Drugs in Congestive Heart Failure Flashcards
Hypertrophy
Increase in the size of the heart - also increase size of individual cells
Trying to combat the extra work required
Remodelling
Long term changes
Dilation of the heart, increase in connective tissue (fibrosis), loss of heart cells, emergence of unusual cells
Causes a high level of mortality
3 purposes of drugs to treat CHF
- Unload the heart (decrease preload and afterload)
- Increase the strength of contraction of the heart (not super great)
- Block the effects of the SNS and RAS (block compensatory responses)
Why are diuretics effective?
They decrease salt and water retention!
Decrease preload, decrease afterload (decrease BP), decrease edema, decrease hypertrophy to some extent
Diuretics: Loop
Act at the loop of Henle
Very powerful
Enhance the secretion of K into the urine (can get hypokalemia)
Useful to reduce the amount of fluid (less edema)
Diuretics: K-sparing
Aldosterone receptor antagonists
Act at the collecting tubule
Mild diuresis
Decrease mortality and increase heart function
Block aldosterone because it may contribute to the development of fibrosis
4 functions of drugs that inhibit the RAS
ACE inhibitors, AII receptor blockers, renin inhibitors
- Reduce total peripheral resistance (dilates arteries and veins, so decrease pre and afterload)
- Decrease aldosterone secretion from adrenal glands (decreases Na and H2O, decreases preload)
- Decrease long term remodelling of ventricles (decrease: fibrosis, hypertrophy, cell loss, mortality)
- Decrease bradykinin breakdown (its a vasodilator usually broken down by ACE)
Cardiac glycosides: Digoxin
Increases contractility
Used as anti-arrhythmic drug
Inhibits the Na-K ATPase, causes increased Na in cell, inhibits the Na-Ca exchanger, more Ca in cell = more contraction
Increases CO so SNS activity decreases: causes reduced RAS, decrease BP/HR/Na and H2O retention/preload
Has toxic effects (AV block, narrow TI)
Beta blockers
Decrease high SNS activity
Ex: Carvedilol (blocks beta 1 (decrease HR/renin) 2 (not useful) and alpha 1 (decrease afterload))
Reduces signs and symptoms of CHF, slows progression of CHF, decreases mortality, reduces remodelling
Carvedilol
Highly non selective beta blocker
Blocks beta 1 (decrease HR/renin)
Blocks beta 2 (not useful)
Blocks alpha 1 (decrease afterload)
Toxic Effects of Digoxin
- AV node - can cause AV block and arrest
- Ventricles - it has a very narrow TW
In the elderly particularly:
its eliminated by the kidneys and renal function declines with age