Heart Failure Flashcards
High output vs. Low output HF
- High output HF maintains a normal CO (can be caused by thyroid issues or anemia)
- Low output HF has decreased CO
The Vicious Cycle of HF
- 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
Treatment Strategies of HF
- 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)
Diuretic Therapy in HF
- 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
Vasodilators in HF
- Goal is the reduce preload and afterload
- These include ACE, ARB, and traditional vasodilators
ACE Inhibitors
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
ARB (AT 2 receptor antagonist)
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
Nitroprusside
IV vasodilator
- is converted to NO which dilates both A and V
- SE hypotension, reflex tachycardia, ischemia
Nitroglycerin
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
Hydralazine
oral and IV
-relaxes smooth muscle in arteries(decreased afterload)
Isosorbide Dinitrate
oral
-is converted to NO to dilate veins(decreased preload)
Concurrent administration of Hydralazine and Isosorbide Dinitrate
- aka BiDIl
- used for patients who cannot take an ACE inhibitor such as pregnant women and african american women
- increases survival
Inotropic agents
increase contractility to increase CO
Digoxin (digitalis drugs)
- 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
Dopamine
Beta 1, Alpha 1, and dopaminergic agonist
-IV inotrope/vasopressor
Dobutamine
Beta 1 agonist
- increases force of contraction without raising HR very much
- for short term use (possibly decompensated HF)
- SE include tachycardia and tolerance
Phosphodiesterase Inhibitors
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
Beta Blockers in HF
- 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
Combination therapy in HF
ACE and BB are DOC. We can add in inotropes and diuretics where appropriate
Course of Therapy in HF
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
