The principles of volume resuscitation are based on the normal body response to hemorrhage. This response has been examined in mild hemorrhage (< 15% loss in blood volume), when volume resuscitation is not necessary. The response is described in three stages.
Stage 1. The first hours after the onset of blood loss is characterized by movement of interstitial fluid into the capillaries. This transcapillary refill helps maintain blood volume but leaves an interstitial fluid deficit.
Stage 2. The loss of body fluids leads to activation of the renin-angiotensin-aldosterone system. This results in sodium conservation by the kidneys. Because sodium distributes primarily in the interstitial space, the retained sodium replenishes the interstitial fluid deficit.
Stage 3. Within a few hours after the onset of hemorrhage, the marrow begins to increase the production of erythrocytes. This response occurs more gradually, and complete replacement of erythrocytes can take up to 2 months.
According to the response to mild hemorrhage described above, the goal of acute volume resuscitation for blood loss should be to replenish interstitial fluid deficits. This is why crystalloid (electrolyte) fluids are used in the resuscitation of acute blood loss, as is discussed later.
The clinical consequences of hypovolemia are determined by the rapidity and magnitude of volume loss and by the responsiveness of individual patients to volume loss. Most cases of mild blood loss are relatively free of clinical manifestations. In fact, hypovolemia may be clinically silent until the volume loss exceeds 30% of the blood volume.
The American College of Surgeons identifies four categories of acute blood loss based on the percent loss of blood volume.
Class I. Loss of 15% or less of the total blood volume. This degree of blood loss is usually fully compensated by transcapillary refill. Because blood volume is maintained, clinical manifestations of hypovolemia are minimal or absent.
Class II. Loss of 15 to 30% of the blood volume. The clinical findings at this stage may include resting tachycardia and orthostatic changes in heart rate and blood pressure. However, resting tachycardia can be an inconsistent finding, and orthostatic changes in pulse and blood pressure are too insensitive to be considered reliable manifestations. A positive tilt test, defined as an increase in pulse rate greater than 30 beats/minute or a drop in systolic pressure greater than 30 mm Hg on assuming the upright position, can be used as corroborative evidence for blood loss, but a negative result has no meaning. When the tilt test is performed, the lower legs must be in a dependent position (sitting without legs dangling is inappropriate). Also, because changes in pulse and pressure are variable within the first minute after changing positions, a waiting period of at least 1 minute after changing positions is recommended before the vital signs are recorded.
Class III. Loss of 30 to 40% of the blood volume usually marks the onset of hypovolemic shock, with a decrease in blood pressure and urine output. There is evidence that the tachycardia-vasoconstrictor response to hemorrhage can be lost at this stage of blood loss. When this occurs, the decrease in blood pressure can be sudden and profound.
Class IV. Loss of more than 40% of blood volume is a harbinger of circulatory collapse. Therefore, when hypovolemia is accompanied by marked hypotension, oliguria, or other evidence of organ failure, prompt volume resuscitation is mandatory.
The clinical evaluation of blood loss is far from precise, even when employing invasive hemodynamic monitoring. The following are some important points regarding the clinical parameters used to evaluate patients with suspected or documented blood loss.
However, when blood loss is severe enough to produce hypotension, the blood pressure can be a valuable guide in the resuscitative effort. As mentioned in Chapter 9, the noninvasive methods of measuring blood pressure often yield spuriously low measurements in patients with hypovolemia (presumably because of the vasoconstrictor response to volume loss). Therefore, when hypovolemia begins to produce a change in noninvasive blood pressure measurements, the pressure should be monitored by direct intraarterial recordings.
CARDIAC FILLING PRESSURES
Although cardiac filling pressures (i.e., the central venous pressure [CVP] and wedge pressure) are monitored routinely in patients with acute blood loss, these pressures show a poor correlation with the presence and extent of volume loss. In particular, these pressures often show little change until the blood loss is severe (i.e., greater than 30% of the blood volume). This insensitivity can be explained in two ways. First, the CVP and wedge pressures are normally low pressures (particularly the CVP, which is normally less than 5 mm Hg), and thus there is little margin for a detectable change in hypovolemia. Second, hypovolemia can be accompanied by a decrease in ventricular distensibility (presumably as a result of sympathetic activation), and when this occurs, the CVP and wedge pressures will be higher than expected at any given ventricular volume. In one animal study of hypovolemia, decreases in ventricular compliance resulted in a two-fold increase in the wedge (left-ventricular end-diastolic) pressure despite a 50% reduction in the end-diastolic volume.
Positional changes in cardiac filling pressures may be a more sensitive marker of hypovolemia. In one report, hypovolemia failed to produce a change in the CVP when it was measured in the supine position; however, when the patients were placed in an upright position, the CVP decreased 4 to 5 mm Hg. Therefore, performing orthostatic maneuvers may help improve the sensitivity of cardiac filling pressures in hypovolemia.
The normal response to a decrease in cardiac output (O2 delivery) is an increase in oxygen extraction in the systemic microcirculation. This is a compensatory response aimed at keeping oxygen uptake normal when oxygen delivery is compromised. However, there is a limit to the increase in oxygen extraction, and when this limit is reached, decreases in cardiac output are accompanied by proportional decreases in oxygen uptake into the tissues. Therefore, an increase in O2 extraction can be a marker of systemic hypoperfusion, and a maximum increases in O2 extraction can be a marker of hypovolemic shock.
Oxygen extraction can be monitored without a pulmonary artery catheter by combining pulse oximetry (for arterial O2 saturation) with measurements of oxygen saturation in blood samples obtained from a CVP catheter (the O2 saturation in the superior vena cava is normally close to the mixed venous O2 saturation). The expected changes in O2 extraction and mixed venous O2 saturation in progressive hypovolemia are shown below.
SaO2 SvO2 SaO2 – SvO2
Normal >95% >65% 20-30%
Hypovolemia >95% 50-65% 30-50%
Hypovolemic shock >95% <50% >50%
The transition from compensated hypovolemia to hypovolemic shock takes place when the oxygen extraction reaches 50 to 60% and the mixed venous O2 saturation falls to 50%. Therefore, an O2 extraction greater than 30% is a marker of hemodynamically significant hypovolemia, and an O2 extraction greater than 50% indicates possible hypovolemia shock. When the O2 extraction exceeds 50%, a blood lactate level will help identify hypovolemic shock (a lactate level greater than 4 mmol/L indicates a shock state). Oxygen extraction can also be increased by hypermetabolism or in response to anemia, and these conditions must also be considered in the interpretation of an increased O2 extraction.
A decrease in cardiac output will decrease the PCO2 in exhaled gas, and because the PCO2 in exhaled gas can be measured noninvasively, this provides a potentially useful method for monitoring the severity of hypovolemia. Intubation is not necessary, because exhaled CO2 can be monitored using standard nasal cannulas used to deliver supplemental oxygen.
The end-tidal PCO2 before volume infusion is very low at 10 mm Hg (the end-tidal PCO2 is normally within 3 mm Hg of the arterial PCO2). After volume resuscitation with 4.5 L of intravenous fluids, the end-tidal PCO2 has risen to 30 mm Hg, indicating that the cardiac output has increased in response to the volume infusion. Because the end-tidal PCO2 is measured on a breath-by-breath basis, it provides an on-line measure of the success or failure of volume resuscitation.
End-tidal CO2 monitoring has been recommended for evaluating the response to cardiopulmonary resuscitation, and it should have a similar role in the evaluation of hypovolemia.
Both physicians and nurses share a common propensity to use the hematocrit as an estimate of acute blood loss. The error of this practice is indicated in the following statement taken from the Advanced Trauma Life Support Course student manual, published by the American College of Surgeons: “Use of the hematocrit to estimate acute blood loss is unreliable and inappropriate”. Changes in hematocrit show a poor correlation with blood volume deficits and red cell volume deficits in acute hemorrhage. In fact, loss of whole blood is not expected to change the hematocrit because the relative proportions of plasma and red cell volume are unchanged. The decrease in hematocrit occurs when the kidney begins to conserve sodium (as described previously), which takes 8 to 12 hours to become evident. Another factor that drops the hematocrit in acute hemorrhage is the administration of intravenous (asanguinous) fluids.
The influence of volume resuscitation on the hematocrit is illustrated in Figure 14.2. Each column in this figure is partitioned to indicate the relative proportions of plasma and erythrocytes in the blood. The columns on the left show that acute blood loss decreases blood volume but does not change the hematocrit. The columns on the right show the influence of blood and asanguinous fluids on the hematocrit. Saline infusion increases the plasma volume selectively and thereby decreases the hematocrit. Infusion of whole blood expands the plasma and erythrocyte fractions proportionately, and thus does not alter the hematocrit. Therefore, in the first hours after the onset of blood loss, the hematocrit is a reflection of the resuscitation effort, not the extent of blood loss. The administration of intravenous (asanguinous) fluids is expected to produce a dilutional decrease in the hematocrit, even in the absence of blood loss, and thus a decrease in the hematocrit during volume resuscitation is a dilutional effect, and it is not an indication of ongoing blood loss.
RATE OF VOLUME RESUSCITATION
The mortality in hypovolemic shock is directly related to the magnitude and duration of the ischemic insult, and thus prompt replacement of volume deficits is the hallmark of successful management. The ability to infuse volume rapidly is thus an important consideration in the management of hypovolemia. The following is a brief description of the factors that influence the rate of volume infusion.
VASCULAR ACCESS SITE
Although there is a tendency to cannulate the large central veins for volume resuscitation, cannulation of peripheral veins is preferred. The larger size of the central veins is not an important consideration in volume resuscitation because the rate of volume infusion is determined by the dimensions of the vascular catheter, not by the size of the vein. Cannulation of the large central veins requires catheters that are at least 5 inches in length, whereas cannulation of peripheral veins can be accomplished with catheters that are 2 inches in length. Shorter catheters permit more rapid rates of volume infusion, and thus cannulation of peripheral veins is more favorable for rapid volume resuscitation. Central venous cannulation is reserved for monitoring cardiac filling pressures and venous O2 saturation unless very-large-bore introducer catheters are used for volume resuscitation.
The rate of laminar or streamlined flow will vary directly with the fourth power of the inner radius of the catheter. Thus, if the radius of a catheter is doubled, the flow rate through the catheter will increase sixteenfold; that is, (2r)4 = 16r. Changes in catheter length will have a proportional influence on flow rate; that is, if the length is doubled, the infusion rate will decrease by one-half. Because central venous catheters are 3 to 4 times longer than peripheral venous catheters, the infusion rate through central catheters will be as much as 75% less than the infusion rate through peripheral catheters (of equal diameter).
The fluid in this case is water, and the gradient for flow is the force of gravity. Note that for catheters of equivalent diameter (16 gauge), flow is 1.5 to 3 times faster in the shorter (2 inch) catheter. This demonstrates why shorter peripheral catheters are preferred for the resuscitation of hemorrhage.
Because the radius of a tube has a much stronger influence on flow rate than the length of the tube, rapid infusion rates are more easily achieved by increasing the diameter of a catheter rather than decreasing its length. Rapid volume infusion, defined as the infusion of at least 5 L of fluid hourly, is thus best accomplished by using large-bore introducer catheters normally used in conjunction with multilumen central venous catheters. These devices are 5 to 6 inches in length and are available in 8.5 French (2.7 mm outer diameter) and 9 French (3 mm outer diameter) sizes. They are normally used as intravascular conduits or sheaths for multilumen central venous and pulmonary artery catheters, and they allow these catheters to be inserted and removed without sacrificing the central venous access site. However, introducer catheters can be used as stand-alone infusion devices when rapid infusion is desirable. Thus, when introducer catheters are used for rapid volume infusion, the side infusion port on the catheter must be bypassed.
The force responsible for flow in this case is gravity, and the infusion device is a 16-gauge, 2-inch catheter similar to the ones used to cannulate peripheral veins. The acellular fluids (i.e., water and 5% albumin) have the highest flow rates, whereas the erythrocyte concentrate (packed RBCs) has the slowest flow rate. This demonstrates the inverse relationship between viscosity and flow rate in the Hagen-Poiseuille equation.
There is a popular misconception that colloid fluids such as plasma or albumin solutions flow more sluggishly than water or electrolyte solutions. However, because viscosity is primarily a function of cellular density, all acellular fluids should have equivalent flow properties. Therefore, colloid solutions (containing large molecular weight substances) will infuse just as rapidly as crystalloid (electrolyte) solutions.
Autotransfusion maneuvers are meant to promote venous return by shifting blood volume from the legs toward the heart. There are two autotransfusion methods: body tilt and pneumatic compression. Unfortunately, neither method is successful in achieving the desired effect, as described below.
THE TRENDELENBURG POSITION
Elevation of the pelvis above the horizontal plane in the supine position was introduced in the latter part of the 19th century as a method of facilitating surgical exposure of the pelvic organs. The originator was a surgeon named Friedrich Trendelenburg, who specialized in the surgical correction of vesicovaginal fistulas. The body position that now bears his name was later adopted as an antishock position during World War I and gained widespread popularity despite a lack of evidence for its efficacy. This popularity continues, as does the lack of evidence for efficacy.
The hemodynamic measurements were obtained in the supine position, and then repeated after the patients were placed in a position with the legs elevated 45 degrees above the horizontal plane and the head placed 15 degrees below the horizontal plane. As shown in the table, the change in position was associated with significant increases in the mean arterial pressure, wedge (left-ventricular filling) pressure, and systemic vascular resistance, while the cardiac output remained the same. This lack of an effect on the cardiac output indicates that the Trendelenburg position does not promote venous return to the heart. The increase in the wedge pressure can be due to an increase in intrathoracic pressure (transmitted into the pulmonary capillaries) caused by cephalad displacement of the diaphragm during the body tilt. The increase in blood pressure during body tilt is likely due to systemic vasoconstriction (indicated by the rise in systemic vascular resistance). These observations are consistent with other studies in animals and humans.
Why the Trendelenburg Position Cannot Work
The inability of the Trendelenburg position to augment cardiac output is not surprising, and it is explained by the high capacitance (distensibility) of the venous circulation. To augment cardiac output, the Trendelenburg position must increase the pressure gradient from peripheral to central veins, which would then increase venous return. However, the venous system is a high-capacitance system designed to absorb pressure and act as a volume reservoir. Thus, when pressure is applied to a vein, the vein distends and increases its volume capacity. This distensibility then limits any change in venous pressure, and this, in turn, counteracts any increase in the pressure gradient between peripheral and central veins. The venous system is more likely to transmit pressure when the veins are volume overloaded and less distensible. In other words, the Trendelenburg position is more likely to be effective (i.e., to augment venous return) during volume overload, not volume depletion.
Thus, the Trendelenburg position has not been, and never will be, effective in promoting venous return (cardiac output) in hypovolemia. As such, this maneuver should be abandoned for the management of hypovolemia. It remains axiomatic that the effective treatment for hypovolemia is volume replacement.
Pneumatic compression of leg veins has also been used to promote venous return in acute hemorrhage. However, as described for the Trendelenburg position, pneumatic compression of peripheral veins seems to augment the blood pressure by increasing peripheral vascular resistance (particularly in the abdomen), and not by increasing venous return. In fact, this maneuver can actually promote blood loss in penetrating thoracic injuries. At the present time, pneumatic “antishock” trousers are used predominantly for prehospital stabilization of trauma victims (i.e., when inflated, pneumatic trousers can produce a tourniquet effect that helps control pelvic and intraabdominal hemorrhage).