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The overarching indication for transfusing packed red blood cells (RBCs) is to improve oxygen delivery (
). One of the primary roles of RBCs is to transport oxygen from the lung to tissue to allow aerobic metabolism.
is dependent upon the cardiac output (CO) and the arterial oxygen content (CaO 2 ) by the following equation:
Where arterial oxygen content equals the following:
Hg, hemoglobin; S a O 2 , arterial oxygen saturation; P a O 2 , arterial oxygen partial pressure
In other words, oxygen delivery to tissue,
, is dependent upon the amount of oxygen in the blood, CaO 2 , and the rate, CO, that blood is delivered. There are circumstances (e.g., hemorrhage) in which the
is inadequate to meet the body’s metabolic oxygen demands (
). Transfusing RBCs will increase the Hg level, thereby, increasing CaO 2 , which increases
. Also, transfusing RBCs (and other blood products) will increase the heart’s preload and subsequent stroke volume (recall Frank-Starling law), leading to an increase in CO which also increases
. Recall, CO = stroke volume × heart rate. Therefore transfusing RBCs will increase
by increasing both oxygen content and CO.
, usually exceeds oxygen consumption,
, by a factor of 4 (1000 mL/min vs. 250 mL/min). In other words, oxygen supply to tissue greatly exceeds tissue oxygen demands at rest. However, when
is inadequate to meet
demands, a compensatory increase in “oxygen extraction” occurs to maintain
. Normally, the oxygen extraction ratio (O 2 ER) is 20% to 30% where O 2 ER =
/
. For example, if
, is normally 250 mL/min and
, is 1000 mL/min, then the O 2 ER = 25%. This corresponds to a mixed venous saturation (S mv O 2 ) equal to 70% to 80%. Note, that a S mv O 2 requires right heart catheterization with a pulmonary artery catheter to sample blood from the pulmonary artery. Normally, a compensatory increase in CO will occur to maintain adequate
in the setting of increased
(e.g., exercise). If the increase in CO fails to maintain adequate
, then the oxygen extraction ratio will increase causing the S mv O 2 less than 70%. Once these compensatory mechanisms are exhausted, cells switch to anaerobic metabolism (i.e., lactic acidosis). For example, a clinical correlate associated with inadequate
is cardiogenic shock caused by inadequate CO or hemorrhagic shock caused by inadequate oxygen content from acute blood loss anemia and inadequate CO from hypovolemia.
is defined as the critical oxygen delivery needed to satisfy the metabolic demands for oxygen consumption. In a euvolemic patient with normal cardiac function, the
is normally not reached until the Hg concentration decreases to 3.5 g/dL. However, the specific Hg level depends upon the patient’s oxygen requirement. For example, in high metabolic states (e.g., sepsis, burns, trauma) there is an increase in
; therefore
is reached at a higher concentration of Hg. Comorbidities, such as coronary artery disease also affects the Hg concentration at which
is reached.
cannot be directly measured in the typical clinical setting. Surrogate variables include:
Vital signs: hypotension, tachycardia, urine output
Labs: lactic acid, base deficit
Signs of myocardial ischemia: new ST-segment depression greater than 0.1 mV, new ST-segment elevation greater than 0.2 mV, regional wall motion abnormalities by echocardiography
Decreased mixed venous O 2 saturation (< 50%)
Acute normovolemic anemia occurs secondary to the replacement of intraoperative blood loss with crystalloid solution. The compensatory physiological changes include sympathetic stimulation (tachycardia, increased CO), decreased blood viscosity (decreases afterload, increases preload, improves capillary flow), and redistribution of blood flow to tissues that are more oxygen dependent (i.e., heart and brain). Notably, the heart and brain have the highest O 2 ER at baseline and cannot tolerate a decrease in
by increasing oxygen extraction compared with other tissues.
A low mixed venous saturation (S mv O 2 < 60%) implies that the body is increasing its O 2 ER because of decreased
. This implies that either the CO and/or oxygen content is insufficient to meet the metabolic demands of the body. This is commonly seen in the setting of cardiogenic and hemorrhagic shock.
Some patients may present with shock physiology (anaerobic metabolism as indicated by lactic acidosis) not because of inadequate
but rather because of inability to use oxygen because of impairment of oxidative phosphorylation. This can be seen in septic shock (endotoxin-mediated inhibition of pyruvate dehydrogenase), cyanide toxicity (inhibits electron transport chain), propofol infusion syndrome (inhibits electron transport chain).
The heart has the highest O 2 ER and consumes more oxygen by mass compare to any other organ. This is evident by the fact that the coronary sinus has the lowest oxygen saturation in the entire body (SvO 2 ≈ 40%), which also explains why the mixed venous saturation from the pulmonary artery (SmvO 2 ≈ 70%) is lower than the central venous saturation from the superior and inferior vena cava (ScvO 2 ≈ 75%). It also explains the rationale in maintaining a higher Hg in patients with coronary artery disease as the heart’s oxygen demands can increase up to a factor of five when stressed (e.g., tachycardia caused by shock physiology), but has limited ability to compensate for anemia by increasing its O 2 ER.
The Transfusion Requirements in Critical Care Trial attempted to answer this question. Within the trial, groups were divided into a restrictive trigger of 7 g/dL (to target a Hg between 7 and 9 g/dL) and a liberal trigger of 10 g/dL (to target a Hg between 10 and 12 g/dL). The 30-day mortality was found to be lower in the restrictive group, with organ dysfunction being comparable between the two groups. Further, the restrictive group received less blood transfusions during the intensive care unit (ICU) stay. It was determined from this trial that the transfusion trigger for most patients in the ICU should be a Hg less than 7 g/dL. However, patients with hemodynamic instability or evidence of cardiac ischemia may need a higher Hg threshold.
Current American Society of Anesthesiology (2015) guidelines recommend to strongly consider transfusion of RBC when the Hg is less than 6 g/dL, that transfusion is rarely needed when the Hg is greater than 10 g/dL, and that clinical indications (e.g., ongoing blood loss) should guide transfusion triggers when the Hg is between 6 and 10 g/dL.
Leukoreduction is the process by which white blood cells are removed from donor blood through the use of a filter. It is reported to have the following benefits: (1) reduces the risk of febrile, nonhemolytic transfusion reactions, and (2) reduces the transmission of infectious agents, such as Epstein-Barr virus, cytomegalovirus, human T-cell lymphocytic virus, prion disease (Creutzfeldt-Jakob disease), malaria, leishmaniasis, human granulocytic anaplasmosis, and yersinia enterocolitis. Universal leukoreduction is currently practiced in mostly all developed countries, aside from the United States, where its adherence is not mandated (because of costs/benefit concerns). However, in practice the vast majority (> 80%–90%) of hospitals in the United States adhere to universal leukoreduction of all blood products.
Infectious transmission
Transfusion reactions (see Table 11.1 )
Diagnostic Entity | Onset | Major Signs and Symptoms | Differentiating Features |
---|---|---|---|
Transfusion-related acute lung injury (TRALI) | Minutes to hours | Dyspnea, respiratory distress, hypoxemia, cyanosis, pulmonary edema, fever, tachycardia | Nonhydrostatic pulmonary edema, frequent fever, transient leukopenia |
Transfusion-associated circulatory overload (TACO) | Minutes to hours | Dyspnea, respiratory distress, hypoxemia, cyanosis, pulmonary edema, evidence of hypervolemia (jugular venous distention, peripheral edema, elevated BNP), hypertension | Hydrostatic pulmonary edema, absent fever, hypertension, evidence of hypervolemia, evidence of increased left atrial pressure, elevated BNP, responds to diuretics |
Anaphylactic reactions | Minutes to hours | Bronchospasm, respiratory distress, hypotension, cyanosis, generalized erythema and urticaria, mucous membrane edema | Rash, urticaria, and edema present; hypotension and bronchospasm prominent |
Bacterial contamination of blood products | Minutes | Fever, rigors, hypotension, and vascular collapse | Fever, rigors, and vascular collapse predominant; most common with platelets |
Hemolytic transfusion reaction | Minutes | Fever, rigors, hypotension, hemoglobinuria, disseminated intravascular coagulation | Usually with red blood cell transfusion, hemolysis |
Immunomodulatory effects
Blood transfusion is extremely safe in this day and age. The risk of transmission of hepatitis C or human immunodeficiency virus (HIV) from a unit of blood is rare in developed nations (one in few million on average) and is highly dependent upon the population. For example, in Canada the risk of hepatitis C and HIV with blood transfusion is reported to be 1 in 13 and 21 million, respectively. However, there will always remain some risk, albeit rare, of infection with blood transfusion. These include pathogens that are routinely tested, including those without a screening test. The pathogens routinely tested include the following: hepatitis, HIV, syphilis, human T-cell lymphotropic virus, West Nile virus, and cytomegalovirus. Other pathogens that may be transmitted include prion-mediated disease (Creutzfeldt-Jakob disease) in the United Kingdom, parasitic diseases, such as Chagas disease, and malaria in underdeveloped regions of the world.
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