04.21 - CHF Pharm (Ostrom) Flashcards
Tx for Stage A CHF
Preventive Measures, ACEi’s and ARB’s
___ is a vasodilator that acts directly on vascular SM
Hydralazine
2 “other” Considerations for Diuretic Tx in CHF
ACEi’s and ARB’s also have diuretic effects; Spirinolactone, Eplerenone have benefits beyond diuretic effect
3 BB’s approved for CHF
Metoprolol, Carvedilol, Bisoprolol (Carved Bison Meat)
3 most common AE’s of ACEi’s
First dose hypotension, Na depletion, Dry Cough
3 most common AE’s of Aliskerin
First dose hypotension, Hyperkalemia, Angioedema
3 most common AE’s of ARB’s
First dose hypotension, Hyperkalemia, Hepatic Dysfunction
4 Drugs that interact with Digoxin
Quinidine, Amiodarone, Verapamil, Diuretics
ACEi effect on Bradykinin
Increase levels due to inhibitor of metabolism
ACEi’s end in
pril
Advantage of ACEi’s
Little effect on lipids or sexual function
Advantage of Milrinone over Dobutamine
Milrinone doesn’t desensitize receptors
Aldosterone and AngII combine to stimulate
fibrosis in cardiac tissue
Angiotensin Receptor Antagonists end in
tan
Arterial Vasodilators alone may what change in Frank-Starling Curve
Left and Upward
Arterial Vasodilators work best when combined with
Inotrope and Diuretic
At what stage do you add beta blockers
B (NYHA I)
At what stage do you add Diuretic, Digoxin
C (NYHA II, III)
BB approved for CHF only in Europe
Nebivolol
BB least likely to induce increase TPR cause by reflex vasoconstriction
Carvedilol: alpha1 antagonist
BB that potentiates NO in vasculature; approved for HTN but not CHF
Nevivolol
Benefit of Nesiritide is comparable to
IV nitroglycerin but hypotension may persist longer
Can hemodynamic drugs slow progression of CHF?
No
Diuretics effects on Preload, CO
Reduce Preload, Do NOT increase CO
Do Diuretics improve survival or prognosis in CHF?
No (except for spironolactone/Eplerenone)
Dobutamine and Milrinone can cause
Arrhythmias
Does mortality change in CHF with Digoxin
Yes, reduced
Drug interactions of Aliskerin
Inhibits P-Glycoprotein (Erythromycin, Amiodarone)
Effect on K of Spirinolactone
K-Sparing
Hemodynamic effects of Natriuretic Peptides
(1) Reduce vent filling pressure; (2) Inhibit renin, aldosterone release; (3) Inhibit Na reabs; (4) Selective afferent arteriole vasodilation
How can Loop Diuretics cause arrhythmias
Hypokalemia
How do Arterial Vasodilators Increase CO
Reduce Afterload
How do beta blockers affect receptor numbers
Increase (reverse desensitization)
How do you favor gene regulation pathway over inotropic pathway
Slower, sustained catecholamine signaling (BAR internalization)
How does BP change with Atropine?
Doesn’t
How does Digoxin affect Pressure-Volume Curve
Shifts upward: CO increases at each level of preload
How is Digoxin excreted
Kidneys
In which patients is benefit of Digoxin greatest
EF < 0.25, Cardiac Enlargement, NYHA III/IV
Increased Aldosterone may worsen
LV function
Interactions of Diuretics
NSAIDs reduce efficacy
Leading cause of death in Class II, III CHF?
Arrhythmias
Long term hemodynamic effects of BB’s in CHF
Inc CO, Decreased LVEDP
Main ACEi adverse effect
Dry Cough
Mitogenic effects of Ang II
Hypertrophy of myocytes and vascular SM; Cardiac and vascular fibrosis, remodeling; Atherosclerosis
MOA of Aliskerin
Renin inhibitor
MOA of Dobutamine
Beta-1-selective agonist: Intropic effects thru cAMP, PKA
MOA of Hydrochlorothiazide
Diuretic
MOA of Milrinone
PDE inhibitor: Increase cAMP level
MOA of Neseritide (3)
(1) Vaso, Venodilation; (2) Increase GFR, Decrease Na reab; (3) Suppress Renin-Ag and SNS
Most commonly used Diuretics
Furosemide (Loop); Spirinolactone (Aldosterone ant)
Most powerful diuretic class
Loop
Need to combine arterial vasodilator with __ to reduce both preload and afterload
Venodilator (nitrate)
Preganancy status of ACEi’s
Fetotoxic
Primary Vasodilators:
Hydralazine, Nitrates
Renin inhibitor
Aliskiren
Role of Bradykinin
Vasodilator and antifibrotic mediator (downregulated by ACEi’s)
Role of Phosphobalmin
Regulates SR pump that removes Ca2
Short term hemodynamic effects of BB’s in CHF
Dec CO, BP
T/F: BB’s always decrease function in CHF?
False, actually improve
T/F: BB’s can’t slow progression of CHF
FALSE
Tachyphylaxis
Depletion of presynaptic vesicles within matter of minutes
Toxicities of Digoxin
AV Block, Atrial/Vent Arrhythmias, Visual Changes (Halos)
Toxicities of Diuretics
Electrolyte disturbances, Ototoxicity (Loop)
Toxicity of Hydralazine
Nausea, Anorexia, +FANA
Tx for Stage B CHF
Preventive, ACEi’s, ARB’s, Beta Blockers
Tx for Stage C CHF
Preventive, ACEi’s, ARB’s, BB’s, Digoxin/ Spironolactone
Tx for Stage D CHF
Preventive, ACEi’s, ARB’s, BB’s, Digoxin/ Spironolactone, IV inotropes, Transplant
Use of Hydralazine is limited to what patients
Can’t tolerate ACEi’s
Use of Nesiritide should be limited to those who
do not respond to nitroglycerin
What attenuates deleterious effects of high levels of NE and Epi?
Beta blockers
What does reduced afterload do to pressure-volume curve
Left and Upward
What is counterintuitive about BB’s in CHF tx?
Slow progression
What is Lusitropy
Activation of beta receptors also activates SR pump that removes Ca2+
What is needed for rapid onset of Digoxin action
Loading dose
What is Nesiritide
Recombinant b-type natriuretic peptide (BNP)
What is primary goal of tx in patients with early (A and B) CHF?
Reign in overactivation of neurohormonal mediators, such as catecholamines and Ang 2
What limits long-term dobutamine use
Desensitization of receptors; Arrhythmias
What prevents vasodilator effect of Dobutamine?
BB therapy (creates unoppose a1 agonist)
When is Nesiritide indicated?
IV tx of decompensated class IV (decompensated) CHF
Which anti-HTN drugs should never be given to pregnant or nursing women?
ACEi’s or ARB’s
Which does not increase vasodilator Bradykinin
ARB’s
Which is more effective at reducing CHF endopoints: ARB’s or ACEi’s?
Equal
Which is preferred: ACEi’s or ARB’s?
ACEi’s, unless patient can’t tolerate side effects
Which shows aldosterone “escape”?: ACEi or ARB
ACEi
Who responds less favorably to ACEi’s
Aas or Low-renin HTN patients
