Cyanotic defects are those in which un-oxygenated blood is mixed with oxygenated blood in the systemic circulation.
Improvements in surgical techniques have significantly increased the outlook for children with these defects.
Compensatory mechanisms A number of compensatory mechanisms occur in cyanotic defects in response to decreased arterial oxygen saturation.
These include polycythemia and the characteristic squatting posture seen with teratology of fallout.
Chronic arterial oxygen saturation in cyanotic heart disease causes decreased tissue, oxygenation, which stimulates erythropoiesis, This results in the production of large numbers of red blood cells, a condition known as polycythemia.
This compensatory response is to carry supplemental oxygen by means of: • increased quantity erythrocytes.
• Increase volume of blood • Forcing the heart to work even harder • Circulation is impeded, especially in the capillaries, the blood that is able to carry additional oxygen is not able to reach the peripheral circulation • Dehydration presents further hazards t the child because of the increased hemoconcentration • Polycythemia is evident in hematologic test • Increased ratio of red cells to plasma • Hemoglobin levels are usually elevated Posturing Posturing is a compensatory mechanism automatically learned by the child with teratogy of Fallot.
During infancy, the most characteristic positions are either flaccid with the extremities extended or side lying with the knees bent towards the chest (knee-chest position).
Continual muscle contraction demands additional oxygen.
Flaccidity is usually a sign of severe cardiovascular compromise.
The knee-chest position and, later in childhood, the squatting position serve two purposes.
First, flexing the legs decreases venous return from the lower extremities, which have very low oxygen content, especially after exercise.
Consequently a smaller volume of this blood enters the right ventricle so that the blood shunted into the aorta has a higher oxygen content.
Second, squatting increases systemic vascular resistance, which diverts right ventricular blood from the aorta into the pulmonary artery, increasing pulmonary blood flow.
This increases the amount of oxygenated blood in the left side of the heart and eventually into the systemic circulation.
Though with the advancement of medical science and clinical diagnostic and treatment methods, the infant mortality rate as a result of congenital heart disease of the cyanotic type has drastically reduced when compared to the time of the 70s and the 80s.
Hence handling and controlling of such ailments have proven to be highly successful in our modern era, especially my surgical method.
Yet, they still poise a threat to infant mortality and should be taken very seriously.
Improvements in surgical techniques have significantly increased the outlook for children with these defects.
Compensatory mechanisms A number of compensatory mechanisms occur in cyanotic defects in response to decreased arterial oxygen saturation.
These include polycythemia and the characteristic squatting posture seen with teratology of fallout.
Chronic arterial oxygen saturation in cyanotic heart disease causes decreased tissue, oxygenation, which stimulates erythropoiesis, This results in the production of large numbers of red blood cells, a condition known as polycythemia.
This compensatory response is to carry supplemental oxygen by means of: • increased quantity erythrocytes.
• Increase volume of blood • Forcing the heart to work even harder • Circulation is impeded, especially in the capillaries, the blood that is able to carry additional oxygen is not able to reach the peripheral circulation • Dehydration presents further hazards t the child because of the increased hemoconcentration • Polycythemia is evident in hematologic test • Increased ratio of red cells to plasma • Hemoglobin levels are usually elevated Posturing Posturing is a compensatory mechanism automatically learned by the child with teratogy of Fallot.
During infancy, the most characteristic positions are either flaccid with the extremities extended or side lying with the knees bent towards the chest (knee-chest position).
Continual muscle contraction demands additional oxygen.
Flaccidity is usually a sign of severe cardiovascular compromise.
The knee-chest position and, later in childhood, the squatting position serve two purposes.
First, flexing the legs decreases venous return from the lower extremities, which have very low oxygen content, especially after exercise.
Consequently a smaller volume of this blood enters the right ventricle so that the blood shunted into the aorta has a higher oxygen content.
Second, squatting increases systemic vascular resistance, which diverts right ventricular blood from the aorta into the pulmonary artery, increasing pulmonary blood flow.
This increases the amount of oxygenated blood in the left side of the heart and eventually into the systemic circulation.
Though with the advancement of medical science and clinical diagnostic and treatment methods, the infant mortality rate as a result of congenital heart disease of the cyanotic type has drastically reduced when compared to the time of the 70s and the 80s.
Hence handling and controlling of such ailments have proven to be highly successful in our modern era, especially my surgical method.
Yet, they still poise a threat to infant mortality and should be taken very seriously.
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