Control of Ventilation Flashcards
Where is the basic pattern of breathing generated
Medulla oblongata
5 factors involved in sensory input
- Central chemoreceptors
- Peripheral chemoreceptors
- Irritant receptors
- Muscle stretch receptors
- Pulmonary srtetch receptors
What are the 2 discrete areas in the medulla oblongata
- Dorsal respiratory group
- Ventral respiratory group
What is control of breathing influenced by
Pneumotaxic centre - expiration
Apneustic centre
DRG NEURONS
- ______ generator
- involved in insp or exp
- Rhythm generator
- Basic resp patter for INSPIRATION
- repetitive generation of ramps of neural activity
- results in contraction of inspiratory muscles
- abruptly shuts off at the end of inspiration (expiration is passive)
Where does the initial AP generation for breathing come from
Pre-Botzinger complex
Are DRG neurons stable or unstable
Intrinsically unstable
Capable of spontaneous depolarisation
Like the pacemaker of the SA node
How doe DRG neurons fire
APs via phrenic and IC nerves - stimulates diaphragm and external intercostals
=> thoracic cavity expands
=> -ve pressure
=> inspiration
Cells stop firing, inspiratory muscles relax, passive exp begins
(some DRG nerves extend into VRG)
What connects peripheral and joint chemoreceptors, lungs and airways to the DRG
Sensory impulses are carried in the vagus and glossopharyngeal nerves
What is the VRG responsible for
Inspiration and expiration
Augments ventilatory pattern - rhythm i.e. activity of DRG when resp drive is high
What does the VRG provide
powerful exp signals to abdominal muscles - ventilation under conditions of high demand (exercise)
Parasympathetic output of the VRG
Bronchioles (bronchoconstriction to decrease airflow)
Heart - inhibitory
What is the Pre-Botzinger Complex
Interneurons
Part of VRG
Resp rhythm generation
What does the PBC inhibit
VRG insp neurons
DRG insp neurons
What does the PBC stimulate
VRG exp neurons
2 components of the pontine resp group
Pneumotaxic centre
Apneustic centre
4 roles of the pneumotaxic centre
- Co-ordinates insp -> exp transition
- Prevents over-expansion of lungs
- Modifies acrtivity in VRG (exp) - directly promotes exp
- Modifies activity in apneustic centre - indirectly inhibits its promotion of insp
What switches off the ramping effect of insp
pneumotaxic area
What does the apneustic centre modify
DRG insp activity
Activates and prolongs insp - deepens breath
- prolonged excitatory ramps
- prolonged acitivity in the diaphragm
What is apneusis
Where is apneusis seen
Breathing pattern associated with apneustic stimulation
Deep gasping inspiration with a brief, insufficient release
Seen in damage to pons or upper medulla
e.g. stroke/trauma (quadriplegia), ketamine overdose
What neurons are in close proximity in medulla
Resp and CVS neurons in close proximity => HR variability in synchrony with resp
_____ ________ in the VRG triggers parasympathetic innervation to the _____ via _____ nerve
Nucleus ambiguus in the VRG triggers parasympathetic innervation to the heart via the vagus nerve
What does inspiration trigger
inhibitory signals in the nucleus ambiguus and consequently the vagus nerve remains unstimulated
=> HR increases
Conversely, in exp nucleus ambiguus neurons are activated and HR decreases
How does resp sinus arrythmia help with alveolar ventilation and perfusion
Improves efficiency of pulmonary gas exchange, which helps to match timing of alveolar ventilation and perfusion
Could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during ebb of perfusion
Where does the voluntary control of resp stem from
what is control via
cerebral cortex
controlled via pyramidal tracts but limited
- bypasses resp centres
- short term
automatic control will regain precedence especially PCO2
What does the limbic system refer to
hypothalamus can influence ventilation
fear
pain
emotion
What do chemoreceptors monitor
Vascularity
Blood chemistry
- PaCO2
- PaO2
- pH
highly vascular
Is there a lot of O2 removed from blood
Negligible removal of O2 from blood
Hypercapnia response
Via central chemoreceptors - medulla
Stimulate increased activity from resp centres
Increased ventilation to decrease CO2
Not direct effect of CO2 rather H+
CO2 crosses BBB, H+ does not
Carbonic acid in cerebral spinal fluid
Response divide between central and peripheral chemoreceptors
CENTRAL - 80%
PERIPHERAL - 20%
Peripheral chemoreceptor response
PaCO2 increase => acidosis, due to increased [H+]
(not as strong a response as in CNS but 5x faster)
increase in medullary centre activity via glossopharyngeal and vagal nerves
Increase in ventilation => decrease in PaCO2
What is the initial acute response to an increase in PaCO2
Increased ventilation
What is the long-term adaptation of central chemoreceptors
Choroid plexus cells (form CSF) add HCO3- to CSF and remove H+ from blood
Added HCO3- to blood => increased CSF pH => inhibition of stimulus for increased ventilation
What is the only NON-ADAPTING receptor in the body
Peripheral chemoreceptor - decreased PaO2 (hypoxia) drives respiration
what happens when there is a prolonged elevation of PaCO2 (50-60 mmHg)
Adaptation of central chemoreceptors
What is the driving force for respiration
Peripheral chemoreceptors - PaO2 (hypoxic drive)
Why are COPD patients not treated with 100% O2
Potentially removes stimulus for respiration
O2 should not be with-held in hypoxaemic COPD patients as tissue oxygenation is over-riding priority but needs careful monitoring
Are central chemoreceptors sensitive to PO2
NO - INSENSITIVE
What do peripheral chemoreceptors mediate
When is there a response
Hypoxic response
Response when PaO2 drops to 60 mmHg
- increased firing in peripheral chemoreceptors
- increased resp centre activity
- increased ventilation
- increased PaO2
How does hypoxia stimulate peripheral chemoreceptors
GLOMUS CELLS
O2 sensitive K+ channels
O2 sensor is on the ECF side
Where are slowly adapting stretch receptors located
SM of longer airways
What is the stimulus for SARs
Hyperinflation => rapid firing
continued inflation - slowly adapt to lower firing rate
What are the effects of SARs
Where do they act
Prolonged expiration and shortened inspiration
Act directly on DRG
Indirectly on PONS
What happens in conditions of altered lung mechanical properties
- airway
- SAR activity
- Increased airway R - asthma, emphysema, mucus plugs etc
- Increased SAR activity slows resp rate by lengthening expiration
What is the Hering-Breuer reflex
INFLATION
Activated after large inflation > 1.2 L (exercise)
Lung inflation inhibits further inflation
reflex provided by SAr (afferent limb)
DEFLATION
Lung deflation prevents further deflation
HOWEVER adults have more prominent central responses/signals
Where are rapidly adapting stretch reflexes/irritant receptors located
between epithelial cells
What do RARs respond to
Mechanical and chemical irritant stimuli and to many inflammatory and immunological mediators
What are RARs activated by
Lung distension or chemical and particulate irritants
- lung oedema
- emoblism
- dust
- cigarette smoke
- ammonia
What are the 2 effects of RARs
- Cough
- Increased inspiration via DRG - increased lung vol
Short-term reflex of RAR
Rapidly adapts
SAR take over
Decreased lung volume
What is sleep apnoea
Temporary suspension of breathing
What are apnoeic episodes associated with
O2 de-saturation
Obstructive sleep apnoea
Pharynx (usually held open by muscles that relax during sleep) collapses
Caused by excess fat deposits in soft tissue of pharynx or fat masses in the neck
Nasal obstruction
Enlarged tonsils
Large tongue
Certain shapes of palate
Gravity
Central sleep apnoea
Less common
CNS signal to resp muscles stops completely
Damage to central resp centre or resp neuromuscular junctions
Can trigger seizures or sudden death
What do the long silent periods of apnoea cause
Increase in PCO2
Decrease in PO2
Treatment of sleep apnoea
Continuous Positive Airway Pressure
Most common
Keeps airways open by means of pressurised air
Nose or facial mask connective by flexible tube to CPAP machine
Stimulus for immersion/diving reflex
Contact of head, face, resp tract with cold liquid
the colder the water, the stronger the physiological responses
Result of immersion/diving reflex
Apnoea
Bradycardia
Laryngeal spasm
Peripheral vasoconstriction (not lungs, heart, brain)
Afferent pathways for respiration
Via somatic sensory nerves of face and nasal cavity
Very active in infants up to 6 months - survive longer than adults when deprived of O2 underwater
Importance of immersion reflex
Foetus in utero - breathing practice increases further into gestation
Totally immersed in liquid - active immersion reflex
Advantages of immersion reflex
Prevents unnecessary resp movements
Relieves workload on the heart - bradycardia, hypotension
BF to vital organs (HLB) - selective vasoconstriction
