The carotid bodies are chemosensitive cells at the bifurcation of the common carotid that respond to changes in oxygen tension and, to a lesser extent, ph. In contrast to central chemoreceptors, which primarily respond to PAO2 and the aortic bodies [output via cn x], which have primarily circulatory effects (bradycardia, hypertension, adrenal stimulation, and also bronchoconstriction), carotid bodies are most sensitive to PAO2. At a pao2 of approximately 55-60 mmhg, they send their impulses via CN IX to the medulla, increasing ventilatory drive (increased respiratory rate, tidal volume, and minute ventilation). Thus, patients who rely on hypoxic respiratory drive will typically have resting PAO2 around 60 mm Hg.
These cells are thought to be primarily dopaminergic, therefore, antidopaminergic drugs may decrease peripheral response to hypoxemia.
Attenuation of the hypoxic response during anesthesia with volatile agents as well as both opioids and benzodiazepines and may be attributed to an effect on the carotid bodies. Carotid body denervation may occur after carotid endarterectomy as a result of surgical disruption. Unilateral loss of function may result in an impaired ventilatory response to mild hypoxemia. Bilateral carotid endarterectomy is associated with loss of the normal ventilatory response to acute hypoxia and an increased resting partial pressure of arterial carbon dioxide. In this situation, the central chemoreceptors are the primary sensors for maintaining ventilation, and serious respiratory depression may result from opioid administration.
- Location: bifurcation of internal and external carotid
- Threshold for Neuronal Activity: paO2 of 100 mm Hg
- Threshold for Increased Ventilation: paO2 of 55-60 mm Hg
- Inhibition: volatile agents; benzodiazepines, opioids
Note that a bilateral carotid endarterectomy would result in significant impairment of the hypoxic drive.