Abstract
Purpose: To investigate the mechanism of acidosis developing after saline infusion (dilutional acidosis or hyperchloremic acidosis). Methods: We simulated normal extracellular fluid dilution by infusing distilled water, normal saline and lactated Ringer's solution. Simulations were performed either in a closed system or in a system open to alveolar gases using software based on the standard laws of mass action and mass conservation. In vitro experiments diluting human plasma were performed to validate the model. Results: In our computerized model with constant pKs, diluting extracellular fluid modeled as a closed system with distilled water, normal saline or lactated Ringer's solution is not associated with any pH modification, since all its determinants (strong ion difference, CO2 content and weak acid concentration) decrease at the same degree, maintaining their relative proportions unchanged. Experimental data confirmed the simulation results for normal saline and lactated Ringer's solution, whereas distilled water dilution caused pH to increase. This is due to the increase of carbonic pK induced by the dramatic decrease of ionic strength. Acidosis developed only when the system was open to gases due to the increased CO2 content, both in its dissociated (bicarbonate) and undissociated form (dissolved CO2). Conclusions: The increase in proton concentration observed after dilution of the extracellular system derives from the reaction of CO2 hydration, which occurs only when the system is open to the gases. Both Stewart's approach and the traditional approach may account for these results.
| Original language | English |
|---|---|
| Pages (from-to) | 2033-2043 |
| Number of pages | 11 |
| Journal | Intensive Care Medicine |
| Volume | 35 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Dec 2009 |
Fingerprint
Keywords
- Acid-base equilibrium
- CO content
- Metabolic acidosis
- Stewart's approach
- Volume resuscitation
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
Cite this
Dilutional acidosis : Where do the protons come from? / Gattinoni, Luciano; Carlesso, E.; Maiocchi, G.; Polli, F.; Cadringher, P.
In: Intensive Care Medicine, Vol. 35, No. 12, 12.2009, p. 2033-2043.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dilutional acidosis
T2 - Where do the protons come from?
AU - Gattinoni, Luciano
AU - Carlesso, E.
AU - Maiocchi, G.
AU - Polli, F.
AU - Cadringher, P.
PY - 2009/12
Y1 - 2009/12
N2 - Purpose: To investigate the mechanism of acidosis developing after saline infusion (dilutional acidosis or hyperchloremic acidosis). Methods: We simulated normal extracellular fluid dilution by infusing distilled water, normal saline and lactated Ringer's solution. Simulations were performed either in a closed system or in a system open to alveolar gases using software based on the standard laws of mass action and mass conservation. In vitro experiments diluting human plasma were performed to validate the model. Results: In our computerized model with constant pKs, diluting extracellular fluid modeled as a closed system with distilled water, normal saline or lactated Ringer's solution is not associated with any pH modification, since all its determinants (strong ion difference, CO2 content and weak acid concentration) decrease at the same degree, maintaining their relative proportions unchanged. Experimental data confirmed the simulation results for normal saline and lactated Ringer's solution, whereas distilled water dilution caused pH to increase. This is due to the increase of carbonic pK induced by the dramatic decrease of ionic strength. Acidosis developed only when the system was open to gases due to the increased CO2 content, both in its dissociated (bicarbonate) and undissociated form (dissolved CO2). Conclusions: The increase in proton concentration observed after dilution of the extracellular system derives from the reaction of CO2 hydration, which occurs only when the system is open to the gases. Both Stewart's approach and the traditional approach may account for these results.
AB - Purpose: To investigate the mechanism of acidosis developing after saline infusion (dilutional acidosis or hyperchloremic acidosis). Methods: We simulated normal extracellular fluid dilution by infusing distilled water, normal saline and lactated Ringer's solution. Simulations were performed either in a closed system or in a system open to alveolar gases using software based on the standard laws of mass action and mass conservation. In vitro experiments diluting human plasma were performed to validate the model. Results: In our computerized model with constant pKs, diluting extracellular fluid modeled as a closed system with distilled water, normal saline or lactated Ringer's solution is not associated with any pH modification, since all its determinants (strong ion difference, CO2 content and weak acid concentration) decrease at the same degree, maintaining their relative proportions unchanged. Experimental data confirmed the simulation results for normal saline and lactated Ringer's solution, whereas distilled water dilution caused pH to increase. This is due to the increase of carbonic pK induced by the dramatic decrease of ionic strength. Acidosis developed only when the system was open to gases due to the increased CO2 content, both in its dissociated (bicarbonate) and undissociated form (dissolved CO2). Conclusions: The increase in proton concentration observed after dilution of the extracellular system derives from the reaction of CO2 hydration, which occurs only when the system is open to the gases. Both Stewart's approach and the traditional approach may account for these results.
KW - Acid-base equilibrium
KW - CO content
KW - Metabolic acidosis
KW - Stewart's approach
KW - Volume resuscitation
UR - http://www.scopus.com/inward/record.url?scp=70949087375&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70949087375&partnerID=8YFLogxK
U2 - 10.1007/s00134-009-1653-7
DO - 10.1007/s00134-009-1653-7
M3 - Article
C2 - 19763537
AN - SCOPUS:70949087375
VL - 35
SP - 2033
EP - 2043
JO - Intensive Care Medicine
JF - Intensive Care Medicine
SN - 0342-4642
IS - 12
ER -