Venous Oximetry – The concept of SvO2 and ScvO2

Abbreviations:

• SvO2 - True mixed venous oxygen saturation      
• ScvO2 - Central venous oxygen saturation  
• VO2 – Consumption of oxygen        
• DO2 – Delivery of oxygen

Determining the adequacy of tissue oxygenation in critically ill patients is central to ascertain the health of the patient. Unfortunately, normal values in blood pressure, central venous pressure, heart rate, and blood gases do not rule out tissue hypoxia or imbalances between whole-body oxygen supply and demand. This discrepancy has led to increased interest in more direct indicators of adequacy of tissue oxygenation such as mixed and central venous oxygen saturations.

The normal cardiovascular response of increasing VO2 is to increase O2 extraction and cardiac output. Usually VO2 is independent of DO2 since tissues can maintain O2 needs by increasing O2 extraction when DO2 decreases. However, this mechanism has its limits. Below a so-called critical DO2 compensatory increase in O2 extraction is exhausted, and VO2 becomes dependent on DO2. In this case tissue hypoxia occurs, and a rise in serum lactate levels may be observed.

A decrease in SvO2 and ScvO2 represents an increased metabolic stress, either DO2 does not increase in such a way to
cover an increased VO2, or DO2 drops because of decrease in either arterial O2 content, cardiac output, or both. The magnitude of the decrease indicates the extent to which the physiological reserves are stressed.

The cardiocirculatory system may be challenged by two different conditions. Firstly, a drop in DO2 can be induced by anemia, hypoxia, hypovolemia, or heart failure. Secondly, fever, pain, stress etc. may also decrease SvO2 or ScvO2 by increasing whole-body VO2.

Pulmonary artery catheterization allows obtaining true mixed venous oxygen saturation (SvO2) while measuring central venous oxygen saturation (ScvO2) via central venous catheter reflects principally the degree of oxygen extraction from the brain and the upper part of the body. SvO2 reflects the relationship between whole-body O2 consumption and cardiac output. Indeed, it has been shown that the SvO2 is well correlated with the ratio of O2 supply to demand.

The central venous catheter sampling site usually resides in the superior vena cava. Thus central venous blood sampling reflects the venous blood of the upper body but neglects venous blood from the lower body (i.e., intra-abdominal organs). As shown below, venous O2 saturations differ among several organ systems since they extract different amounts of O2. ScvO2 is usually less than SvO2 by about 2–3% because the lower body extracts less O2 than the upper body making inferior vena caval O2 saturation higher. The primary cause of the lower O2 extraction is that many of the vascular circuits that drain into the inferior vena cava use blood flow for nonoxidative phosphorylation needs (e.g., renal blood flow, portal flow, hepatic blood flow). However, SvO2 and ScvO2 change in parallel when the whole body ratio of O2 supply to demand is altered.

The difference between the absolute value of ScvO2 and SvO2 changes under conditions of shock. In septic shock, ScvO2 often exceeds SvO2 by about 8%. During cardiogenic or hypovolemic shock mesenteric and renal blood flow decreases followed by an increase in O2 extraction in these organs. In septic shock, regional O2 consumption of the gastrointestinal tract and hence regional O2 extraction increases despite elevated regional blood flows. On the other hand, cerebral blood flow is maintained over some period in shock. This would cause a delayed drop of ScvO2 in comparison to SvO2, and the
correlation between these two parameters would worsen. Some authors therefore argued that ScvO2 cannot be used as surrogate for SvO2 under conditions of circulatory shock.

Limitations:

Venous oximetry can reflect the adequacy of tissue oxygenation only if the tissue is still capable of extracting O2. In the case of arteriovenous shunting on the microcirculatory level or cell death, SvO2 and ScvO2 may not decrease or even show elevated values despite severe tissue hypoxia. As demonstrated in patients after prolonged cardiac arrest, venous hyperoxia with an ScvO2 higher than 80% is indicative of impaired oxygen use.

Conclusion:

While measurement of SvO2 requires the insertion of a pulmonary artery catheter, measurement of ScvO2 requires only central venous catheterization. ScvO2 directed early goal-directed therapy improves survival in patients with septic shock
who are treated in an emergency department. However, ScvO2 values may differ from SvO2 values, and this difference varies in direction and magnitude with cardiovascular insufficiency. ScvO2 should not be used alone in the assessment of the cardiocirculatory system but combined with other cardio-circulatory parameters and indicators of organ perfusion such as serum lactate concentration and urine output.

Ref: M. R. Pinsky · L. Brochard · J. Mancebo; Applied Physiology in Intensive Care Medicine, Springer-Verlag Berlin Heidelberg 2006

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TRALI – Treatment and Outcome

Treatment:

• If the reaction is recognized during transfusion, then the transfusion should be stopped immediately.
• The treatment of TRALI is primarily supportive and similar to that for other forms of ALI. Supplemental oxygen is an essential part of treatment. For mild cases, supportive care may suffice.
• For more severe cases, intravenous fluids, vasopressor agents, and mechanical ventilation may be necessary. Mechanical ventilatory support may be required in more than 70% of patients. A low tidal volume, lung protective strategy has been advised for these patients.
• Generally, administration of diuretics is detrimental and must be avoided, as the pulmonary edema is not because of fluid overload. The only setting where diuretics may possibly be indicated is in the patient with fluid overload who develops TRALI.
• The use of steroids remains controversial.
• Anecdotally, cardiopulmonary bypass and extracorporeal membrane oxygenation have been successfully used.
• Prostaglandin administration and plasmapheresis have only been anecdotally reported and cannot be routinely recommended.

Outcome:

Compared with ARDS, TRALI is a transient phenomenon and has lower mortality; the majority of patients recover within 4 days with supportive care. There does not appear to be late pulmonary fibrosis or parenchymal destruction; long-term lung function in survivors appears to be the same as patients who did not experience TRALI. However, in a minority of cases, (5% to 15%), the disease is fatal .

Ref: Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

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TRALI – Clinical Presentation and Diagnosis

A high index of suspicion is needed to make the diagnosis of TRALI. The diagnosis of TRALI is primarily clinical and radiographic. As per the Canadian consensus conference, the diagnosis of TRALI is “not dependent on the results of laboratory tests or any proposed pathophysiologic mechanisms”

The symptoms commonly occur within 2 hours after the start of transfusion, with almost all reactions occurring by 6 hours. These symptoms may be rather severe and include dyspnea, hypoxemia, cyanosis, bilateral pulmonary edema, cough, fever, and chills. Both hypertension and hypotension have been reported in the presence of normal cardiac function. The hypotension may be unresponsive to intravenous fluid administration. Production of voluminous frothy secretions and an increase in airway pressures in intubated patients have also been noted. Radiographs of the chest show findings typical of ARDS. The pulmonary edema may be initially localized to the dependent or perihilar areas of the lungs, but more often it becomes generalized relatively rapidly with both alveolar and interstitial infiltrates, without cardiac enlargement or engorged
pulmonary vessels, also noted on radiography are the absence of cardiac enlargement and pulmonary vascular engorgement. Occasionally, a florid radiologic picture exists. This is described as “white out” of the lungs. The radiographic severity of lung injury often contrasts dramatically with the minimal auscultatory findings physical examination.

The central principle for diagnosing TRALI is exclusion of hydrostatic (cardiogenic) pulmonary edema. In the setting of blood transfusion, hydrostatic pulmonary edema occurring within 6 hours is referred to as transfusion-associated cardiac overload. The clinical manifestations of transfusion-associated cardiac overload include tachypnea/respiratory distress, cyanosis, tachycardia, and hypertension. Other conditions that are considered in the differential diagnosis of TRALI include allergic/anaphylactic reactions and transfusion of contaminated blood products.

The central venous and wedge pressures are typically low or
normal in TRALI but may be elevated if TRALI occurs in the setting of heart failure. Serum B type natriuretic peptide (BNP) levels may or may not be helpful in excluding cardiogenic edema, as elevated BNP levels have been reported in patients with ALI in the absence of left ventricular dysfunction. Finally, sampling of pulmonary edema fluid, shortly after lung injury, from the endotracheal tube (if present) may help in determining the etiology of the fluid. Pulmonary edema fluid in TRALI, like other causes of pulmonary capillary leak, has an elevated protein content.

Arterial blood gas analysis shows hypoxia, where a PaO2/FiO2 ratio less than 300 is consistent with ALI. Laboratory findings may also include hemoconcentration, leukopenia, neutropenia, hypocomplementemia, and hypoalbuminemia. The leukopenia is transient and thought to result from aggregation of circulating leukocytes in the pulmonary vasculature.

Serologic tests are important in confirming the diagnosis of TRALI. The basic principle is examination of sera from the donor for anti-HLA or anti-HNA antibodies. HLA antibody testing methods include lymphocytotoxicity, leuko-agglutination, and the flow panel reactive antibody assays. This latter method can detect antibodies as well as identify their specificities and is more sensitive than other techniques. Evaluation of neutrophil specific antibodies entails granulocyte agglutination and granulocyte immunofluorescence assays; notably, this latter assay does not necessarily distinguish between HLA I and HNA antibodies. DNA typing of granulocyte antigens may also be done. Although testing for neutrophil-priming activity and for antibodies in the recipient may provide important information about TRALI etiogenesis, they are not considered as part of the routine work-up.

Notification of the blood bank is advised to further evaluate the donor and their blood products for future donation or transfusion. Per the Canadian consensus conference, a donor can be considered as implicated in a TRALI reaction only if they are found to have anti-HLA or anti-HNA antibodies that are specific for antigens on the recipient’s leukocytes or via a positive cross-match.

Ref : Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

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