Congestive heart failure Flashcards
1
Q
Diuretics
A
furosemide, bumetanide, torsemide, ethacrynic acid (if allergic to sulfonamides), thiazides (for mild forms of CHF)
- Most common: furosemide, bumetanide, torsemide
- Ethacrynic acid can be used if the patient is allergic to sulfonamides
- Thiazides only for mild CHF
- Sodium restriction
2
Q
ACE inhibitors
A
- Renin is released in heart failure due to:
- Reduced renal perfusion
- Increased SYM tone
- Antihypertensive drugs that stimulate renin secretion
- Diuretics by decreasing delivery of Na to the macula densa
- Vasodilators by reducing renal perfusion pressure
- Drugs that inhibit feedback inhibition (ang 2 binding to JG cells)
- ACEi diminish cardiac work
- Decrease afterload - reduced angiotensin vasoconstriction
- Decreased preload - reduced aldosterone release and fluid volume
- Effective drugs: captopril, enalapril, lisinopril, ramipril, quinapril
3
Q
ARBs
A
- Drugs: azilsartan, candesartan, eprosartan, irbesartan, losartan, olmisartan, telmisartan, or valsartan
- Two important differences to ACEi
- More specific - don’t affect bradykinin metabolism (no cough) - only hit the angiotensin aspect
- More complete inhibition - because enzymes other than ACE can convert angio 1->2
4
Q
other vasodilators
A
nitroprusside, nitroglycerine, hydralazine + isosorbide dinitrate
- Sodium nitroprusside
- IV infusiton for decompensated CHF
- Balanced: vasodilates and arteriole dilates
- Oral nitroglycerine or isosorbide dinitrate dilates veins more than arteries = lowering preload more than afterload
5
Q
CCBs
A
amlodipine, felodipine
Amlodipine, felodipine (dihydropuridines) - relax art SM and produce vasodilatation
Verapamil and diltiazem inhibit cardiac contraction (SA node impuls generation and AV node conduction)
Don’t use these in treatment of CHF because they depress the heart
6
Q
beta blockers
A
bisoprolol, carvedilol, metoprolol
- Produce negative inotropic effects-> worsen ventricular function and can be potenitlaly harmful in CHF
- Despite this may clinical studies who that long term treatment with certain b-blockers (bisprolol, carvedilol, metoprolol, and nebivolol) improves symptoms by slowing HR and contraction velocity to improve
- CO, exercise tol, ventricular fucntion
- Bisprolol, carvedilol and metoprolol - show reduced mortality in severe stable HF, (not seen with bucindolol)
7
Q
aldosterone antagonists
A
spironolactone, eplerenone
- Spironolactone and eplerone have been shown to reduce mortality in HF
- Potential AE
- Hyperkalemia
- Gynecomastica (eplerenone doesn’t do this)
8
Q
digoxin
A
inotropic drug
- Certain drugs can enhance the tox: quinidine, amiodarone, captopril, verapamil, diltiazem and cyclosporine - many antibiotics increase digoxin absorption
- Digoxin tox
- Excreted by kidneys - be careful if not perfused well
- Early signs: GI
- Anorexia, nausea, vomiting, diarrhe, abdominal discomfort
- Later signs: cardiac
- Stimulate arrythmias (worse one is v-fib)
- Treatment of tox
- Discontinue digoxin
- Correct hypokalemia and hypomagnesemia
- Lidocaine if arrhythmic
- Digoxin antibodies (fab fragment) - digibind
9
Q
inamrinone
A
inotropic drug
- Other inotropes (PDE inhibitors)
- Inamrinone (amrinone), milrinone are given by injection
- Increase cAMP = increase Ca flux into the heart
- Like digoxin use for acute HF but not chronically
10
Q
milrinone
A
inotropic drug
- Other inotropes (PDE inhibitors)
- Inamrinone (amrinone), milrinone are given by injection
- Increase cAMP = increase Ca flux into the heart
- Like digoxin use for acute HF but not chronically
11
Q
dobutamine
A
b-adrenergic and dopaminergic agonists
- Other inotropes (b- adrenergic and dopaminergic agonists)
- Dopamine and b1 agonsts like dobutamine are infused IV to increase contractility in acute CHF
- B2-agonsits like albuterol, pirbuterol relax vasular smooth muscles and have been tested as vasodilators in CHF
