Your heart has 4 chambers: an atrium and a ventricle each on the right and left sides. Between heartbeats, blood flows into the atria. It then passes into the ventricles and is pumped out to the body. The percentage of the blood contained in a ventricle that is pumped out when the heart contracts is the ejection fraction, or EF 2. The EF is a measure of how well the heart is working. Normal EFs are greater than or equal to 50 percent. A heart attack, high blood pressure, abnormal heart rhythms and other diseases can reduce the EF to abnormal levels. There are several strategies for improving EF with medications.
If you are experiencing serious medical symptoms, seek emergency treatment immediately.
Strengthening the Heart Muscle
Digitalis is one of the oldest drugs still in use, principally administered as a derivative known as digoxin (Lanoxin). Ventricular muscle shortens to force blood out of the heart. Digoxin increases the strength and rapidity of that shortening. It may also help control abnormal heart rhythms that reduce EF. Other drugs similarly increase pumping action, such as milrinone (Primacor) and dobutamine (Dobutrex). These drugs are not routinely recommended for heart failure and are reserved for highly monitored treatment of acute heart failure that's resistant to other therapies.
Reducing Blood Vessel Resistance to Flow
Arteries also have muscles. The more they contract, the smaller the channel through which blood flows and the greater the strain on the heart muscle. Angiotensin, a naturally occurring hormone, is a very potent constrictor of blood vessels. Drugs that inhibit angiotensin formation or block its ability to link to the blood vessel help to relax the vessel muscles and are the foundation of the Heart Failure Society of America guidelines. Examples include captopril (Capoten), enalapril (Vasotec), valsartan (Diovan) and losartan (Cozaar). The heart can eject more blood per beat due to that relaxation, improving EF. A combination of the drugs hydralazine and isosorbide (Bidil) may be effective in patients who are resistant to -- or intolerant of -- the angiotensin inhibitors.
Relaxing the Heart Muscle
In response to decreased EF, the body releases substances such as epinephrine that increase the rate and strength of ventricular contraction. While temporarily effective, chronic elevations of those compounds cause stiffening of the heart muscle and decrease its motion. Beta blockers are drugs that counteract those actions, decreasing the tension in the wall of the heart and improving contraction ability. The three that are recommended are carvedilol (Coreg), metoprolol succinate (Toprol XL) and bisoprolol (Zebeta). Beta blockers are most often used in combination with angiotensin inhibitors.
Decreasing Fluid Load
The kidneys often do not function normally in decreased EF conditions, and excess fluid may be retained. This results in an increased load on the heart. Diuretics increase the elimination of water and salts and are commonly combined with other classes of drugs in treating low EF. Examples are furosemide (Lasix) and spironolactone (Aldactone).
Your heart has 4 chambers: an atrium and a ventricle each on the right and left sides. The EF is a measure of how well the heart is working. Ventricular muscle shortens to force blood out of the heart. Other drugs similarly increase pumping action, such as milrinone and dobutamine . The heart can eject more blood per beat due to that relaxation, improving EF. Beta blockers are drugs that counteract those actions, decreasing the tension in the wall of the heart and improving contraction ability. The kidneys often do not function normally in decreased EF conditions, and excess fluid may be retained.
- Agency for Healthcare Research Quality: National Guideline Clearinghouse -- Heart Failure in Patients With Reduced Ejection Fraction -- HFSA 2010 Comprehensive Heart Failure Practice Guideline
- British Medical Journal: Benefits of β Blockers in Patients With Heart Failure and Reduced Ejection Fraction -- Network Meta-Analysis
- Circulation: Contemporary Reviews in Cardiovascular Medicine
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