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Bianco, Carl. "How Congestive Heart Failure Works." 01 August 2000. HowStuffWorks.com. <http://health.howstuffworks.com/congestive-heart.htm> 06 July 2008.

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Causes of CHF

CHF is not a specific diagnosis, but is a result of another underlying condition. Finding the underlying condition is important because the treatment often depends on what that condition is. Many conditions can lead to CHF:

High blood pressure (hypertension) increases the work of the heart. The heart has to pump blood against higher resistance and must therefore generate more force. The added strain on the heart muscle can cause failure. This is one of the most common causes of CHF in the United States.
Coronary artery disease causes ischemia, inadequate oxygen supply to the heart muscle, which can damage or destroy heart muscle tissue, leading to failure. Coronary artery disease is the other most common cause of CHF in the United States.
Valvular heart disease causes improper blood flow through the heart, which increases the heart's workload. There are three main types of faulty heart valves:
- Narrow (stenotic) valves restrict the flow of blood. To generate enough pressure to pump blood through a narrow valve, the heart has to work much harder.
- Leaky (regurgitant) valves allow blood to flow back through after it has been pumped out. The heart must pump more blood with each heartbeat (the blood coming in normally plus blood leaking back), greatly increasing its workload.
- Endocarditis is an infection of the heart valves that can damage them.
Abnormal heart rhythms (arrhythmias) interrupt the normal filling and pumping cycle. If the heart beats too slow (bradycardia), then not enough blood gets pumped out. If the heart beats too fast (tachycardia), then there is not enough time for the heart to fill with blood. In either case, cardiac output is reduced causing the heart to fail.
Overactive thyroid gland (hyperthyroidism) increases the overall rate of metabolism in the body. The heart must circulate blood more frequently so that the body's tissues get an adequate amount of oxygen. This increased work can cause the heart to fail.
A severe decrease in red blood cells (anemia) reduces the supply of oxygen in circulated blood (blood cells carry oxygen). To provide adequate amounts of oxygen to bodily tissues, the heart must circulate blood more frequently. This extra work can cause the heart to fail.
Diseases that affect the heart muscle itself (cardiomyopathy) result in inadequate contraction of the heart. This decreases the cardiac output, which leads to CHF. Technically, cardiomyopathy only means diseases that originate and primarily affect the myocardium. However, many physicians also use the term in "ischemic cardiomyopathy," a condition resulting from the scarring caused by coronary artery disease. Diseases that cause cardiomyopathy include:
- Infections (viral, bacterial, AIDS, Lyme disease, rheumatic fever, etc.)
- Toxins (alcohol, cocaine, radiation, chemotherapy, etc.)
- Nutritional deficiencies (thiamine deficiency causing beri-beri)
- Connective tissue disorders (lupus, rheumatoid arthritis, etc.)
- Neuromuscular diseases (muscular dystrophy)
- Infiltrative (amyloidosis, sarcoidosis, cancer)
- Idiopathic (unknown)
- Peripartum cardiomyopathy
- Familial
Diseases that affect the pericardium (the sac surrounding the heart) restrict the ability of the heart to stretch when it fills. The filling is reduced, thereby diminishing cardiac output. A thickened or scarred sac (constrictive pericarditis) or fluid within the sac (pericardial tamponade) both reduce the ability of the heart to fill.
Birth defects in the formation of the heart (congenital heart disease) produce an additional workload on the heart eventually causing it to fail. These defects involve abnormal formation of the walls between different chambers of the heart (hole in the heart), abnormal formation of the heart valves, or abnormal positions of the blood vessels that bring blood to or from the heart.

Many other factors, called precipitating factors, place an extra burden on a failed heart. Identifying the precipitating factor, as well as the initial cause of CHF, is important for directing proper treatment. Precipitating factors include:

Stopping prescribed medications
Excessive intake of fluids or salt
Uncontrolled hypertension
Infection
Heart attack
Ischemia (lack of blood to heart muscle)
Cardiac arrhythmia (abnormal heart rhythm)
Anemia
Pulmonary embolus (blood clot in lung)
Hyperthyroidism (overactive thyroid)
Hypoxia (low level of oxygen in blood usually due to lung disease)
New heart valve malfunction

CHF often develops slowly over many years. As the heart fails, the body compensates to maintain the cardiac output and blood flow to the organs. Although these compensatory mechanisms are useful, they often cause further heart damage and worsen CHF. This compensation usually delays the development of CHF symptoms.

Sympathetic Nervous System
The sympathetic nervous system is part of the autonomic nervous system, which works at the subconscious level and controls the workings of many organs (e.g., heart, blood vessels, glands, intestines and bladder). Sympathetic nerves secrete a chemical called norepinephrine, which belongs to a class of chemicals called catecholamines or adrenergics. Norepinephrine binds to different receptors on various organs and can have a number of effects on those organs. These receptors are:

Alpha-adrenergic receptors These receptors constrict blood vessels (arteries, veins) and enlarge (dilate) pupils.
Beta-1-adrenergic receptors These receptors increase both the heart's rate and the force of the heart's contraction.
Beta-2-adrenergic receptors These receptors dilate both cardiac blood vessels and bronchial air passages.

When the heart begins to fail, the first thing the body does is activate the sympathetic nervous system. Sympathetic nerve stimulation increases the heart rate and the force of contraction and constricts the body's veins. These factors work together to increase cardiac output. However, sympathetic nerve stimulation also constricts arteries, which increases blood pressure. The increase in pressure forces the heart to work harder and use more oxygen, which is thought to cause further deterioration of the heart over time.

The body then decreases the blood flow to the kidneys. This activates the renin-angiotensin-aldosterone system. The decreased blood flow causes the kidney to release an enzyme called renin. Renin converts an inactive plasma protein, angiotensinogen, into an active hormone called angiotensin II. Angiotensin II is a powerful constrictor of both arteries and veins and stimulates the adrenal gland to secrete a hormone called aldosterone. Aldosterone causes the kidneys to retain salt and water which increases blood volume. The increased blood volume helps to maintain cardiac output by increasing the filling of the heart. However, the increased blood volume, along with the vasoconstriction, also increases blood pressure. This increased pressure causes edema and an increased workload, which may further weaken the heart.

The body also increases the secretion of a hormone in the pituitary gland called anti-diuretic hormone (ADH). This causes the kidney to retain more fluid, which increases blood volume and helps cardiac output, but also increases blood pressure, which makes the weakened heart work even harder.

There are also changes in the heart muscle itself. The thickness of the muscle layer increases (hypertrophy), enabling the heart to contract with greater force to maintain cardiac output. This increases the need for oxygen, however, and eventually leads to further deterioration. The heart can also enlarge by stretching and thinning its walls (dilation). Initially this may help increase output by increasing the amount of blood that the heart can hold, but the dilation eventually fails and leads to further worsening of the disease.

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