Neural and Chemical Control of Respiration Flashcards
homeostasis of blood gases
-nervous system interaction with the respiratory system is designed to maintain normal blood levels of oxygen, carbon dioxide, and hydrogens
key points
- brainstem generates basic breathing rhythm and is influenced by ventilatory reflexes
- respiration rate and depth is controlled by blood gas concentrations and lung stretch receptors
- arterial Pco2 is most important factor for control of respiratory drive at rest
- central chemoreceptors detect changes in arterial Pco2- really changes in H concentration
- peripheral chemoreceptors detect changes in arterial Po2, PCo2, and pH
inspiratory output
- ventral and dorsal respiratory group both active
- send out impulses to phrenic nerve and spinal nerves to external intercostals
- DRG and VRG connected via spinal respiratory motoneurons to the phrenic nerve
central pattern generator
- breathing is neurogenic
- located in medullary respiratory center
- below the floor of the 4th ventricle of the brain
- has both dorsal and ventral respiratory groups
- CPG sends a rhythmic drive to the motorneurons controlling respiratory muscles and controls rate and tidal volume
- CPG receives input from higher brain centers and from peripheral and central chemoreceptors
expiratory output
-the medullary VRG is connected via spinal respiratory motoneurons to spinal nerves that innervate the internal intercostals and abd muscles
AP frequency
- phrenic/ external intercostal
- APs increase during inspiration for relaxed breathing
- expiration muscles not having much APs
- vigorous breathing increases the APs in abd/intercostal expiration muscles (hyperpnea)
- tidal volume increases as well as frequency
Hering-Breuer Inflation Reflex
-during deep inspirations, lung inflation activates stretch receptors that inhibit further inflation via vagal afferents and phrenic efferents
respiratory center
- just above the medulla
- pontine respiratory group controls center- in pons
- controlled by the hypothalamus
- brain stem is relay station
- has VRG and DRG (in NTS) and other controls
BOT
- botzinger complex
- pacemaker of breathing
- pharmacological target
- expiratory neurons
- in venttrolateral medulla essential for pacemaker
DRG
- bilaterally in the NTS
- inspiratory neurons
- initiator of activity of the phrenic nerves
- sends many collateral neurons to the VRG
- receives vagal afferents from chemoreceptors
VRG
- located bilaterally in the retrofacial nucleus, nucleus ambiguous, and nucleus retroambifualis
- inspiratory and expiratory neurons
- contains BOT
pontine respiratory group
- pneumotaxic center
- located in nucleus parabrachialis medialis and the KF nucleus of the pons
- fine tunes respiratory pattern and modulates pattern in response to vagal afferents responding to hypercapnea or hypoxia
Level I transection
- with vagus has normal breathing
- without vagus has decreased frequency and increased tidal volume
Level II transection
- with vagus has dec frequency and increased tidal volume
- without vagus has apneusis
level III transection
- just below pons
- gasping with vagus
- more sporadic gasping without vagus
Level IV transection
- below DRG
- apnea
- CPG above here
Cheyne stokes respiration
- abnormal pattern characterized by alternating periods of hyperpnea and apnea, each cycle from 30s to 2 min
- altered arterial partial pressures of oxygen and carbon dioxide
- injuries to resp centers, chronic heart failure, CO, strokes, brain tumors
cluster breathing
- stroke, head trauma, pressure, lesion in lower pontine region of brainstem
- closely groups series of shallow breaths similar in size separated by intervals of apnea and indicative of poor prognosis
ataxic breathing
- lesion in medullary respiratory center
- completely irregular inspirations and expirations with irregular pauses and increasing periods of apnea
kussmaul breathing
- abnormal form of deep and labored desperate and gasping breathing associated with severe metabolic acidosis, particularly diabetic
- shallow rapid hyperventilation becomes kissmaul as acidosis progresses
central chemoreceptors
-activated primarily by hydrogen ions via blood CO2 crossing the blood brain barrier and generating hydrogen ions
peripheral chemoreceptors
-activated by low blood partial pressures of oxygen, high partial pressures of co2, high H
alveolar CO2
- major controller of respiration rate
- after intense hyperventilation, there is a period of apnea because CO2 is so low
- once CO2 levels reach normal, breathing starts
- also produces cheyne stokes rhythm
increasing PACO2
- increases ventilation to get more out
- sensitivity to carbon dioxide increases with hypoxia
- shifts to left on ventilation vs PaCO2 graph
- smaller increase in co2 will cause increase in ventilation
- response to co2 also altered by sleep, drugs, metabolic acidosis. sleep and drugs make less sensitive, acidosis makes it more sensitive
CO2 and O2
- plotting ventilation against line from CO2
- there is a set point at intersection between sensitivity curve and effector curve
- increasing levels of ventilation reduces CO2
- its a dynamic process
- drugs, acidosis move set point down and up respectively
altering pH
- with constant CO2, low pH increases ventilation greatly
- with changing CO2, its dynamic again, ventilation increases with drop in pH and corrects it
- same effect on PO2 with constant CO2 and then not- first big changes then ventilation doesn’t allow for as big of a change
blood brain barrier
-only CO2 crosses, central receptors respond to H dissociated
peripheral chemoreceptors
-carotid and aortic bodies
-have glomus cells
low O2, closes K channel, cell depolarizes, Ca open, Ca stimulates IX which sends afferent signals to brain to change breathing
-if chemoreceptors are denervated, ventilation decreases, lack of O2
