Pharm Drugs Used To Treat Heart Failure

Front 1

MOA of Cardiac glycosides (eg. digoxin)

Back 1

It inhibit the Na+/K+ ATPase so that more intracellular Na+ is retained; which alters the Na-Ca exchange, so that less Ca is removed from the cell, thus, increasing cardiac contractility.

Front 2

Digoxin is used in

Back 2

Nodal fibrillation and CHF

Front 3

Digoxin toxicity can be precipitated by

Back 3

Hypokalemia

Front 4

Antidote for digoxin toxicity

Back 4

Digoxin antibodies (Fab fragments; Digibind)

Front 5

Phosphodiesterase inhibitors that increase mortality and have been found to have NO beneficial effects with chronic CHF. What is the MOA.

Back 5

Amrinone and milrinone

Inhibits phosphodiesterase isozyme III, found in cardiac and smooth muscle. Inhibition of the enzyme results in increase cAMP, which opens the Ca channel, which leads to increased contractility. It is used for treatment of acute decompensated heart failure.

Front 6

SE of amrinone

Back 6

Thrombocytopenia

Front 7

Beta 1 agonists used in acute CHF, its MOA, and its usefulness.

Back 7

Dobutamine: beta-1 agonist that increases cardiac output. It is used to treat decompensated CHF or cardiogenic shock.

Dopamine: At high dosage, is an alpha1 agonist, which causes vasoconstriction that leads to systolic and diastolic blood pressure. At lower dosage, is a beta and D1 agonist, which increases heart rate and contractility; thereby increasing cardiac output through stimulation of beta-1 receptors (D1 receptors increase renal perfusion).

Dobutamine and dopamine are not used for chronic failure because of tolerance, lack of oral efficacy, and significant arrhthmogenic effects.

Front 8

Diuretics work in CHF by

Back 8

Reducing preload

Front 9

Beta blockers work in CHRONIC CHF by?

Back 9

It can reduced mortality, possibly by decreasing remodeling.

Reducing progression of heart failure. By blocking beta1-receptors, heart rate and contractility are decreased, thereby leading to decreased cardiac output. With decrease cardiac output, there is a reflexive peripheral vasoconstriction (although, with decrease cardiac output and peripheral vasoconstriction, the balance results in decrease blood pressure).


(never use in acute heart failure, especially if systolic dysfunction is marked).

Front 10

Peptide drug used to treat CHF

Back 10

Nesiritide (BNP)

Front 11

MOA of nesiritide and its clinical application?

Back 11

Increasing sodium excretion and decreases arterial and venous tone by being a vasodilator and a diuretic.

Used for acute severe decompensated failure.

Front 12

SE of nesiritide

Back 12

Excessive hypotension and kidney failure

Front 13

Agent used in CHF that is a selective alpha1 and nonselective beta blocker

Back 13

Carvedilol

Front 14

Agent used in acutely decompensated CHF resembling natriuretic peptide

Back 14

Nesiritide (Natrecor)

Front 15

What are the two homeostatic responses to depressed cardiac output, and their consequences?

Back 15

Sympathetic nervous system (tachycardia and vasoconstriction) and renin-angiotension-aldosterone system.

Although these compensatory responses can temporarily improve cardiac output, they also increase the load on the heart, and the increased load contributes to further long-term decline in cardiac function. This results in end-diastolic fiber length to be increased.

Front 16

How does digoxin decrease the compensatory sympathetic and renal responses of heart failure?

Back 16

It increases contractility with ventricular ejection and cardiac output, decreased end-systolic and end-diastolic size, and increase in renal perfusion.

The decreased sympathetic tone reduces heart rate, preload, and afterload.

Front 17

What ECK changes may you see with digoxin?

Back 17

Due to decrease AV conduction velocity, increased PR interval. Along with, shorten QT, and change in repolarization with inversion or flattening of the T wave, and ST depression may occur late.

There can also be premature ventricular beats, bigeminy, ventricular tachycardia, ventricular fibrillation, atrial tachycardia or fibrillation, AV nodal tachycardia, AV blockade.

Front 18

What are the SE, or toxicity from digitalis?

Back 18

Cardiac arrhythmias; GI upset, nausea, vomiting, and diarrhea; blurry yellow vision

Intracellular calcium overload results in delayed afterdepolarizatoin, which may evoke extrasystoles, tachycardia, or fibrillation in any part of the heart. Premature ventricular beats can occur.

Front 19

Although digitalis may improve functional status (reducing symptoms), it may not?

Back 19

Prolong life!

Front 20

The parasympathomimetic action of digitalis may accomplish?

Back 20

Reduction in atrial fibrillation.

Front 21

What are some major exacerbation of digoxin? How should suicidal overdose or acute intoxication from digoxin be treated?

Back 21

Quinidine (displaces digoxin on albumin, increases serum levels of digoxin), renal failure (decrease excretion), and hypokalemia (e.g., from diuretics; therefore, treat with K supplements); hypomagnesium, and hypercalcemia.

Acute intoxication from digoxin can cause hyperkalemia, and should not be treated with supplemental potassium.

Front 22

What is the first line therapy for both systolic and diastolic failure?

Back 22

Diuretics and angiotensin antagonist:

Furosemide for immediate reduction of the pulmonary congestion and severe edema associated with acute heart failure and moderate or severe chronic failure.

hydrochlorothiazide: sometimes sufficient for mild chronic failure

Spironolactone and eplerenone (aldosterone antagonists diuretics) have significant long-term benefits and can reduced mortality in chronic failure.

Angiotensin receptor blockers (e.g., losartan) and ACE inhibitors (e.g., captopril).

Front 23

Nitroprusside is used for and its MOA?

Back 23

It vasodilate via by increase NO in smooth muscle (by incrase cGMP). It dilates the veins a lot more than the arteries; therefore, preload and afterload.

It is used for acute SEVERE decompensated failure. Also, with acute hypertensive crisis.

It can cause excessive hypothension, thiocyanate and cyanide toxicity ("Monday disease" in industrial exposure).

Front 24

Nesiritide MOA, and its clinical application?

Back 24

Atrial peptide vasodilator and diuretic.

It is used for acute severe decompensated failure.

Front 25

What drug has been least useful in heart failure?

Back 25

Calcium channel blockers. Although they cause decreased afterload, they cause too much cardiac depression.

Front 26

What is the best documented mechanism of beneficial action of cardiac glycosides (e.g., digoxin)?

Back 26

An increase in systolic cytoplasmic calcium levels by inhibiting Na/K ATPase and increasing cytoplasmic Na, which in turn slows down the extrusion of Ca2+ by the sodium-calcium exchanger (3 Na is pumped in while 1 Ca is pumped out; therefore, increase in Na prevents Ca from leaving)

Front 27

A PT who has been taking digoxin for several years for atrial fibrillation and chornic heart failure is about to receive atropine for another condition. A common effect of digoxin (at therapeutic blood levels) that can be almost entirely blocked by atropine is?

Back 27

Digoxin increases PR interval (which represents slowing of AV conduction) on ECG, and this parasympathomimetic effects of digitalis can be blocked by muscarinic blockers such as atropine.

Front 28

A 65 year old woman has been admitted to the coronary care unit with a left ventricular myocardial infarction. She develops acute severe heart failure with marked pulmonary edema, but no evidence of peripheral edema or weight gain. What drug will be most helpful?

Back 28

Furosemide, a loop diuretic. Not only does it reduce preload and edema by a powerful diuretic action on the thick ascending limb, it is also a vasodilator on the pulmonary vessels.

Front 29

What is is most likely to contribute to the arrhythmogenic effect of digoxin?

Back 29

Increased intracellular calcium.

Front 30

What drug has been shown to reduce mortality in chronic CHF?

Back 30

Spironolactone

Front 31

Which one of the following drugs is associated with clinically useful or physiologically important positive inotropic effect?

Back 31

Dobutamine.

ACE inhibitors, angiotensin receptor blockers, are very useful in heart failure, but have no inotropic effect.

Front 32

If hemodynamics are measured using the Frank-Starling curve before and after therapy with the PT at rest, successful treatment of acute heart failure will result in?

Back 32

Shorter diastolic fiber length and greater contractility.

Compensatory responses result with increase in fiber length. Heart failure is associated with reduced contractile force, stroke volume, and cardiac output at any diastolic fiber length. Successful therapies attempt to partial reverse these.

Front 33

The DOC in most cases of heart failure is?

Back 33

For both systolic and diastolic heart failure, it is furosemide.

Front 34

What has been shown to prolong life in PTs with chronic CHF but has a negative inotropic effect on cardiac contractility?

Back 34

Beta blockers, such as carvedilol

Front 35

What is a beta-1 selective agonist sometimes used in acute heart failure?

Back 35

Dobutamine

Front 36

What is the DOC in treating suicidal overdose of digitoxin?

Back 36

digoxin antibodies, Digibind.

Front 37

What is the SE of furosemide, hydrochlorothiazide, and spironolactone?

Back 37

Furosemide: ototoxicity, hypovolemia, and hypokalemia.

Hydrochlorothiazide: hypokalemia, hyperglycemia, hyperuricemia, hyperlipidemia.

Spironolactone: hyperkalemia, gynecomastia.

Front 38

Captopril SE?

Back 38

Cough, renal damage, and hyperkalemia.