Heart Failure

Question 1

High output vs. Low output HF

Answer 1

• High output HF maintains a normal CO (can be caused by thyroid issues or anemia)
• Low output HF has decreased CO

Question 2

The Vicious Cycle of HF

Answer 2

• cardiac or pulmonary dysfunction lead to decreased CO. As a result the SNS releases catecholamines, activates the RAA system.
• While both measures improve CO for a short time, they ultimately lead to remodeling, pulmonary and peripheral edema, and worsening of CO.
• See the image in the notes. Remember the Frank-Starling rule of the heart

Question 3

Treatment Strategies of HF

Answer 3

• Treat the cause for secondary HF
• Manage the symptoms in primary HF to increase longevity and quality of life.
• The pharmacological management often requires combating the body’s SNS response. (ex. ACE to stop RAA, vasodilators to decrease afterload and increase CO, etc)

Question 4

Diuretic Therapy in HF

Answer 4

• See diuretics segment for more detail
• Take home point is to try loops, then add a thiazide. Do not increase survival.
• K sparing work well with dig and limit remodeling effects of aldo. Ultimately, these INCREASE SURVIVAL

Question 5

Vasodilators in HF

Answer 5

• Goal is the reduce preload and afterload

- These include ACE, ARB, and traditional vasodilators

Question 6

ACE Inhibitors

Answer 6

captopril, enalapril, lisinopril
Drug of Choice for HF
-Blocks conversion of angiotensin 1 to 2 and degradation of bradykinin leading to vasodilaton (bradykinin causes bronchoconstriction leading to dry cough)
-decreases aldosterone release and subsequently Na and H2O reabsorption

Question 7

ARB (AT 2 receptor antagonist)

Answer 7

losartan, candisartan

• block AT1 receptors to produce effects similar to ACE, but with fewer SE.
• does not affect bradykinin metabolism so no dry cough
• supposedly as effective as ACE, ACE ARB combo being evaluated

Question 8

Nitroprusside

Answer 8

IV vasodilator

• is converted to NO which dilates both A and V
• SE hypotension, reflex tachycardia, ischemia

Question 9

Nitroglycerin

Answer 9

Vasodilator that is IV, sublingual, and topical

• is converted to NO to produce primarily venous(preload) and some arterial(afterload) vasodilation
• SE are hypotension, reflex tachycardia, ischemia, and tolerance

Question 10

Hydralazine

Answer 10

oral and IV

-relaxes smooth muscle in arteries(decreased afterload)

Question 11

Isosorbide Dinitrate

Answer 11

oral

-is converted to NO to dilate veins(decreased preload)

Question 12

Concurrent administration of Hydralazine and Isosorbide Dinitrate

Answer 12

• aka BiDIl
• used for patients who cannot take an ACE inhibitor such as pregnant women and african american women
• increases survival

Question 13

Inotropic agents

Answer 13

increase contractility to increase CO

Question 14

Digoxin (digitalis drugs)

Answer 14

• cardiac glycosides
• Used primarily in pt with atrial arrhythmias, and those refractory to ACE and Beta blocker
• inhibits the Na/K ATPase system which increases intracellular Ca and subsequently the force of contraction
• this increases CO, decreases preload, congestion/edema, and increases renal perfusion.
• also increases the parasympathetic tone, decreases automaticity and AV conduction
• digoxin has shorter HL than digitalis
• SE are primarily NV, arrhythmia
• has very narrow therapeutic window and SE are precipitated by low K

Question 15

Dopamine

Answer 15

Beta 1, Alpha 1, and dopaminergic agonist

-IV inotrope/vasopressor

Question 16

Dobutamine

Answer 16

Beta 1 agonist

• increases force of contraction without raising HR very much
• for short term use (possibly decompensated HF)
• SE include tachycardia and tolerance

Question 17

Phosphodiesterase Inhibitors

Answer 17

Inamrinone and Milrinone (both IV only)

• MOA limits breakdown of cAMP leading to increased levels, increased intracellular Ca, and stronger force of contraction
• also relaxes smooth muscle in vasculature, decreasing preload and afterload
• like dobutamine, these should only be used short term in those decompensated HF pts

Question 18

Beta Blockers in HF

Answer 18

• these are now drugs of choice (along with ACE) in HF
• MOA limits sympathetic activation in the heart which decreases HR and O2 consumption, limits hypertrophy and remodeling, increases ventricular filling times and EF
• beta blockers limit symptoms increase survival

Question 19

Combination therapy in HF

Answer 19

ACE and BB are DOC. We can add in inotropes and diuretics where appropriate

Question 20

Course of Therapy in HF

Answer 20

At risk and asymptomatic pts, limits the risk factors(HTN, diabetes, etc)
Structural dx without symptoms, begin ACE/ARB then BB
Structural dx with symptoms, ACE/ARB and BB if not already on. Then dietary Na restriction, diuretic, Digoxin. Then aldosterone antagonist. Then strong inotropes, LVAD, hospice