Clinical summary of congestive heart failure (CHF)

Congestive heart failure is a heart failure that sends enough blood to the systemic circulation to satisfy the body's metabolism. Causes of heart failure can be classified according to the following changes:

The capacity increases, especially in the case of a left to right shunt to enlarge the right ventricle and compensate for additional blood volume.
2. Increased post-load mainly due to obstructive lesions such as aortic valve stenosis or aortic aneurysm obstruction.
3. Myocardial factors affecting muscle fiber contractility, such as severe anemia or suffocation, cardiac block, acute and low level potassium, glucose, calcium or magnesium myocardial ischemia.
4. Cardiac output required by blood containing oxygen in the body, such as obstructive pulmonary disease, hyperthyroidism, severe anemia, exceeds cardiac output (volume is normal Also).

In children, congestive heart failure occurs most frequently following structural abnormalities resulting in an increase in blood volume and blood pressure. This is usually the symptom caused by the defect in the underlying heart, not the disease itself, because the myocardium is overloaded. The vast majority of children experiencing congestive heart failure are infectious diseases, and more than 50% are less than one month old.

Pathophysiology
Heart failure is often divided into two categories: right atrium or left heart failure. On the right side of failure, the right ventricle can not pump blood into the pulmonary artery, resulting in less blood volume supplemented with oxygen by the lung, increasing pressure in the right atrium and systemic venous circulation. Systemic venous hypertension causes edema in the extremities. In left heart failure, the left ventricle is unstable to pump blood into the systemic circulation, the pressure of the left atrium and pulmonary vein rises. The lungs associated with blood caused associated pulmonary pressure and pulmonary edema.

Although each type produces a different whole-body / pulmonary artery change, clinically it is unusual to only observe right or left insufficiency. Because both sides of the heart are dependent on the proper function of the other side, failure of one chamber causes a reciprocating change in the opposite chamber. For example, in left heart failure, an increase in pulmonary vascular congestion causes right ventricular hypertrophy, decreased myocardial efficiency, and ultimately increased pressure in the right ventricle resulting in a pool of blood in the systemic venous circulation.

Compensation mechanism
Congestive heart disease is actually an impairment of the compensatory mechanism that increases cardiac function according to metabolic demands. Since most signs and symptoms result from decomposition, you must first look at the compensation process trying to preserve cardiac function.

Sympathetic stimulation
As cardiac output decreases, atrial and venous stretch receptors and aortic and carotid baroreceptors stimulate the sympathetic nervous system, which exerts two main effects. It increases the power and rate of myocardial contraction and results in a more efficient pumping action. It also increases venous return by increasing vascular tone, reducing peripheral circulation to the extremities, spleen bed (viscera), and kidney. Stimulation of the sympathetic cholinergic fiber of the skin causes an increase in perspiration, and is particularly noticeable in the scalp at the time of exercise such as crying of feeding.

Kidney system
Reduction of kidney blood flow from sympathetic nerve stimulation adversely affects renal function and bring about a change aiming at increasing venous return due to an increase in blood volume. First, aldosterone production is increased in response to renal blood flow and increased renin secretion from sympathetic stimulation. Aldosterone increases the rate of sodium reabsorption by the distal renal tubule and promotes penetration of water into the blood. The absorbed sodium increases the osmotic concentration of the extracellular fluid, stimulates the release of antidiuretic hormone from the pituitary gland, and promotes the increase of water reabsorption by capillaries.