Treatment of HF Flashcards
Treatment goals for systolic HF
1. Improve quality of life - Reduce or eliminate symptoms -Reduce or eliminate congestion 2. Reduce long term mortality 3. Slow down progression of or reverse cardiac structural abnormalities
- Treat all other cardiac risk factors
Acute Effects of Diuretics in HF
-Sodium excretion and water excretion
-Venodilation decreases VR thus…
-Reduction in filling pressures
Chronic Effects of Diuretics in HF
- Maintain a normal volume state
-Work best when combined with sodium restriction
-Work in conjunction with ACE-I and BB (reduce RAAS)
-Most HF patients need loop diuretics
-Do not favorably affect the natural history of HF
ACE-Is
1. Balanced vasodilators
2. Reduce angiotensin II levels and enhance Kinins (vasodilators)
 3. Multiple types of ACE-Is
5. Fluid overload attenuates the effects of the drug
- volume depletion enhances the side effects
- Gradual titration needed to attempt to achieve high doses for maximum benefit
Side effects: CATCHH:
hypotension, hyperkalemia, angioedema, cough and teratogenic effects
Name the 3 Beta Blockers and the receptor they block
B1: Metoprolol and bispropolol
All: Carvedilol
Beneficial effects of the 3 Beta Blockers adequately tested in systolic HF
-Reduce mortality -Reduce HF related hospitalizations -Increase LV ejection fraction -Reduce symptoms of HF -Partially reduce or reverse the process of remodeling of the LV
How Do BB improve LV function?
1. Increase in LV EF (> 5 EF units) occurs in 50- 70% of patients treated
2. Reversal of LV remodeling -Volume reduction -Mass reduction -Shape change back toward ellipsoid 3. The effect is intrinsic, not load mediated
How to introduce BBs
-Add beta blockers to ACE-I
The combined effect of ACE-I and BB is the most important therapy for systolic HF
Add BBs to stable patients at normal volume status
Begin at low doses and gradually titrate upward to goal dose
 Beneficial effect will not reach a maximum for several months
What about ACE-Is and ARBs together?
No difference in major events; uneffective together
ARB Therapy
Effective for heart failure as an alternative to ACE-I in patients intolerant of ACE-Is.
Equally effective as ACE-I therapy in heart failure and post
• Not 1st line because unlike ACE-I’s, ARBs have not been proven to reduce mortality
Effects of Aldosterone
Regulated by angiotensin-II levels, potassium and catecholamines
Multiple potentially harmful effects for HF in addition to salt and water retention and potassium depletion
-Vasoconstriction
-Fibrosis
-Inflammation
Not suppressed by ACE-I over the long term
Treatment of Heart Failure: Aldosterone Antagonism (MRA)
It appears more effective to block aldosterone + ACE than double block the RAAS with an
ACE-I and ARB
• added to ACE-I and BB when pt has EF less than 35%
- benefit in severe heart failure with spironolactone
- benefit of eplerenone in post MI heart failure
-benefit in mild- moderate heart failure
*** w/spironolactone a parallel increase in hospital admissions and death from hyperkalemia–Need to monitor!
Summary of Aldosterone Antagonists
Established for post MI and severe heart failure patients
Use has been extended to less severe forms of heart
failure.
The serum potassium and renal function should be
monitored closely.
The generic spironolactone is most commonly used
Eplerenone is used when gynecomastia side effects from spironolactone are not tolerable.
Digoxin
- more of a last line because it doesn’t decrease mortality
- only really helps with symptoms
When systolic dysfunction is present and symptoms persist despite use of diuretics, beta blockers and renin-angiotensin- aldosterone inhibitors
When atrial fibrillation and heart failure are present
Best combination of safety and efficacy are at blood levels of 0.5 to 1.0 ng/ml
Toxicity of Digoxin
Heart block and bradycardia
Ectopic and reentrant arrythmias (SVT and VT)
Anorexia, nausea and vomiting
(1st S/E–but may have this from HF itself)
Visual disturbances, confusion
(more specific S/E)
Drug interactions
Digibind for severe toxicity
