antichf Flashcards
indication Digitalis (cardiac glycoside, positive inotrope)
Both Acute and Chronic HF
MOA Digitalis (cardiac glycoside, positive inotrope)
Cellular Mech involves inhibition of Na/K ATPase in cell leading to increased Ca exchange and more Ca in SR. Calcium=contractility.
Drug Action/Pd Digitalis (cardiac glycoside, positive inotrope)
Decreases end-systolic & end-diastolic volumes (more efficient pumping so inc SV), increases CO & then inc renal perfusion, & dec sympathetic tone
PK Digitalis (cardiac glycoside, positive inotrope)
narrow therapeutic window–monitoring is needed, esp if dec GFR (renal clearance)
Route of Admin Digitalis (cardiac glycoside, positive inotrope)
oral usually. Can be reversed with an antibody
Adverse Effects Digitalis (cardiac glycoside, positive inotrope)
Calcium Mech=DAD’s
Notes Digitalis (cardiac glycoside, positive inotrope)
digitalis has another MOA (CNS mech-parasympathetics) used in anti-arrythmics.
indication Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)
Acute HF
MOA Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)
increased cAMP, stimulated by Gs-linked receptors (B1 & B2 on heart), increases opening of Ca channels, inc uptake of Ca into SR, inc pacemaker current, inc rate of conduction.
Drug Action/Pd Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)
note that this is the OPPOSITE of B-Blockers MOA (decrease cAMP) so don’t be confused
Notes Isoproterenol or Dobutamine (Beta agonist, inc cAMP, positive inotropes)
cAMP increases: Chronotropy, Dromotropy (conduction), Inotropy (contractility), and Lusitropy (relaxation)
indication Amirinone or Milrinone (PDE inhibitors, positive inotropes)
Acute HF
MOA Amirinone or Milrinone (PDE inhibitors, positive inotropes)
Remember that PDE normally degrades cAMP. If you stop PDE from degrading cAMP, you increase cAMP concentration
Drug Action/Pd Amirinone or Milrinone (PDE inhibitors, positive inotropes)
increased cAMP has inc chronotropy, dromotropy, inotropy and lusitropy
Route of Admin Amirinone or Milrinone (PDE inhibitors, positive inotropes)
note that this is a DIFFERENT MOA than B-agonists (BUT SAME PATHWAY) and can help overcome existing B-blockade if present.
Notes Amirinone or Milrinone (PDE inhibitors, positive inotropes)
do not confuse amirinone (PDE inhibitor) with amiodarone (class III anti-arrythmic, longest t 1/2), or amiloride (direct K-sparing diuretic)
indication Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)
Chronic and Acute HF
MOA Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)
reduce intravascular volume to reduce filling pressure (decrease preload–but little effect on CO–on flat part of Starling curve); reduce extracellular fluid so reduce peripheral edema (3rd spacing)
Drug Action/Pd Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)
Action depends on drug–Furosemide=vigorous, works on Na/K/2Cl txporter in LOH; Thiazide=DCT action Na/Cl, Aldo antags=mild diuresis
PK Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)
watch ototoxicity of loop diuretics, and remember that loop/thiazides are SULFA drugs and can cause ALLERGIES, also with loop/thiazides see hyperuricemia which can lead to GOUT! If pts are resistant to diuretics overcome by using COMBO therapy (use K-sparing & K-wasting for example)
Adverse Effects Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)
Note that hypokalemia potentiates digitalis toxicity
Notes Diuretics- Furosemide (loop), Thiazide (dct), Spironolactone/eplerenone (K-sparing aldo antags)
note: thiazides are calcium-sparing and are protective against kidney stones, have longer t 1/2 than loop. Don’t run hypok risk (digitalis tox) with K-sparers
Drug Name
Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)
indication Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)
Chronic and Acute HF
MOA Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)
the major action of the arteriolar vasodilators (Hydralazine, Minoxidil) is to reduce afterload on the heart and increase forward CO, ACEI’s/ARB’s also reduce afterload by inhibiting angiotensin effects (vasoconstriction, aldosterone)
Drug Action/Pd Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)
major desired action of Nitrates here is to dilate venous capacitance vessels (reduce venous return), but there are also arteriolar effects.
Adverse Effects Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)
careful with the ACEI/ARB’s (K-savers) and K-sparing diuretics-hyperkalemia
Notes Vasodilators: acute CHF-Nitroprusside, chronic CHF: ACEI’s & ARB’s (Hydralazine/Minoxidil), Prazocin (A1 antag)
remember that AT-II is a potent cardiomyocyte growth factor (hypertrophy) and fibroblast mitogen factor (hyperplasia)
Recommendations for treatment of CHRONIC HF:
Decrease Symptoms: Pulmonary: Venodilators (ACEI’s/ARBS, nitrates) and Diuretics. Prevent Ventricular Remodeling: ACEIs, BB’s and Aldo Antagonists (Spironolactone/eplerone) Prolong Survival of Pt: ACEI’s, BB, Aldo Antagonists, Nitrates + Hydralazine
Recommendations for treatment of Acute HF:
Reduce pulmonary congestion:Loop diuretics (Furosemide) and Venodilators (Nitroglycerin). Increase Cardiac Output: Increase contractility (B-agonists, PDE inhibitors, Digitalis); Afterload reducing agents (Nitroprusside) do NOT give a B-Blocker here
Causes of chronic HF
Ischemic Cardiomyopathy (CAD)=Most common, also dilated or hypertrophic cardiomyopathy.
Causes of acute HF
Acute MI, Arrythmias, Pericardial Tamponade, Massive PE
