG I --> AG II, they also inhibit metabolism of bradykinins (which will cause vasodilation as well as coughing)

ARBs only inhibit the receptor for AG II and do not touch bradykinin metabolism

Front 25

why are ARBs better than ACEIs in terms of improving survival rates?

Back 25

1) there may be an alternative pathway to generate AGII that goes around AG I. so ARBs would stop that anyways at the receptor for AG II.
2) also, ARBs selectively block binding at AT1 receptors (inhibiting vasoconstriction) whereas ACEIs blcok nonspecifically to both AT1 and AT2

Front 26

name the important side effects of ACEIs (4)

Back 26

1. cough
2. angioedema (this is swelling deep under the skin; also caused by elevated bradykinin)
3. hypotension
4. hyperkalemia (remember, diuretics increase Na+ excretino and lead to HYPOkalemia)

Front 27

what are the 3 contraindications for ACEIs and ARBs?

Back 27

1. during pregnancy or in pts who are likely to become pregnant bc they cross placental barrier
2. renal failure
3. bilateral renal artery stenosis

Front 28

how does spironolactone work and what does it do for CHF patient?

Back 28

it's an aldosterone antagonist; so it inhibits aldosterone-induced na/k retention by kidney

- somehow this inhibits fibrosis of the heart and decreases mortality and morbidity in CHF

Front 29

Polytherapy (giving CHF pts 3 drugs) is BETTER/WORSE than monotherapy.

Back 29

better (Patients receiving triple
therapy are least likely to
experience worsening
of heart failure)