Heart Failure (General) Flashcards
What is Heart Failure
Cardiac Output is not enough to meet metabolic demands of body
Progressive Syndrome
Causes of Heart Failure
Decreased Contractility:
- Diseases of Myocardium
- Cardiotoxic Drugs
- Pressure Overload
- Volume Overload
Restriction in Ventricular Filling:
- Diastolic Dysfunction
–> Ventricle Stiffness
Compensatory Mechanism during Heart Failure and their effect
When cardiac function significantly decreases compensatory mechanisms are triggered to maintain adequate CO
–> These mechanism make situation worse instead of better (Counter Regulatory)
Heart Failure
(Counter Regulatory Mechanisms)
Kidney interprets reduced prefusion as ineffective blood volume
- Kidney thinks body is bleeding
–> Stimulate Na+ and H2O retention (RAS)
Vasoconstriction
- Redistribute blood flow from non-essential organs to coronary and cerebral circulations
Ventricular Hypertrophy
- Remodeling of Heart and Hypertrophy
What are the two types of RAS Inhibitors
ACE Inhibitors
Angiotensin Receptor Blockers (ARBs)
RAS Inhibitors Mechanism of Action
Blocks formation of Ang II
- Inhibits release of aldosterone
- Reduced vascular resistance and afterload
- Improve tissue perfusion
- Reduces Na+ reabsorption
Beta-Adrenoceptor Antagonist Mechanism of Action
Reduces heart rate and blood pressure
- Prolongs Diastolic Filling
- Reduces Detrimental remodeling of heart
- Inhibits Renin
Beta-Adrenoceptor Antagonist Dosage
Normal Dose Beta-Adrenoceptor Antagonists reduce CO
- Need to be started at low doses and slowly increased
Aldosterone Receptor Antagonists Mechanism of Action
Competitive Antagonists of Aldosterone Receptor in Kidney
- Inhibits expression of transporters (Changes nuclear receptor’s gene expression)
Overall Effect: Inhibits Na+ reabsorption and Water Retention
What kind of Receptor are Aldosterone Receptors
Mineral Corticoid Receptor (Class 1 Nuclear)
Furosemide Mechanism of Action
Inhibits Na+/K+/2Cl- transporters in loop of Henle
- Potent Diuretic, more water eliminated
–> Decrease Na+ Reabsorption
–> Decrease Water Reabsorption
–> Decrease Blood Volume
Digoxin
- When to use?
Used in heart failure patients with:
- Chronic atrial fibrillation
- Remain symptomatic after ACEI and Diuretic treatments
Digoxin
- What class?
Cardiac Glycoside with Positive Inotropic Effect
- Changes the force of contraction of the heart
Digoxin
- Mechanism of Action
Inhibits Na+/K+ ATPase pump
- Increases Contraction Force
- Slows Heart Beat
- Increases Ventricular Filling
Less Na+ Influx and Less transport of Ca2+
- More Ca2+ in Cardiac Myocyte
–> Stronger Contractions
–> Slower Heartbeat
–> Increased Ventricular Filling
Isosorbide Mononitrate
- Mechanism of Action
Metabolized with release of NO
- Relax veins and Reduces central Venous Pressure
–> Reduces Preload