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.

Inclusion Criteria:

• Septic patients and healthy volunteers

Exclusion Criteria:

• age < 18 years and pregnancy

Patients with sepsis or septic shock admitted to the ICU will be enrolled. Furthermore, healthy volunteers recruited from ICU staff members and relatives will be enrolled as control group.