Even in cases of profound anemia, the body has a tremendous ability to compensate, resulting in a good prognosis for many profoundly anemia patients. This module will focus on fundamental physiological processes relevant to all types of anemia—the compensatory mechanisms that are triggered in the anemic patient.
A deeper understanding of the human body’s ability to compensate for profound anemia, in concert with modern non transfusion-based support modalities, has played a key role in a paradigm shift in the management of Jehovah’s Witness patients, as it has helped physicians to realize that a Witness patient’s conscientious refusal of blood transfusion does not preclude quality care.
What is tolerance of anemia?
The phrase “tolerance of anemia” has been used clinically in two interrelated ways, both of which are relevant to bloodless medicine and surgery:
- the ability of the human body to compensate physiologically for anemia
- a clinician’s decision to “tolerate” the patient’s anemia–not to automatically view subnormal hemoglobin or hematocrit numbers as requiring emergent intervention
According to the World Health Organization (WHO), anemia is defined as hemoglobin (Hb) levels <12.0 g/dL in women and <13.0 g/dL in men. However, normal Hb distribution varies not only with sex but also with ethnicity and physiological status, and the level at which patients become symptomatic varies according to the individual’s circumstances and capacity to respond to blood loss or reduced red cell production. Thus, for any patient, Hb values alone cannot provide the information needed to create an optimal care plan. Rather, it is essential that the physician take into consideration all the individual patient’s clinical signs and symptoms, and “treat the patient, not a number.”
Why is this important?
This is important because many healthcare providers have a deeply held conscientious concern that a moderately or severely anemic patient requires urgent or emergent intervention. This can become particularly problematic when treating Jehovah’s Witnesses and other patients for whom blood transfusion is not an option. A well-intentioned physician or nurse unfamiliar with the compensatory mechanisms of anemia and the strategies of bloodless medicine may fear that a severely anemic patient is going to die imminently unless a blood transfusion is administered. These providers may spend considerable time and energy trying to convince or even coerce a patient to agree to a transfusion against the patient’s conscientious position and wishes. This reaction to an anemic patient can create stress for the provider that can complicate or impede the course of treatment. It may also translate into stress and/or harm to the patient—at very least by delaying appropriate care.
In a video interview found in our “Clinical Pearls” section, Dr. Hiep Dao describes a “paradigm shift” in patient care. High-quality research over the past two decades has demonstrated improved outcomes when less blood is transfused. A select group of providers have gained the skills and confidence needed to successfully treat patients for whom blood transfusion is not an option. Dr. Dao highlights the key role of education in achieving this paradigm shift. Education about the role of compensatory mechanisms in anemia is a key element of that education. Understanding the body’s ability to tolerate anemia helps the healthcare team to assess the patient’s anemia correctly and focus on providing optimal clinical care.
What compensatory mechanisms protect the profoundly anemic patient?
The Survivability of Profound Anemia: Understanding Compensatory Mechanisms
We’ve learned a great deal about severe anemia from animal models. For example, in a porcine model of severe euvolemic anemia, evidence of lactic acidosis—which indicates insufficient tissue oxygen utilization—did not occur until a hemoglobin of 2.7 grams per deciliter. At a hemoglobin of 4, there was no statistical evidence of anemic hypoxic injury in the brain or heart, although other organs were less tolerant.
In humans, we have information dating back several decades indicating that many patients can survive illnesses associated with severe anemia. In fact, in postoperative patients, hemoglobin values as low as 2-3 gm/dl are associated with significant survival rates.
There are multiple databases that support the significant survivability of severe anemia. In one retrospective analysis of propensity-matched patients managed in a protocolized manner with hemoglobin less than 8, survival was similar in bloodless and transfused patients.
So the human body tolerates anemia even when hemoglobin is profoundly reduced. This is due to multiple compensatory mechanisms that help maintain adequate tissue oxygenation when the blood’s oxygen-carrying capacity is diminished.
These mechanisms include:
- Enhanced ability of hemoglobin to unload oxygen;
- Increased extraction of oxygen from the blood as it passes through capillaries;
- Increased cardiac output;
- And redistribution of that cardiac output.
Oxygen delivery to the periphery is determined largely by cardiac output or by means of convection. By the time oxygen reaches the periphery, the partial pressure of oxygen is quite low, and diffusion to the mitochondria where oxygen is utilized occurs down a relatively narrow gradient. The ability of hemoglobin to unload oxygen becomes all the more important when the system is stressed with severe anemia.
The oxygen hemoglobin saturation curve plots the proportion of hemoglobin in its saturated form on the vertical axis against the partial pressure of oxygen in the blood on the horizontal axis. A variety of factors can shift the curve. When shifted to the right, for example, by low pH, high temperature, or high carbon dioxide, oxygen becomes easier to unload and compensates for reduced convective delivery by anemia.
Normally, 25% of the arterial oxygen content is extracted by the peripheral tissues from each milliliter of blood. A reduction in delivery from a fall in cardiac output or anemia is associated with increasing extraction, allowing the body to maintain a normal oxygen consumption.
In the normal resting state, the heart pumps about five liters of blood every minute. When there is a greater demand for oxygen, as during exercise, the heart can increase its output many fold, to as much as 30 liters per minute.
During severe anemia, a rise in both stroke volume and heart rate contribute to an increase in cardiac output. Vasodilation and decreased blood viscosity are important components of this response.
In addition to increasing cardiac output, the body prioritizes the brain and heart. Control of peripheral vascular tone by the nervous system and other local mechanisms allows blood to be redistributed from less vital to more vital organs.
As a response to anemia, small blood vessels in the skin contract, causing a greater resistance to the flow of blood than is present in more vital organs. The result is a partial diversion of blood from the skin to other organs. Blood is also diverted from the kidneys as part of the adaptation to anemia.
The diversion of blood flow from the skin causes one of the cardinal clinical features of anemia: pallor. Pallor is the pale color observed in the skin of a light-skinned anemic individual, and in the mucous membranes and nailbeds of all anemic individuals, regardless of skin color.
It should be noted that anemic patients are pale not because their blood is thin but because the diversion of blood means there is less blood in the skin.
When these compensatory mechanisms are well understood, the care team will be able to operate on the basis of a new paradigm: finding appropriate and effective non-blood solutions instead of reflexively responding to anemia with blood transfusion or viewing transfusion as the sole treatment for anemia. The rationale for this approach is borne out by a large and increasing number of case reports and studies.
In Survival in Individuals with Profound Anemia Treated without the Use of Blood Transfusions, a study of patients undergoing a wide spectrum of medical, surgical and obstetrical cases, Patricia Ford et al. describe the non-blood techniques used in her hospital, demonstrating the survivability of profound anemia without blood transfusion: “Our nonblood approach included simultaneous interventions to stimulate erythropoiesis, control bleeding, enhance hemostasis, minimize iatrogenic blood loss and maintain hemodynamic stability. All patients received erythropoietin and iron with antifibrinolytic agents added for any active bleeding. To keep laboratory sampling at a minimum, physicians were required to rely on their basic clinical assessment skills to manage patients. The need for critical care monitoring, volume resuscitation and oxygen support was determined based on changes in blood pressure, heart rate, urine output, and cognitive function. Patients experienced slower recovery times with more frequent cardiac monitoring and increased length of hospital stays. This series demonstrates that the majority of individuals can survive with Hb levels as low as 2.5 g/dL utilizing simple nonblood strategies. The low mortality rate supports the elimination of any predetermined transfusion trigger.” Dr. Ford’s table summarizes patient outcomes at varying hemoglobin levels:
Survival Rates in Patients with Profound Anemia
|Hb Level (g/dL)
|Proportion Who Survived
It is noteworthy that patients treated for anemia in a bloodless program who are stable and whose hemoglobin is rising are often discharged from the hospital with hemoglobin levels below 7, a level at which many providers would administer a blood transfusion.
The nurse’s role
The nurse, and especially the bloodless program nurse coordinator, should be prepared to remind the healthcare team that a low hemoglobin does not inherently constitute an emergency. The nurse should also be vigilant to see that the precautions provided to clearly identify the patient as enrolled in the bloodless program are in place. These might include wristband, sign on the patient’s door, notation on the patient’s chart, and a copy of the patient’s advance directive.