Clinical Summary of Congestive Heart Failure (CHF)
Posted: Saturday, July 03, 2010
by Funom Theophilus Makama
D Chosen 1
Congestive Heart failure is inability of the heart to pump an adequate amount of blood to the systemic circulation to meet the body's metabolic demands. Causes of heart failure can be classified according to the following changes:
1. Increased volume, especially in case of left-to-right shunts that cause the right ventricle to hypertrophy in order to compensate for the additional blood volume.
3. Myocardial factors that affect the contractility of the muscle fibers, such as myocardial ischemia from severe anemia or asphyxia, heart block, academia and low levels of potassium, glucose, calcium or magnesium.
4. High cardiac output demands, in which the body's need for oxygenated blood exceeds the cardiac output (even though the volume may be normal), such as in obstructive lung disease, hyperthyroidism and severe anemia.
In children, Congestive Heart failure occurs most frequently secondary to structural abnormalities that result in increased blood volume and pressure. It is a symptom caused by an underlying cardiac defect, not a disease in itself, since it is usually the result of an excessive workload imposed on a normal myocardium. The majority of children, who experience Congestive Heart failure are infants, and more than 50% are younger than 1 month of age.
Pathophysiology
Heart failure is often separated into two classifications: right sided or left-sided failure. In right-sided failure, the right ventricle is unable to pump blood into the pulmonary artery, resulting in less blood being oxygenated by the lungs and increased pressure in the right atrium and systemic venous circulation. Systemic venous hypertension causes edema on the extremities. In left-sided failure, the left ventricle is unstable to pump blood into the systemic circulation, resulting in increased pressure in the left atrium and pulmonary veins. The lungs become congested with blood, causing relevated pulmonary pressures and pulmonary edema.
Although, each type produces different systemic/pulmonary artery alterations, clinically it is unusual to observe solely right-or left-sided failure. Since both sides of the heart are dependent on adequate function of the other side, failure of one chamber causes a reciprocal change in the opposite chamber. For example, in left-sided failure increase in pulmonary vascular congestion will cause increased pressure in the right ventricle, resulting in right ventricular hypertrophy, decreased myocardial efficiency, and eventually pooling of blood in the systemic venous circulation.
Compensatory mechanisms
Congestive Heart disease is actually failure of compensatory mechanisms to increase cardiac function in accordance with metabolic requirements. Since most of the signs and symptoms result from decomposition, one must first look at the compensatory processes that attempt to preserve cardiac function.
Sympathetic stimulation
When the cardiac output falls, the atrial and venous stretch receptors and the aortic and carotid baroreceptors stimulate the sympathetic nervous system, which exerts two major effects. It increases the force and rate of myocardial contraction, resulting in a more efficient pumping action. It also increases venous return by increasing the tone of blood vessels and decreasing peripheral circulation to the limbs, splanchnic bed (viscera), and kidneys. Stimulation of the sympathetic cholinergic fibers in the skin causes increased sweating, which is especially prominent on the scalp during periods of exertion, such as crying of feeding.
Renal system
Reduced renal blood flow from sympathetic stimulation has a profpund effect on kidney function and results in changes aimed at increasing venous return through increased blood volume. First, there is an increase in aldosterone production in response to increased rennin secrestion from decreased renal blood flow and sympathetic stimulation. Aldosterone increases the rate of sodium reabsorption by the distal tubules, promoting osmosis of water into the blood. The absorbed sodium increases the osmotic concentration of the extracellular fluid, stimulating release of anti-diuretic hormone from the hypophysis, which promotes increased water reabsorption by the tubules.
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Top-level comments on this article: (1 total)Thank you for this article, which is full of helpful information.
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