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.
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.
Study Type
OBSERVATIONAL
Enrollment
36
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
Measurement of plasma electrolytes, hemoglobin concentration, albumin and phosphates to compute acid-base variables according to Stewart's approach.
IRCCS Fondazione Ca' Granda Ospedale Maggiore Policlinico
Milan, Italy
Non-carbonic buffer power
Non-carbonic buffer power (beta) of whole blood and isolated plasma \[expressed as variations in bicarbonate concentration divided by variations in pH).
Time frame: 1 day
Strong Ion Difference variations induced by carbon dioxide
Variations in Strong Ion Difference of whole blood and plasma \[expressed in milliequivalents per Liter\], induced by acute in vitro changes of carbon dioxide
Time frame: 1 day
Bicarbonate Variations induced by carbon dioxide
Variations in bicarbonate concentration of whole blood and plasma \[expressed in milliequivalents per Liter\], induced by acute in vitro changes of carbon dioxide
Time frame: 1 day
Oxidized albumin
Oxidized albumin \[expressed as percentage of total albumin concentration\]
Time frame: 1 day
Correlation between hematocrit values and Strong Ion Difference variations
Correlation 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.
Time frame: 1 day
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