how low can we go? is there a way to know?

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TRANSFUSION Volume 30 January 1990 Number 1 How low can we go? Is Acute blood loss triggers a number of compensatory mechanisms designed to maintain blood flow to and thus oxygenation of the brain and heart. The extent of the compensation depends upon the rate and magnitude of the blood loss as well as upon the ability of the organism to respond. It is important to recognize that the initial manifestations of acute blood loss are related to hypo- volemia and not to a decrease in circulating red cell mass. The compensatory mechanisms activated by acute blood loss include stimulation of the adrenergic nervous sys- tem, release of vasoactive hormones, hyperventilation, reabsorption of fluid from the interstitium into the vas- cular space, a shift of fluid from the intracellular to the extracellular compartment, and renal conservation of to- tal body water and electrolytes. Cardiac output, the primary determinant of tissue per- fusion, is directly proportional to the venous return to the right side of the heart (preload). During acute blood loss, preload increases as a result of adrenergically me- diated venoconstriction of the systemic venules and small veins. Fifty percent or more of the total blood volume is sequestered in this circulatory bed. Mobilization of this volume increases the preload, which results in an increase in right ventricular end-diastolic pressure and thus of stroke volume. In addition, as a result of sym- pathetic nervous system stimulation, the heart rate in- creases. Because cardiac output is the product of stroke volume and heart rate, the output of the right side of the heart is returned to or toward normal. This increased output of the right side of the heart distends the pul- monary vascular bed, and blood from this low-pressure system is displaced into the left chambers of the heart. Once again, distention of cardiac muscle results in an increased stroke volume, which together with the in- crease in heart rate augments the cardiac output. As blood loss continues, there is a constriction of the vascular sphincters in the circulatory beds of skin, skeletal mus- cle, kidney, and splanchnic viscera. This vasoconstric- tion is mediated not only by the adrenergic nervous system Editorials there a way to know? and circulating catecholamines, but also by activation of the renin-angiotensin system and the secretion of vaso- pressin. Increased systemic vascular resistance (after- load) may indeed reduce the cardiac output. However, blood flow is redistributed to the heart and brain, organs that are capable of regulating their own flow over a wide range of arterial pressures. These mechanisms restore cardiac output to or toward normal within 60 to 120 seconds of the onset of acute blood loss, unless the loss exceeds the ability to compensate. Constriction of the systemic vascular bed leads to an- aerobic metabolism, with the accumulation of fixed acids and a consequent decrease in arterial pH. This acidemia induces hyperventilation the function of which is to maintain the hydrogen ion concentration in the physio- logic range. Spontaneous deep breathing has another beneficial side effect: negative intrathoracic pressure is increased, augmenting venous return to the right side of the heart, which further aids in the maintenance of car- diac output. Catecholamine-enhanced vasomotion in the microcir- culatory beds, along with hypotension, results in a de- creased capillary hydrostatic pressure that promotes the movement of fluid from the interstitial space into the vascular compartment. This shift of extracellular fluid may restore up to 50 percent of the lost blood volume. Somewhat slower, but no less important, is the shift of fluid from the intracellular compartment into the intra- vascular space. This phase of vascular restitution is hy- perosmotically induced. The liberation of a host of vasoactive and metabolically active ligands stimulates the liver to provide a source of glucose, lactate, pyru- vate, phosphate, amino acids, and urea, all of which combine to increase the serum osmotic pressure. This variance, which is in direct proportion to the degree of blood loss, creates an osmotic gradient between the in- travascular, interstitial, and intracellular compartments, with a net shift of fluid into the peripheral circulation. Albumin, which is ultimately responsible for the resto- ration of the circulating volume, follows a similar path- 1

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Page 1: How low can we go? Is there a way to know?

T R A N S F U S I O N Volume 30 January 1990 Number 1

How low can we go? Is

Acute blood loss triggers a number of compensatory mechanisms designed to maintain blood flow to and thus oxygenation of the brain and heart. The extent of the compensation depends upon the rate and magnitude of the blood loss as well as upon the ability of the organism to respond. It is important to recognize that the initial manifestations of acute blood loss are related to hypo- volemia and not to a decrease in circulating red cell mass.

The compensatory mechanisms activated by acute blood loss include stimulation of the adrenergic nervous sys- tem, release of vasoactive hormones, hyperventilation, reabsorption of fluid from the interstitium into the vas- cular space, a shift of fluid from the intracellular to the extracellular compartment, and renal conservation of to- tal body water and electrolytes.

Cardiac output, the primary determinant of tissue per- fusion, is directly proportional to the venous return to the right side of the heart (preload). During acute blood loss, preload increases as a result of adrenergically me- diated venoconstriction of the systemic venules and small veins. Fifty percent or more of the total blood volume is sequestered in this circulatory bed. Mobilization of this volume increases the preload, which results in an increase in right ventricular end-diastolic pressure and thus of stroke volume. In addition, as a result of sym- pathetic nervous system stimulation, the heart rate in- creases. Because cardiac output is the product of stroke volume and heart rate, the output of the right side of the heart is returned to or toward normal. This increased output of the right side of the heart distends the pul- monary vascular bed, and blood from this low-pressure system is displaced into the left chambers of the heart. Once again, distention of cardiac muscle results in an increased stroke volume, which together with the in- crease in heart rate augments the cardiac output. As blood loss continues, there is a constriction of the vascular sphincters in the circulatory beds of skin, skeletal mus- cle, kidney, and splanchnic viscera. This vasoconstric- tion is mediated not only by the adrenergic nervous system

Editorials

there a way to know?

and circulating catecholamines, but also by activation of the renin-angiotensin system and the secretion of vaso- pressin. Increased systemic vascular resistance (after- load) may indeed reduce the cardiac output. However, blood flow is redistributed to the heart and brain, organs that are capable of regulating their own flow over a wide range of arterial pressures. These mechanisms restore cardiac output to or toward normal within 60 to 120 seconds of the onset of acute blood loss, unless the loss exceeds the ability to compensate.

Constriction of the systemic vascular bed leads to an- aerobic metabolism, with the accumulation of fixed acids and a consequent decrease in arterial pH. This acidemia induces hyperventilation the function of which is to maintain the hydrogen ion concentration in the physio- logic range. Spontaneous deep breathing has another beneficial side effect: negative intrathoracic pressure is increased, augmenting venous return to the right side of the heart, which further aids in the maintenance of car- diac output.

Catecholamine-enhanced vasomotion in the microcir- culatory beds, along with hypotension, results in a de- creased capillary hydrostatic pressure that promotes the movement of fluid from the interstitial space into the vascular compartment. This shift of extracellular fluid may restore up to 50 percent of the lost blood volume. Somewhat slower, but no less important, is the shift of fluid from the intracellular compartment into the intra- vascular space. This phase of vascular restitution is hy- perosmotically induced. The liberation of a host of vasoactive and metabolically active ligands stimulates the liver to provide a source of glucose, lactate, pyru- vate, phosphate, amino acids, and urea, all of which combine to increase the serum osmotic pressure. This variance, which is in direct proportion to the degree of blood loss, creates an osmotic gradient between the in- travascular, interstitial, and intracellular compartments, with a net shift of fluid into the peripheral circulation. Albumin, which is ultimately responsible for the resto- ration of the circulating volume, follows a similar path-

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Page 2: How low can we go? Is there a way to know?

2 EDITORIAL TRANSFUSION

Vol. 30. No. 1-1990

way. Increased titers of vasopressin and of the adrenal cortical steroids acting on the kidney result in the con- servation of water and electrolytes, which further re- stores the circulating plasma volume.

Stabilization of a patient who has sustained acute blood loss by the administration of asanguinous fluid, together with the mobilization of interstitial and intracellular fluid, results in significant hemodilution. At this point, the clinician must make the crucial decision. What is the lowest level of hemoglobin that will ensure adequate oxygen delivery to the tissues of a particular patient? The article by Levine et al.' in this issue of TRANS- FUSION is yet another in a series by investigators at Michael Reese Hospital that attempts to redefine the transfusion trigger. In that study, baboons underwent exchange transfusion until they achieved a hematocrit of 15 percent; they were then observed, without adminis- tration of red cells, for a 2-month period. All 19 animals subsequently survived without physiologic or biochem- ical sequelae. Can these studies be extrapolated to hu- mans? Are normovolemic hemodilution and the consequent acute anemia equivalent to resuscitation after the hypovolemia that results from an acute reduction in blood volume? Do the metabolic consequences of acute uncompensated blood loss alter the level at which red cells should be transfused?

For five decades, 10 g per dL was considered to be the lowest accepted hemoglobin level. This value, then, served as the transfusion trigger, in spite of a wealth of clinical experience indicating that patients not only could survive but could function adequately with lower hemo- globin levels if their circulating blood volumes were in the normal range. It has long been recognized that, in the ideal 70-kg subject, total body oxygen consumption approximates 250 mL per minute and oxygen delivery approximates 1000 mL per minute. The oxygen extrac- tion ratio, then, is 0.25 percent, which is indicative of a fourfold reserve. It has also been long accepted that hemoglobin level is but one factor in oxygen transport and that compensatory mechanisms come into play when the hemoglobin content is reduced. Why then the great emphasis on hemoglobin? The answer is simple: the hemoglobin level is easy to measure, whereas the other determinants were, until recently, relatively difficult to obtain. The advent of extensive invasive and noninva- sive monitoring has made it possible to measure all of the factors that contribute to oxygen delivery and con- sumption. Cannulation of a peripheral artery for direct measurement of blood pressure as well as for sampling of arterial blood for gas determinations is relatively com- monplace. The introduction of the balloon-tipped, flow- directed, pulmonary artery catheter has made it possible not only to determine right-sided and left-sided ventric- ular filling pressures but also to obtain true mixed-ve- nous blood for gas analysis. The addition of a thermistor

probe permits the determination of cardiac output by the thermodilution technique. Thus, all of the determina- tions needed to calculate oxygen delivery, oxygen ex- traction ratio, and extraction ratio can be obtained in the clinical setting at minimal risk.

As a result of advances in biomedical technology, it is now possible to measure and continuously record mixed venous oxygen saturation by the use of a fiberoptic re- flective oximetry system incorporated into the pulmo- nary artery catheter. The fiberoptic system interfaces with a microprocessor that uses a spectrophotometric tech- nique involving the use of light-emitting diodes to cal- culate the oxygen saturation. A not dissimilar system is incorporated in the pulse oximeter, which allows for the continuous determination of arterial oxygen saturation. A probe with a light-emitting diode on one side and a light-sensing diode on the other side is placed on an area of the body with pulsatile blood flow, such as a finger. The instrument measures the absorption of specific wavelengths of light relative to the ratios of oxygenated and reduced hemoglobin. A microprocessor corrects for absorption of light by tissue other than blood and cal- culates the oxygen saturation. There are, however, sig- nificant limitations to the use of pulse oximetry, especially in patients who sustain acute blood loss. Hypoperfusion can result in loss of the signal. Moreover, a decrease in saturation does not become evident until the PaO, is less than 100 torr. Nevertheless, the use of these two devices allows for a continuous approximation of arterial and mixed venous saturation and thus of oxygen tension.

The Reese Hospital investigators have repeatedly demonstrated the importance of the oxygen delivery sys- tem for the survival of primates in the presence of acute normovolemic anemia. It is their belief that the crucial point corresponds to a hematocrit of 10 percent and an oxygen extraction ratio of 50 percent. Shoemaker and associates* provided evidence that oxygen debt, calcu- lated from values derived from oxygen delivery and con- sumption, is a determinant of lethal and nonlethal postoperative organ failure. It is evident from these stud- ies that all aspects of oxygen delivery and use, not just the hemoglobin level, must be taken into account in de- termining the need for red cell administration.

In June 1988, the Consensus Conference on Periop- erative Red Cell Transfusion, sponsored by the National Institutes of Health, recommended3 a reduction in the transfusion trigger from 10 g per dL. What is the appro- priate level? Transfusion is rarely indicated when the hemoglobin level exceeds 10 g per dL; it is usually in- dicated when the level is below 7 g per dL. The oxygen extraction ratio, the mixed venous oxygen tension, and the clinical status of the patient should be helpful in determining the need for transfusion in those patients whose hemoglobin level is between 7 and 10 g per dL. Some patients with hemoglobin levels of 10 g per dL

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TRANSFUSION 1990-Vol. 30. No. 1 EDITORIAL 3

may well require an increased red cell mass to ensure adequate oxygen delivery. By the same token, some pa- tients may do well with levels less than 7 g per dL. The widespread use of invasive monitoring and the deter- mination of a number of physiologic values should help to define the transfusion trigger for each individual patient.

Linda Stehling, MD Howard L. Zauder, MD, PhD Department of Anesthesiology

University of New Merico

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2.

3.

School of Medicine Albuquerque, NM

References Levine E, Rosen A, Sehgal L, et al. Physiologic effects of acute anemia: implications for a reduced transfusion trigger. Transfusion

Shoemaker WC, Appel PL, Kram HB. Tissue oxygen debt as a determinant of lethal and nonlethal postoperative organ failure. Crit Care Med 1988;16:1117-20. Office of Medical Applications aad Research. National Institutes of Health. Perioperative red cell transfusion. JAMA

1990;30:11-14.

1988;260:2700-3.