Physiology and pathophysiology of blood volume regulation.
Adequate cardiac output and tissue perfusion is dependent on intravascular blood volume and its adequate return to the heart. Considering the overall functions of the cardiovascular system in ensuring appropriate flow to the peripheral microcirculation, it is not surprising that conflicts of interest may occur when an organism is exposed to stresses. Of particular importance are the stresses in which there are increased oxygen demands, decreased oxygen availability and concomitant requirements for thermoregulation. When there is depletion of intravascular blood volume, the splanchnic circulation is in effect an "autologous blood bank" for maintaining venous return until trans-capillary refill and haemodilution occurs. With the acute haematological stress response centralisation of blood, secondary contraction of the venous capacitance occurs, as seen with acute hypoxia. This results in overfilling of the heart, activation of atrial volume receptors, release of atrial natriuretic peptide and subsequent reduction of the plasma volume by rapid shifting of plasma into the lymphatic capacitance (via spleen) and transcapillary efflux throughout the circulation. In this overview the physiology and pathophysiology of blood volume, red cell mass and plasma volume regulation is reviewed.
Isbister
J P
JP
Haematology and Transfusion Medicine Department, Royal North Shore Hospital of Sydney, St Leonards, NSW, Australia. jisbiste@med.su.oz.au
D000222:Adaptation, Physiological; D009320:Atrial Natriuretic Factor / Q000502:physiology; D001810:Blood Volume / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology*; D005440:Fluid Therapy; D006400:Hematocrit; D006801:Humans; D010953:Plasma Volume; D013312:Stress, Physiological / Q000503:physiopathology