Safe and effective critical care requires that bedside respiratory therapists and nurses understand blood gas analysis as it relates to external and internal respiration and the resulting cell metabolism. Such basic information is crucial to understanding acute respiratory failure, acute ventilatory failure, acidosis versus acidemia, hypoxia versus hypoxemia, cardiopulmonary homeostasis, deadspace-producing disease, alveolar deadspace, ventilation in excess of perfusion, and shunt-producing disease. Acute respiratory failure is a broad, nonspecific term with limited clinical value. Acute ventilatory failure is a specific blood gas diagnosis (
, pH < 7.30), and the term does not refer to oxygen status; it does reflect external respiratory inadequacy. Acidosis refers to a broad pathophysiologic state, whereas acidemia specifies excess free hydrogen ion in arterial blood (pH < normal). Hypoxia refers to tissue oxygen status and cannot be directly measured, whereas hypoxemia is
below normal and is directly measurable. Arterial hypoxemia does not reflect tissue oxygenation, however; that is best seen in mixed venous blood oxygen (pulmonary arterial PO2 < 35 mm Hg = tissue hypoxia). Abnormal systemic blood gases reflect uncompensated cardiopulmonary disease, and serial blood analysis is necessary for management. Increased deadspace means increased energy expenditure for ventila-tion, which encroaches on vital reserves. Mechanical ventilation increases deadspace, while common clinical causes of deadspace are acute pulmonary embolus and uneven perfusion. When cardiac output is decreased, one must watch for increased deadspace and increased work of breathing. Ventilation in excess of perfusion is significant in alveolar septal destruction and with mechanical hyperventilation; increasing minute ventilation does not necessarily increase alveolar ventilation. Although hypoxemia can usually be equated with shunting, the effect on PO2 depends on hemoglobin saturation of shunted blood. Anatomic shunting results from congenital heart disease, intrapulmonary fistulas, and vascular lung tumors. Most physiologic shunting is caused by atelectasis, while ventilation/perfusion inequality is the form of shunting most easily correctable by oxygen therapy.
