Renal compensatory mechanisms
Severe anemia causes the redistribution of blood supply to vital organs such as the brain and heart. This results in a decrease in renal blood flow causing the activation of the renin-angiotensin-aldosterone-system. Activation of this system results in increased production of aldosterone by the adrenal glands. Aldosterone causes increased retention of salt and water by the kidneys. This compensatory mechanism increases blood volume and renal blood flow without altering tissue hypoxia in other organs (Gaspad, 2005 as cited in Coyer & Lash, 2008).
The decrease in renal blood flow also stimulates the production of anti-diuretic hormone which increases water re-absorption in the renal tubules.
Activation of the RAAS mechanism stimulates the thirst centers in the hypothalamus.
Low hemoglobin concentration reduces the viscosity of blood and the latter decreases systemic vascular resistance (SVR). Reduction of systemic vascular resistance prompts an increase in stroke volume and subsequently, cardiac output. Low arterial oxygen concentrations secondary to increased destruction of sickled red blood cells causes tissue hypoxia. Tissue hypoxia causes vasodilation in an effort to increase peripheral blood flow. This vasodilation is thought to trigger an increase in cardiac output. Tissue hypoxia also activates the sympathetic nervous system which causes an increase in heart rate and heart contractility. Increased heart contractility increases stroke volume and concomitantly, cardiac output. The latter is a product of heart rate and stroke volume. Increase in cardiac output enhances the speed of delivery as well as the volume of blood delivered to tissues (Coyer & Lash, 2008).
The sympathetic system also increases the rate and depth of respiration in an effort to increase hemoglobin oxygenation.
Decreased oxygenation of the kidneys results in hypoxia. Hypoxia activates a factor found in the regulatory region of the erythropoietin gene called the hypoxia inducible factor-1 (HIF-1). This factor enhances the production of erythropoietin by the proximal tubular cells as well as the peritubular interstitial cells. Erythropoietin stimulates erythroid precursors in the bone marrow to produce extra red blood cells. Increased production of red blood cells causes widening of the bones (Coyer and Lash, 2008).
Decrease in PH
Blood PH influences the direction of the oxygen disassociation curve. In anemia, the PH of blood decreases due to accumulation of lactate, a product of anaerobic cell metabolism. In the presence of tissue hypoxia, cells switch from aerobic to anaerobic respiration. A decrease in PH causes significant rightward shifts of the oxyhemoglobin curve due to the BOHR effect. This shift enhances oxygen release at tissue level. It is postulated that the increased release of oxygen in patients with sickle cell anemia is double that of persons with normal hemoglobin for a similar shift. The body counters the increase in PH by increasing renal excretion of hydrogen ions and excretion of carbon dioxide at the lungs (Cotter, 2001).
Rapid RBC breakdown
Excessive hemolysis of sickled red blood cells results in increased bilirubin levels and urobilinogen, a by-product of biluribin metabolism. The body compensates for increased bilirubin concentration in blood by increasing their excretion in feaces and urine (Cotter, 2008, p. 15).
Dehydration and hypoxemia
Sickle cell crisis is triggered by amongst other factors dehydration and hypoxemia. The body prevents dehydration by stimulating the thirst center, the production of aldostrerone which increases water and sodium retention and anti-diuretic hormone which stimulates the renal tubules to retain more water. The body counteracts the effects of hypoxemia by enhancing the release of oxygen to tissues, redistributing blood to vital organs, increasing respiratory rate and cardiac output.
Coyer, S. M. & Lash, A. A. (2008). Pathophysiology of anemia and nursing care
complications. MEDSURG Nursing, 17(2), 77-83.
Cotter, S. (2001). Hematology. Jackson, WY: Teton NewMedia.