DETERMINATION OF HYPERLACTATEMIA AND ACIDOSIS IN ADULT PATIENTS WITH CARDIAC DISEASES AND DYSFUNCTIONS
It has been postulated that acidosis, which is co-morbid in cardiac dysfunctions usually not occurs only due to high lactate concentration in blood (hyperlactatemia), but some other components such as un-measured anions are known to significantly induce characteristic acidemia in patients also contribute to it. The present study describes the determination of different components of metabolic acidosis in cardiac dysfunction and cardiac arrest patients in order to assess the degree to which lactate is responsible for the acidosis. Fifty five adult patients with cardiac dysfunctions and cardiac arrest who were brought to the hospital for treatment or admitted to the hospital were included in present study. All biochemical, blood gases and related parameters were determined by standard methods using auto-analyzers. Stewart's (1983) quantitative biophysical methods and formula were used for apparent strong ion difference “SIDa” and strong ionic gap “SIG”, to evaluate unmeasured and measured ions. The average age of the patients was 58.4 years, including 39 (70.90%) males and 16 (29.09%) females. All assessed variables were found significantly different between the two groups, except the concentration of sodium, ionized calcium and SIDa. Cardiac dysfunction patients also showed low potassium (hyperkalemia) and chloride (hypochloremia) and elevated lactate concentration (hyperlactatemia) in blood, whereas higher anion gap and SIG were also noted to be manifested. Lactate as an independent component was observed to be a notable assessor of acidemia. It was concluded that although lactate accounts for only less than 50% of acidemia it did influence the occurrence of metabolic acidosis and subsequent acidemia in patients. Moreover, amplification in unmeasured anions (SIG) and phosphate is also related to the major portion of acidemia.