Shock Clinical Trial
Official title:
PCO2 Gab as a Marker of Tissue Adequacy of Cardiac Output in Sever Shock State, Compared to Other Tissue Perfusion Indicators.
1. To assess validity of of central and pulmonary veno - arterial CO2 gradient to predict fluid responsiveness and to guide fluid management and determine the cut off point to continue or stop resuscitation. 2. comparison between PCO2 gab and left ventricular outflow tract velocity time integral to determine whether to continue or stop resuscitation and whether PCO2 gab is a surrogate of cardiac output or not.
Assessing the adequacy of oxygen delivery with oxygen requirements is one of the key-goal of hemodynamic resuscitation. Clinical examination, lactate and central or mixed venous oxygen saturation (SvO2 an ScvO2 respectively) all have their limitations (Gavelli et al., 2019). The veno- arterial difference in CO2 tension (delta CO2 or PCO2 gap) is not indicator of anaerobic metabolism since it is influenced by the oxygen consumption. By contrast, it reliably indicates whether blood flow to remove is sufficient to carry CO2 from prepheral tissues to the lung in view of its clearance: it, thus, reflects the adequacy of cardiac output with the metabolic condition (valley et al., 2013). The gap is a marker of adequacy of venous blood flow to remove CO2 produced rather than a marker of tissue hypoxia (Vallet et al., 2013). The gab can be calculated from simultaneous sampling of central venous blood from a central vein catheter and arterial blood. Determining the delta PCO2 during resuscitation of septic shock Patients might be useful when deciding when to continue resuscitation despite a central venous oxygen saturation>70% associated with elevated blood lactate levels. because a high blood lactate level is not a discriminatory factor in determining the source of that stress, an increased delta PCO2 (>6 mmHg) could be used to identify Patients who still remain inadequately resuscitated. Fluid responsiveness in shocked patients is conventionally defined as an increase of at least 10% to 15% in stroke volume in response to a fluid challenge. Assessment of response to a fluid challenge can be guided with echocardiography. It is achieved by measuring left ventricular outflow tract velocity time integral (LVOT VI) immediately before and after fluid challenge (miller et al; 2016). ;
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