Flashcards in Drugs for Heart Failure - Kruse Deck (49):
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?
- 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
Common symptoms of all heart failure (5)
- Decreased exercise tolerance
- Shortness of breath
- Drug class?
- Things to be cautious of when administering? (3)
- Results? (2)
- INDICATED WHEN?
- 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?
- 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
- Used for what (in HF)?
- 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
Antagonism of ____ from the RAAS system is a cornerstone for HF management
Negative effects of angiotensin 2 in HF (6)
- Na/H20 retention
- Increased catecholamines (sympathetics)
- 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
Substance that directly slows myocardial and vascular remodeling by angiotensin 2
Bradykinin (increased w/ ACE inhibitors)
Which is better 1st: ACEI or ARB? Why?
ACEI - increased bradykinin --> slowed tissue remodeling
When to give an ARB?
Side effects from ACEI (cough, angioedema)
2 functions of vasodilators in HF
- Reduce preload (venous dilators)
- Reduce afterload (arteriolar dilators)
MoA of vasodilators
N.O. --> G.C. --> cGMP --> relaxation
Adverse effects of venodilators
- Postural hypotension
Arteriolar dilator drug
Use of Hydralazine in HF
- Decrease afterload (BP), increased C.O.
How are vasodilators really used?
Veno and arteriolar TOGETHER
- Fluid retention
- Lupus-like symptoms
Nitroprusside - MoA
Arteriolar AND venous dilator (via N.O.)
Nitroprusside - clinical use
- Acute cardiac decompensation
- HTN emergencies
3 beta blockers that reduce mortality in HF
- Bisoprolol (Beta-1)
- Carvedilol (Beta-1, Beta-2, and alpha-1)
- Metoprolol (Beta-1)
Results of beta blockers in HF
- Decreased myocardial remodeling
- Slight EF rise over time
- Decreased HR (oxygen demand, etc.)
How to safely remove sodium in HF?
- Loop diuretic + supplements
- K-sparing diuretics
Potassium levels are especially important when giving which drug?
HF + edema...best first drug?
HF w/o edema...best first drug?
ACEI (or ARB)
How to know which vasodilator to use?
Based on patient symptoms
Patient w/ dyspnea, pulmonary congestion, high atrial diastolic volume (filling pressure)...
Which vasodilator to give?
Venous dilators (nitro, isosorbide)
How to administer beta blockers in HF?
LOW DOSES - prevent worsening of HF via too much sympathetic antagonism
Are effects of beta blockers in HF immediate?
NO, may take months
When is Digoxin given?
If ACEI and diuretics fail to control symptoms