Abstract

The cardiac and respiratory adjustments in chronic anemia and their clinical manifestations have been reviewed. When the oxygen carrying capacity of the blood is diminished, an adequate supply of oxygen to the tissues is maintained by an increased cardiac output, an increased velocity of blood flow, and a relatively more complete abstraction of the oxygen from the blood as it passes through the capillaries. With the increased blood flow, the average peripheral resistance is decreased but the state of the small blood vessels is not uniform everywhere; the blood flow in the hands and kidneys, for instance, may be reduced, while that of other parts of the body is increased. The total oxygen consumption of the body in anemia is not strikingly altered. The blood volume generally is slightly reduced but the plasma volume is normal.

The deviations from the normal values vary from patient to patient, but generally are definite when the hemoglobin values are less than 50 per cent and are greatest at the lowest levels of hemoglobin concentration.

The close interrelationship between the cardiovascular and respiratory systems is exemplified by the coincident changes in the respiratory system in anemia. The rate and depth of respiration often are increased together with a lowering in the vital capacity and its subdivisions, the reserve and complemental air volumes. The resid- ual air is somewhat increased. These deviations from the normal are similar to those observed in pulmonary congestion or edema and denote a loss of elasticity and expansibility favoring the occurrence of exertional dyspnea. The arterial blood saturation is usually normal at rest but, during exertion, a significant lowering becomes apparent.

The importance of hemoglobin in the transport of carbon dioxide is reviewed; the decreased availability of hemoglobin as a buffer in carbon dioxide transport in anemia is compensated by the increased ventilation of the blood in the lungs, rendering the arterial blood somewhat alkalotic. The red cells also play an important role in regard to the respiratory enzyme, carbonic anhydrase. In the anemias due to blood loss, malnutrition, chronic infection, uremia, or leukemia, the blood carbonic anhydrase activity is parallel to the decrease in hemoglobin level leading to a deficiency not only of oxygen carrying capacity but also a decreased ability to absorb carbon dioxide from the tissues and to release it in the lungs. The following factors, many of which are closely interrelated, are operative in the production of dyspnea in anemic patients: the increased respiratory minute volume, the decreased vital capacity and its subdivisions, the abnormalities in carbon dioxide transport and dissociation, the reduced arterial oxygen capacity and the decreased blood oxygen saturation during effort, and the frequently observed elevated blood lactic acid values.

The symptoms and signs exhibited by anemic patients, including palpitation and breathlessness on exertion, tachycardia, cardiac dilatation and hypertrophy, are described. In addition to an apical systolic murmur, other systolic and diastolic murmurs are occasionally heard. The arterial blood pressure is frequently lowered in anemia; the venous pressure is generally within the limits of normal. Electrocardiographic abnormalities occur in approximately one-quarter of anemic patients but are minor and not specific in character.

The occurrence of angina pectoris, congestive failure, and intermittent claudication in some patients with the development of anemia, and disappearance of these conditions as the anemia is alleviated, is discussed with particular reference to the underlying physiologic mechanisms.

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