Page 1235 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

842 PART 7: Hematologic and Oncologic Disorders

CHAPTER Anemia and Red Blood Cell high P O 2 and unloading in the tissues at low P O 2 values. Hemoglobin O
2
binding affinity can be altered by various disease states and may play a
89 Transfusion in Critically significant adaptive role in response to anemia. ) is the product of blood
Ill Patients flow or cardiac output (CO) and arterial O content (Ca O 2 ). The relation-
The amount of O delivered to tissues (D O 2
2
ship is expressed as 2
Kevin P. Desrosiers
Howard L. Corwin D O 2 = Ca O 2 × CO
Under most circumstances, arterial O content may be approximated
2
by the O bound to hemoglobin.
KEY POINTS 2
https://kat.cr/user/tahir99/
(in mL/L) = %Sat × 1.39 (mL/g) × [Hb] (g/dL)
• Anemia is common in the critically ill and often results in a large Ca O 2
number of red blood cell transfusions. The relationship becomes
• Anemia can be tolerated in many critically ill patients. = CO × (%Sat × 1.39 × [Hb])
D O 2
• The risks of red blood cell transfusions have expanded and are well
documented. Tissue hypoxia (and anoxia) will occur if O delivery is decreased to
2
• Little data support efficacy of red blood cell transfusions in many a level where tissues no longer have enough O delivery to meet their
2
metabolic demands and may be caused by decreased O delivery due to
clinical situations in which they are given. a decrease in Hb, cardiac output, or Hb saturation. Each of the determi-
2
• Avoiding red blood cell transfusion is a positive outcome. nants of D O 2 has substantial physiologic reserves which allows the body
to compensate for either an increase in O requirement or a decrease in
2
. In general, the amount of O delivered
one of the determinants of D O 2 2
to tissues exceeds resting O requirements by a factor of two- to four-
2
Historically, red blood cell (RBC) transfusions have been viewed as a safe fold; additionally, the tissues themselves can increase oxygen extraction
and effective means of improving oxygen delivery to tissues. Beginning from the blood to compensate for decreased delivery. Therefore, there is
in the early 1980s, transfusion practice began to come under scrutiny. significant physiologic reserve that allows maintenance of tissue oxygen-
Initially, this was primarily driven by concerns related to the risks of trans- ation despite significant degrees of anemia.
fusion-related infection. However, today other concerns have continued
to drive the debate over transfusion practice. What started as a concern
for RBC transfusion risks over the last two decades has shifted to include THE PHYSIOLOGIC RESPONSE TO ANEMIA
a more critical examination of RBC transfusion benefits. These issues are The initial response to anemia is a shift in the oxygen dissociation curve
particularly important in the critically ill patient population. to the right as modulated by an increase in production of 2,3-DPG in
RBCs. This shift allows for the unloading of oxygen to the tissues at
3,5
PATHOPHYSIOLOGY OF ANEMIA IN CRITICAL ILLNESS higher partial pressures of oxygen, ensuring adequate oxygen delivery
despite the reduction in RBC mass. As anemia progresses, the cardiac
Anemia is best defined as a reduction in RBC mass. As RBC mass mea- output will increase by an increase in the heart rate to preserve the deliv-
surement is not practical in day-to-day clinical practice, hemoglobin ery of oxygen in the setting of decreased oxygen content. As RBC mass
3
(Hb) concentration and/or hematocrit (HCT) are the common sur- is reduced in anemia, the viscosity of the blood decreases. This reduc-
rogates used for RBC mass. While this works well in the steady state, it tion in viscosity leads to an increase in regional blood flow at the tissue
may present problems in nonsteady states such as resuscitation where and organ level, driving up local perfusion area and pressures leading
Hb and HCT might not accurately reflect RBC mass. The definition of to increased oxygen extraction. While a change in viscosity may be the
3
“normal” Hb currently is defined using standardized values referent to trigger for increased regional blood flow, there has been suggestion that
the Scripps-Kaiser database from 1998 to 2002. Anemia is of particular local blood vessel dilatation may be mediated by the release of nitric
1
importance in the critically ill; 95% of critically ill patients are anemic by oxide (NO) from the RBCs. In order for these mechanisms to work
6
the third hospital day and the presence of this anemia results in a large properly, the patient must be at or near a euvolemic state. In consider-
number of RBC transfusions. 2 ing these regulatory mechanisms, it is important to understand that the
Critically ill patients have an underproduction anemia, which com- transfusion of RBCs will increase viscosity by adding stored RBCs that
bined with blood loss, most commonly from phlebotomy, explains the may not have the same vasoactive capabilities of native RBCs. As such,
high prevalence of anemia seen in critically ill patients. Over 90% of ICU a transfusion of RBCs may inhibit compensatory mechanisms for low
3
patients have low serum iron (Fe), total iron binding capacity (TIBC), oxygen states, without significantly increasing oxygen delivery.
and Fe/TIBC ratio, but have a normal or, more usually, an elevated serum There is evidence that low levels of Hb can be tolerated in healthy
ferritin level. On the other hand, nutritional deficiencies are uncommon. subjects. Hematocrits of 10% to 20% have been achieved in experimental
4
At the same time, serum erythropoietin (EPO) levels are only mildly studies using normovolemic hemodilution without untoward effects.
7,8
elevated, with little evidence of reticulocyte response to endogenous EPO. Weiskopf and colleagues studied patients who underwent isovolemic
The blunted EPO response observed in the critically ill appears to result reduction of Hb to 7, 6, and 5 g/dL. No evidence of reduced oxygen deliv-
from inhibition of the EPO gene by inflammatory mediators. These same ery was detected at any of the tested values of Hb; however, there was a
inflammatory cytokines directly inhibit RBC production by the bone subtle reversible reduction in reaction time and impaired immediate and
marrow and may produce the distinct abnormalities of iron metabolism. delayed memory observed at Hb below 6 g/dL. An important source
9,10
Anemia of critical illness therefore is a distinct clinical entity characterized of data regarding the impact of anemia on surgical outcome comes from
by blunted EPO production and abnormalities in iron metabolism similar studies of Jehovah’s Witness patients. Carson has demonstrated that
to what is commonly referred to as the anemia of chronic disease. the risk of death in these patients at Hb between 7 and 8 g/dL is low.
Hemoglobin is a complex molecule to which oxygen binds. The O - However, the odds of death increase by 2.5 for each gram decrease in
2
carrying capacity of hemoglobin, or binding affinity to O , is represented Hb below 8 g/dL. The mortality is very high at Hb levels below 5 g/dL.
11
2
by a sinusoidal relationship between the Hb saturation and the partial It should be noted that these data are from patients who refuse all RBC
). In this relationship, referred to as the oxy- transfusions. There is time to intervene between a low Hb and resulting
pressure of oxygen (P O 2
hemoglobin dissociation curve, O loading takes place in the lungs at morbidity or mortality in most patients.
2

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