Lecture 6: Respiration Regulation Flashcards
Central control of respiratory skeletal muscles
Medulla oblongata
Medullary respiratory center parts
- Dorsal Respiratory Group (inspiratory neurons)
- Ventral Respiratory Group
(pre-Botzinger complex, expiratory neurons)
Pre-Botzinger complex
Pacemaker respiratory rhythm generator
Apneustic center
Lower pons area that finetunes medullary inspiratory neurons; terminates inspiration
Pneumotaxic center
Upper pons area aka pontine respiratory group that smooths inspiration-expiration transition; modulates stimuli responses and signals to medullary inhib. C interneurons
Hering-Breuer reflex
Pulmonary stretch receptors in airway smooth muscle cut off inspiration at large volume w/ vagal signals to medullary insp. B neurons
Peripheral chemoreceptors
Carotid + aortic bodies that monitor arterial PO2, CO2, and H+ and signal to medullary insp. A neurons
Central chemoreceptors
Primarily monitor brain ECF H+ and are thus stimulated by PCO2; responsible for majority of PCO2 response and signals to medullary insp. A neurons
Effect of very high PCO2 on ventilation
Very high PCO2 can directly inhibit ventilation through the medulla
Metabolic acidosis/alkalosis
High/low H+ due to changes in metabolism, not respiration e.g. lactic acidosis
Limiting factors during intense exercise
Cardiac output is the limiter in exercise, not ventilation
Other factors that stimulate ventilation
- Joint/muscle mechanoreceptor reflexes
- Increase in body temp.
- Central brain command
- Increase in blood epi
- Increase in blood K+ due to working muscles
- Learned neural responses
Juxtacapillary (J) receptors
Sensors in lung interstitum/capillary walls that are stimulated by increased lung interstitial pressure due to fluid; signal to slow vagal C-fibers
Augmented firing of efferent respiratory impulses
Describes ramp-like increase in frequency at onset of inspiration, then rapid decrease at end of inspiration for inspiratory neurons
How can respiratory depth by increased neurally?
- Increase motor unit firing frequency
- Increase motor unit recruitment
- Increase duration of impulse bursts
How is respiratory rate controlled neurally?
- Controlling interval duration between impulse volleys
- Controlling duration of impulse bursts
Dorsal Respiratory Group
- Mostly inspiratory neurons (STN)
- Primary initiator of phrenic nerve activity for diaphragm
- Receives input from carotid/aortic chemoreceptors/baroreceptors and lung stretch receptors
Ventral Respiratory Group
- Mix of insp./exp. neurons
- Contains pre-Botzinger complex
DRG self-cycling circuit
- A/B: medullary insp. neurons (not motor)
- C: inhib. interneuron
Mutual inhibition in breathing control
VRG neurons reciprocally inhibit insp. neurons; no neuron firing occurs during opposite respiratory phase
Type I Glomus cells
Cells in peripheral chemoreceptors that sense PO2, H+, PCO2
How do Type I glomus cells signal?
Decrease in PO2 or increase in H+/CO2 are reflected IC and close K+ channels; depolarization opens Ca2+ channels triggering NT release
Effects of chronically high/low CO2
Chemoreceptors become desensitized due to increased bicarb. buffering
Irritant receptors
Receptors between airway epithelial cells that send impulses to vagal afferents triggering bronchoconstriction and hyperpnea
Cheyne-Stokes breathing
Caused by delayed ventilatory responses to PCO2; hypervent. diminishing to apnea increasing to hypervent.; common in cardiac failure due to reduced brain blood flow -> slower CSF PCO2 equilibration
Apneustic breathing
Caused by brain stem injury; deep extremely long inspirations and brief expiration
Sleep apnea
Obstructive: mechanical blockage e.g. relaxed pharyngeal muscles
Central: decreased ventilatory drive; apnea w/ no respiratory effort
