Respiratory Control Rhythmogenesis - Karius Flashcards
Hypoxia
low O2 in the blood
Apnea
stuck in expiration
- damage to medullary or spinal area
- immediate high CO2, H+, low O2
Hypoventilation
high CO2, causing more rapid breathing
Rate of breathing is determines by what calculation
Ve = f x TV
active phrenic nerve causes
inhalation
DRG location
Dorsal Respiratory Group
Part of Nucleus Solitarius
DRG function
Pattern Generator for depth in TV
= gets sensory input from skin and world and phrenic N activates diaphragm for depth in breathing
VRG location
Ventral Respiratory Group
Nucleus Abiguous and Retreo Amigualis
VRG Function
Pattern generator also for TV
sends signal to the inhalation and exhalation muscles for depth of breathing
ROSTRAL part = to inhalation muscles motor neurons
CAUDAL part = to exhalation muscles motor neurons
PRG location
MORE rostral to the Botzinger complex
PRG function
ENDING inspiration
LESION = APNEUSIS
*has some role in timing of breathing (ending inspiration faster = higher frequency)
Pre-Botzinger complex location
Rostral to the VRG
Pre-Botzinger complex function
RHYTHM of breathing = FREQUENCY
- part of central pattern generator (core rhythm)
- very important in infants
what medullary complex is activated first
- the Pre-Botzinger setting frequency + PRG (stop inhalation also involved in f indirectly
- then the VRG/DRG for TV depth of breathing
Apneusis
cant stop inspiration stuck in inspiration *phrenic nerve never turns off - due to pontine damage - slight delay, however then high CO2, H+, and low O2
what nerve does the PRG use to turn of phrenic nerve (inspiration)
CX 10
it can also on its own
tachypnea
rapid and shallow breathing
* that and dry cough are signs or pulmonary edema
what do chemoreceptors detect
low O2, high CO2 and H+
Central Chemoreceptors
location
activated by
causes what end goal
- VENTRAL, lateral of medulla
- PaCO2 (crossed into the CSF)
- increase firing of the Pre-Botzinger + DRG/VRG to increase f and TV of breathing
= DRIVE TO BREATH
Peripheral Chemoreceptors
location
activated by
causes what end goal
- CAROTID BODY, Aortic Arch sinus
- PaCO2, PHa, PaO2
- increase firing of Pre-Botzinger + DRG/VRG to increase f and TV of breathing
= DETECT CHANGE IN BREATHING
3 types of mechanoreceptors
- slow adapting
- Rapidly Adapting
- J- receptors
Slow adapting Receptors : location activated by end goal purpose for existing
- Airways
- stretch of the bronchioles or airway
- STOP inhalation and start expiration
(PRG) - babies for normal breathing
adults during exercise
Rapidly adapting Receptors : location activated by end goal purpose for existing
- Airways
- irritation
- mucous cough
- protect the airway
J Receptors : location activated by end goal purpose for existing
- Alveoli
- pulmonary edema
- tachypnea (pre-Botz. + DRG/VRG) AND DRY COUGH
- protect respiratory circuit
cortical control of breathing happens when
and how is this done
while talking or holding breath for example
the cortex sends signal directly to the MUSCLES for respiration (BYPASS THE medulla + pons)
central pattern receptors
Pre-Betz, DRG, VRG, PRG
what do standard neurons do if low O2 or high CO2 or high H+
Decreasing firing rate
= causes Respiratory rate (minute ventilation rate) to decrease
= causing more lowering O2 and highering of CO2,H+
what prevents the + feedback loop that the standard neurons create
Chemoreceptors that —-I lowering of respiration rate
= increase firing rate to increase breathing rate
how do central chemoreceptors work
the steps in the function
- tissues make CO2 + ATP from fuel
- CO2 is carried as HCO-3 is the arterial system
- CO2 can cross the BBB into the CSF
- it converts back CO2 + H2O –> HCO-3 + H+
- the PaCO2 is sensed by the ventral medulla central chemoreceptors (when PaCO2 > 40mmHg)
- central chemoreceptors fire —->
- Pre-Betz. (increase f)
- DRG/VRG (sends Phrenic N to diaphragm to increase TV)
how do peripheral chemoreceptors work
the steps in the function
- they are located in sinusoids that are in the carotid body and some in aortic arch (SENSE LOW O2, and also high CO2,H+)
- low O2 causes increased ROS, Lactic acid, and low ATP
- K+ leak channels SHUT DOWN
- peripheral chemoreceptors DEPOLARIZE
- LCAT channels open (CA influx)
- more depolarization —-> release DOPAMINE
- activates the CN 9
- increase firing to Pre-Betz + DRG/VRG
= increased VC
Sinusoids are composed of what 3 things
- LOTS OF BLOOD (to bring O2,CO2,H+ levels)
- Type 1 cells : gomus cells = sense the O2, CO2, H+ levels = PERIPHERAL CHEMORECEPTORS
- Type 2 cells : sustentacular cells
what kind of receptors are mechanical receptors
Pulmonary Stretch Receptors
purpose of the mechanical receptros
the CPG about LUNG VOLUME and how fast it is changing (using the pulmonary stretch receptors)
step by step function of the slow adapting pulmonary stretch receptors
- sense stretch in the airway from inhalation
- CN 10 fires —-> all over respiratory centers (CPG *PRG)
- STOP INHALATION , START expiration
(Hering-Breuer reflex)
step by step function of the Rapidly adapting Pulmonary stretch receptors
- sense irritation in the airway
- CN 10 fires to CPG medulla
- mucous coughing
step by step function of the Juxtaglomerular (J) receptors
- senses pulmonary edema irritation on the alveolar capillaries
- activate CN 10 firing to CPG medulla
- dry coughing + tachypnea
- increases interpleural P
