Drugs for Heart Failure - Kruse Flashcards
(49 cards)
Typical direct cause of heart failure
Decreased contractility of the myocardium –> insufficient oxygen supply to the body
Historically, drug therapy for heart failure has typically focused on what 2 end results?
But ____
- Volume overload (diuretics)
- Myocardial dysfunction/weakness (inotropic agents)
NOT ENOUGH to improve survival
Agents that act directly on _____ seem to be more valuable in the long run
Organs other than the heart that are involved in hemodynamic consequences of HF
Today, primary treatment for long term HF is aimed at doing what?
Mainly via altering what two compensatory systems?
Reducing preload and afterload
- RAAS - Sympathetics
Common symptoms of all heart failure (5)
- Tachycardia
- Decreased exercise tolerance
- Shortness of breath
- Edema
- Cardiomegaly
Digoxin
- Drug class?
- Things to be cautious of when administering? (3)
- MoA?
- Results? (2)
- INDICATED WHEN?
- Toxicity?
- Cure?
- Cardiac glycoside
- Dose ∆ w/ renal problems, vasodilators, or sympathomimetics
- Inhibits Na/K ATPase of sarcolemma –> increased calcium build-up
- INCREASED CONTRACTILITY AND increased K+ efflux –> SHORTENED AP
- INDICATED in HF w/ S3 or A. FIB.
- Toxicity = ANY arrhythmia (next card)
- Give K+ (decrease K+ outflow) and antidigoxin fab Ab
Describe how arrhythmias can develop with digitalis toxicity
- Decreased atrial refractory period –> ectopic atrial contractions –> A. tach. –> A. fib
- Increased ventricular refractory period –> AV dissociation –> ectopic ventricular contractions –> V tach. –> V fib.
Classic EKG finding for digitalis toxicity
Downward “U-shaped” ST segment
“-rinone” - drug class?
Bipyridines - PDE3 inhibitors
MoA of bipyridines (“-rinone”)
PDE3 inhibition –> increased cAMP –> increased Ca++ (contractility) and increased SM (vascular) dilation
End results of bipyridines (2)
- Increased contractility
- Decreased preload and afterload
Use of bipyridines
SHORT-TERM relief in HF
Toxicities of each of the bipyridines
Inamrinone - GI, arrhythmias, thrombocytopenia, liver enzymes
Milrinone - arrhythmias ONLY
A patient is on Inamrinone for short-term HF but is having complications with bleeding. Replacement drug?
Milrinone
Dobutamine
- MoA
- Direct result
- Overall result
- DOC for what?
- Side effects? (2)
- Beta-1 agonist
- AC –> cAMP –> PKA –> increased Ca++ (contractility)
- Increased stroke volume (cardiac output)
- DOC for SYSTOLIC DYSFUNCTION in HF
- S.E. = tachycardia, arrhythmias
Dopamine
- Used for what (in HF)?
- How?
- Raising BP in vasodilation circulatory collapse (sepsis, anaphylaxis)
- HIGH DOSE –> alpha-1 and beta-1 agonist –> peripheral vascular constriction and increased contractility
When should dopamine use be avoided? Why?
CAD patients - tachycardia (increased O2 demand) may provoke ischemia
Diuretic class shown to improve survival in advanced HF? Why?
Aldosterone antagonists - aldosterone causes myocardial and vascular fibrosis and remodeling, and baroreceptor dysfunction
Main aldosterone antagonists used
- Spironolactone
- Eplerenone
Antagonism of ____ from the RAAS system is a cornerstone for HF management
Angiotensin 2
Negative effects of angiotensin 2 in HF (6)
- Na/H20 retention
- Increased catecholamines (sympathetics)
- Arrhythmogenic
- Vascular hyperplasia
- Myocardial hypertrophy
- Myocyte death
Inhibiting Angiotensin 2 will do what? (multiple)
- Reduce preload
- Reduce afterload
- Decrease sympathetics
- Reduce aldosterone
- Reduce myocardial/vascular remodeling
Problem with loop diuretics in HF?
K+ wasting –> arrhythmias
Why are ACE inhibitors maybe even better than aldosterone inhibitors?
ACE inhibitors ALSO inhibit aldosterone secretion
