Hemorrhage and Hypovolemia

The circulatory system operates with a relatively small volume and a volume-responsive pump. This is an energy-efficient design, but it quickly falters when volume is lost. While most internal organs like the lungs, liver, and kidneys can lose as much as 75% of their functional mass without life-threatening organ failure, loss of less than 50% of the blood volume can be fatal. This intolerance to blood loss is the dominant concern in the bleeding patient.

I. Body Fluids & Blood Loss

A. Distribution of Body Fluids

The volume of selected body fluids in adults is shown in Table 7.1 (1). The following points deserve mention:

Total body fluid (in liters) accounts for about 60% of the lean body weight in males (600 mL/kg) and 50% of the lean body weight in females (500 mL/kg).
Blood volume represents only 11–12% of the total body fluids.
Plasma volume is about 25% of interstitial fluid volume. This relationship is important for understanding the volume effects of sodium-rich crystalloid fluids, which is described later in the chapter.

Table 7.1 Volume of Selected Body Fluids in Adults

Body Fluid	Men		Women
Body Fluid	mL/kg	75 kg^†	mL/kg	60 kg^†
Total Body Fluid	600	45 L	500	30 L
Interstitial Fluid	150	11.3 L	125	7.5 L
Whole Blood	66	5 L	60	3.6 L
Red Blood Cells	26	2. L	24	1.4 L
Plasma	40	3 L	36	2.2 L
^† Lean body weight for an average adult male and female. Volume of blood, red blood cells, and plasma (in mL/kg) from Reference 1.

B. Severity of Blood Loss

The American College of Surgeons has proposed the following classification system for acute blood loss (2).

1. Class I

Loss of <15% of the blood volume (or <10 mL/kg).
This degree of blood loss is usually fully compensated by interstitial fluid shifts (transcapillary refill), so that blood volume is maintained and clinical findings are minimal or absent.

2. Class II

Loss of 15–30% of the blood volume (or 10–20 mL/kg).
This represents the compensated phase of hypo-volemia, where blood pressure is maintained by systemic vasoconstriction. Postural changes in pulse rate and blood pressure may be evident, but these findings are inconsistent.
The extremities become cool at this stage, and urine output falls, but does not reach oliguric levels (<0.5 ml/kg/hr).

3. Class III

Loss of 30–40% of the blood volume (or 20–30 mL/kg).
This stage marks the onset of decompensated blood loss or hemorrhagic shock, where the vasoconstrictor response is no longer able to sustain blood pressure and organ perfusion.
Clinical findings can include supine hypotension, cold extremities, confusion, oliguria (urine output <0.5 mL/kg/hr) and increased lactate levels in blood.

4. Class IV

Loss of >40% of blood volume (or >30 mL/kg).
This degree of blood loss results in progressive hemorrhagic shock, and includes massive blood loss; i.e., loss of >50% of the blood volume in 3 hours.
Clinical findings include limb cyanosis, evidence of multiorgan dysfunction (e.g., lethargy, oliguria, increased liver enzymes, etc.) and progressive lactic acidosis.

II. Clinical Evaluation

The clinical detection of hypovolemia is so flawed that is has been called a comedy of errors (3).

A. Vital Signs

The reliability of vital signs in the detection of acute blood loss is shown in Table 7.2 (4,5). Note the following:

Supine tachycardia and supine hypotension are absent
(i.e., low sensitivity) in a majority of patients with blood volume deficits up to 1.1 liters (i.e., up to a 25% loss of blood volume in average sized males).
Postural pulse increments (≥30 beats/min) and postural hypotension (decrease in systolic pressure ≥20 mm Hg) are uncommon when blood loss is less than 630 mL, but with greater blood loss, postural pulse increments are a sensitive and specific marker of hypovolemia.

Table 7.2 Accuracy of Vital Signs in Detecting Hypovolemia

Abnormal Finding	Sensitivity/Specificity
Abnormal Finding	Blood Loss (450–630 mL)^†	Blood Loss (630–1150 mL)^ξ
Supine Tachycardia¹	0 / 96%	12% / 96%
Supine Hypotension²	13% / 97%	33% / 97%
Postural Pulse Increment³	22% / 98%	97% / 98%
Postural Hypotension⁴
Age <65 yrs	9% / 94%	Not studied
Age ≥65 yrs	27% / 86%	Not studied
¹ Pulse rate >100 beats/min. ² Systolic pressure <95 mm Hg. ³ Increase in pulse rate >30 beats/min. ⁴ Decrease in systolic pressure >20 mm Hg. ^† Equivalent to loss of 10–12% of blood volume in an average-sized male. ^ξ Equivalent to loss of 12–25% of blood volume in an average-sized male. From References 4 and 5.

B. Central Venous Pressure

The central venous pressure (CVP) has traditionally played a prominent role in the evaluation of intravascular volume. However, clinical studies have consistently shown a poor correlation between the CVP and objective measures of blood volume (6). This is demonstrated in Figure 7.1 (7).
The consistent lack of correlation between CVP and blood volume measurements has prompted the recommendation that the CVP should never be used to evaluate blood volume (6).

FIGURE 7.1 Scatter plot showing paired measurements of circulating blood volume (CBV) and central venous pressure (CVP) in a group of postoperative patients. Correlation coefficient (r) and p value indicate no significant relationship between the two measurements. Redrawn from Reference 7.

C. Venous O₂ Saturation

The O₂ saturation in the superior vena cava (ScvO₂) is a surrogate measure of the mixed venous O₂ saturation in the pulmonary arteries (SvO₂), and is a marker of the balance between systemic O₂ delivery (DO₂) and O₂ consumption (VO₂) (see Equation 6.15).
Hypovolemia will prompt a decrease in cardiac output and a subsequent decrease in DO₂, which will result in
a decrease in ScvO₂. The normal ScvO₂ is 70–80%, so in a patient with suspected hypovolemia, an ScvO₂ <70% will help to confirm the diagnosis (for more on the ScvO₂, see Chapter 6, Sections I-F and III-D).

D. Hemoglobin/Hematocrit

Acute hemorrhage involves the loss of whole blood, which is not expected to alter the hemoglobin concentration or hematocrit. This is supported by studies showing a poor correlation between changes in hematocrit and blood volume deficits (or erythrocyte deficits) in acute hemorrhage (8).
Any decrease in hemoglobin or hematocrit in acute hemorrhage is a reflection of volume resuscitation with asanguinous fluids (e.g., saline), which expands the plasma volume and causes a dilutional decrease in hemoglobin and hematocrit (9).
For the reasons stated above, the hemoglobin and hematocrit should NEVER be used to evaluate the extent of acute blood loss (2).

E. Serum Lactate

In the setting of acute blood loss, an elevated serum lactate level (generally >2 mmol/L) is evidence of hemorrhagic shock, even in the absence of hypotension. (See Chapter 6, Section III-E for information on lactate as a marker of tissue hypoxia.)
Lactate levels also have prognostic value; i.e.,
- The magnitude of elevation in lactate levels has a close correlation with the risk of a fatal outcome (10).
- The rate of decline in lactate levels (lactate clearance) is also related to outcome (see Chapter 6, Figure 6.2).
  In one study of trauma victims with hemorrhagic shock, there were no deaths when lactate levels returned to normal within 24 hours, while 86% of the patients died when lactate levels remained elevated after 48 hours (11). Therefore, normalization of lactate levels within 24 hours can be used as an end-point of resuscitation for hemorrhagic shock (see later).

F. Arterial Base Deficit

The base deficit is the amount (in millimoles) of base needed to titrate one liter of whole blood to a pH of 7.40 (at a PCO₂ of 40 mm Hg); it is considered a more specific marker of metabolic acidosis than the serum bicarbonate (12).
The normal range for base deficit is +2 to −2 mmol/L. Increases in base deficit are classified as mild (−3 to −5 mmol/L), moderate (−6 to −14 mmol/L), or severe (≥−15 mmol/L).
In the bleeding patient, there is a direct correlation between the severity of the base deficit and the magnitude of blood loss, and rapid correction of the base deficit is associated with more favorable outcomes (13).
Monitoring the base deficit has been a popular practice in trauma resuscitation, but the base deficit is essentially a surrogate measure of lactic acidosis, and it has less predictive value than serum lactate levels in trauma patients (14). Since lactate levels are easily obtained, there is no justification for monitoring the base deficit.