Cardiac failure Flashcards
What are the adverse consequences of heart failure?
Impaired cardiac output = muscle fatigue and activation of RAAS = Na+ retension = less diuresis = high venous pressure and oedema
What are the 3 main underlying causes of heart failure? How does this lead to impaired CO?
- High afterload (resistance to CO) = less blood ejected per heartbeat
- Heart valves not closing properly = less blood available to eject per heartbeat
- Heart muscle disease (AMI, etc) = less blood ejected per heartbeat
What are the 5 principles of treatment for cardiac failure? (How do we treat it?)
- Relieve underlying condition
- Relieve aggravating conditions (anaemia)
- Reduce preload to reduce oedema
- Increase CO to reduce muscle fatigue
- Reduce TPR to reduce skeletal and cardiac muscle fatigue
What are the 3 positive inotropes used to treat cardiac failure?
Cardioglycosides, B1 agonists, and phosphodiesterase (PDE) inhibitors
Why are positive inotropes used to treat cardiac failure?
It increases Ca2+ levels = more Ca2+ to bind to troponin = stimulates heart muscle contraction
How do cardioglycosides work?
Inhibits Na/K-ATPase = more intracellular Na+ = Na+ gradient is changed = Na/Ca exchanger can’t work = calcium cannot be transported out of the cell
How do B1 agonists work?
Activates cardiac B1 receptors = activates adenylyl cyclase = more synthesis of cAMP = cAMP inhibits inactivation of calcium current = current is active for longer = intracellular calcium level increases
How do phosphodiesterase (PDE) inhibitors work?
Inhibits phosphodiesterase = inhibits emtabolism of cAMP = cAMP inhibits inactivation of calcium current = calcium current is active for longer = more intracellular calcium
How do venodilators like glyceryl trinitrate (GTN) work?
Dilates central veins = reduce venous pressure = less pressure in right atrium and pulmonary circuit = less LVEDP = lower CO
Why are diuretics like furosemide used in treating heart failure?
They reduce blood volume = less central venous pressure = reduces preload
How dooes an arteriolar dilator like hydralazine work?
Hydralazine prevents the oxidation of nitric oxide (NO) by inhibiting NADH oxidase = arteriolar dilation = easier perfusion of blood to the body
Why do we also use prazosin (A1 antagonist) in treating heart failure?
It reduces preload and afterload by dilating arteries and veins. This can help reduce oedema and cardiac work while increasing perfusion.
Why are we using ACE inhibitors and ARBs in treating cardiac failure?
They reduce afterload and preload (through diuretic and natriuretic effects & vasodilation). This reduces oedema and muscle fatigue
Why are beta-blockers used in treating cardiac failure?
It inhibits heart remodeling = lower death risk.
