Editing Chemoreceptor (section)

=== Heart rate ===
The response to stimulation of chemoreceptors on the heart rate is complicated. Chemoreceptors in the heart or nearby large arteries, as well as chemoreceptors in the lungs, can affect heart rate. Activation of these peripheral chemoreceptors from sensing decreased O<sub>2</sub>, increased CO<sub>2</sub> and a decreased pH is relayed to cardiac centers by the [[vagus nerve|vagus]] and [[glossopharyngeal nerve|glossopharyngeal nerves]] to the [medulla oblongata|medulla] of the brainstem. This increases the sympathetic nervous stimulation on the heart and a corresponding increase in heart rate and [[myocardial contractility|contractility]] in most cases.<ref>{{Cite web|url=http://www.columbia.edu/~kj3/Chapter4.htm|title=Chapter 4|website=www.columbia.edu|access-date=2017-01-29}}</ref> These factors include activation of [[stretch receptors]] due to increased ventilation and the release of circulating catecholamines.

However, if respiratory activity is arrested (e.g. in a patient with a high cervical spinal cord injury), then the primary cardiac reflex to transient [[hypercapnia]] and [[Hypoxia (medical)|hypoxia]] is a profound [[bradycardia]] and coronary [[vasodilation]] through vagal stimulation and systemic vasoconstriction by sympathetic stimulation.<ref>{{cite journal |last1=Berk |first1=James L. |last2=Levy |first2=Matthew N. |title=Profound Reflex Bradycardia Produced by Transient Hypoxia or Hypercapnia in Man |journal=European Surgical Research |date=1977 |volume=9 |issue=2 |pages=75–84 |doi=10.1159/000127928 |pmid=852474 }}</ref> In normal cases, if there is reflexive increase in respiratory activity in response to chemoreceptor activation, the increased sympathetic activity on the cardiovascular system would act to increase heart rate and contractility.