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C HAPTER 11 / Laboratory Tests Using Blood 259
inflammatory diseases, and hepatitis. Decreased levels are seen in with prior events will have a normal D-dimer level, thus limiting
severe liver disease, DIC, leukemia, and obstetric complications. the test’s usefulness. D-dimer testing has been studied to help de-
Thrombolytic therapy may also affect fibrinogen levels. 3 termine the length of time needed for anticoagulation therapy.
Palareti et al. 78 found that patients with an abnormal D-dimer
Protein C and Protein S level one month after discontinuing anticoagulation therapy had
a significantly higher risk of recurrent venous thromboembolism
Protein C, with cofactor protein S, is a natural anticoagulant pro- than patients who continued anticoagulation since they had an
tein whose function is to degrade activated factors V and VIII. De- abnormal D-dimer level.
ficiency in either protein C or S can lead to a hypercoagulable state,
which may cause venous thrombosis. In order for protein C to be
activated, it needs to interact with the thrombin–thrombomodulin ARTERIAL BLOOD GASES
complex on the surface of endothelial calls. Protein C is vitamin K-
2
dependent and indirectly promotes fibrinolysis. Hereditary pro- Arterial blood gases are frequently assessed in the patient with car-
tein C deficiency accounts for approximately 3% to 9% of patients diac disease. Tissue oxygenation, carbon dioxide removal, and
with venous thrombosis. Hereditary protein S deficiency accounts acid–base status are analyzed through the assay of arterial blood
for 2% to 7% of patients with venous thrombosis. 12 gases. Arterial blood gas results guide treatment decisions in ven-
Acquired conditions that cause protein C or protein S defi- tilated patients and critically ill, nonventilated patients. Knowl-
ciency include liver disease, vitamin K deficiency or warfarin use, edge of the normal blood gas values and the meaning of deviation
or consumption of protein C or protein S from thrombosis, DIC, from normal are essential to treatment decisions. A complete dis-
or surgery. Protein S deficiency may also be acquired by use of es- cussion of these parameters can be found in Chapter 7.
trogen, including oral contraceptives or estrogen replacement The arterial oxygen saturation (SaO 2 ) and the mixed venous
therapy, or pregnancy. Protein S may also be decreased in oxygen saturation (SvO 2 ) reflect the relation between oxygen sup-
nephrotic syndrome, HIV infection, or varicella infection. A rapid ply and demand and the extent of overall tissue utilization of O 2 .
fall in protein C or protein S can be caused by initiating warfarin Continuous monitoring of SaO 2 (oxygen supply) can be achieved
therapy without first reducing other coagulation factors with he- through pulse oximetry; laboratory analysis, however, is useful in
parin. This rapid fall in protein C or protein S can cause hyper- distinguishing the SaO 2 at PaO 2 levels above 65 mmHg. A
coagulability and cause warfarin-induced skin necrosis. Warfarin- fiberoptic pulmonary artery catheter is capable of evaluating SvO 2
induced skin necrosis causes thrombosis of skin vessels, which can levels continuously. This information is useful in determining the
lead to infarction and necrosis. Treatment requires discontinua- ideal mode of respiratory intervention, the effect of nursing care
tion of warfarin and vitamin K administration. 2,3,12 on tissue O 2 demands, physiologic alterations requiring increased
Warfarin should be discontinued for at least 10 days prior to supply of O 2 , and the reflection of physiologic changes on cardiac
testing for protein C or protein S. Reference range for protein C output. Calibration of the SvO 2 catheter oximeter should be per-
or protein S is reported as a percentage of the amount expected in formed every 24 hours by laboratory co-oximeter saturation
normal plasma. The reference range is approximately 70% to analysis. Table 11-4 provides normal values for SaO 2 and SvO 2 .
140%. 12 Chapter 21 describes hemodynamic monitoring.
D-Dimer (Fibrin Degradation
Fragment) BLOOD CHEMISTRIES
D-dimer is an assay used to measure the amount of clot break- The body’s homeostatic mechanisms are responsible for a stable
down products specific for cross-linked fragments derived from internal environment. The chemical regulation of cellular and
fibrin. A positive test indicates that thrombus is forming. This test plasma metabolites is among the most precise mechanisms in the
is most useful in the inpatient and outpatient setting, along with body. During periods of critical illness, these mechanisms may be
compression ultrasound and chest computed tomography for the inadequate or dramatically altered. The functional alterations that
diagnosis of deep vein thrombosis or PE. D-dimer may also be result from altered values are sometimes life threatening. An
used along with fibrin degradation products in the diagnosis of awareness of the factors affecting blood chemistry homeostasis, as
DIC. 2 well as the consequences of elevated or decreased levels, aids the
For the diagnosis of PE, D-dimer has a good sensitivity and nurse in making appropriate patient care decisions.
negative predictive value, but poor specificity. D-dimer levels are Some blood chemistry tests are drawn routinely on admission
abnormal in 95% of patients with PE; however, they are abnormal to the hospital to establish the patient’s baseline. Other tests are
3
in only 50% of patients with subsegmental PE. Patients with performed frequently over a day and may indicate the need for in-
normal D-dimer levels have a 95% likelihood of not having PE, tervention in the form of altered therapy and treatment modali-
and therefore the test offers an excellent negative predictive value. ties. “Normal” or reference values may differ between laboratories
In the outpatient setting when deep vein thrombosis is suspected, or among populations. Typical reference ranges for selected blood
if the D-dimer test is negative, compression ultrasound of the legs chemistry values can be found in Table 11-4.
is not necessary. 2,77 D-dimer levels are normal in only 25% of pa-
tients without PE and so have low specificity. Among patients Serum Electrolytes
without PE, D-dimer levels are commonly abnormal in hospital-
ized patients, particularly those with malignancy or recent surgery. Sodium
A normal D-dimer level can exclude recurrent PE in patients Sodium is the major cation in the extracellular space. It has sev-
with prior venous thrombosis and/or PE. However, fewer patients eral major functions: maintenance of osmotic pressure, regulation