Heart Failure Flashcards
Define heart failure
- inability of heart to pump blood at rate that can keep up with the needs of tissues
- any structural or functional disorder that impairs the ability of the ventricle to fill with or eject blood
- main clinical symptoms: dyspnea, fatigue, fluid retention
Define the NYHA classes of heart failure
- Class I: with cardiac disease but no limitations on physical activity
- Class II: with cardiac disease, comfortable at rest but slight limitation on physical activity
- Class III: with cardiac disease, comfortable at rest but marked limitation on physical activity
- Class IV: with cardiac disease, symptoms at rest and inability to carry out any physical activity
What neurohormonal levels are elevated in patients with heart failure?
- norepinephrine (increases HR)
- angiotensin II
- aldosterone
- endothelin
- vasopressin
- cytokines
- all of these play a major role in remodeling of the heart - work to increase prelaod and afterload which is acutely good but chronically causes damage to the myocardium and kidneys
Describe stage A in the development of heart failure, according to the JACC
Stage A: at high risk for HF but no evidence of disease (HTN, diabetes, obesity, family history, on cardiotoxic drugs)
- Therapy: try to control risk factors, encourage exercise, in rare cases use ACEI or ARB
Describe stage B in heart failure, according to the JACC
Stage B: structural heart disease but no signs or symptoms (previous MI, LVH, low EF, valve disease)
- Therapy: control risk factors, ACEI or ARB, sometimes β blockers
Describe stage C in heart failure, according to the JACC
Stage C: structural heart disease with prior or current symptoms (SOB, fatigue, reduced exercise tolerance)
- Therapy: control risk factors, restrict salt intake, ACEI or ARB, diuretics for fluid retention, β blocker, sometimes digoxin, sometimes pacemaker or defibrillator
Describe stage D in heart failure, according to JACC
Stage D: refractory heart failure requiring specialized interventions (symptoms at rest with maximal medical therapy)
- Therapy: appropriate measures from other stages, and make decisions about end of life care
What are the beneficial hemodynamic effects of ACEIs in the setting of heart failure?
- arteriovenous vasodilation, which reduces pulmonary capillary wedge pressure and LVEDP (less lung congestion), decreases systemic vascular resistance and BP, increases CO and exercise tolerance
What are three important things that don’t develop when using ACEIs when compared to other vasodilators?
- no neurohormonal activation
- no reflex tachycardia
- no development of tolerance
Name the angiotensin receptor blockers, a benefit to use over ACEIs, and potential side effects
- losartan, irbesartan (most commonly prescribed)
- valsartan, candesartan, olmesartan, telmisarten
- benefit: no cough! (does not effect bradykinin levels)
- SE: decreases GFR, raises potassium, hypotension, potential for angioedema
What are the roles of diuretics in heart failure?
- decreases the volume/preload to improve symptoms of congestion
- improves arterial distensibility
HOWEVER, no direct effect on CO and neurohormonal activation of norepi/angiotensin II
Besides ACEIs, what other drug can reduce remodeling and decrease risk of death?
- spironolactone or eplerenone (aldosterone antagonists)
- often used in conjunction with ACEI
- aldosterone worsens fibrosis in heart and is elevated in CHF patients
What is important to remember about β blockers in the context of CHF?
- can inhibit the adverse effects of SNS
- start at very low dose and increase slowly if tolerated
- bisoprolol, metoprolol, and carvedilol have been proved to reduce risk of death and hospitalization
How does digoxin work?
- inhibits the cardiac Na-K ATPase, which results in higher intracellular Na
- this reduces activity of Na/Ca exchanger, which results in higher intracellular Ca
- this increases contractility
- also has effect on neuronal Na-K ATPase, which results in increased vagal activity to decrease HR
What are the hemodynamic effects of digoxin?
- increases cardiac output, LVEF, natriuresis
- decreased LVEDP, neurohormonal activation
