About the Condition


There is no established definition for severe chronic anemia in the literature. Some studies use a hemoglobin cutoff of < 5 g/dl and a duration of > 4 months.

In 1922, Fahr and Ronzone wrote: “It is a well known fact that persons suffering from severe chronic anemias do not show the signs of anoxemia when at rest even when the oxygen carrying capacity of each cubic centimeter of blood is below the normal venous unsaturation”.

Castle and Minot emphasized in 1936 that anemic patients “may show, while at complete rest, very little discomfort from a reduction of the red blood cells and hemoglobin values to about one-fifth of normal”.

In 1969, Duke and Abelemann wrote: “In many patients with chronic anemia, a rapid circulation time and increased cardiac output have indicated the existence of a hyperkinetic state, usually accompanied by an increased tissue extraction of oxygen. When patients were studied both before and following therapy, there was usually reversion to a normal circulatory state. It has been postulated that the hyperkinetic response to anemia in patients at rest occurs only when the concentration of hemoglobin falls beneath 7 g/100 ml”.

The bottom line is that patients with severe chronic anemia use a series of physiological adaptations to meet their oxygen needs. The cardiovascular adaptation to chronic severe anemia differs from that to acute anemia. Here, we will focus on cardiovascular adaptation to chronic severe anemia.

Such changes include:

  • Stimulation of respiration resulting in increased minute ventilation which optimizes the partial pressure of oxygen in arterial blood (PaO2 ) and Hb oxygen saturation (SaO2).
  • Decreased blood viscosity leading to decreased vascular resistance, increased stroke volume and increased cardiac output.
  • Shift of oxygen dissociation curve to right resulting in increased offloading of oxygen in tissues.
  • Redistribution of blood flow to critical organs.

Heart rate plays a minimal if any role in increasing cardiac output in a patient with severe chronic anemia (it is, however, a more relevant mechanism in acute anemia).

The concept of critical oxygen delivery helps to place these various adaptations into context (for example, the increased extraction of oxygen results in a shift of the oxygen delivery-oxygen consumption curve to the right) and to highlight the precarious position of patients with chronic severe anemia on the supply-dependent part of the curve.

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