Congestive Heart Failure 101

Precipitating Factors

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.