Metabolic acidosis developing during cardiopulmonary bypass is related to a decrease in strong ion difference

Perfusion ◽  
2004 ◽  
Vol 19 (3) ◽  
pp. 145-152 ◽  
Author(s):  
R Peter Alston ◽  
Laura Cormack ◽  
Catherine Collinson
Keyword(s):  
Metabolic Acidosis ◽  
Lactate Concentration ◽  
Gas Analysis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Outcome Variable ◽  
Royal Infirmary ◽  
Strong Ion Difference ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood

Metabolic acidosis is a frequent complication of cardio-pulmonary bypass (CPB). Commonly, its cause is ascribed to hypoperfusion; however, iatrogenic causes, related to the composition and volume of intravascular fluids that are administered, are increasingly being recognized. The aim of this study was to determine if metabolic acidosis during CPB was associated with hypoperfusion, change in strong ion difference (SID) or haemodilution. Forty-nine patients undergoing cardiac surgery using CPB in the Royal Infirmary of Edinburgh (RIE) or the HCI, Clydebank were included in the study. Arterial blood samples were aspirated before induction of anaesthesia and the end of CPB. Samples were subjected to blood gas analysis and measurement of electrolytes and lactate. Changes in concentrations were then calculated. Change variables that were found to be significant (p B-0.1) univariate correlates of the change in hydrogen ion concentration were identified and entered into a multivariate regression model with hydrogen ion concentra tion at the end of CPB as the outcome variable (r2=0.65, p<0.001). Change variance in hydrogen ion concentration was created by first entering the baseline hydrogen ion concentration into the model. Next, any variance resulting from the respiratory component of acidosis was removed by entering the change in arterial carbon dioxide tension (regression coefficient (β)=0.67, p<0.01). Change in SID (β=-0.34, p<0.01) and surgical institution (β=-0.40, p<0.01) were then found to be predictors of the remaining variance whilst change in concentration of lactate (β in=0.16, p=0.07) and volume of intravascular fluid that was administered (β=-0.07, p=0.52) were rejected from the model. These findings suggest that the metabolic acidosis developing during CPB is partially the result of iatrogenic decrease in SID rather than hypoperfusion, as estimated by lactate concentration, or haemodilution.

A physiological approach to acid–base disorders: The roles of ion transport and body fluid compartments

2020 ◽  
pp. 2182-2198
Author(s):  
Julian Seifter
Keyword(s):  
Metabolic Acidosis ◽  
Gas Analysis ◽  
Hydrogen Ion ◽  
Anion Gap ◽  
Ion Concentration ◽  
Hydrogen Ions ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood Gas ◽  
Fluid Compartments

The normal pH of human extracellular fluid is maintained within the range of 7.35 to 7.45. The four main types of acid–base disorders can be defined by the relationship between the three variables, pH, Pco2, and HCO3 –. Respiratory disturbances begin with an increase or decrease in pulmonary carbon dioxide clearance which—through a shift in the equilibrium between CO2, H2O, and HCO3 –—favours a decreased hydrogen ion concentration (respiratory alkalosis) or an increased hydrogen ion concentration (respiratory acidosis) respectively. Metabolic acidosis may result when hydrogen ions are added with a nonbicarbonate anion, A−, in the form of HA, in which case bicarbonate is consumed, or when bicarbonate is removed as the sodium or potassium salt, increasing hydrogen ion concentration. Metabolic alkalosis is caused by removal of hydrogen ions or addition of bicarbonate. Laboratory tests usually performed in pursuit of diagnosis, aside from arterial blood gas analysis, include a basic metabolic profile with electrolytes (sodium, potassium, chloride, bicarbonate), blood urea nitrogen, and creatinine. Calculation of the serum anion gap, which is determined by subtracting the sum of chloride and bicarbonate from the serum sodium concentration, is useful. The normal value is 10 to 12 mEq/litre. An elevated value is diagnostic of metabolic acidosis, helpful in the differential diagnosis of the specific metabolic acidosis, and useful in determining the presence of a mixed metabolic disturbance. Acid–base disorders can be associated with (1) transport processes across epithelial cells lining transcellular spaces in the kidney, gastrointestinal tract, and skin; (2) transport of acid anions from intracellular to extracellular spaces—anion gap acidosis; and (3) intake.

Changing the priming solution from Ringer’s to Hartmann’s solution is associated with less metabolic acidosis during cardiopulmonary bypass

Perfusion ◽  
2007 ◽  
Vol 22 (6) ◽  
pp. 385-389 ◽  
Author(s):  
RP Alston ◽  
C Theodosiou ◽  
K Sanger
Keyword(s):  
Metabolic Acidosis ◽  
Cardiopulmonary Bypass ◽  
Repeated Measures ◽  
Haemoglobin Concentration ◽  
Hydrogen Ion ◽  
Volume Replacement ◽  
Ion Concentration ◽  
Intravascular Volume ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood

Background and objective: Previously, it was noted that changing the solutions used for priming and intravascular volume replacement from Hartmann’s to Ringer’s resulted in a more profound metabolic acidosis developing during cardiopulmonary bypass (CPB). The aim of this study was to examine the effects of changing the solutions back to Hartmann’s on metabolic acidosis that develops during CPB in patients undergoing heart surgery. Methods: Two groups of patients were studied sequentially: the first received Ringer’s (n = 63) and the second Hartmann’s solution (n = 66). Arterial blood samples were taken before induction of anaesthesia and towards the end of CPB. Samples were analysed in a blood gas analyser. Results: Hydrogen ion concentration increased from 38 (4) to 41 (7) mm/L in the Ringer’s group, but decreased from 38 (5) to 36 (6) mmol L-1 in the Hartmann’s group. Changes in PaCO2 (0.77, p < 0.001) and volume of fluid administered (r = 0.23, p < 0.01) were significant univariate correlates of change in hydrogen ion concentration, but haemoglobin concentration was not (r < 0.01, p = 0.97). Analysis of variance for repeated measures found significant between subject effects on the change in hydrogen ion concentration during CPB caused by the choice of intravascular solution used (p < 0.001) and PaCO2 (p = 0.001), but not as a result of the volume of solution administered (p > 0.10). Conclusions: Changing the solutions used for priming and intravascular volume replacement from Ringer’s to Hartmann’s was associated with a reduction in metabolic acidosis that developed during CPB.

Changes in blood gases and acid-base balance in the exercising dog

1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie
Keyword(s):  
Venous Blood ◽  
Blood Gases ◽  
Respiratory Alkalosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Mixed Venous Blood ◽  
Acid Base Balance ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood ◽  
Mixed Venous

Effects of varying rates of treadmill work on blood gases and hydrogen ion concentrations of four healthy young dogs were determined by analyses of blood for O2 and CO2 contents, Po2, Pco2, and pH. Changes in these parameters were also observed during 30-min recovery periods from hard work. Arterial and mixed venous blood samples were obtained simultaneously during work through a polyethylene catheter in the right ventricle and an indwelling needle in an exteriorized carotid artery. Mixed venous O2 content, Po2 and O2 saturation fell with increased work, whereas arterial values showed little or no change. Mixed venous CO2 content, Pco2, and hydrogen ion concentration exhibited little change from resting levels in two dogs but increased significantly in two others during exercise. These values always decreased in the arterial blood during exercise, indicating the presence of respiratory alkalosis. On cessation of exercise, hyperventilation increased the degree of respiratory alkalosis, causing it to be reflected on the venous side of the circulation. Submitted on January 8, 1962

scholarly journals Red Cell 2,3-Diphosphoglycerate and Intracellular Arterial pH in Acidosis and Alkalosis

Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 740-746 ◽  
Author(s):  
Jane F. Desforges ◽  
Philip Slawsky
Keyword(s):  
Whole Blood ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Red Cell ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Weak Organic Acid ◽  
Arterial Blood ◽  
Blood Ph ◽  
Clinical Conditions

Abstract With the use of 14C-DMO (14C-5, 5-dimethyl-2,3-oxazolidinedione), a weak organic acid, we measured the intraerythrocytic hydrogen ion concentration in 16 acidotic and alkalotic patients. Whole blood pH, red cell 2,3-diphosphoglycerate, hemoglobin, oxyhemoglobin, plasma pCO2, and plasma bicarbonate were measured simultaneously on heparinized arterial blood. The results show: (1) hydrogen ion concentration in the red cell varies directly with that of whole blood, (2) red cell concentration of 2,3-diphosphoglycerate varies inversely with the whole blood hydrogen ion concentration, and (3) red cell 2,3-diphosphoglycerate concentration also varies inversely with the intracellular hydrogen ion concentration. There were no significant relationships between the arterial total hemoglobin or oxyhemoglobin and intracellular or whole blood pH, nor was there any relationship between plasma pCO2 or plasma bicarbonate and intracellular or whole blood pH. We concluded that in a number of clinical conditions in which the hydrogen ion concentration is altered, the cellular pH parallels that of the whole blood and that the 2,3-diphosphoglycerate concentration varies with the hydrogen ion concentration.

Effect of norepinephrine on myocardial intracellular hydrogen ion concentration

1975 ◽  
Vol 229 (2) ◽  
pp. 344-349 ◽  
Author(s):  
KM Riegle ◽  
RL Clancy
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Beta Blockade ◽  
Hydrogen Ion Concentration ◽  
Rat Hearts ◽  
Buffer Value

The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.

Effect of pH on metabolic and cardiorespiratory responses during progressive exercise

1984 ◽  
Vol 57 (5) ◽  
pp. 1558-1563 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
N. L. Jones
Keyword(s):  
Power Output ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Peak Power Output ◽  
Plasma Lactate ◽  
Exercise Tests ◽  
Hydrogen Ion Concentration ◽  
Co2 Output

Six healthy male subjects performed three exercise tests in which the power output was increased by 100 kpm/min each minute until exhaustion. The studies were carried out after oral administration of CaCO3 (control), NH4Cl (metabolic acidosis), and NaHCO3 (metabolic alkalosis). Ventilation (VE), O2 intake (VO2), and CO2 output (VCO2) were monitored continuously. Arterialized-venous blood samples were drawn at specific times and analyzed for pH, PCO2, and lactate concentration. Resting pH (mean +/- SE) was lowest in acidosis (7.29 +/- 0.01) and highest in alkalosis (7.46 +/- 0.02). A lower peak power output (kpm/min) was achieved in acidosis (1,717 +/- 95) compared with control (1,867 +/- 120) alkalosis (1,867 +/- 125). Submaximal VO2 and VCO2 were similar, but peak VO2 and VCO2 were lower in acidosis. Plasma lactate concentration was lower at rest and during exercise in acidosis. Although lactate accumulation was reduced in acidosis, increases in hydrogen ion concentration were similar in the three conditions. We conclude that acid-base changes influence the maximum power output that may be sustained in incremental dynamic exercise and modify plasma lactate appearance, but have little effect on hydrogen ion appearance in plasma.

Sign in / Sign up

Export Citation Format

Share Document