Acute Hemodynamic Effects of Red Cell Volume Reduction in Polycythemia of Cyanotic Congenital Heart Disease

Acute reduction in red cell volume (RCV) without significant alterations of blood volume in 22 patients with severe polycythemia secondary to cyanotic congenital heart disease resulted in a decrease in peripheral vascular resistance and an increase in stroke volume, systemic blood flow (SBF), and systemic oxygen transport. These changes are probably related to the decreased blood viscosity and yield shear stress associated with lower red cell concentrations. Hypervolemia in hypoxic polycythemia should be maintained in order to sustain an adequate SBF. In contrast to acute phlebotomy which may be expected to decrease blood oxygen content and SBF, the replacement of whole blood with plasma or 5% albumin is shown to result in an increased systemic blood flow and oxygen delivery.

[1]  A. Rosenthal,et al.  Blood volume changes in cyanotic congenital heart disease. , 1971, The American journal of cardiology.

[2]  S. Kontras,et al.  Hyperviscosity in congenital heart disease. , 1970, The Journal of pediatrics.

[3]  M. Conrad,et al.  Heparin treatment of haemorrhagic diathesis in cyanotic congenital heart-disease. , 1967, Lancet.

[4]  R. Replogle,et al.  Factors influencing the viscosity of blood. , 1967, Surgery, gynecology & obstetrics.

[5]  H. Meiselman,et al.  Clinical implications of blood rheology studies. , 1967, Circulation.

[6]  R. Wells.  Blood flow in the microcirculation of man and the flow properties of blood: a correlative study. , 1967, Bibliotheca anatomica.

[7]  D. Gairdner,et al.  Acid-base changes following exchange transfusion with citrated blood. , 1965, Archives of disease in childhood.

[8]  C. W. Walter,et al.  Simultaneous Determination of the Volume of Red Cells and Plasma for Survival Studies of Stored Blood , 1965, Transfusion.

[9]  J. Murray,et al.  The circulatory effects of hematocrit variations in normovolemic and hypervolemic dogs. , 1963, The Journal of clinical investigation.

[10]  E. Merrill,et al.  Rheology of human blood, near and at zero flow. Effects of temperature and hematocrit level. , 1963, Biophysical journal.

[11]  C. R. Dauwalter,et al.  A Rotational Viscometer Using an A.C. Torque to Balance Loop and Air Bearing , 1963 .

[12]  J. Murray,et al.  Systemic oxygen transport in induced normovolemic anemia and polycythemia. , 1962, The American journal of physiology.

[13]  D. Vérel.  Blood Volume Changes in Cyanotic Congenital Heart Disease and Polycythemia Rubra Vera , 1961, Circulation.

[14]  J L PATTERSON,et al.  General and regional circulatory responses to change in blood pH and carbon dioxide tension. , 1961, The Journal of clinical investigation.

[15]  L. Cobb,et al.  Circulatory effects of chronic hypervolemia in polycythemia vera. , 1960, The Journal of clinical investigation.

[16]  C. Ferencz.  The pulmonary vascular bed in tetralogy of Fallot. I. Changes associated with pulmonic stenosis. , 1960, Bulletin of the Johns Hopkins Hospital.

[17]  A. Guyton,et al.  Effects of polycythemia and anemia on cardiac output and other circulatory factors , 1959 .

[18]  L. Werko,et al.  The effect of experimentally induced hypervolemia on cardiac function in normal subjects and patients with mitral stenosis. , 1959, The Journal of clinical investigation.

[19]  Z. Fejfar.  Cardiac output and its regulation. , 1957, Acta cardiologica.

[20]  F. Sunahara,et al.  Cardiovascular effects of acutely produced anemia in the normal dog. , 1953, The American journal of physiology.

[21]  A. Nadas,et al.  Hematologic adjustments to cyanotic congenital heart disease. , 1953, Pediatrics.

[22]  M. N. Levy,et al.  The Influence of Erythrocyte Concentration upon the Pressure‐Flow Relationships in the Dog's Hind Limb , 1953, Circulation research.

[23]  R. Hartmann.  A hemorrhagic disorder occurring in patients with cyanotic congenital heart disease. , 1952, Bulletin of the Johns Hopkins Hospital.

[24]  O. Ratnoff,et al.  A new method for the determination of fibrinogen in small samples of plasma. , 1951, The Journal of laboratory and clinical medicine.

[25]  M. Berthrong,et al.  Cerebral lesions in congenital heart disease. , 1951, Journal of neuropathology and experimental neurology.

[26]  S. Natelson,et al.  III. THE FATE OF CITRATE IN ERYTHROBLASTOTIC INFANTS TREATED WITH EXCHANGE TRANSFUSION. , 1949, The Journal of clinical investigation.

[27]  J. Pincus,et al.  The fate of citrate in erythroblastotic infants treated with exchange transfusion. , 1949, The Journal of clinical investigation.

[28]  A. Rich.  A hitherto unrecognized tendency to the development of widespread pulmonary vascular obstruction in patients with congenital pulmonary stenosis (tetralogy of Fallot). , 1948, Bulletin of the Johns Hopkins Hospital.

[29]  E. J. Smith.  A children's hospital in a medical center , 1947 .