ACIDOSIS ALKALOSIS

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.