GapCO2 and Respiratory Rate in Patients Under Volume Mechanical Ventilation

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

28 participants

Study Classification

OBSERVATIONAL

Study Start Date

2015-10-31

Study Completion Date

2016-12-31

Brief Summary

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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.

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Detailed Description

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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.

Conditions

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Shock

Study Design

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Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Study Groups

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respiratory rate is 10 breaths/min

GapCO2=Pv-aCO2 = PvCO2 - PaCO2;

Effects of venous-to-arterial CO2 tension difference after increased respiratory rate.