scholarly journals Change in strong ion difference and metabolic acidosis after heart surgery

2020 ◽  
Vol 34 ◽  
pp. S11-S12
Author(s):  
C.Y.B. Wang ◽  
P. Alston
Keyword(s):  
Metabolic Acidosis ◽  
Heart Surgery ◽  
Strong Ion Difference

Pathophysiology and causes of metabolic acidosis in the critically ill

2016 ◽  
Author(s):  
Patrick J. Neligan ◽  
Clifford S. Deutschman
Keyword(s):  
Metabolic Acidosis ◽  
Isotonic Saline ◽  
Lactate Production ◽  
Weak Acid ◽  
Strong Ion Difference ◽  
Waste Products ◽  
Renal Tubular ◽  
Specific Symptoms ◽  
Symptoms And Signs ◽  
Intracellular Glucose

Critical illness is typically characterized by changes in the balance of water and electrolytes in the extracellular space, resulting in the accumulation of anionic compounds that manifests as metabolic acidosis. Metabolic acidosis manifests with tachypnoea, tachycardia, vasodilatation, headache and a variety of other non-specific symptoms and signs. It is caused by a reduction in the strong ion difference (SID) or an increase in weak acid concentration (albumin or phosphate). Increased SID results from hyperchloraemia, haemodilution or accumulation of metabolic by-products. A reduction in SID results in a corresponding reduction is serum bicarbonate. There is a corresponding increase in alveolar ventilation and reduced PaCO2. Lactic acidosis results from increased lactate production or reduced clearance. Ketoacidosis is associated with reduced intracellular glucose availability for metabolism, and is associated with insulin deficiency and starvation. Hyperchloraemic acidosis is associated with excessive administration of isotonic saline solution, renal tubular acidosis and ureteric re-implantation. Renal acidosis is associated with hyperchloraemia, hyperphosphataemia, and the accumulation of medley nitrogenous waste products.

scholarly journals PENDEKATAN STEWART DALAM pH DARAH YANG MENDASARI ASIDOSIS METABOLIK

2018 ◽  
Vol 19 (2) ◽  
pp. 79
Author(s):  
Efrida Efrida ◽  
Ida Parwati ◽  
Ike Sri Redjeki
Keyword(s):  
Metabolic Acidosis ◽  
Ph Value ◽  
Total Concentration ◽  
Ph Measurement ◽  
Strong Ion Difference ◽  
Cross Sectional ◽  
Stewart Approach ◽  
Blood Ph ◽  
Base Disorder ◽  
The Mean

Metabolic acidosis is the most frequent acid-base disorder in patients of the Intensive Care Unit. By conventional approach based onpH value, [HCO3–], and base deficit (BD) from blood gas analyzer (BGA) measurement are often inappropriate with the clinical stateand inadequate in explaining the mechanism of the metabolic acidosis. The Stewart approach states that the blood pH is determinedby a strong ion difference (SID), the carbon dioxide tension (pCO2), the total concentration of non-volatile weak acid. The Stewartapproach may give a better understanding of the mechanisms that underlie the metabolic acidosis. The purpose of this study is to knowthe correlation of blood pH value measurement from BGA and calculation based on Stewart approach and identifying the mechanismsthat underlie a metabolic acidosis. In this study an analytic observational cross-sectional method was used. The examined subjectsconsisted of 71 patients who were admitted with a metabolic acidosis at the ICU from July up to August 2007. All patients were measuredfor their blood pH, pCO2, [HCO3–], BD, sodium, potassium, calcium, magnesium, chloride, lactate, albumin, and phosphate. The resultwas reported as the mean and standard deviation. The data were analyzed by Pearson’s correlation test and linier multiple regression.Statistical significance was determined at p < 0.05. The mean values of blood pH measurement from BGA and blood pH calculationbased on the Stewart approach were 7.33 (0.11) and 7.49 (0.11) (r = 0.681; p < 0.001). Most patients had two underlying mechanisms ofmetabolic acidosis. Hyperlactatemia was present in 61.8%, hyperchloremia was present in 58.2% of patients. Based on this study so far,by using the Stewart approach there is an excellent and significant correlation between the blood pH measurement from BGA and bloodpH calculation. Hyperlactatemia and hyperchloremia are the main causes of the metabolic acidosis in patients of the ICU ward.

scholarly journals Experimental protocol for metabolic acidosis induction by intravenous administration of hydrochloric acid in sheep

2019 ◽  
Vol 71 (1) ◽  
pp. 53-60 ◽  
Author(s):  
F.T.N.M.A. Romão ◽  
J.M. Curti ◽  
P.F.V. Pereira ◽  
K.K.M.C. Flaiban ◽  
J.A.N. Lisbôa
Keyword(s):  
Metabolic Acidosis ◽  
Side Effects ◽  
Hydrochloric Acid ◽  
Intravenous Administration ◽  
Total Concentration ◽  
Carbon Dioxide Partial Pressure ◽  
Strong Ion Difference ◽  
Experimental Protocol ◽  
Hyperchloremic Acidosis ◽  
Fractional Excretion Of Sodium

ABSTRACT The aim of this study was to assess the magnitude and duration of blood and urine changes and the side effects of hyperchloremic acidosis induced by the intravenous administration of hydrochloric acid in sheep. Five healthy, crossbred adult ewes, with a mean body weight of 44±2.9kg were used. The hydrochloric acid solution was administered intravenously at a rate of 25mL/kg/h for 4 hours continuously. Venous blood and urine samples were collected and pH values, blood carbon dioxide partial pressure, bicarbonate, base excess, strong ion difference, anion gap, total concentration of nonvolatile buffers, creatinine, plasma L-lactate, plasma and urine sodium, potassium, and chloride were determined. The experimental protocol induced severe hyperchloremic acidosis at the end of the infusion, with a decreased plasma strong ion difference. The fractional excretion of sodium and chloride remained increased during 4 hours after the infusion. Aciduria was observed at approximately 24 hours. Twenty-four hours after the infusion, the animals showed mild and compensated metabolic acidosis. This protocol was effective in inducing severe and long-lasting hyperchloremic acidosis and did not cause serious side effects. Therefore, this protocol can be used safely in adult sheep for studies on the treatment of this condition.

Respiration and Acid-Base Physiology of the Spotted Gar, A Bimodal Breather: III. Response to a Transfer from Fresh Water to 50% Sea Water, and Control of Ventilation

1982 ◽  
Vol 96 (1) ◽  
pp. 295-306
Author(s):  
NEAL J. SMATRESK ◽  
JAMES N. CAMERON
Keyword(s):  
Metabolic Acidosis ◽  
Fresh Water ◽  
Lung Volume ◽  
Sea Water ◽  
Pulmonary Ventilation ◽  
Strong Ion Difference ◽  
Lung Inflation ◽  
Air Breathing ◽  
Spotted Gar ◽  
Gill Ventilation

Transfer from fresh water to 50% sea water (SW) at 26 °C increased the blood osmolarity of spotted gar (Lepisosteus oculatus) from 275 to 310 mosmol during the first 24 h. It then returned slowly to freshwater levels by 5 days after the transfer. The arterial pH dropped sharply, from 7.69 in fresh water to 7.46 in 50% SW, as a result of a small elevation in the blood CO2 partial pressure, and a marked metabolic acidosis. The respiratory (CO2) portion of the acidosis appeared to be a result of the reduction in branchial ventilation, and possibly permeability as well. The metabolic portion of the acidosis was not due to the accumulation of lactic acid, but probably involved a disruption of the extracellular strong ion difference in the saltier medium. The metabolic acidosis did not diminish during 5 days. The rate of air breathing rose from 7 to 20 bph during 50 % SW exposure. The control of pulmonary ventilation was directly responsive to the availability of O2, in general increasing when O2 was limiting (e.g. 50% SW transfer, hypoxia) and decreasing in hyperoxia. CO2 had no affect on the rate of air breathing. Withdrawal from 5–20% of total lung volume elicited an immediate air breath during hypoxia, but the response was inconsistent in normally aerated water. Lung inflation with O2 prolonged the interval between air breaths, but inflation with N2 did not change the rate of air breathing. Thus, pulmonary ventilation was secondarily controlled by lung volume. Gill ventilation frequency fell in 50 % SW, despite a respiratory and metabolic acidosis, while gill ventilation increased in response to treatment with acetazolamide. Hyperoxia caused a marked depression of gill ventilation, despite a respiratory acidosis. The gill ventilation rate appears to be most closely linked to oxygen, but may be affected indirectly by CO2 through the Root or Bohr effects.

Rapid Saline Infusion Produces Hyperchloremic Acidosis in Patients Undergoing Gynecologic Surgery 

1999 ◽  
Vol 90 (5) ◽  
pp. 1265-1270 ◽  
Author(s):  
Stefan Scheingraber ◽  
Markus Rehm ◽  
Christiane Sehmisch ◽  
Udilo Finsterer
Keyword(s):  
Metabolic Acidosis ◽  
Total Protein ◽  
Gynecologic Surgery ◽  
Strong Ion Difference ◽  
Serum Bicarbonate ◽  
Bicarbonate Concentration ◽  
Stewart Approach ◽  
Ringer’S Solution ◽  
Lactated Ringer's Solution ◽  
Hasselbalch Equation

Background Changes in acid-base balance caused by infusion of a 0.9% saline solution during anesthesia and surgery are poorly characterized. Therefore, the authors evaluated these phenomena in a dose-response study. Methods Two groups of 12 patients each who were undergoing major intraabdominal gynecologic surgery were assigned randomly to receive 0.9% saline or lactated Ringer's solution in a dosage of 30 ml x kg(-1) x h(-1). The pH, arterial carbon dioxide tension, and serum concentrations of sodium, potassium, chloride, lactate, and total protein were measured in 30-min intervals. The serum bicarbonate concentration was calculated using the Henderson-Hasselbalch equation and also using the Stewart approach from the strong ion difference and the amount of weak plasma acid. The strong ion difference was calculated as serum sodium + serum potassium - serum chloride - serum lactate. The amount of weak plasma acid was calculated as the serum total protein concentration in g/dl x 2.43. Results Infusion of 0.9% saline, but not lactated Ringer's solution, caused a metabolic acidosis with hyperchloremia and a concomitant decrease in the strong ion difference. Calculating the serum bicarbonate concentration using the Henderson-Hasselbalch equation or the Stewart approach produced equivalent results. Conclusions Infusion of approximately 30 ml x kg(-1) x h(-1) saline during anesthesia and surgery inevitably leads to metabolic acidosis, which is not observed after administration of lactated Ringer's solution. The acidosis is associated with hyperchloremia.

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.

scholarly journals Hyperchloraemia causes metabolic acidosis by reducing strong ion difference

Anaesthesia ◽  
2000 ◽  
Vol 55 (1) ◽  
pp. 94-94 ◽  
Author(s):  
P. Dorje ◽  
S. E. Bree ◽  
G. Adhikary ◽  
D. I. Mclaren
Keyword(s):  
Metabolic Acidosis ◽  
Strong Ion Difference
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