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
Bi-V Pacemaker Results
-ICD to prevent SCD (common form of HF death)
- For symptomatic patients w/EF
Neprilysin
NEP=neutral endopeptidase
Enzyme that breaks down natriuretic peptides (ANPs, BNPs)
Entresto: Sacubitril/valsartan
ARB and Neprilysin Inhibitor that simultaneously inhibits RAS and NEP!
- Indication: to reduce the risk of cardiovascular death and hospitalization for heart failure in patients with chronic heart failure (NYHA Class II- IV) and reduced ejection fraction
• Used in place of ACEi or ARB
- Give lower starting doses to patient ACEi/ARB naïve
- Hypotension most significant reason for discontinuation
Ivabradine
- It is a hyperpolarization activated cyclic nucleotide-gated channel blocker
- Reduces pacemaker activity in SAN by inhibiting If channels
- Result: Reduced HR without affecting ventricular repolarization or contractility
• Idea behind ivabradine is that those with higher HR tend to have worse outcomes (HR>70bpm)
*bradycardia and atrial fibrillation may be serious concerns
*Indication: to reduce the risk of HOSPITALIZATION for worsening heart failure in patients with stable, symptomatic chronic heart failure
• LVEF ≤ 35%
• in sinus rhythm with resting heart rate ≥ 70 beats per min
• can’t give to afib or those who
have a contraindication to beta-blocker use
Vasodilators
Most common: hydralazine and isosorbide dinitrate
Additional tx in refractory pts
Reduction in mortality and hospitalizations
*hydralazine-nitrate combo alternative tx for thise w/poor renal fxn (can’t have ACE-I or ARB)
Cardiogenic Shock (Decompensated HF)
Treat with IV diuretics and inotropic Therapy:
- Milirinone
- Dobutamine
- Dopamine
All very different
They all increase contractility and CO
Milirinone
- Phosphodiesterase inhibitor
- doesn’t require alpha and beta receptors so may be good for pts in full beta block - Raises levels of cAMP –> increases contractility
(also HR a little) - Vasodilator
- especially in veins and pulmonary vasculature - Combined inotropic and preload reducing actions
- Most beneficial in HF pts w/low CO, congestion, and increased SVR and PulmonaryVR
- Decreases BP
Dobutamine
Stimulates B1 and a little B2
-since HF pts have less B1, then not as much of a response as in normal people
- Increase inotropy and lesser degree chronotropy
- Tends to cause reduction in SVR while increasing SV and CO
- Tolerance after 72 hours of IV
- W/more it starts to get a-1
Dopamine
- Beta 1 and dopa receptors
- Greater A1 receptor action than dobutamine
- Ex dependent on dose
- Low: dopaminergic response
- Middle: Stimulate B1: +inotropic and +chronotropic
- Large: Greater a-1 stimulation
- Increases BP
- if venoconstriction also occurs, then it can increase preload
Tx of End Stage HF
- IV inotropes (oral doesn’t work anymore)
- LV Assist Devices
- in series w/LV
- suck blood out of weak LV and pump though aorta - Cardiac Transplant
- Palliative Care
