CHF Drugs- Leah (3)* Flashcards
Five general classes of drugs to treat CHF
Vasodilators B blockers Diuretics \+ Ionotropic drugs ACEi/ARBs
What are two types of CHF?
Which is treated with standard drug therapy ?
- CHF with preserved or reduced ejection fraction
- most drugs treat with reduced ejection fraction
- What is the main “physiologic” problem in CHF w/ reduced EF?
- What are secondary problems?
- Reduced CO
- Reduced CO activates compensatory mechanisms–> ^ preload (good), edema, congestion–> hypertrophy
- Mechanisms include sympathetics and RAAS
- Must treat this along with reduced EF*
What are the two main goals of CHF treatment?
- increase cardiac output
2. decrease negative effects of compensatory mechanisms
In the normal heart, which has greater effect on stroke volume: preload or afterload?
What effect does ^ TPR (^ afterload) have on CO in the normal heart?
- Preload has higher effect than afterload in the normal heart (as in during exercise).
- Increases return of blood to heart = ^ output
*Increasing TPR does NOT dangerously reduce CO in the normal heart (as occurs during fight or flight)
In the diseased heart, which has greater effect on stroke volume: preload or afterload?
In the CHF heart, what effect does ^ TPR
(^ after load) have on CO?
- In CHF, increasing preload will NOT effectively increase cardiac output
- Heart can’t pump well, no matter how much blood it gets.
- Increasing afterload/ peripheral resistance can dramatically decrease CO.
Effect of arterial dilation in CHF?
DECREASE afterload–> ^SV –> ^ CO + DECREASE compensatory mechanisms (somewhat)
Effect of venous dilation in CHF (2)?
- DECREASE preload/ LVEDV/ SV/ CO
- DECREASES negative compensatory effects, like congestion, edema, and hypertrophy
What are the vasodilators for treating CHF?
7 classes
- nitroprusside
- nitrates
- hydralazine
- ACEi
- ARBs
- Nesiritide
- PDEi (both cardiac and vascular effects)
Of the vasodilators, which are only used for IV treatment of ACUTE CHF exacerbation? (3/7)
- nitroprusside
- nesiritide
- PDEi
Of the vasodilators, which are used for chronic treatment of CHF? (4/7)
- nitrates (remember tolerance here!)
- ACEi
- ARBs
- Hydralazine
Of the vasodilators, which predominanty dilate arteries? (3/7)
- hydralazine
- ACEi
- ARBs
Of the vasodilators, which predominately dilates the venous system? (1)
NITRATES effect mostly VEINS
- Only dilate arteries at very high concentrations
- this was a step prep question.
- **MOA for NG is NOT dilation of coronary arteries!!!!!*
Of the vasodilators, which dilate both the venous and arterial system (3)?
-nitroprusside (equal effects on vv’s, aa’s)
-nesiritide
-PDEi
(same drugs that are only used acutely the drugs that effect both arteries and veins)
What is the first line vasodilator for CHRONIC CHF?
Second choice?
- 1st choice is ACEi’s
- All CHF patients that can tolerate ACEi’s take them.
- 2nd choice = ARBs
Special consideration when treating CHF in African Americans?
-Many do not respond to ACEi’s, ARBS, BBs, or aldosterone blockers alone.
-They will often need combination therapy.
*Commonly the combo therapy is Hydralazine/ ISDN
(This was one of the CHF quiz questions.)
How does nesiritide (vasodilator) work?
- Recombinant BNP (naturitic peptide)
- Activates PARTICULATE guanylyl cyclase/ ^cGMP –> Arterial + venous dilation
How do phosphodiesterase inhibitors (type 3) work to treat acute CHF?
Inhib PDE-III–>DECREASE cAMP breakdown (^cAMP)
- ++cardiac contractility (^CO)
- Arterial and venous dilation
*Note: Type FIVE PDEi’s reduce cGMP breakdown/ keep the penis “filled” (The -afil drugs are type 5.)
What are the two PDEi inhibitors on the market?
Which is most commonly used?
- Milronone (most commonly used)
- Inamironone
- ONE* They are the “ONEs” used today.
- “ONE” =3letters—> PDEi type 3
Why aren’t PDEi good for chronic use? (2)
- proarrhythmic = QT ^^
- cause hypotension
What are three B blockers used in the treatment of CHF?
- metoprolol
- bisoprolol
- carvedilol
(MEet me at the BIStro and bring the CAR. I can’t walk home because of my CHF!)
How do B blockers improve the outcome of CHF? (3)
- prevent remodeling (by decreasing NE/catecholamine)
- decrease O2 demand
- prevent arrhythmias
Special consideration when starting a patient on a B blocker for CHF (2)?
Dose must be gradually titrated; CHF must be compensated
Never give B blocker to someone with a really low EF.
Digoxin: MOA
This was an Rx question
Inhibits Na-K ATPase–> Inhibit Na/Ca XGE–>
- ^ intracellular Na+ and Ca++
- ^ serum K+
(normal function of Na-K = K+ in, Na+ out)