Flashcards in CHF Drugs- Leah (3)* Deck (44)
Five general classes of drugs to treat CHF
+ Ionotropic drugs
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
1. What is the main "physiologic" problem in CHF w/ reduced EF?
2. What are secondary problems?
1. Reduced CO
2. 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?
1. 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. PDEi (both cardiac and vascular effects)
Of the vasodilators, which are only used for IV treatment of ACUTE CHF exacerbation? (3/7)
Of the vasodilators, which are used for chronic treatment of CHF? (4/7)
-nitrates (remember tolerance here!)
Of the vasodilators, which predominanty dilate arteries? (3/7)
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)
(same drugs that are only used acutely the drugs that effect both arteries and veins)
What is the first line vasodilator for CHRONIC CHF?
- 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)
1. ++cardiac contractility (^CO)
2. 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)
*ONE* They are the "ONEs" used today.
* "ONE" =3letters---> PDEi type 3
Why aren't PDEi good for chronic use? (2)
-proarrhythmic = QT ^^
What are three B blockers used in the treatment of CHF?
(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
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.)
*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)
How does dignoxin effect the SA node, AV node? contractility? CHF compensatory mechanisms?
1. Vagomimetic: DECREASE AV/SA node rates
(possible AV block at high dose)
*This is because Na/ K block decreases extracellular Na, which is needed for nodal depolarization.
2. INCREASES contractility
*This is because decreasing extracellular Na prevents Na/Ca exchange to ^^ Ca levels.
3. DECREASES compensatory mechanisms (via ^ cntrxn)
Two important kinetic issues to remember with digoxin?
-You HAVE to renal adjust
"DI-d you renally adjust for DIgoxin?"
-Incomplete absorption; various generics have failed for this reason.
Aside from CHF, for what reasons might digoxin be used therapeutically?
-Decrease V-rate in Afib/flutter
What are 4 of the symptoms of digoxin toxicity?
#1: GI upset
3. CNS effects: delirium, hallucination, etc.
4. Visual: GREEN-YELLOW Halos
"DIGO: Delirium, I(eye), GI upset, Out-of-control heart"
Under what 4 conditions is digoxin toxicity most likely?
(You're preventing the entry of K+ into the cell, add a lack of potassium to this, and you are in trouble!)
2. HYPERCALCEMIA (You're adding Ca to cells with digoxin, giving extra = bad)
3. RENAL/ THYROID FAILURE (renally excreted)
4. ACIDOSIS (Acidosis inhibits Na/K channels.)