Flashcards in Drugs For Heart Failure (Kruse) Deck (43):
What are some adverse effects of loops?
Sulfonamide hypersensitivity (not ethacrinic acid)
This cardiac glycoside is used in the tx of heart failure, tachyarrhythmias, and shock. It is well absorbed and widely distributed
What is the MOA of digoxin?
Inhibits membrane-bound Na/K ATPase and increase myocardial contractility (50-100% in individuals with HF)
Digoxin-induced elevated intracellular Ca increases the activity of Ca-dependent ___ channels.
Increased Ca-dependent K channel activity promotes K efflux and a more rapid repolarization
The most common cardiac manifestation of digoxin toxicity is ___
If allowed to progress, the tachycardia may deteriorate into fibrillation that could be fatal unless corrected
At toxic doses of digoxin, what occurs in the atrial muscle?
Decreased refractory period
At toxic doses of digoxin, what occurs at the AV node?
Decreased refractory period
At toxic doses of digoxin, what occurs in the purkinje system and ventricular muscle?
Describe the ECG findings when digoxin is effective at a therapeutic, non-toxic dose:
Increased PR interval
Decreased QT interval
At high doses, what type of drug (or drug name) can potentiate the toxic effects of digoxin?
Furosemide (loop diuretic)
Digoxin and K bind to competing sites on the ___
What class of agents can increase both the force of heart contraction and produce vasodilation?
Milrinone is a ___
What is the MOA of bipyridines?
Cause selective inhibition of PDE3 phosphodiesterase enzyme (PDE3 degrades cAMP)
What are bipyridines approved for?
SHORT-TERM support of circulation in ADVANCED HF
Chronic tx does not show improvement in quality or length of life and may increase mortality
What is the 1st step in the tx of heart failure?
Control HTN, hyperlipidemia, glucose metabolism (diabetes), obesity
How does digoxin ultimately increase myocardial contractility?
Increasing the releasable Ca from the SR (more accumulates in SR d/t its MOA)
Parasympathomimetic effects of digoxin are inhibited by __
Where is cholinergic innervation more concentrated in the heart?
Increased actions of digoxin on atrial and AV nodes comapred to purkinje or ventricular function
What is the most common site of digoxin toxicity outside of the heart?
GI --> anorexia, nausea, vomitting, and diarrhea
___kalemia can reduce the effects of digoxin (especially the toxic effects
___kalemia can potentiate the toxic effects of digoxin
How are bipyridines administered?
Only available for parenteral
These compounds are non-specific PDE inhibitors and their use in HF is limited by their lack of specificity and concomitant side effects
Caffeine and theophylline
What toxicity is associated with Milrinone?
What are the prototypical B-adrenergic and dopaminergic agonists?
Dobutamine (B agonist)
Dopamine (Dopaminergic agonist)
What are the MOA of B-adrenergic and dopaminergic agonists?
Act via stimulation of cardiac myocyte dopamine D1 receptor (Dopamine) and B1-adrenergic receptor (Dobutamine)
___ is the B agonist of choice for management of pts with systolic dysfunction and HF. It increases stroke volume d/t its positive inotropic action and an increase in CO
At high doses ___ causes peripheral arterial and venous constriction via a-adrenergic receptor stimulation, which may be desirable in pts where circulatory failure is the result of vasodilation (sepsis, anaphylaxis)
These diuretics are widely used in the treatment of heart failure
Loops --> furosemide, bumetanide, and torsemide are most commonly used
These diuretics are most frequently used in tx of systemic HTN and have a more restricted role in tx of HF
What are the prototypical aldosterone antagonists?
Spironolactone and eplerenone
This ADH antagonist can tx HF and SIADH and is administered parenterally with a 1/2 life of 5-10 hrs
This ADH antagonist is a selective antagonist of V2 ADH rcepetors that is given PO
What toxicities are associate with ADH antagonists?
Conivaptan can cause hypernatremia, nephrogenic DI
What drug class can be given to potentiate the effects of diuretics in HF?
What drug class can be given to potentiate the effects of diuretics in HF if a pt is intolerant to a specific drug class that causes a characteristic cough and angioedema?
Act through AT1 receptors
What is the MOA of Isosorbide dinitrate?
Releases NO and activates guanylyl cyclase; is a VENODILATOR
Used in acute and chronic HF as well as angina
What arteriolar dilator is used in combo with nitrates to reduce mortality in pts w/ HF? What are its toxicities?
Tachycardia, fluid retention, lupus-like syndrome
This drug is used for acute cardiac decompensation and hypertensive emergencies (malignant HTN)
Combined arteriolar and venodilator
___ is a recombinant form of human BNP that has been approved for tx of acutely decompensated HF with dyspnea at rest or with minimal activity
What is the MOA of Nesiritide?
Binds to GC receptor on vascular smooth muscle and endothelial cells, increasing intracellular cGMP, resulting in smooth muscle relaxation
___=B1 selective blocker, off-label use for HF in USA
___=Nonselective B blocker and a-1 selective blocker
___=B1 selective blocker, mild-to-moderate HF