Chemoreceptors are stimulated by a change in the chemical composition of their immediate environment. There are many types of chemoreceptor spread throughout the body which help to control different processes including taste, smell and breathing.
This article will focus on how the respiratory system is regulated by chemoreceptors and discuss their clinical relevance.
Peripheral chemoreceptors are located in both the carotid body and the aortic body. They detect large changes in the partial pressure of oxygen (pO2) as the arterial blood supply leaves the heart. When low levels of oxygen are detected, afferent impulses travel via the glossopharyngeal and vagus nerves to the medulla oblongata and the pons in the brainstem. A number of responses are then coordinated which aim to restore pO2.
- The respiratory rate and tidal volume are increased to allow more oxygen to enter the lungs and subsequently diffuse into the blood.
- Blood flow is directed towards the kidneys and the brain (as these organs are the most sensitive to hypoxia).
- Cardiac Output is increased in order to maintain blood flow, and therefore oxygen supply to the body’s tissues.
Central chemoreceptors are located in the medulla oblongata of the brainstem. They detect changes in the arterial partial pressure of carbon dioxide (pCO2). When changes are detected, the receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation to restore normal pCO2.
- Detection of an increase in pCO2 leads to an increase in ventilation. More CO2 is exhaled, the pCO2 decreases and returns to normal.
- Detection of a decrease in pCO2 leads to a decrease in ventilation. Less CO2 is retained in the lungs, the pCO2 increases and returns to normal.
The mechanism behind how central chemoreceptors detect changes in arterial pCO2 is more complex, and is related to changes in the pH of the Cerebral Spinal Fluid (CSF).
The pH of the CSF is established by the ratio of pCO2 : [HCO3–].
The HCO3– levels remain relatively constant, whereas CO2 freely diffuses across the blood brain barrier, from the arterial blood supply into the CSF. CO2 reacts with H2O, producing carbonic acid, which lowers the pH. This means that the pH of the CSF is inversely proportional to the arterial pCO2.
- A small decrease in pCO2 leads to an increase in the pH of the CSF, which stimulates the respiratory centres to decrease ventilation.
- A small increase in pCO2 leads to a decease in the pH of the CSF, which stimulates the respiratory centres to increase ventilation.
However if pCO2 levels stay abnormal for a longer period of time, e.g. three days or more, choroid plexus cells within the blood brain barrier allow HCO3– ions to enter the CSF. Movement of HCO3– ions alters the pH which in turn resets the pCO2 to a different value. This can be relevant in certain diseases, such as Chronic Obstructive Pulmonary Disease (COPD).
Clinical Relevance – Hypoventilation
Hypoventilation is a decrease in the rate of ventilation which leads to a build-up of carbon dioxide within the body, commonly known as hypercapnia. This causes the blood to become acidic when dissolved, and can be dangerous as it can cause vital proteins, such as enzymes, to denature.
Common causes include: COPD, chest wall deformities, neurological defects and obesity.
Clinical Relevance – Hyperventilation
Hyperventilation is an increase in the rate of ventilation that leads to a depletion of carbon dioxide within the body, known clinically as hypocapnia, causing our blood to become more alkaline. This decreases free calcium levels and can lead to symptoms such as pins and needles (paraesthesia) or muscle cramps, due to the increased excitability of nerves and muscles
Common causes include: anxiety, heart failure and pulmonary Embolism.