Blood component transfusion is generally provided as supportive therapy for correction of one or more hematologic and/or hemostatic
deficiencies, until the underlying disease process can be controlled or corrected. Blood component administration and its
immediate endpoints often are only one part of a general therapeutic plan. Although appropriate endpoints may be achieved
in terms of measurable parameters or clinical response, the clinician needs evidence that the traditional "outcomes" are relevant
in relation to the final outcome for the patient. However, evidence-based support of many transfusion practices, in many
clinical settings, is limited. Therefore, the clinician must base the administration of component therapy on good understanding
of the problem in terms of pathophysiology and indicators of severity. Indiscriminate administration of blood products may
pose unnecessary risk to the patient. The basic principles of component therapy are:
a. transfuse only what is needed
b. transfuse only when there is a clinically significant problem
c. weigh benefits, risks and alternatives to transfusion therapy
Compensatory mechanisms for anemia
Adequate oxygen supply is a key factor in maintaining body function and cell homeostasis. Therefore there is a normal physiologic
response to anemia, which helps maintain this oxygen supply to the peripheral tissues. This physiological response to anemia
consists of cardiac and peripheral tissue adaptations as well as changes in red blood cell (RBC) 2,3-diphosphoglycerate (2,3-DPG).
Cardiac output (CO) is increased by an accompanying decrease in vascular resistance as viscosity decreases with anemia, in
addition, increasing heart rate and/or stroke volume. As the heart normally extracts ~80 % of O2 delivered, increased cardiac O2 extraction is achieved largely by increasing coronary artery flow by coronary artery vasodilation. Animal studies suggest
that lower limit of cardiac tolerance for anemia in the presence of normal cardiovascular system is in the hemoglobin (Hb)
range of ~3-5 g/dL.
Peripheral tissue compensation for anemia is to increase O2 delivery by increasing blood flow through vascular beds, to recruit more capillaries, or in the case of supply-dependent
tissues, to increase oxygen extraction. These compensatory mechanisms may, however, be limited and dependent on circulating
intravascular volume as well as on red blood cell mass in the case of the splanchnic bed, muscles, and skin. With chronic
anemia, RBC intracellular 2,3-DPG concentrations also increase, shifting the oxyhemoglobin dissociation curve to the right,
thereby facilitating tissue off-loading of O2.
It should be noted that a Hb / Hct that is adequate in a stable setting, may no longer by adequate in the same patient in
a stressful postoperative setting, ie. awake, shivering, in pain, with a systemic inflammatory response after surgery. A
recent study in Jehovah's Witnesses indicates that postoperative morbidity and mortality begin to rise when the Hb is < 5
g/dL in patients without cardiovascular compromise.
The decision to transfuse should be supported by the need to relieve clinical signs and symptoms of impaired oxygen transport
and to minimize morbidity and mortality. The question of the lowest safe hematocrit continues to remain unanswered and likely
varies between different patient species, breed, comorbidities and underlying pathophysiologic states.