The central venous blood is inadequate to assess the arterial oxygenation as the venous oxygen partial pressure (PvO2) reflects primarily the tissue oxygenation. However, the arterial oxygenation status may be assessed from pulsoximetry. If this is available, as in most of the critically ill patients, the central venous blood analysis provides further clinical relevant information. Primarily the central venous oxygen saturation (SatvO2) is an extremely sensitive monitor of respiratory hemodynamic and metabolic status. In fact: SatvO2=SataO2 – (VO2/Q)*(1/(Hb*1.36) SatvO2=lung – (Metabolism/Haemodynamic)*(1/Anemia) As shown whatever change in lung function, metabolism, haemodynamic or anaemia affects SatvO2. Indeed SatvO2 is extremely sensitive (not specific) monitor of basic vital functions. Moreover it may be used as target of therapy during resuscitation. In unselected population of critically ill patients it has been shown that targeting SatvO2 equal or greater than 70% is equivalent as to target to a normal cardiac output. In septic patients targeting to SatvO2 equal or greater than 70% has been shown to provide survival benefits. Indeed sampling the central venous blood in patients in which pulsoximetry is available provides information on tissue oxygenation and hemodynamic setup not derivable from arterial sampling. For what the ventilatory status and the acid-base equilibrium is concerned it is important to emphasize that central venous blood may provide the same information as the arterial blood. PaCO2 and the central venous carbon dioxide tension (PvCO2) are strongly correlated (at least in steady state patients). Obviously the normal PvCO2 is not 40 mmHg but is 3-3.5 mmHg higher. The same applies for BE. It is important to note that the normal BE in the venous blood is =1.5 mmol greater than arterial one. To compute exactly the venous BE the reference normal values should be the ones of the venous and not of the arterial blood, i.e., as an example, pH = 7.38 and HCO3- = 25.7. Keeping the normal values of the central venous blood in mind it is easy to quantify both the ventilatory status and acid-base equilibrium. Indeed the central venous blood not only provides the same information on ventilation and acid-base equilibrium as the arterial blood but also provides information on tissue oxygenation and hemodynamic adequacy. The most complete set of information, however, is provided by the simultaneous sampling of arterial and central venous blood. In this case the cause of the oxygenation defect may be measured by measuring the shunt fraction. The venous arterial difference allows a better assessment of hemodynamic set-up. The PvCO2 to PaCO2 difference, due to an unsteady state period, may give insights on tissue acidosis, which sharply increases PvCO2, before a new equilibrium is reached.

Central venous blood gas analysis / L. Gattinoni. ((Intervento presentato al 23. convegno SMART : Simposio Mostra Anestesia Rianimazione e Terapia Intensiva tenutosi a Milano nel 2012.

Central venous blood gas analysis

L. Gattinoni
Primo
2012

Abstract

The central venous blood is inadequate to assess the arterial oxygenation as the venous oxygen partial pressure (PvO2) reflects primarily the tissue oxygenation. However, the arterial oxygenation status may be assessed from pulsoximetry. If this is available, as in most of the critically ill patients, the central venous blood analysis provides further clinical relevant information. Primarily the central venous oxygen saturation (SatvO2) is an extremely sensitive monitor of respiratory hemodynamic and metabolic status. In fact: SatvO2=SataO2 – (VO2/Q)*(1/(Hb*1.36) SatvO2=lung – (Metabolism/Haemodynamic)*(1/Anemia) As shown whatever change in lung function, metabolism, haemodynamic or anaemia affects SatvO2. Indeed SatvO2 is extremely sensitive (not specific) monitor of basic vital functions. Moreover it may be used as target of therapy during resuscitation. In unselected population of critically ill patients it has been shown that targeting SatvO2 equal or greater than 70% is equivalent as to target to a normal cardiac output. In septic patients targeting to SatvO2 equal or greater than 70% has been shown to provide survival benefits. Indeed sampling the central venous blood in patients in which pulsoximetry is available provides information on tissue oxygenation and hemodynamic setup not derivable from arterial sampling. For what the ventilatory status and the acid-base equilibrium is concerned it is important to emphasize that central venous blood may provide the same information as the arterial blood. PaCO2 and the central venous carbon dioxide tension (PvCO2) are strongly correlated (at least in steady state patients). Obviously the normal PvCO2 is not 40 mmHg but is 3-3.5 mmHg higher. The same applies for BE. It is important to note that the normal BE in the venous blood is =1.5 mmol greater than arterial one. To compute exactly the venous BE the reference normal values should be the ones of the venous and not of the arterial blood, i.e., as an example, pH = 7.38 and HCO3- = 25.7. Keeping the normal values of the central venous blood in mind it is easy to quantify both the ventilatory status and acid-base equilibrium. Indeed the central venous blood not only provides the same information on ventilation and acid-base equilibrium as the arterial blood but also provides information on tissue oxygenation and hemodynamic adequacy. The most complete set of information, however, is provided by the simultaneous sampling of arterial and central venous blood. In this case the cause of the oxygenation defect may be measured by measuring the shunt fraction. The venous arterial difference allows a better assessment of hemodynamic set-up. The PvCO2 to PaCO2 difference, due to an unsteady state period, may give insights on tissue acidosis, which sharply increases PvCO2, before a new equilibrium is reached.
9-mag-2012
Settore MED/41 - Anestesiologia
Central venous blood gas analysis / L. Gattinoni. ((Intervento presentato al 23. convegno SMART : Simposio Mostra Anestesia Rianimazione e Terapia Intensiva tenutosi a Milano nel 2012.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/173493
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