The heart, our hardest working organ, is a pump made of muscle. It is the most efficient muscle in the body. Generating its own electrical impulses, the heart beats continuously without rest for as long as we live. Congestive heart failure is a health condition in which the pumping ability of the heart becomes weak.(1) The heart just doesn't have the oomph it used to. It no longer beats with enough force to properly circulate blood throughout the body. When the heart loses pumping strength, excess sodium and water may accumulate in the tissues, causing "congestion" of fluid that puts an even greater burden on the circulatory system. People sometimes have signs of congestive heart failure without any symptoms of congestion, however, so doctors now prefer the term "heart failure." Heart failure can be caused by a variety of cardiac disorders, so it is actually a clinical syndrome rather than a specific disease.(2)

Doctors use the term "ejection fraction" to describe the amount of blood propelled out from the heart to the body. The heart normally ejects about 60% of its blood volume in one beat. With heart failure it may pump as little as 20 to 30 percent. The entire circulatory system becomes sluggish, putting more strain on the weak heart. With the circulatory system overloaded like this, the volume of blood returning to the heart through the veins increases. A normal heart responds by increasing the force of its contractions. In heart failure, the heart is simply not up to the task.

Doctors speak about the "contractility" of the heart when describing the shortening and lengthening of it's muscle fibers as it beats. When the heart muscle fails to function properly, contractility drops off. A number of heart-related problems can cause a loss of contractility, including heart attacks, coronary artery disease, rheumatic heart disease, and persistent irregular heartbeat. Certain medications, beta-blockers and duanorubicin, for example, can impact contractility too.

As the heart muscle loses strength, it tries to compensate in an effort to keep moving blood through its chambers and out to the body. One of the ways it does this is to beat faster, in response to prodding from the body. Here is how this works. Low blood output from the heart results in reduced blood circulation to the tissues. Tissues and cells are deprived of the oxygen they need. The body then sends an alarm signal to the heart in an attempt to give it a kick. This signal is delivered by the hormone norepinephrine, which speeds up the heartbeat. (Norepinephrine works with the sympathetic nervous system, the body's "fight or flight mechanism that is designed to gear us up in the face of stress.) When the sympathetic nervous system activates, the heart pumps more blood so the body has the oxygen it needs to jump into action. Unfortunately, noepinephrine constricts blood vessels in the skin, the digestive system, and kidneys, choking off their blood supply.

This extra demand on the heart to beat faster has additional consequences that compound the heart's predicament. Timing between the heart's contractions and relaxations--called "systole and diastole"--is thrown off. (When you have your blood pressure taken, the "systolic" pressure is the contraction and the "diastolic" pressure is the relaxation.) In heart failure, the muscle has less time to relax between beats. Diastole is shorter, and the heart cannot fill up with returning venous blood as it should. This ultimately makes it harder for the heart muscle fibers to relax. In order for a muscle cell to relax it has to move calcium inside the cell to the outside. Heart cells have a more difficult time doing this when diastole shortens. The muscle fibers cells also need more oxygen when all this is happening. Not a very pretty picture for a worn out heart.

And there is more. In heart failure, less blood circulates through the kidneys. They react by releasing a protein called "rennin" that causes retention of sodium and water. Excess fluid accumulates in the tissues surrounding blood vessels, increasing blood pressure and the heart's workload. A normal heart has an extra capacity for harder work in response to increased blood volumes returning by way of the veins. In heart failure, this reserve is exhausted.

The body responds to any loss of blood output from the heart by constricting the blood vessels. In addition to norepinephrine, a number of other hormones participate in this process. The body redistributes blood to make sure the brain and heart have enough to keep us alive. This is a normal body function, but in heart failure it only compounds the problem by making the heart fight harder to keep up. It is easy to see that heart failure is a vicious circle for the weary heart.

In chronic (long-term) heart failure, the heart muscle adapts by becoming thicker. Doctors call this "ventricular hypertrophy." But thicker does not mean stronger. Just the opposite, the abnormally thick heart wall is stiff and dysfunctional.