scholarly journals Hypoproteinemia, strong-ion difference, and acid-base status in critically ill patients

1998 ◽  
Vol 84 (5) ◽  
pp. 1740-1748 ◽  
Author(s):  
Peter Wilkes

The present study was a prospective, nonrandomized, observational examination of the relationship among hypoproteinemia and electrolyte and acid-base status in a critical care population of patients. A total of 219 arterial blood samples reviewed from 91 patients was analyzed for arterial blood gas, electrolytes, lactate, and total protein. Plasma strong-ion difference ([SID]) was calculated from [Na+] + [K+] − [Cl−] − [La−]. Total protein concentration was used to derive the total concentration of weak acid ([A]tot). [A]tot encompassed a range of 18.7 to 9.0 meq/l, whereas [SID] varied from 48.1 to 26.6 meq/l and was directly correlated with [A]tot. The decline in [SID] was primarily attributable to an increase in [Cl−]. A direct correlation was also noted between[Formula: see text] and [SID], but not between [Formula: see text] and [A]tot. The decrease in [SID] and [Formula: see text] was such that neither [H+] nor [[Formula: see text]] changed significantly with [A]tot.

2001 ◽  
Vol 91 (3) ◽  
pp. 1364-1371 ◽  
Author(s):  
Peter D. Constable

The strong ion approach provides a quantitative physicochemical method for describing the mechanism for an acid-base disturbance. The approach requires species-specific values for the total concentration of plasma nonvolatile buffers (Atot) and the effective dissociation constant for plasma nonvolatile buffers ( K a), but these values have not been determined for human plasma. Accordingly, the purpose of this study was to calculate accurate Atot and K a values using data obtained from in vitro strong ion titration and CO2tonometry. The calculated values for Atot (24.1 mmol/l) and K a (1.05 × 10−7) were significantly ( P < 0.05) different from the experimentally determined values for horse plasma and differed from the empirically assumed values for human plasma (Atot = 19.0 meq/l and K a = 3.0 × 10−7). The derivatives of pH with respect to the three independent variables [strong ion difference (SID), Pco 2, and Atot] of the strong ion approach were calculated as follows: [Formula: see text] [Formula: see text], [Formula: see text]where S is solubility of CO2 in plasma. The derivatives provide a useful method for calculating the effect of independent changes in SID+, Pco 2, and Atot on plasma pH. The calculated values for Atot and K a should facilitate application of the strong ion approach to acid-base disturbances in humans.


Author(s):  
Jeremy B. Richards ◽  
David H. Roberts

An arterial blood gas (ABG) provides clinically useful information about an individual's acid–base status, the partial pressure of arterial carbon dioxide, the partial pressure of arterial oxygen, and the arterial oxygen saturation. Hypoxia, dyspnea, or suspected acid–base disturbance are clear indications to check an ABG. Altered mental status, critical illness, and acute respiratory distress syndrome (ARDS) are specific clinical syndromes or presentations that warrant checking an ABG. An ABG is helpful in evaluating pulmonary pathophysiology as the presence and severity of hypoxia and/or hypercapnia can be quantified. Because an ABG can rapidly provide information about oxygenation, ventilation, and acid–base status, ABGs are particularly useful and common in the critical care setting.


2018 ◽  
Vol 35 (5) ◽  
pp. 511-518
Author(s):  
Scott E. Rudkin ◽  
Craig L. Anderson ◽  
Tristan R. Grogan ◽  
David A. Elashoff ◽  
Richard M. Treger

Background and Objectives: In severe circulatory failure agreement between arterial and mixed venous or central venous values is poor; venous values are more reflective of tissue acid–base imbalance. No prior study has examined the relationship between peripheral venous blood gas (VBG) values and arterial blood gas (ABG) values in hemodynamic compromise. The objective of this study was to examine the correlation between hemodynamic parameters, specifically systolic blood pressure (SBP) and the arterial–peripheral venous (A-PV) difference for all commonly used acid–base parameters (pH, Pco 2, and bicarbonate). Design, Setting, Participants, and Measurements: Data were obtained prospectively from adult patients with trauma. When an ABG was obtained for clinical purposes, a VBG was drawn as soon as possible. Patients were excluded if the ABG and VBG were drawn >10 minutes apart. Results: The correlations between A-PV pH, A-PV Pco 2, and A-PV bicarbonate and SBP were not statistically significant ( P = .55, .17, and .09, respectively). Although patients with hypotension had a lower mean arterial and peripheral venous pH and bicarbonate compared to hemodynamically stable patients, mean A-PV differences for pH and Pco 2 were not statistically different ( P = .24 and .16, respectively) between hypotensive and normotensive groups. Conclusions: In hypovolemic shock, the peripheral VBG does not demonstrate a higher CO2 concentration and lower pH compared to arterial blood. Therefore, the peripheral VBG is not a surrogate for the tissue acid–base status in hypovolemic shock, likely due to peripheral vasoconstriction and central shunting of blood to essential organs. This contrasts with the selective venous respiratory acidosis previously demonstrated in central venous and mixed venous measurements in circulatory failure, which is more reflective of acid–base imbalance at the tissue level than arterial blood. Further work needs to be done to better define the relationship between ABG and both central and peripheral VBG values in various types of shock.


1989 ◽  
Vol 58 (4) ◽  
pp. 382-388 ◽  
Author(s):  
Susan A. Ward ◽  
Karlman Wasserman ◽  
James A. Davis ◽  
Brian J. Whipp

1987 ◽  
Vol 252 (2) ◽  
pp. R348-R352 ◽  
Author(s):  
M. Shimizu ◽  
D. R. Jones

Measurements of all the major independent variables [arterial CO2 tension (PaCO2); strong-ion difference ([SID]), and total protein content, which approximate total weak acid concentration in plasma] are essential for understanding changes in acid-base balance in plasma. During involuntary submergence of 1, 2, or 4 min, PaCO2 in ducks increased and arterial pH (pHa) decreased. During 1-min dives there were no significant changes in any strong ions. In both 2- and 4-min dives, there was a significant increase in [lactate-], but because of an increase in equal magnitude of [Na+], [SID] did not change. During recovery from all dives the plasma remained acidotic for several minutes, although PaCO2 fell below predive levels in less than 1 min. [Lactate-] increased in the recovery period. There were no changes in total protein content during submergence or recovery. Breathing 100% O2 before 2-min dives caused a reduction in [lactate-] production and release during and after the dive, although due to a marked increased in PaCO2, pHa fell as low as in 4-min dives after breathing air. After 1 min of recovery, pHa returned to normal along with the restoration of the predive level of PaCO2. We conclude that the acidosis during involuntary submergence is due solely to an increase in PaCO2, whereas in recovery it is caused by decreased [SID].


Toxics ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 22
Author(s):  
Hyo-Wook Gil ◽  
Min Hong ◽  
HwaMin Lee ◽  
Nam-jun Cho ◽  
Eun-Young Lee ◽  
...  

We investigated clinical impacts of various acid-base approaches (physiologic, base excess (BE)-based, and physicochemical) on mortality in patients with acute pesticide intoxication and mutual intercorrelated effects using principal component analysis (PCA). This retrospective study included patients admitted from January 2015 to December 2019 because of pesticide intoxication. We compared parameters assessing the acid-base status between two groups, survivors and non-survivors. Associations between parameters and 30-days mortality were investigated. A total of 797 patients were analyzed. In non-survivors, pH, bicarbonate concentration (HCO3−), total concentration of carbon dioxide (tCO2), BE, and effective strong ion difference (SIDe) were lower and apparent strong ion difference (SIDa), strong ion gap (SIG), total concentration of weak acids, and corrected anion gap (corAG) were higher than in survivors. In the multivariable logistic analysis, BE, corAG, SIDa, and SIDe were associated with mortality. PCA identified four principal components related to mortality. SIDe, HCO3−, tCO2, BE, SIG, and corAG were loaded to principal component 1 (PC1), referred as total buffer bases to receive and handle generated acids. PC1 was an important factor in predicting mortality irrespective of the pesticide category. PC3, loaded mainly with pCO2, suggested respiratory components of the acid-base system. PC3 was associated with 30-days mortality, especially in organophosphate or carbamate poisoning. Our study showed that acid-base abnormalities were associated with mortality in patients with acute pesticide poisoning. We reduced these variables into four PCs, resembling the physicochemical approach, revealed that PCs representing total buffer bases and respiratory components played an important role in acute pesticide poisoning.


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