As an approximate of the difference between venous-to-arterial CO2 tension (∆PCO2), ∆PCO2 is proportional to CO2 production and inversely related to cardiac output (Fick equation). Anaerobic CO2 production is thought to occur when tissue hypoxia is present, mostly because of buffering of bicarbonate ions by the protons produced in excess secondary to the hydrolysis of adenosine triphosphate. Therefore ∆PCO2 has been proposed as a marker of tissue hypoxia.
An increased ∆PCO2 (\> 6 mmHg) could be used to identify patients who still remain inadequately resuscitated, when deciding when to continue resuscitation despite a central venous oxygen saturation (ScvO2) \> 70% associated with elevated blood lactate levels. Under steady states of both VO2 and VCO2, P (v-a) CO2 was observed to increase in parallel with the reduction in cardiac output. However, spontaneous breathing and hyperventilation may reduce PaCO2 and prevent the CO2 stagnation-induced rise in PvCO2. To date,these studies of ∆PCO2 and respiratory rate in septic shock patients Under Volume Mechanical Ventilation are rarely.
Study Type
OBSERVATIONAL
Enrollment
28
respiratory rate was started at 10 breaths/min and added by 2 breaths/min every 60 min up to 16 breaths/min
Effects of respiratory rate on venous-to-arterial CO2 tension difference in septic shock patients Under Volume Mechanical Ventilation
Time frame: 1 year
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