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Drugs for treating heart failure. A. Introduction. Heart failure (HF) is due to the inability of the ventricles to pump sufficient blood thru-out the body. There are a number of causes of heart failure:. diabetes. from:http://www.nhlbi.nih.gov/health/dci/images/heart_coronary_artery.gif.

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a introduction
A. Introduction
  • Heart failure (HF) is due to the inability of the ventricles to pump sufficient blood thru-out the body.
from http www nhlbi nih gov health dci images heart coronary artery gif
from:http://www.nhlbi.nih.gov/health/dci/images/heart_coronary_artery.giffrom:http://www.nhlbi.nih.gov/health/dci/images/heart_coronary_artery.gif
  • coronary artery disease
slide10
About 20% of patients diagnosed with heart failure die within 1 year of diagnosis, about 50% die within 5 years.
slide11
There is NO cure for heart failure. Treatment goals involve treating/removing the underlying causes in order to improve the quality of life and/or extend life expectancy.
b pathophysiology of heart failure
B. Pathophysiology of heart failure
  • Two important factors which affect cardiac output, and therefore affect how heart failure is treated, are preload and afterload
1 preload
1. Preload
  • Immediately before the chambers of the heart contract they are filled to their maximum capacity with blood.
2 afterload
2. Afterload
  • For the left ventricle to pump blood out of the heart, it must overcome a fairly substantial pressure in the aorta.
slide17
Afterload is the pressure in the aorta that must be overcome for blood to be ejected from the left side of the heart.
3 left heart failure aka chf
3. Left heart failure aka CHF
  • If heart failure is on the left side (more common), excess blood accumulates in the left ventricle.
slide23
This results in classic symptoms: cough, shortness of breath, especially when a patient is prone
4 right heart failure
4. Right heart failure
  • Here, blood “backs up” into peripheral veins.
slide25
This results in classic symptoms: swelling of feet, ankles (peripheral edema) and engorgement of organs such as liver
5 cardiac output
5. Cardiac Output
  • Cardiac output (the amount of blood pumped by the heart per minute) is significantly decreased during heart failure.
c drug class mechanisms of action in treating heart failure
C. Drug class mechanisms of action in treating heart failure
  • There are a number of different mechanisms of action when considering how to treat heart failure:
slide30
1. Certain drugs increase the force of contraction. This is called a positive inotropic effect and is characteristic of:
  • a. cardiac glycosides
  • b. phosphodiesterase inhibitors
slide31
2. Certain drugs decrease the heart rate. This is characteristic of the adrenergic (beta) blockers.
slide32
3. Certain drugs relax vascular smooth muscle which dilates blood vessels and lowers blood pressure. This is characteristic of the vasodilators.
slide34
5. Certain drugs affect the renin-angiotensin-aldosterone (RAA) system. This is characteristic of the ACE inhibitors
slide35
6. Certain drugs reduce both preload and afterload. This is characteristic of the natriuretic peptides.
1a cardiac glycoside therapy of heart failure
1a. Cardiac glycoside therapy of heart failure
  • The cardiac glycosides are derived from the foxglove plants, Digitalis purpurea and

Digitalis lanata

slide37
They have been used to treat heart disorders for over 2000 years, and were

the mainstay of heart failure treatment until the discovery of the ACE inhibitors

slide38
Cardiac glycosides have 2 primary actions:
  • 1. Increasing the force of contraction allows the heart to eject more blood per beat which increases cardiac output and improves circulation.
slide40

Digoxin stimulates the vagus nerve, which slows the activity of the sinoatrial (SA) and atrioventricular (AV) nodes

slide41

This reduced heart rate (known as a negative chronotropic effect) is seen as a lengthening of the PR interval on an ECG.

slide42
The specific mechanism of action of the cardiac glycosides is inhibition of the

Na1+- K1+-ATPase pump.

slide45
The increased concentration of Na1+ stimulates the Na1+-Ca2+ exchange mechanism, leading to an increase in intracellular Ca2+.
slide47
The primary cardiac glycoside available in the U.S. is digoxin (Digitek, Lanoxicaps, Lanoxin).
slide49
The antidote for digoxin is called digoxin immune fab (Digibind). It binds digoxin and has a rapid onset of action, less than 1 minute after IV infusion.
slide50
It is necessary to have an antidote available as nearly 1/3 of patients taking cardiac glycosides develop symptoms of toxicity.
slide52
Symptoms of toxicity: pulse rate below 60 beats/min., confusion, nausea, diarrhea, yellow-green halos around lights, hallucinations
slide53
Vincent van Gogh’s “The Starry Night” (1889) is believed, by some physicians, to show evidence of digoxin (aka digitalis) toxicity, in the way he created yellow-green halos around the stars.
1b phosphodiesterase inhibitor therapy of heart failure
1b. Phosphodiesterase inhibitor therapy of heart failure
  • Phosphodiesterase inhibitors are used for short-term control of acute/advanced heart failure that is unresponsive to the “more conventional” ( i.e. diuretics and ACE inhibitors) treatments.
slide56
These drugs block phosphodiesterase in cardiac and smooth muscle which prevents the hydrolysis of cAMP.
slide58
Phosphodiesterase inhibitors have 2 primary actions:
  • 1. Increasing the force of contraction (similar to the cardiac glycosides)
  • 2. vasodilation
slide59
They are generally used for only 2-3 days because they may produce potentially serious adverse effects (ventricular arrhythmias, severe hypotension, thrombocytopenia)
slide60
Phosphodiesterase inhibitors include:
  • inamrinone (Inocor): IV, peak effect in 10 min.
  • milrinone (Primacor): IV, peak effect in 2 min.
2 beta adrenergic blocker therapy of heart failure
2. Beta adrenergic blocker therapy of heart failure
  • Selective beta blockers target beta1 receptors in the heart and kidneys. They are used in combination with other drugs to slow the progression of heart failure and to prolong patient survival.
slide64

However, there is increased activation of the sympathetic nervous system in patients with heart failure that causes tachycardia and increases stress on the heart.

slide65

Beta blockers slow the heart rate, which allows the heart to both fill and function more effectively.

slide66
Beta blockers used in the treatment of heart failure include:
  • acebutolol: (Sectral)
  • atenolol (Tenormin)
  • bisoprolol (Zebeta)
  • esmolol (Brevibloc)
slide67

The “preferred” beta blockers for the treatment of heart failure are:

  • carvedilol (Coreg)
  • metoprolol (Lopressor)
3 vasodilator therapy of heart failure
3. Vasodilator therapy of heart failure
  • Vasodilators generally play a minor role in the drug therapy of heart failure.
slide71
They reduce the symptoms of heart failure by decreasingcardiac oxygen demand.
slide72
Vasodilators indicated for the treatment of heart failure include:
  • hydralazine (Apresoline): acts on smooth muscle of arterioles, increases heart rate and cardiac output
slide73
isosorbide dinitrate (Isordil, Sorbitrate): causes venodilation, particularly in the larger veins and vena cava
slide74

This reduces both venous return to the heart and preload, allowing the heart to pump more forcefully.

4 diuretic therapy of heart failure
4. Diuretic therapy of heart failure
  • Diuretics are one of the “more conventional” treatments for heart failure.
slide77

Diuretic therapy, as well as sodium restriction is recommended for patients with mild heart failure

slide80
They reduce fluid overload and lower blood pressure which reduces the workload on the heart and increases cardiac output.
slide82
To control mild heart failure in patients with normal kidney function:
  • chlorothiazide (Diuril) or hydrochlorothiazide (Hydrodiuril)
  • methylclothiazide (Enduron, Aquatensen)
slide83
For patients with more advanced heart failure, low kidney function, and/or more severe edema:
  • furosemide (Lasix)
  • bumetanide (Bumex)
  • torsemide (Demadex)
slide84

Some studies have shown that treatment of heart failure with a potassium sparing diuretic reduces mortality.

slide85

These diuretics are more effective when the aldosterone level is elevated as they are either:

slide86

competitive inhibitors of the aldosterone receptor, or

  • decrease aldosterone activity by blocking Na1+ channels in the collecting ducts
slide87

Potassium sparing diuretics used in the treatment of heart failure include:

  • spironolactone (Aldactone)
  • eplerenone (Indira)
  • amiloride (Midamor)
  • triamterene (Dyrenium)
5 ace inhibitor acei therapy of hf
5. ACE inhibitor (ACEI) therapy of HF
  • ACE inhibitors have become the preferred drugs for the treatment of heart failure.
slide89

They inhibit angiotensin II. Angiotensin II causes vasoconstriction, and release of aldosterone and ADH.

slide92
ACE inhibitors which have been approved by the FDA in the treatment of heart failure include:
  • captopril (capoten)
  • enalapril maleate (Vasotec)
  • fosinopril (Monopril)
  • lisinopril (Prinivil, Zestril)
  • quinapril (Accupril)
  • ramipril (Altace)
6 natriuretic peptide therapy of hf
6. Natriuretic peptide therapy of HF
  • Natriuretic peptide was approved in 2001 for the treatment of heart failure.
slide94
It is a small peptide hormone structurally identical to a hormone secreted by the heart, beta-type natriuretic peptide (hBNP)
slide95
When heart failure occurs, the ventricles secrete hBNP in response to the increased stretching of the ventricular walls.
slide96
hBNP acts on the kidney, increasing excretion of Na1+ and water, thus lowering blood pressure.
slide98
The natriuretic peptide which has been approved for the treatment of heart failure is nesiritide (Natrecor).
slide99
It is approved only for severe heart failure because of the potentially serious side effects: apnea, hypotension, arrhythmias.