Clinical Review: Hemorrhagic Shock PDF

Available online http://ccforum.com/content/8/5/373 Review Clinical review: Hemorrhagic shock Guillermo Gutierrez1, H David Reines2 and Marian E Wulf-Gutierrez3 1Professor, Pulmonary and Critical Care Medicine Division, Department of Medicine, The George Washington University Medical Center, Washing...

Available online http://ccforum.com/content/8/5/373 Review Clinical review: Hemorrhagic shock Guillermo Gutierrez1, H David Reines2 and Marian E Wulf-Gutierrez3 1Professor, Pulmonary and Critical Care Medicine Division, Department of Medicine, The George Washington University Medical Center, Washington, District of Columbia, USA 2Professor, Virginia Commonwealth University and Vice-Chairman, Department of Surgery, Inova Fairfax Hospital, Falls Church, Virginia, USA 3Associate Professor, Department of Obstetrics and Gynecology, The George Washington University, Inova Fairfax Hospital, Falls Church, Virginia, USA Corresponding author: Guillermo Gutierrez, [email protected] Published online: 2 April 2004 This article is online at http://ccforum.com/content/8/5/373 © 2004 BioMed Central Ltd Critical Care 2004, 8:373-381 (DOI 10.1186/cc2851) See Letter, page 396 Abstract This review addresses the pathophysiology and treatment of hemorrhagic shock – a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. Hemorrhagic shock can be rapidly fatal. The primary goals are to stop the bleeding and to restore circulating blood volume. Resuscitation may well depend on the estimated severity of hemorrhage. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. The optimal method of resuscitation has not been clearly established. A hemoglobin level of 7–8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia. However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters. Keywords blood loss, estimated blood volume, hemorrhage, oxygen consumption, oxygen delivery, shock, transfusion Introduction Life-threatening decreases in blood pressure often are associated with a state of shock – a condition in which tissue perfusion is not capable of sustaining aerobic metabolism. Shock can be produced by decreases in cardiac output (cardiogenic), by sepsis (distributive), or by decreases in intravascular volume (hypovolemic). The latter may be caused by dehydration from vomiting or diarrhea, by severe environmental fluid losses, or by rapid and substantial loss of blood. A less common form of shock (cytopathic) may occur when the mitochondria are incapable of producing the energy required to sustain cellular function. Agents that interfere with oxidative phosphorylation, such as cyanide, carbon monoxide and rotenone, can produce this type of shock. Hemorrhage is a medical emergency that is frequently encountered by physicians in emergency rooms, operating rooms, and intensive care units. Significant loss of intravascular volume may lead sequentially to hemodynamic instability, decreased tissue perfusion, cellular hypoxia, organ damage, and death. This review addresses the pathophysiology and treatment of hypovolemic shock produced by hemorrhage, which is also known as hemorrhagic shock. Physiologic considerations in hemorrhagic shock Estimating blood loss The average adult blood volume represents 7% of body weight (or 70 ml/kg of body weight). Estimated blood CaO2 = arterial oxygen content; DO2 = oxygen delivery; EBV = estimated blood volume; VO2 = oxygen consumption. 373 Critical Care October 2004 Vol 8 No 5 Gutierrez et al. Table 1 Classification of hemorrhage Class Parameter I II III IV Blood loss (ml) 2000 Blood loss (%) 40% Pulse rate (beats/min) 100 >120 >140 Blood pressure Normal Decreased Decreased Decreased Respiratory rate (breaths/min) 14–20 20–30 30–40 >35 >30 20–30 5–15 Negligible Normal Anxious Confused Lethargic Urine output (ml/hour) CNS symptoms Modified from Committee on Trauma. CNS = central nervous system. volume (EBV) for a 70 kg person is approximately 5 l. Blood volume varies with age and physiologic state. When indexed to body weight, older individuals have a smaller blood volume. Children have EBVs of 8–9% of body weight, with infants having an EBV as high as 9–10% of their total body weight. Estimating blood loss is complicated by several factors, including urinary losses and the development of tissue edema. To help guide volume replacement, hemorrhage can be divided into four classes (Table 1). Class I is a nonshock state, such as occurs when donating a unit of blood, whereas class IV is a preterminal event requiring immediate therapy. Massive hemorrhage may be defined as loss of total EBV within a 24-hour period, or loss of half of the EBV in a 3-hour period. A relatively simple way to estimate acute blood loss is by considering the intravascular space as a single compartment, in which hemoglobin changes according to the degree of blood loss and fluid replacement (Fig. 1). When volume losses are not replaced during hemorrhage, hemoglobin concentration will remain constant. In that condition a rough estimate of blood loss may be obtained using the classification provided in Table 1. Conversely, when blood losses are sequentially replaced by isovolemic fluid infusion, the estimated blood loss may be obtained as follows : EBL = EBV × ln(Hi/Hf) Where Hi and Hf denote the initial and final hematocrit. Implicit in this equation is the absence of significant urinary losses or the leakage of intravascular fluid into the tissues. For example, a decrease in hematocrit from 40% to 26% with complete fluid replacement of blood losses corresponds to an estimated blood loss of 2.1 l. 374 Intravenous fluid infusion in the absence of bleeding also will lower hemoglobin concentration. Using the one-compartment Figure 1 Fluid replacement Intravascular space Tissue leakage Blood loss One compartment model of the vascular space. model, a first approximation to hemodilution with intravenous fluids is as follows: Hf = EBV × Hi/(EBV + volume infused) This is the lowest possible estimate of Hf, because fluid administration and expansion of intravascular fluid volume will trigger compensatory mechanisms to increase glomerular filtration rate and decrease plasma volume. Transfusing packed red cells in a person who is not actively bleeding will increase hemoglobin concentration by 1 g/dl (or 3% hematocrit) per unit of packed red blood cell transfused. It is impossible to estimate the effect of blood transfusion on volume or hemoglobin concentration in actively bleeding individuals. Measures of central venous or, preferably, Available online http://ccforum.com/content/8/5/373 pulmonary artery pressures are needed to estimate the degree of fluid replacement that may be required. Alterations in systemic oxygen delivery during hemorrhagic shock Decreases in circulating blood volume during severe hemorrhage can depress cardiac output and lower organ perfusion pressure. Severe hemorrhage impairs the delivery of oxygen and nutrients to the tissues and produces a state of shock. A clearer understanding of the pathophysiology of hemorrhagic shock may be obtained by defining the process of oxygen delivery and utilization by the tissues. Total oxygen delivery (DO2 [mlO2/min per m2]) is the product of cardiac index (l/min per m2) and arterial oxygen content (CaO2 [mlO2/l blood]). CaO2 is calculated as 13.4 × [Hb] × SaO2 + 0.03 PaO2, where [Hb] represents the concentration of hemoglobin in blood (g/dl), SaO2 is the hemoglobin oxygen saturation and PaO2 is the partial pressure of oxygen in arterial blood. Under normal aerobic conditions, systemic oxygen consumption (VO2) is proportional to the metabolic rate and varies according to the body’s energy needs. VO2 may be calculated using Fick’s principle as the difference between the rates of oxygen delivered and oxygen leaving the tissues: VO2 = cardiac index × (CaO2 – CmvO2), where CmvO2 is the oxygen content of mixed venous blood. Calculation of VO2 using Fick’s equation does not account for pulmonary oxygen consumption, which may be substantial during acute lung injury. Another useful parameter when defining tissue oxygenation is the fraction of oxygen consumed to oxygen delivered to the tissues, termed the oxygen extraction ratio and calculated as (CaO2 – CmvO2)/CaO2. The relationship of oxygen delivery to oxygen consumption during hemorrhagic shock Rapid decreases in blood volume may lead to decreases in cardiac output and in DO2 with little change in VO2, because blood flow is preferentially distributed to tissues with greater metabolic requirements. Increased efficiency in oxygen utilization during hypoxia is reflected by a rise in oxygen extraction ratio. Lowering regional vascular resistance by adenosine, prostaglandins, and nitric oxide induces hypoxic redistribution of blood flow [8,9]. In spite of this organspecific microvascular response, all organs, with the possible exception of the heart, experience decreases in blood flow during severe hypovolemia. Another targeted response to hemorrhage is an increase in the number of open capillaries in organs that are capable of this. For example, in skeletal muscle only a fraction of capillaries are usually open to accommodate the passage of erythrocytes whereas the remaining capillaries allow only passage of plasma. During hemorrhage the number of open capillaries increases in proportion to the degree of tissue hypoxia. Capillary recruitment shortens the diffusion distance from red blood cells to the surrounding tissue and increases the capillary surface area available for oxygen diffusion. The overall effect of capillary recruitment is the maintenance of tissue oxygen flux at a lower capillary oxygen tension, which is a vital response in organs on the edge of hypoxia. Severe and sustained decreases in DO2 eventually overwhelm the microvascular responses to hypoxia. As tissue oxygen flux falters, mitochondria cannot sustain aerobic metabolism and VO2 decreases. The rate of DO2 associated with the initial decline in VO2 is defined as the critical DO2 (DO2crit). Animal experiments show that DO2crit is a remarkably constant parameter regardless of the method used to decrease DO2, be it anemia, hypoxemia, or hypovolemia. Hypovolemia and isovolemic anemia Patients with massive hemorrhage may experience conditions ranging from severe hypovolemia, in which blood volume decreases with no changes in hemoglobin concentration, to isovolemic anemia, in which extreme decreases in hemoglobin concentration occur with normal or even increased blood volume. Hypovolemia occurs in rapidly bleeding individuals who are not receiving intravenous fluids. The importance of circulating blood volume has been demonstrated in animals subjected to the sequential removal of blood aliquots from a central vein. These experiments show that VO2 remains constant as the circulating blood volume decreases. VO2 falls precipitously and death rapidly ensues below a DO2crit of 8–10 mlO2/min per kg. At this critical juncture, decreases in blood volume approach 50% with no changes in hemoglobin concentration. Hypovolemia is associated with substantial decreases in cardiac output and mixed venous oxygen tension. Aggressive fluid replacement may produce the condition of isovolemic anemia, which is characterized by adequate blood volume but decreased hemoglobin concentration and low oxygen carrying capacity. Isovolemic anemia occurs when blood for transfusion is not readily available or in individuals who are bleeding but refuse to accept blood products. Experimental isovolemic anemia is produced by drawing blood aliquots from a central vein and replacing the exact amount of blood removed with a colloidal solution such as albumin. Animals subjected to progressive isovolemic anemia also exhibit a DO2crit in the neighborhood of 10 mlO2/min per kg. DO2crit is reached at a hemoglobin concentration of approximately 4.0 g/dl (corresponding to a hematocrit