Resp - Ventilation Control Flashcards
Respiratory control centers in brainstem
pons
medullary resp center
parts of medullary resp center
pattern generator
dorsal resp group (DRG)
ventral resp group (VRG)
parts of pons resp center
integrator
pneumotaxic center
apneustic center
dorsal resp group
pacemaker of inspiration
responsible for continuous (tonic) inspiratory drive
DRG how it works
intrinsically oscillate
APs transmitted via phrenic nerve to diaphragm/inspiratory muscles to initiate inspiration
inspiratory neurons: fire –> inspire, cease fire –> expire
VRG
quiescent during quiet breathing
Pre-botzinger complex
play a role in forced expiration
Pre-Botzinger complex actions
expiratory neurons: inhibit inspiratory neurons in DRG
inspiration/expiration control center responses
- latent period
- inspiration: up DRG firing, then stop at end
- expiration: up DRG (brakes) in phase I, then cease in phase 2
DRG neuron types
1 alpha
1 beta
both are inspiratory
1 alpha actions
prevent over distension
inhibited by lung inflation (high V)
Hering Breuer inflation reflex
1 beta actions
prevent extreme deflation
excited by lung deflation
Hering Breuer deflation reflex
Hering Breuer inflation reflex
inhibits inspiring when lung volume is high
use pulmonary stretch receptors in SM of airway
inhibit DRG inspiratory neurons
pneumotaxic center
tells DRG to turn off inspiratory neurons
downs TV
up RR
dominates pons
apneustic center
stops inspiratory neurons from being turned off
apneusis
no pneumotaxic brakes
prolonged inspiratory gasps w/ brief expirations
central chemoreceptor
in CSF, respond to CO2 that comes in and dissociates into H+
tell respiratory control center to up ventilation to lower PCO2
most important mech to control ventilation at rest
CO2-induced H+ in CSF
why we cant die by holding our breath
central chemoreceptor change in sensitivity
prolonged hypoventilation
bicarb used to buffer H+
receptors cant tell theres more CO2
hypoxic drive becomes primary resp stim
peripheral chemoreceptor sensitive to…
hypoxia (PaO2 >. 60)
hypercapnia (weakly)
acidosis
PCO2 and PO2 (together) effects on ventilation
- ventilation goes up as PCO2 goes up – BUT if PO2 is low also, ventilation goes up more quickly as PCO2 goes up (increases sensitivity to hypercapnia)
- ventilation goes up as PO2 goes down – BUT if PCO2 is high also, ventilation will go up more quickly as PO2 goes down (increases sensitivity to hypoxia)
submaximal exercise and ventilation
ventilation up in few seconds
then up slowly to plateau
maximal exercise and ventilation
up ventilation disproportionately
due to lactic acid stim carotid bodies (peripheral chemo)
why make lactic acid during exercise
increased ATP demand - glycolysis, glyconeogenesis
mitochondrial saturation –> goes to lactate
fast twitch units recruited (use more glycolysis)
athletes and ventilation
lower ventilation
same lung structure
up oxidative capacity of muscles - less lactic acid made
