antichf

Question 1

indication Digitalis (cardiac glycoside, positive inotrope)

Answer 1

Both Acute and Chronic HF

Question 2

MOA Digitalis (cardiac glycoside, positive inotrope)

Answer 2

Cellular Mech involves inhibition of Na/K ATPase in cell leading to increased Ca exchange and more Ca in SR. Calcium=contractility.

Question 3

Drug Action/Pd Digitalis (cardiac glycoside, positive inotrope)

Answer 3

Decreases end-systolic & end-diastolic volumes (more efficient pumping so inc SV), increases CO & then inc renal perfusion, & dec sympathetic tone

Question 4

PK Digitalis (cardiac glycoside, positive inotrope)

Answer 4

narrow therapeutic window–monitoring is needed, esp if dec GFR (renal clearance)

Question 5

Route of Admin Digitalis (cardiac glycoside, positive inotrope)

Answer 5

oral usually. Can be reversed with an antibody

Question 6

Adverse Effects Digitalis (cardiac glycoside, positive inotrope)

Answer 6

Calcium Mech=DAD’s

Question 7

Notes Digitalis (cardiac glycoside, positive inotrope)

Answer 7

digitalis has another MOA (CNS mech-parasympathetics) used in anti-arrythmics.

Question 8

indication Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)

Answer 8

Acute HF

Question 9

MOA Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)

Answer 9

increased cAMP, stimulated by Gs-linked receptors (B1 & B2 on heart), increases opening of Ca channels, inc uptake of Ca into SR, inc pacemaker current, inc rate of conduction.

Question 10

Drug Action/Pd Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)

Answer 10

note that this is the OPPOSITE of B-Blockers MOA (decrease cAMP) so don’t be confused

Question 11

Notes Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)

Answer 11

cAMP increases: Chronotropy, Dromotropy (conduction), Inotropy (contractility), and Lusitropy (relaxation)

Question 12

indication Amirinone or Milrinone (PDE inhibitors, positive inotropes)

Answer 12

Acute HF

Question 13

MOA Amirinone or Milrinone (PDE inhibitors, positive inotropes)

Answer 13

Remember that PDE normally degrades cAMP. If you stop PDE from degrading cAMP, you increase cAMP concentration

Question 14

Drug Action/Pd Amirinone or Milrinone (PDE inhibitors, positive inotropes)

Answer 14

increased cAMP has inc chronotropy, dromotropy, inotropy and lusitropy

Question 15

Route of Admin Amirinone or Milrinone (PDE inhibitors, positive inotropes)

Answer 15

note that this is a DIFFERENT MOA than B-agonists (BUT SAME PATHWAY) and can help overcome existing B-blockade if present.

Question 16

Notes Amirinone or Milrinone (PDE inhibitors, positive inotropes)

Answer 16

do not confuse amirinone (PDE inhibitor) with amiodarone (class III anti-arrythmic, longest t 1/2), or amiloride (direct K-sparing diuretic)

Question 17

indication Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)

Answer 17

Chronic and Acute HF

Question 18

MOA Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)

Answer 18

reduce intravascular volume to reduce filling pressure (decrease preload–but little effect on CO–on flat part of Starling curve); reduce extracellular fluid so reduce peripheral edema (3rd spacing)

Question 19

Drug Action/Pd Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)

Answer 19

Action depends on drug–Furosemide=vigorous, works on Na/K/2Cl txporter in LOH; Thiazide=DCT action Na/Cl, Aldo antags=mild diuresis

Question 20

PK Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)

Answer 20

watch ototoxicity of loop diuretics, and remember that loop/thiazides are SULFA drugs and can cause ALLERGIES, also with loop/thiazides see hyperuricemia which can lead to GOUT! If pts are resistant to diuretics overcome by using COMBO therapy (use K-sparing & K-wasting for example)

Question 22

Adverse Effects Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)

Answer 22

Note that hypokalemia potentiates digitalis toxicity

Question 23

Notes Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)

Answer 23

note: thiazides are calcium-sparing and are protective against kidney stones, have longer t 1/2 than loop. Don’t run hypok risk (digitalis tox) with K-sparers

Question 24

Drug Name

Answer 24

Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)

Question 25

indication Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)

Answer 25

Chronic and Acute HF

Question 26

MOA Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)

Answer 26

the major action of the arteriolar vasodilators (Hydralazine, Minoxidil) is to reduce afterload on the heart and increase forward CO, ACEI’s/ARB’s also reduce afterload by inhibiting angiotensin effects (vasoconstriction, aldosterone)

Question 27

Drug Action/Pd Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)

Answer 27

major desired action of Nitrates here is to dilate venous capacitance vessels (reduce venous return), but there are also arteriolar effects.

Question 28

Adverse Effects Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)

Answer 28

careful with the ACEI/ARB’s (K-savers) and K-sparing diuretics-hyperkalemia

Question 29

Notes Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)

Answer 29

remember that AT-II is a potent cardiomyocyte growth factor (hypertrophy) and fibroblast mitogen factor (hyperplasia)

Question 30

Recommendations for treatment of CHRONIC HF:

Answer 30

Decrease Symptoms: Pulmonary: Venodilators (ACEI’s/ARBS, nitrates) and Diuretics. Prevent Ventricular Remodeling: ACEIs, BB’s and Aldo Antagonists (Spironolactone/eplerone) Prolong Survival of Pt: ACEI’s, BB, Aldo Antagonists, Nitrates + Hydralazine

Question 31

Recommendations for treatment of Acute HF:

Answer 31

Reduce pulmonary congestion:Loop diuretics (Furosemide) and Venodilators (Nitroglycerin). Increase Cardiac Output: Increase contractility (B-agonists, PDE inhibitors, Digitalis); Afterload reducing agents (Nitroprusside) do NOT give a B-Blocker here

Question 32

Causes of chronic HF

Answer 32

Ischemic Cardiomyopathy (CAD)=Most common, also dilated or hypertrophic cardiomyopathy.

Question 33

Causes of acute HF

Answer 33

Acute MI, Arrythmias, Pericardial Tamponade, Massive PE