Ventilatory Patterns and the Apnea Test
Central Pattern Generator for Breathing. In health, the anatomic origin of the cyclic pattern of breathing is the brainstem. Sectioning the brainstem above the pons leaves breathing unaffected when the vagus nerve (cranial nerve X) carrying afferent information from the lungs is intact. Vagotomy results in a reduction in the breathing frequency and an increase in tidal volume. Transection below the medulla results in complete cessation of breathing. Sectioning above the central medulla results in rhythmic but irregular breathing, with vagotomy slowing the irregular pattern. Transection at the level of the upper pons leads to a slowing of respiration and an increase in tidal volume. If both vagus nerves are cut, the result is the cessation of breathing at full inspiration (called apneusis), or inspiratory spasms interrupted by intermittent expirations (called apneustic breathing). The central pattern generator for breathing is located within the medullary center.
The areas of
the brainstem that modulate ventilation are co-localized to the same structure
containing the central pattern generator. The areas that are sensitive to
changes in hydrogen ion concentration and blood composition of respiratory
gases (chemosensitive areas) are localized to the ventral surface of the
medulla, bilaterally, at the level of cranial nerve roots VIII to XI.
These areas are
very superficial, lying about 200 μM below the surface.
Additional chemosensitive areas have also been found caudally in the area of the
XII cranial nerve root (hypoglossal). All of these central chemoreceptors are
sensitive to local changes in cerebrospinal fluid pH induced by rising Paco2.
Failure to respond to an adequate Paco2 stimulus indicates a failure
in the medullary respiratory centers.
The apnea test is performed if the brainstem reflexes are all absent, and it is a requirement of brain death testing (see Plate 6-8). There are a number of techniques that are used to perform this test in the intensive care unit. However, the essential feature in brain death is that the patient must have complete absence of respiratory effort by formal testing using the endogenous increase in arterial partial pressure of carbon dioxide (Paco2) as the stimulus to breathing. At baseline, the patient should start with a Paco2 of approximately 40 mm Hg. The stimulus to breathing is considered adequate when there has been a rise in Paco2 by 20 mm Hg to some value greater than 60 mm Hg.
