Agents of Heart Failure Flashcards
Afterload
- force which pushing back against heart
blood out is opening door, afterload is pushing back and closing the door
Diuretics (heart)
patients with heart failure often have pulmonary congestion, which means too much fluid around lungs and too much fluid being pushed to heart
- diuretics turn down flow of fluid being delivered to the heart, decreasing filling pressures to normal range
Inotropic Agents
- increase Ca in heart so there is a stronger force of contraction
B Agonists
- stimulate heart to make beat faster; increases force of contraction
Vasodilators
- decrease preload and afterload
- ACE inhibitors and ARBs
- makes easier to push through door
B antagonists
- reduce arrhythmogenesis
- curtail remodeling
- reduce undesired sympathetic effects
- – make so catecholamines can’t overstimulate heart
Short Term Ionotropes for Acute Heart Failure
What do they do?
- increase cardiac output
Digoxin (long card)
Inotropic
- short circuits/blocks sodium ATPase, destroying NA gradient
- Na accumulates in cell = Ca stuck in cell
- increase Ca in cell = greater force of contraction
- ** narrow TI = v. dangerous = does NOT increase lifespan (can kill you if K increases in cell)
- can cause many forms of arrhythmias
Inotropic Agents (4)
- cardiac glycosides
- B1 agonists
- Ca sensitizers
- bypyridines
B1 stimulates:
adenylcyclase which effects cAMP, increasing Ca in cell
Bypyridines
MILRINONE
- act on phosphodiesterase 3
- increases cAMP = increased Ca into cell = increased contractility force
- SHORT TERM use only
Milrinone
Bypyridine
Digoxin
Inotrope
Angiotensin II Effects
- vasoconstriction
- Na retention
- effects cardiac remodeling
Dobutamine
B- agonist
- stimulates heart; doesn’t effect BP