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Clinical Trial Summary

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.


Clinical Trial Description

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 Design


Related Conditions & MeSH terms


NCT number NCT02867943
Study type Observational
Source 105 Hospital of Chinese People's Liberation Army
Contact
Status Active, not recruiting
Phase N/A
Start date October 2015
Completion date December 2016

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