Skip to content

Non Carbonic Buffer Power of Critical Ill Patients With Sepsis

Changes in Acid-base Variables Induced by Acute Variations in Partial Pressure of Carbon Dioxide in Whole Blood and Isolated Plasma of Septic Critically Ill Patients and Healthy Volunteers: an In-vitro Study

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT03503214
Enrollment
36
Registered
2018-04-19
Start date
2018-03-07
Completion date
2019-02-20
Last updated
2019-04-25

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Acid-Base Imbalance, Respiratory Acidosis, Respiratory Alkalosis

Keywords

Acid-base equilibrium, Stewart's approach, In vitro study, Respiratory acid-base derangements

Brief summary

Alterations of acid-base equilibrium are very common in critically ill patients and understanding their pathophysiology can be important to improve clinical treatment. The human organism is protected against acid-base disorders by several compensatory mechanisms that minimize pH variations in case of blood variations in carbon dioxide content. The aim of the present study is to quantify the buffer power, i.e. the capacity to limit pH variations in response to carbon dioxide changes, in critically ill septic patients and compare these results with data collected from healthy volunteers.

Detailed description

Alterations of acid-base equilibrium are very common in critically ill patients and understanding their pathophysiology can be important to improve clinical treatment. The human body is protected against acid-base disorders by several compensatory mechanisms that minimize pH variations in response to acid-base derangements. The present study focuses on the acute compensatory mechanisms of respiratory acid-base derangements, i.e., respiratory acidosis and respiratory alkalosis. In this case the non-carbonic buffers are constituted by albumin and phosphates in plasma, with the addition of hemoglobin in whole blood. Aim of the present in-vitro study is to measure the buffer power of non-carbonic weak acids contained in whole blood and isolated plasma, assess the relative contribution of red blood cells and plasma proteins and perform a comparison between septic patients and healthy controls.

Interventions

DIAGNOSTIC_TESTIn vitro determination of non-carbonic buffer power

In vitro measurement of the non-carbonic buffer power by the means of equilibration of whole blood and isolated plasma with gas mixtures containing different concentrations of carbon dioxide

DIAGNOSTIC_TESTClassic description of acid-base status

Measurement of plasma electrolytes, hemoglobin concentration, albumin and phosphates to compute acid-base variables according to Stewart's approach.

Sponsors

Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico
Lead SponsorOTHER

Study design

Observational model
CASE_CONTROL
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes

Inclusion criteria

* Septic patients and healthy volunteers

Exclusion criteria

* age \< 18 years and pregnancy

Design outcomes

Primary

MeasureTime frameDescription
Non-carbonic buffer power1 dayNon-carbonic buffer power (beta) of whole blood and isolated plasma \[expressed as variations in bicarbonate concentration divided by variations in pH).

Secondary

MeasureTime frameDescription
Strong Ion Difference variations induced by carbon dioxide1 dayVariations in Strong Ion Difference of whole blood and plasma \[expressed in milliequivalents per Liter\], induced by acute in vitro changes of carbon dioxide
Bicarbonate Variations induced by carbon dioxide1 dayVariations in bicarbonate concentration of whole blood and plasma \[expressed in milliequivalents per Liter\], induced by acute in vitro changes of carbon dioxide
Oxidized albumin1 dayOxidized albumin \[expressed as percentage of total albumin concentration\]
Correlation between hematocrit values and Strong Ion Difference variations1 dayCorrelation between hematocrit \[expressed as percentage\] values and Strong Ion Difference variations \[expressed in mEq/L\] induced by acute in vitro changes of Carbon Dioxide. Acute variations in partial pressure of carbon dioxide cause changes in Strong Ion Difference. The hypothesis is that the magnitude of Strong Ion Difference variations correlate to the hematocrit, being the red blood cell the major source of electrolytes. The higher the hematocrit, the higher the possible change in Strong Ion Difference induced by acute variations in partial pressure of carbon dioxide.

Countries

Italy

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026