ACID-BASE ABNORMALITIES
The value of the Stewart approach is that it allows us to use
a simple model for explaining acid-based disturbances, because all abnormalities
can be explained in terms of SID, ATOT
, or PCO2
.
Traditionally, acid-base disturbances have been classified as caused by alterations
in arterial carbon dioxide (PaCO2
) tension
(e.g., respiratory acidosis or alkalosis), and alterations in blood chemistry metabolic
acidosis, or alkalosis. This remains a useful classification, although respiratory
and metabolic abnormalities rarely occur independently of one another.
Respiratory Acid-Base Abnormalities
Respiratory acidosis occurs when there is an acute rise in PaCO2
,
principally because of respiratory failure (see Chapter
74
and Chapter 75
).
Clinically, there are signs of CO2
retention: cyanosis, vasodilatation,
and narcosis. Respiratory alkalosis occurs when there is an acute decrease in PaCO2
caused by hyperventilation. The patient presents with symptoms and signs of vasoconstriction:
light-headedness, visual disturbances, dizziness, and perhaps hypocalcemia because
of increased binding of calcium to albumin. The latter condition is caused by an
increase in the available negative charge on albumin in alkaline states. Acute hypocalcemia
is associated with paresthesia and tetany.
Respiratory acidosis causes a rapid increase in [H+
].
Compensation for hypercarbia is slow, requiring increased urinary excretion of chloride.
[8]
There is a concomitant increase in the serum
bicarbonate, reflecting a higher total CO2
load, rather than compensation.
The acuity of respiratory failure can be deduced by looking at the relative ratio
of CO2
to HCO3
-
( Table
41-1
). Many investigators have suggested that respiratory acidosis may
not necessarily be harmful. There has been extensive clinical experience with "permissive
hypercapnia" for acute respiratory failure, which appears to be well tolerated.[9]
[11]
[12]
