Control of Respiration Flashcards
The dorsal respiratory group of nuclei control what part of respiration?
Normal inspiration
Explain what is happening in this image.
During inspiration, there is a gradual ramp up of firing of neurons. This prevents rapid contraction of the diaphragm and allows for slow, controlled inhalation.
When the lungs have expanded to the tidal volume, the pneumotoxic center in the brainstem shuts off inhalation.
During expriation, there is an initial phase where there is still some firing of neurons at a lower level which prevents rapid relaxation of the diaphragm and allows for slow, controlled exhalation.
After phase 1, when neural signals turn off, the recoil of lungs and chest wall cause remainder of expiration.
Anything that increases […] will increase the pH of the blood
HCO3-
What does the hering - breuer reflex control?
- Rate or volume of lung inflation or deflation to prevent overexpansion of lungs
- Modulated by stretch receptors in smooth muscle fo lungs
- Controlled by CN10
Describe the peripheral mechanisms we have in place to respond to changes in partial pressure of O2, CO2 and [H+].
Carotid body (CN9) and Aortic Arch (CN10)
- Responds to decreasing PaO2, increasing PaCO2 and increasing [H+]
- Response to CO2 is much faster than central response, so this helps regulate changes that occur on the order of seconds
Anything that increases […] and […] will decrease the pH of the blood.
H+
CO2
Describe in general an overview of how respiration is controlled by structures in the brain.
Breathing is spontaneously initiated in the CNS, which provides input to the brainstem (nuclei in the medulla) to generate breathing. The impulses from this center stimulate muscles of inspiration to contract. The medullary control center is modified by a number of peripheral input areas as well as higher cortical influences.
Explain the changes that occur to ventilation, PaCO2, the blood, the brain and the kidneys with increasing altitude.
CO2 + H2O <=> H2CO3 <=> H+ + HCO3-
The increased respiration that is generated by increased excretion of HCO3- by the kidneys is due to an increase in H+ that results from a rightward shift of the above equation
Voluntary control of respiration is controlled by […]
corticospinal tracts
The carotid body (and aortic body) respond to […] not […] in the blood
PaO2
oxygen content
What mechanisms are responsible for increasing breathing during exercise?
Muscle spindles, golgi tendon organs and proprioceptors in the skeletal muscle, tendons and joints sense that exercise is occuring and send signals to the brain to increase the total volume and respiratory rate even before CO2 or H+ increase (anticipatory)
Describe what the ventilation response would be when PaCO2 increases in the following clinical situations:
- Metabolic acidosis
- Sleep
- Narcotics, obstructive sleep disorder
- Deep anesthesia
- Ventilation increase is augmented due to presence of both high H+ and increasing PaCO2
- Ventilation response to PaCO2 is less than our response when awake
- Ventilation response to increasing PaCO2 is less than when awake due to suppression of many neural systems by narcotics or decreased oxygen in apnea
- Ventilation response to increasing PaCO2 is heavily depressed, why people put under anesthesia need to be put on ventilator to remove CO2
Where do output fibers from the DRG go and what do they do?
- Majority go to contralateral spinal cord and synapse on motor neurons of the phrenic nerve, which arises from levels C3, C4, and C5. Phrenic nerve controls muscles of normal inspiration (diaphragm and external intercostals). Some continue on to synapse on motor neurons in thoracic spinal cord which then innervate external intercostals.
- Sends some fibers to VRG so that when more inspiration is needed the DRG can tell the VRG to help increase respiration by activating additional muscles
Describe (in general) the signaling that occurs at the synapse between the carotid artery, carotid body, and CN 9 fibers that innervate carotid body.
Decreased O2 –> closes K+ channels –> causes increased membrane potential –> depolarization –> calcium channel opens –> calcium enters –> neurotransmitter released (not yet known at this time that the NT is)