The simple mechanism to diagnose whose having acid base disorder. The table doesnt tell us yet about chronic and acute respiratory acid base disorder
As you can see in the figure we have a significant elevation or decrease in
acute respiratory acid base disorder. This can be explain as follow : Respiratory Alkalosis
Respiratory alkalosis is caused by hyperventilation, which results in
excessive loss of CO2. Hyperventilation can be caused by direct stimulation of the medullary respiratory center, by hypoxemia (which stimulates peripheral chemoreceptors), or by mechanical ventilation. The arterial blood profile seen in respiratory alkalosis is The following sequence of events occurs in the generation of respiratory alkalosis to produce this blood profile : 1. Loss of CO2. Hyperventilation causes an excessive loss of CO2 and a decrease in PCO2. The decreased PCO2 is the primary disturbance in respiratory alkalosis and, as predicted by the Henderson-Hasselbalch equation, causes an increase in pH (pH = 6.1 + log HCO3/CO2). The decreased PCO2, by mass action, also causes a decreased concentration of HCO3. 2. Buffering. Buffering occurs exclusively in ICF, particularly in red blood cells. In this case, CO2 leaves the cells and intracellular pH increases. 3. Respiratory compensation. As with respiratory acidosis, there is no respiratory compensation for respiratory alkalosis because respiration is the cause of the disorder. 4. Renal compensation. Renal compensation for respiratory alkalosis consists of decreased excretion of H+ as titratable acid and NH4+ and decreased synthesis and reabsorption of new HCO3. Decreased reabsorption of HCO3 decreases the HCO3 concentration even further than did the effect of mass action alone. The Henderson-Hasselbalch equation can be used to understand why the decreased HCO3 concentration is a compensatory response: This renal compensation differentiate acute and chronic respiratory alkalosis : In acute respiratory alkalosis, renal compensation has not yet occurred and pH is quite high (there is a decrease in the denominator of the Henderson- Hasselbalch equation but little decrease in the numerator). In chronic respiratory alkalosis, renal compensation is occurring, which further decreases the blood HCO3 concentration and tends to normalize both the ratio of HCO3/CO2 and the pH. The difference between acute and chronic respiratory alkalosis lies in renal compensation. Again, on the basis of the absence or presence of renal compensation, the renal rules give different calculations for the expected change in HCO3 concentration in acute and chronic respiratory alkalosis. Therefore chronic respiratory alkalosis often misintrepretate as a normal condition which less elevate pH, less decrease in HCO3- , but significance decrease in PCO2. Respiratory Acidosis Respiratory acidosis is caused by hypoventilation, which results in retention of CO2. The retention of CO2 can be caused by inhibition of the medullary respiratory center, paralysis of respiratory muscles, airway
obstruction, or failure to exchange CO2 between pulmonary capillary blood
and alveolar gas. The arterial blood profile seen in respiratory acidosis is The following sequence of events occurs in the generation of respiratory acidosis to produce this blood profile: 1. Retention of CO2. Hypoventilation causes retention of CO2 and an increase in PCO2. The increased PCO2 is the primary disturbance in respiratory acidosis and, as predicted by the Henderson-Hasselbalch equation, causes a decrease in pH (pH = 6.1 + log HCO3/CO2). The increased PCO2, by mass action, also causes an increased concentration of HCO3. 2. Buffering. Buffering of the excess CO2 occurs exclusively in ICF, especially in red blood cells. To utilize these intracellular buffers, CO2 diffuses across the cell membranes. Within the cells, CO2 is converted to H+ and HCO3 and the H+ is buffered by intracellular proteins (e.g., hemoglobin) and by organic phosphates. 3. Respiratory compensation. There is no respiratory compensation for respiratory acidosis, since respiration is the cause of this disorder. 4. Renal compensation. Renal compensation for respiratory acidosis consists of increased H+ excretion as titratable acid and NH4+ and increased synthesis and reabsorption of new HCO3. Reabsorption of new HCO3 increases the HCO3 concentration even further than the effect of mass action alone. The HendersonHasselbalch equation can be used tounderstand why the increased HCO3 concentration is a compensatory response. Thus, In acute respiratory acidosis, renal compensation has not yet occurred, and the pH tends to be quite low (there is an increase in the denominator in the Henderson-Hasselbalch equation but little increase in the numerator). On the other hand, in chronic respiratory acidosis, renal compensation is occurring, which increases the HCO3 concentration and tends to normalize both the ratio of HCO3/CO2 and the pH. The difference between acute and chronic respiratory acidosis lies in the renal compensation. the absence or presence of renal compensation, the renal rules give different calculations for the expected change in HCO3 concentration that occurs in acute and chronic respiratory acidosis. Therefore chronic respiratory acidosis often misintrepretate as a normal condition which less decrease pH, less elevate in HCO3- , but significance elevation in PCO2.