Carotid endarterectomy benefits and risks of the procedure is required on an individual patient basis. Peri-operative CEA risks for combined 30 day mortality and stroke risk should be < 3% for asymptomatic patients and ≤ 6% for symptomatic patients. Symptomatic patients typically have either transient ischemic attack (TIA) or minor stroke, defined as a focal neurologic defect affecting one side of the body, speech, or vision. Asymptomatic patients have narrowing of their carotid arteries, but have not experienced a TIA or stroke. Carotid stenosis is diagnosed with ultrasound doppler studies of the neck arteries, magnetic resonance angiography (MRA) or computed tomography angiography
Carotid body acid-base transporters (e.g. Na-H) which raise intracellular pH, and activates transporters (e.g. Cl-HCO) which decrease it. Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in P sensing. Another mechanism is through oxygen sensitive potassium channels. A drop in dissolved oxygen lead to closing of these channels which results in depolarization. This leads to release of the neurotransmitter dopamine in the glossopharyngeal and vagus afferente to the vasomotor area. The type I (glomus) cells in the carotid (and aortic bodies) are derived from neuroectoderm and are thus electrically excitable.