Secondary Polycythemia. Whenever the tissues become hypoxic because of too little oxygen in the breathed air, such as at high altitudes, or because of failure of oxy gen delivery to the tissues, such as in cardiac failure, the blood-forming organs automatically produce large quantities of extra RBCs. This condition is called secondary polycythemia, and the RBC count commonly rises to 6 to 7 million/mm3, about 30 percent above normal.

A common type of secondary polycythemia, called physiological polycythemia, occurs in natives who live at altitudes of 14,000 to 17,000 feet, where the atmospheric oxygen is very low. The blood count is generally 6 to 7 million/mm3; this blood count allows these people to perform reasonably high levels of continuous work even in a rarefied atmosphere.

Polycythemia Vera (Erythremia). In addition to physiological polycythemia, a pathological condition known as polycythemia vera exists, in which the RBC count may be 7 to 8 million/mm³ and the hematocrit may be 60 to 70 percent instead of the normal 40 to 45 percent. Polycythemia vera is caused by a genetic aberration in the hemocytoblastic cells that produce the blood cells. The blast cells no longer stop producing RBCs when too many cells are already present. This causes excess production of RBCs in the same manner that a breast tumor causes excess production of a specific type of breast cell. It usually causes excess production of white blood cells and platelets as well.

In polycythemia vera, not only does the hematocrit increase, but the total blood volume also increases, sometimes to almost twice normal. As a result, the entire vascular system becomes intensely engorged. Also, many blood capillaries become plugged by the viscous blood; the viscosity of the blood in polycythemia vera sometimes increases from the normal of 3 times the viscosity of water to 10 times that of water.

EFFECT OF POLYCYTHEMIA ON FUNCTION OF THE CIRCULATORY SYSTEM

Because of the greatly increased viscosity of the blood in polycythemia, blood flow through the peripheral blood vessels is often very sluggish. In accordance with the factors that regulate return of blood to the heart, as dis cussed in Chapter 20, increasing blood viscosity decreases the rate of venous return to the heart. Conversely, the blood volume is greatly increased in polycythemia, which tends to increase venous return. Actually, the cardiac output in polycythemia is not far from normal because these two factors more or less neutralize each other.

The arterial pressure is also normal in most people with polycythemia, although in about one third of them, the arterial pressure is elevated. This means that the blood pressure–regulating mechanisms can usually offset the tendency for increased blood viscosity to increase peripheral resistance and, thereby, increase arterial pressure. Beyond certain limits, however, these regulations fail and hypertension develops.

The color of the skin depends to a great extent on the quantity of blood in the skin subpapillary venous plexus. In polycythemia vera, the quantity of blood in this plexus is greatly increased. Further, because the blood passes sluggishly through the skin capillaries before entering the venous plexus, a larger than normal quantity of hemoglobin is deoxygenated. The blue color of all this deoxygenated hemoglobin masks the red color of the oxygenated hemoglobin. Therefore, a person with polycythemia vera ordinarily has a ruddy complexion with a bluish (cyanotic) tint to the skin.

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مواضيع ذات صلة

Anemias

Clinical Manifestations of Infective Endocarditis

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Acute circulatory failure (cardiogenic shock)

Pulmonary hypertension

Pulmonary thromboembolism

Giant cell (temporal) arteritis

ابيضاض الدم النقوي المزمن Chronic myelocytic leukaemias

Abdominal aortic aneurysm

Infective endocarditis

تليف النقيMyelofibrosis

فقر الدم اللا مصنع ( اللا تنسجي ) Aplastic anemia