Resp - Ventilation Control Flashcards

1
Q

Respiratory control centers in brainstem

A

pons

medullary resp center

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2
Q

parts of medullary resp center

A

pattern generator
dorsal resp group (DRG)
ventral resp group (VRG)

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3
Q

parts of pons resp center

A

integrator
pneumotaxic center
apneustic center

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4
Q

dorsal resp group

A

pacemaker of inspiration

responsible for continuous (tonic) inspiratory drive

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5
Q

DRG how it works

A

intrinsically oscillate
APs transmitted via phrenic nerve to diaphragm/inspiratory muscles to initiate inspiration
inspiratory neurons: fire –> inspire, cease fire –> expire

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6
Q

VRG

A

quiescent during quiet breathing
Pre-botzinger complex
play a role in forced expiration

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7
Q

Pre-Botzinger complex actions

A

expiratory neurons: inhibit inspiratory neurons in DRG

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8
Q

inspiration/expiration control center responses

A
  1. latent period
  2. inspiration: up DRG firing, then stop at end
  3. expiration: up DRG (brakes) in phase I, then cease in phase 2
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9
Q

DRG neuron types

A

1 alpha
1 beta
both are inspiratory

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10
Q

1 alpha actions

A

prevent over distension
inhibited by lung inflation (high V)
Hering Breuer inflation reflex

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11
Q

1 beta actions

A

prevent extreme deflation
excited by lung deflation
Hering Breuer deflation reflex

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12
Q

Hering Breuer inflation reflex

A

inhibits inspiring when lung volume is high
use pulmonary stretch receptors in SM of airway
inhibit DRG inspiratory neurons

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13
Q

pneumotaxic center

A

tells DRG to turn off inspiratory neurons
downs TV
up RR
dominates pons

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14
Q

apneustic center

A

stops inspiratory neurons from being turned off

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15
Q

apneusis

A

no pneumotaxic brakes

prolonged inspiratory gasps w/ brief expirations

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16
Q

central chemoreceptor

A

in CSF, respond to CO2 that comes in and dissociates into H+

tell respiratory control center to up ventilation to lower PCO2

17
Q

most important mech to control ventilation at rest

A

CO2-induced H+ in CSF

why we cant die by holding our breath

18
Q

central chemoreceptor change in sensitivity

A

prolonged hypoventilation
bicarb used to buffer H+
receptors cant tell theres more CO2
hypoxic drive becomes primary resp stim

19
Q

peripheral chemoreceptor sensitive to…

A

hypoxia (PaO2 >. 60)
hypercapnia (weakly)
acidosis

20
Q

PCO2 and PO2 (together) effects on ventilation

A
  1. 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)
  2. 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)
21
Q

submaximal exercise and ventilation

A

ventilation up in few seconds

then up slowly to plateau

22
Q

maximal exercise and ventilation

A

up ventilation disproportionately

due to lactic acid stim carotid bodies (peripheral chemo)

23
Q

why make lactic acid during exercise

A

increased ATP demand - glycolysis, glyconeogenesis
mitochondrial saturation –> goes to lactate
fast twitch units recruited (use more glycolysis)

24
Q

athletes and ventilation

A

lower ventilation
same lung structure
up oxidative capacity of muscles - less lactic acid made

25
Q

apnea - why?

A

sleep - central chemo less sensitive to PCO2

26
Q

SIDS - why?

A

immaturity of respiratory control mechanisms (brain stem or chemoreceptors - carotid*)