Treatment of CHF Flashcards
Class I CHF is defined by what?
Low ejection fraction
Class I is treated by>
ACEi or ARBs
Why are ACEi and ARBs good CHF treatments>
THey prevent and reverse the myogenic effects of ANgiotensin II such as: hypertrophy of cardiac myocytes hypertrophy of vascular smooth muscle cardiac and ventricular fibrosis atherosclerosis
What effect do ACEi and ARBs have on Bradykinin
They increase its concentration, It is a vasodilator and also an antifibrotic mediator
What are the harmful drug interactions with ACEi?
Diuretic therapies EXCEPT spironolactone
Contraindications for ACEi and ARBs
angioedema (mostly just ACEi), pregnancy, renal insufficiency, hepatic insufficiency
Keep in mind the pregnancy issue
ok
Why were beta blockers previously contraindicated in CHF?
Because Beta receptors are the delivery site for sympathetic action on the heart so it makes sense that you wouldn’t want to block this if the pump is failing
How are Beta blockers helpful in management of CHF
They attenuate the not so great effects of chronic high epinephrine and norepinephrine such as: increased myocardial oxygen consumption beta receptor downregulation arrhythmias fibrosis and myocyte apoptosis
Short term hemodynamic effects of beta blockers
reduced cardiac output and reduced blood pressure
Long term effects of beta blockers in CHF?
increased CO, decreased LVEDP…it may get worse before it gets better
Beta blockers in summary
Reverse desensitization, increase receptor number, restore fast signaling modes (contractility) over slow signaling modes (gene expression).
What beta blockers are used in CHF
Metoprolol
What drug do you add when pts become class II
diuretics
What diuretics are most commonly used
High ceiling Diuretics like Furosemide or Bumetanide
Explain teh diuretic effects of ACEi’s and ARBs
They reduce sodium retention by preventing aldosterone release, their effect is not always sufficient tp prevent edema, the dose of the diuretic should be lowered
How to spironolactone and epelerone have benefits beyond their diuretic effect
Aldosterone can have mitogenic and fibrogenic effects on the myocardium that stimulate fibrosis- spironolactone blocks this
Digoxin mechanism
inhibits the Na/K ATPase transporter which leads to increased intracellular calcium levels and increased ionotrophy (contractility)
Digoxin toxicity
Very narrow therapeutic window and a great deal of variability b/w patients.
Arrhythmias, blurred vision, yellow halo, headache, fatigue, dizziness, seizures. Use Digi bind to reomve it in life threatening situations
Digoxin drug interactions
tons of them. ANything that changes its metabolism may move it out of the therapeutic wondow.
Quinidine decreases levels, Amiodarone, VERAPAMIL
Greatest benefit of digoxin sen in what pts
those with ejection fraction of 25% and less and with cardiac enlargement
Add what to therapy for class III
Digoxin
Add what to Therapy for class IV
Strong vasodilators transplants and deveices
Hydralazine
vasodilator
