Control of breathing Oct5 M1 Flashcards
2 resp control neurons aggregates and location
medulla. VRG and DRG
what DRG does
inspiration, situation beyond normal tidal breath
what VRG does
inspiration and expiration, normal breathing
what controls phrenic nerve mainly
DRG (NTS)
DRG components (1)
NTS (nucleus tractus sollitarius)
VRG components (2)
nucleus ambiguous retrofacial nucleus (pre botz complex and botz complex)
what pre botz complex does and location in VRG
pacemaker. (all others are modulators)
rostral end of VRG
botz complex function
involved in expiration
ninth and tenth cranial nerve name + job
glossopharyngeal. vagus. carry info on PO2, PCO2, pH and BP from aorta and carotid bodies to central controller
what additional info vagus nerve carries
stretch receptors (PSRs), C-fibers, juxta-capillary receptors) in the lugns
3 cell types in carotid bodies and important one and why
type 1: glomus cell (important senses O2)
type 2: sustentacular cells
NF: fibres of carotid sinus nerve
central chemoreceptors location and mechanism
ventrolateral surface of medulla. sense pH
location of CO2 chemoreceptors in the brain
retrotrapozoid nucleus (RTN) or retrofacial nucleus,
RTN nucleus closely related to what nucleus
pre-botz complex
how ventilation changes with O2 drop if eucapnic vs hypercapnic
greater increase of ventilation for same O2 drop if hypercapnic
chemoreceptor activation mechanism (in carotid body)
hypoxia: hemoxygenase 2 (HO 2) shuts off, no more CO prod, CSE not inhibited anymore and can produce hydrogen sulfide, opens K+ channel, opens Ca channel, ntr vesicles release
response to hypoxia and why
rapid shallow breathing: stay in linear portion of PV curve
response to hypercapnia and why
slow deep breathing to minimize deadspace ventilation (Vd over VT) and optimize CO2 elim
sensors other than chemo and pulmonary
chest wall receptors (golgi tendons, muscle spindles)
upper airway dilator muscle sensors
def of hyperventilation
reduced PaCO2
causes of hyperventilation
metabolic acidosis drugs CNS problem lung disease psychogenic
ultimate consequence of increase in PACO2
generalized acidosis and syncope
why high FiO2 worsens high PaCO2 (3)
- blunts ventilatory drive
- blunts hypoxic vasoconstriction in poorly ventilated regions
- more HbO2, less HbCO2, more CO2 in blood
how treat high PaCO2
controlled supp O2 91-93%
hypoventilation def
high PaCO2
causes of hypoventilation
metabolic drugs CNS chest wall deormities neuromuscular parenchymal disease congenital central hypovent syndrome
Ondine’s curse or congenital central hypoventilation syndrome
impaired CO2 chemosensitivity, no air hunger, sleep ane
congenital central hypoventilation syndrome cause
mutation in Phox2b
