Acid–base and electrolyte disorders are nearly ubiquitous in hospitalized patients and often originate from or manifest as neurological illness. Prompt recognition of the presence and degree of acid–base disorders through analysis of arterial blood gas can have a significant clinical impact in terms of diagnosis and treatment, particularly in the setting of increased intracranial pressure, respiratory muscle weakness, and seizures. Sodium abnormalities, such as diabetes insipidus, the syndrome of inappropriate antidiuretic hormone secretion, and cerebral salt wasting, are often encountered in neurological patients in association with their primary illness. Correction of hyponatremia and hypernatremia should be gradual to avoid central pontinemyelinolysis and cerebral edema. Abnormalities of potassium, calcium, and magnesium are also common and can cause serious neurologic and systemic abnormalities that warrant prompt recognition and correction.
The maintenance of acid–base homeostasis is essential for life and is strictly regulated by the body. Disruptions in the system outside of the physiologic range can have widespread and deleterious effects on human physiology, as acid–base status plays an integral role in protein and membrane functioning.1,2 Prompt and correct interpretation of acid–base derangements can be as challenging as clinically impactful.
The carbonic acid–bicarbonate buffer system is the main physiological determinant of acid–base status in the body and is represented by the following reaction:3
This depicts the bidirectional conversion of carbon dioxide and water to form carbonic acid, which rapidly dissociates to form bicarbonate and hydrogen ions. In vivo, the three main variables that can be altered are the partial pressure of CO2 (PaCO2), bicarbonate, and hydrogen ions. Changes in PaCO2 and/or bicarbonate ultimately affect the amount of hydrogen ions by driving the equation to the left or right. The pH, or negative log of the hydrogen-ion concentration, quantifies the acid–base status in a particular individual. The terms acidemia and alkalemia refer to abnormally low and high pH, respectively. Alterations in pH can be categorized according to the primary etiology—“respiratory” (characterized by changes in PaCO2 from alteration in minute ventilation) or “metabolic” (characterized by changes in bicarbonate) forming the four primary conditions affecting pH: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. While clinical context can be extremely helpful in determining a patient’s acid–base status, the arterial blood gas (ABG) provides crucial information about the severity, etiology, and chronicity of acid–base abnormalities.
An ABG should be obtained whenever there is a suspicion of acid–base disturbance based on clinical context and symptomatology to confirm the presence and ascertain the type and degree of the acid–base disorder. The pH can be used first to delineate whether the patient has acidemia (pH <7.35) or="" alkalemia="" (ph="">7.45). Next, the PaCO2 and bicarbonate levels should be integrated to determine the primary mechanism ...7.35)>