Disturbances of acid-base equilibrium occur in a wide variety of critical illnesses and are among the most commonly encountered
disorders in the intensive care unit (ICU). In addition to reflecting the seriousness of the underlying disease, disturbances
in hydrogen ion concentration ([H+]) have important physiologic effects.
A blood pH less than normal is called acidemia; the underlying process causing the acidemia is called acidosis. Similarly,
alkalemia and alkalosis refer to an increased pH and the underlying process, respectively. Acidosis and alkalosis can be further
classified based on whether it is a primary change in PCO2 (respiratory) or HCO3
- (metabolic) that alters the extracellular [H+]. Although an acidosis and alkalosis may coexist, there can be only one resulting pH. Therefore, acidemia and alkalemia are
mutually exclusive conditions, where as acidosis and alkalosis are not.
The approach to acid-base derangements should emphasize a search for a cause, rather than an immediate attempt to normalize
the pH. Many disorders are mild and do not require treatment. Further, treatment may be more detrimental than the acid-base
disorder itself. More importantly, the clinician must fully consider the possible underlying pathologic state(s). This approach
may facilitate a directed intervention that will benefit the patient more than normalization of the pH.'
Physiologic effects of acidemia and alkalemia
Precise H+ regulation is essential because the activities of almost all enzyme systems in the body are influenced by [H+]. Therefore, perturbations in [H+] may alter virtually all cell and body functions, leading to widespread physiologic change of clinical importance. However,
in any given patient, the effects of acidemia and alkalemia may be difficult to discern because any physiologic consequences
may be influenced by the underlying illness causing the acid-base disorder.
Metabolic acidemia causes stimulation of the sympathetic-adrenal axis (increasing vascular resistance), decrease the affinity
of hemoglobin for oxygen (shift the oxyhemoglobin dissociation curve to the left) and increases the free concentration (and
potential for toxicity) of many drugs by decreasing their protein binding. In severe acidemia, stimulation of the sympathetic-adrenal
axis is countered by a depressed responsiveness of adrenergic receptors to circulating catecholamines. Severe acidemia typically
causes a decrease in cardiac output and vasodilation, despite sympathetic stimulation. Additional influences of severe acidemia
include altered renal and hepatic blood flow, altered enzymatic function, promotion of cardiac arrhythmias, depressed mental
status, as well as induction of hyperkalemia and increased ionized calcium levels.
Acute respiratory acidemia causes marked increases in cerebral blood flow. As PCO2 increases, patients may become confused, irritable, anxious (symptoms difficult to differentiate from hypoxemia), with possible
loss of consciousness and seizures. Acute hypercapnia causes depression of diaphragmatic contractility, which may contribute
to the downward spiral of respiratory failure in patients with acute CO2 retention.
Acidemia is better tolerated than is alkalemia. While a pH of 7.2 is typically well tolerated, a pH of 7.6 is associated with
significant mortality. Respiratory alkalosis lowers blood pressure and calculated systemic vascular resistance. Most vascular
beds demonstrate vasodilation but vasoconstriction predominates in the cerebral circulation. Both respiratory and metabolic
alkalemia can lead to seizures. The clinical effect of alkalemia-induced changes in oxygen delivery is small but in patients
with ongoing tissue hypoxia the increased hemoglobin oxygen affinity (shift of the oxyhemoglobin dissociation curve to the
right) may be detrimental and clinically significant. Alkalemia may decrease ionized calcium levels, due to increased calcium
binding to proteins, and hypokalemia due to transcellular exchange with H+.