Control of breating Flashcards
wk 6
What is the function of the Dorsal Resp Group (DRG)?
Determines timing of resp cycle
(PSR activation each inspiration = rhythmic pattern of breathing)
What are the effectors activated by the DRG?
Diaphragm and Ext intercostal muscles
What is the function of the Ventral Respiratory Group? *(VRG)
Contributes to extra resp drive in cases of increased demand
Coordinates info from cortical input, peripheral sensory info and visceral and cardiovascular inputs
what resp functions does the VRG NOT do?
- inactive during normal quite breathing
- doesn’t generate resp rythym
What is the innervation of the DRG and VRG respectively?
DRG= Pulmonary stretch receptors and mechanoreceptors
VRG= chemoreceptors and higher brain centres
what are the components of the VRG and what neurons are they responsible for?
Botzinger complex and Casual VRG = expiratory neurons
Rostral VRG = inspiratory neurons
how can the inspiratory ramp be altered?
1- Rate (lung V/Depth) (signal intensity)
2- Termination point (freq)
What is the inspiratory ramp signal?
cyclical cycle (2s duration, 3s pause) of increased DRG and VRG to allow for controlled lung filling.
What is the purpose of the pause in the inspiratory lung ramp?
passive exhalation via elastic recoil of chest wall and lungs
What is the pre-botzinger complex and where is it?
Needed for rhythmogenesis and signals DRG
It is in the VRG but is FUNCTIOANLLY SEPARATE
What is rhythmogenesis?
removal of rhythmic inspiratory activity
Explain the cycle of quiet breathing
Insp muscles contract –> inspiration –> DRG inhibited –> insp muscles relax –> passiv expir –> DRG active
Explain the cycle of forced breathing
insp muscles contract, exp relax –> inspiration –> DRG and insp centre of VRG inhibited, Exp centre of VRG active
–> insp relax, exp contract –> active expiration –>
DRH and insp centre of VRG active and Exp centre of VRH inhibited –>
PRG vs DRG and VRG
DRG and VRG = generates reso rythym
PRG = fine control of resp rythym
What is the function of the Apneustic centre and Pneumotaxic centre respectively?
A= Prolongs resp = increased Vt and decreased f
P= Ramp off earlier = decreased Vt and increased f
How does cortical override work?
may bypass the medullary respiratory centre to act directly on respiratory muscle LMNs
Role of Upper Resp tract in reflexes
Contains receptors in nose, pharynx and larynx that are sensitive to toxins, irritants and temp
Origin of cough reflex
What are the two types of pulmonary stretch receptors and what are they sensitive to?
Slowly adapting stretch receptors (SARs) =
Lung volume
Rapidly adapting stretch receptors (RARs) =
Changes in Vt, f or Cl
Nociceptive and chemosenstitive
What is the role of the Hering-Breuer inflation reflex?
Inhibits inspiration in response to increased Pulmonary transmural pressure gradient (increased Lung stretch)
Where are the TASK-2 and GPR4 chemoreceptors located?
RTN neurons
Describe the action of RTN neurons
selectively target pon-to-medullary region to help generate resp rythym and pattern
What are the two peripheral chemoreceptors and what nerves do they use to input into medulla?
Aortic bodies
Vagus nerve
Carotid bodies
Glossopharyngeal nerve
What are the peripheral chemoreceptors most sensitive to?
Changes in arterial H+
Non-CO2 generated H+
Most sensitive to low PaO2
What effects do the peripheral chemoreceptors have?
Increase rate and depth of breathing
Bradycardia
HTN
Increased bronchomotor tone and adrenal secretion
Describe the flow of events that occurs when there is increased Arterial PCO2
arterial chemoreceptors stimulated –> DRG stimulated –> increased f –> increased elimination of Co2 –> decreased P arteial CO2 –> homeostasis restored
What does increased CO2 have a stronger acute effect than chronic effect?
renal mechanisms increase blood HCO3
HCO3 crosses BB and binds to H = decreased CSF
What is the advantage of fainting?
horizontal position = heart doesn’t have to pump against gravity to maintain cerebral perfusion
What is Owles point?
Point when relative hyperventilation is associated with lactic acidosis
Describe the Ventilatory response to light-mod exercise
Arterial Blood gases stable
Increased VE matched w increased VO2
Describe the Ventilatory response to heavy exercise
Increased VE > increased Vo2
What is Primary Hypoventilation Syndrome (Ondine’s curse)
Long periods of apnoea even whilst awake
Might die during sleep due to lack of automatic resp control in sleep.
What is the cause and management of Pri Hypoventilation Syndrome?
Cause
Congenital (PHOX2B mutation)
Acquired post brain injury
management
Mechanical ventilation
Diaphragmatic pacing
what is Cheyne-Strokes Respiration and who does it often impact?
Periodic breathing abnormality that occurs in high altitide or in preterm newborns.
Cycles every 40-60s
What causes central sleep apnoea?
transient pause in central drive to breath
How does the preBotC aid with arousal?
Rebreathing exhale air during prone sleeping
Altered blood gases initiates arousal response
Successful arousal = head lifting and repositioning
How does preBotC aid with Autoresuscutation?
If arousal fails = more sevre hypoxic stare
Transition to gasping mediated by preBotC
Gasping = arousal
How does impaired pre-Bötzinger complex function lead to SIDS?
impaired sigh and gasp generation → irreversible hypoxic insult → asphyxiation
What is the presentation of CO poisioning?
Non-specific (headaches, fatigue, malaise, confusion nausea, chets pain and SOB).
Late stage = cherry-red lips, peripheral cyanosis and retinal haemorrhages
What impact does CO poisoning have on the Oxygen-Hb dissociation curve?
Downward shift: CO displaces O2 from Hb = decreased HbO2 sat
Left Shift: CO increases affinity of Hb for O2 = deceased O2 unloading
How do opioids cause respiratory depression?
Depresses Resp Rythym
Decreased sensitivity of peripheral chemoreceptors to hypercapnia and hypoxia
Increased Up airway res
Decreased lung complaince
What opioid receptor subtype controls resp?
Mu-opioid receptor (MOPr) controls resp via MOP B-arrestin pathway
where does DRG send out put to?
Phrenic motor neurons for diaphragm contraction
spinal interneurons (C1-2) for ext intercostal muscles
VRG and PRG
where does the rVRG receive input from?
PreBotC
DRG
PRG
Chemoreceptors
High Brain centres
Where does the cVRG recieve input from?
PreBotC
rVRG
PRG
Chemoreceptors
High Brain centres
Where does the BotC recieve input from?
Nucleus Tracts Solitus (info from chemoreceptors)
DRG
r + c VRG
PreBotC
Where does the rVRG send an output to?
phrenic motor neurons (activate)
thoracic motor neurons
PreBotC and BotC
Where does the cVRG send an output to?
abdominal motor neurons
internal IC motor neurons
BotC and NTS
Where does the BotC send an output to?
Phrenic motor neurons (inhibits)
PreBotC
rVRG/cVRG
What is Corticol control of breathing and what limits it?
voluntary conscious control of breathing
If hold breath (trying to control) will decrease PoO2 and increased PCO2. The increase in PCO2 creates gasping (involunteyr via PreBoT)
the increased CO2 is detected by chemoreceptors (increased HCO3 = crosses BBB and binds H+)
what is the indirect and direct impact of Increased PaCO2?
indirect = medulla RTH (central CR detects CSF H+)
direct = stimulates peripheral CRs
acute vs chronic PaCO2 effect on resp drive.
Acute = strong
-central = rapid
-peripheral = elevated PaCO2 amplitude
Chronic= weak
-kidneys adapt to chronic hypercapnia as HCO3 buffers H+
-desensitises chemoreceptors
explain the glomerular filtration?
blood enters glomerlus via afferent arterioles –> Pressures force water through the GFB. PGC does filtration whilst capsular and blood calcioid P opposes filtrate.
