Control of breathing Oct5 M1 Flashcards Preview

Bloc B - Respiration > Control of breathing Oct5 M1 > Flashcards

Flashcards in Control of breathing Oct5 M1 Deck (28)
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1
Q

2 resp control neurons aggregates and location

A

medulla. VRG and DRG

2
Q

what DRG does

A

inspiration, situation beyond normal tidal breath

3
Q

what VRG does

A

inspiration and expiration, normal breathing

4
Q

what controls phrenic nerve mainly

A

DRG (NTS)

5
Q

DRG components (1)

A

NTS (nucleus tractus sollitarius)

6
Q

VRG components (2)

A
nucleus ambiguous
retrofacial nucleus (pre botz complex and botz complex)
7
Q

what pre botz complex does and location in VRG

A

pacemaker. (all others are modulators)

rostral end of VRG

8
Q

botz complex function

A

involved in expiration

9
Q

ninth and tenth cranial nerve name + job

A

glossopharyngeal. vagus. carry info on PO2, PCO2, pH and BP from aorta and carotid bodies to central controller

10
Q

what additional info vagus nerve carries

A

stretch receptors (PSRs), C-fibers, juxta-capillary receptors) in the lugns

11
Q

3 cell types in carotid bodies and important one and why

A

type 1: glomus cell (important senses O2)
type 2: sustentacular cells
NF: fibres of carotid sinus nerve

12
Q

central chemoreceptors location and mechanism

A

ventrolateral surface of medulla. sense pH

13
Q

location of CO2 chemoreceptors in the brain

A

retrotrapozoid nucleus (RTN) or retrofacial nucleus,

14
Q

RTN nucleus closely related to what nucleus

A

pre-botz complex

15
Q

how ventilation changes with O2 drop if eucapnic vs hypercapnic

A

greater increase of ventilation for same O2 drop if hypercapnic

16
Q

chemoreceptor activation mechanism (in carotid body)

A

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

17
Q

response to hypoxia and why

A

rapid shallow breathing: stay in linear portion of PV curve

18
Q

response to hypercapnia and why

A

slow deep breathing to minimize deadspace ventilation (Vd over VT) and optimize CO2 elim

19
Q

sensors other than chemo and pulmonary

A

chest wall receptors (golgi tendons, muscle spindles)

upper airway dilator muscle sensors

20
Q

def of hyperventilation

A

reduced PaCO2

21
Q

causes of hyperventilation

A
metabolic acidosis
drugs
CNS problem
lung disease
psychogenic
22
Q

ultimate consequence of increase in PACO2

A

generalized acidosis and syncope

23
Q

why high FiO2 worsens high PaCO2 (3)

A
  • blunts ventilatory drive
  • blunts hypoxic vasoconstriction in poorly ventilated regions
  • more HbO2, less HbCO2, more CO2 in blood
24
Q

how treat high PaCO2

A

controlled supp O2 91-93%

25
Q

hypoventilation def

A

high PaCO2

26
Q

causes of hypoventilation

A
metabolic
drugs
CNS
chest wall deormities
neuromuscular
parenchymal disease
congenital central hypovent syndrome
27
Q

Ondine’s curse or congenital central hypoventilation syndrome

A

impaired CO2 chemosensitivity, no air hunger, sleep ane

28
Q

congenital central hypoventilation syndrome cause

A

mutation in Phox2b