Drugs For Heart Failure

Front 1

3 major approaches to treating cardiac failure

Back 1

1)increase cardiac output
2)reduce blood volume
3)reduce afterload

Front 2

3 major mechanisms that a failing heart undergoes to try and compensate for the failure

Back 2

1)increase adrenergic activity (increase heart rate and vasoconstriction resulting in increased preload)
2)retention of fliuds (increases peripheral resistance and retention of sodium and water)
3)hypertrophy of cardiac muscle

Front 3

Digoxin

Back 3

Digoxin; Derived from foxglove; A cardian glycoside used aith other agents for the treatment of CHF. It is a positive ionotropic agent that increases cardiac output but has a low therapeutic index therefore, has a high probability of causing toxicity. It inhibits the cellular enzyme, Na/K activated ATPase which is found in all body cells so Digoxin is considered the universal poison. The inhibition of this enzyme causes an increase in intracellular Na in the heart cells, which leads to the Na/Ca exchanger bringing in Ca eventually leading to a sustained contraction. Tolerance and excretion are compromised in the elderly due to diminution

Front 4

Three major mechanisms that a failing heart evokes to enhance cardian output?

Back 4

1) increased adrenergic activity
2) retention of fluids
3)hypertropy of cardiac muscle

Front 5

cardiac glycoside that inhibits Na/K ATPase. increases force of contraction (positive inotropic agent). Incrase cardiac output. Universal poison. Hard to control the drug concentration. Takes days to take effect. Inhibited by potassium, therefore, hyperkalemia reduces it's conc and hypokalemia increases its conc. known to control ventricular rates in atrial fibrillation and atrial flutter by increasing vagal activity through the AV node although cacium channel blockers are more effective.

Back 5

digoxin

Front 6

Treatment of digoxin toxicity?

Back 6

potassium administration and antidigoxin immunotherapy

Front 7

First line therapy for CHF?

Back 7

ACE inhibtors (-pril) and beta blockers (-olol)

Front 8

positive inotropic agents that increase cardiac output and decrease ventricular filling pressure.

Back 8

beta-adrenergic agonists (Dobutamine and Dopamine)

Front 9

Recommended in pts with left ventricular dysfunction and recent MI. Effective in the managment of pts with chronic CHF. Standard in use after MI. INCREASE serum K levels. AE includes dry cough and fetotoxicity. Lowers vascular resistance, venous tone and blood pressure without reflex increase of CO, rate or contractility. Diminishes bradykinin (vasodilator) inactivation. Decreases secretion of aldosterone. Reduces angiotension II.

Back 9

ACE inhibitors (-pril)

Front 10

specific angiotension II antagonist that blocks the AT1 receptor that mediates the vasopressor and aldosterone effects. Mainly used for HT but is FDA approved to treat heart failure in pts intolerant to ACE inhibitors

Back 10

Volsartan (angiotensin receptor blocker)

Front 11

Most useful in pts whom the principal sympotom is dyspnea. Most helpful in reducing filling pressures and sympotoms of pulmonary congestion. Dilates veins and venules.

Back 11

Nitrates

Front 12

beta blocker used exclusively for CHF. Is a combined alpha and nonselective beta blocker. Believed to be due to a reduced remodeling (hypertrophy). Also used in the managment of HT

Back 12

Carvedilol

Front 13

Intravenous preparation of human B-type natriuretic peptide (BNP), a naturally occuring hormone produced in the ventricles of the heart. Produced atrial and venous dilation, decrease TPR, decreased arterial pressure, decreased right atrial pressure, and deceased mean pulmonary arterial pressure. Causes universal renal failue

Back 13

Nesiritide