Control of Breathing Flashcards
– Describe the neural mechanisms that establish the respiratory rhythm – Distinguish between the respiratory centers that establish the rhythm and those that regulate the rhythm – Explain the role of peripheral & central chemoreceptors in the control of ventilation – Delineate the ventilatory responses to hypoxemia & hypercapnia
Components of the respiratory control system - integrator
-neural network in the brainstem
Components of the respiratory control system - sensor
- main = chemosensors sensing changes in CO2, O2 and pH
- contributors = lungs, cardiovascular, skeletal muscles, tendons of respiratory muscles
Components of the respiratory control system - effector
-respiratory muscles
Inspiration = diaphragm and external intercostals
Expiration = internal intercostals & abdominal
Respiratory control system response to stimulus (increase in PCO2)
1) Arterial blood PCO2 increases (or decreasing pH or PO2)
2) Detected by central chemo-receptors in the medulla and peripheral chemoreceptors in aortic and carotid bodies
3) Send input via nerve impulses to inspiratory area in medualla oblongata
4) Send output via nerve impulses to effectors the diaphragm and other muscles of respiration - these contract more forcefully and more frequently (hyperventillation)
5) Decrease in arterial blood PCO2 and increase in pH and PO2
- feedbacks to chemoreceptors = return to homeostasi, shuts systemm down
Components of neural control (3)
- Factors that generate alternating inspiration/expiration rhythm
- Factors that regulate the magnitude of ventilation (rate and depth)
- Factors that modify resp. activity for other purposes - speech, cough, sneeze
Model of respiratory control during quiet breathing
- Sensory input from central chemoreceptors, peripheral chemoreceptors, pulmonary stretch receptors, irritant receptors, proprioreceptors as well as the pons and cortex (vouluntary control)
- Info goes to the medulla - inspiratory neurons of DRG and VRG
- Sends out info to effectors that dictate the breathing rhythm
Respiratory muscles and their inervation + how do nerves fire and for what purpose
1 Inspiration:
a) diaphragm - phrenic nerve
b) external intercostal muscle - external intercostal nerve
2. Expiration:
- internal intercostal - internal intercostal nerve
Fire in oscillating patterns (so get contraction and relaxation - producing inspiration and expiration respectively i.e. oscillating increase/decrease in tension and increase/decrease in volume)
Inspiration quiet breathing vs. active ventiallation
- Frequency of firing (both phrenic nerve and external intercostal nerve) increases during active ventillation
- causes inspiraotry muscle tension to increase
- and thereby increases lung volume
Expiration quiet breathing vs. active ventillation
- no firing of internal intercostal nerve during quiet, fires during active ventillation
- therefore no expiratory muscle tension in quiet and oscillating in active
- lung volume inscreased during active
Components that generate the breathing rhythm (2 control centers)
1) Respiratory control centers of medulla
2) Respiratory control centers of pons
Medullary respiratory neurons (rhythmicity center) - 2 groups of neurons + their function
1) The dorsal respiratory group (DRG)
2) the ventral respiratory group (VRG)
-2 groups are bilaterally paired
-cross communication between them
Both are responsible for initiation and regulation of breathing
Dorsal respiratory group (DRG) function
- inspiratory neurons
- discharge during inspiration & stop discharging during expiration
Ramp signal
- generated by the DRG
- a weak burst of APs that gradually increase in amplitude then ceases for the next 3 sec until a new cycle begins
- functions to initiate inspiration + provides a gradual increase in lung volume during inspiration
Ventral respiratory group (VRG) -when active
-activated during heavy breathing (i.e. exercise) due to increased activity of inspiratory neurons during these conditions
Role of activated VRG
- discharge signal that
i) inhibits inspiratory group
ii) stimulates muscles of expiration
Pontine respiratory centre components
- 2 pontine centres that modify the rate & pattern of respiration
a) apneustic centre
b) pneumotaxic centre
Apneustic centre location
- in the lower 1/3 of pons
- close to medullary groups
Apneustic centre function
- sends stimulatory discharge to inspiratory neurons (dorsal respiratory group i.e. vagus and glossopharyngeal, and ventral respi group) -promoting inspiration
- removal of its stimulatory effect = respiration becomes shallow and irregular
Pneumotaxic centre location
-upper 2/3 of pons
Pneumotaxic centre function
- major role = regulation of respiratory volume and rate
- controlling cessation of inspiratory ramp signal from DIG and can also switch off apneustic centre –> so that expiration occurs
Outcome of hypoactivation of pneumotaxic centre
-prolonged deep inspiration with limited brief expiration
Outcome of hyperactivation of pneumotaxic centre
-shallow inspiration
Central pattern generator function
-establishes respiratory cycle
Overall control of activity of respiratory centre
1) Involuntary (automatic) control
- chemoreceptor reflexes
- neurogenic reflexes
2) Voluntary control
Peripheral input to respiratory centers (5)
- chemoreceptors
- pulmonary stretch receptors (SARs)
- Irritant receptors (RARs)
- mechanoreceptors
- muscle and joint proprioreceptors
2 pathways chemical regulation of respiratory centre (chemoreceptor reflexes)
1) Central chemoreceptor pathway
2) Peripheral (arterial) chemoreceptor pathway
Stimulus for these two pathways
-these chemoreceptors sense changes in PaCO2, PaO2 and pH
Location of central chemosensitive area
Lying just beneath ventral surface of medulla
Central chemosensitive area - where do relay to?
Relay to respiratory centres in medulla and pons
What is the central chemosensitive area most sensitive too
-Changes in PaCO2, H+ conc but not to PaO2
Central chemosensitive area - importance
-under normal respiratory conditions 75-85% of respiratory drive is due to stimulation of central chemoreceptors by PaCO2
Central chemosenstive area - how does it work
-direct stimulant for neurons of central chemoreceptors = H+ ions
-H+ cannot cross BBB but CO2 can
-concentration of H+ depends on CO2 (CO2 +H2O –> HCO3- + H+)
So CO2 cross the barrier then becomes H+
-so central cehmosensive area is directly responsive to H+ and indirectly responsive to CO2 and not responsive to O2
Peripheral chemoreceptors types
-specialized cells in direct contact with arterial blood includes carotid bodies, (and aortic bodies??)
Peripheral chemoreceptors - what sensitive too
- respond to changes in PO2, or PH
- little through PCO2 directly
Effects of arterial O2 on ventillation
- not much of a change until P O2 < 60 mmHg
- at this level peripheral chemoreceptors are activated and ventilation increases
Effects of arterial CO2 on ventillation
- both central and peripheral chemoreceptors - but CO2 must be converted to H+ first (small direct effect of CO2 on peripheral chemorecceptors)
- as pCO2 increases above normal resting level (40 mm Hg) ventillation increases
Neurologenic reflexes (6)
1) Hering-Breuer inflation reflex
2) Hering-Breuer deflation reflex
3) J-receptor reflex
4) Cough and sneezing reflexes
5) Baroreceptor reflex
6) Other influences via hypothalamus
Hering-Breuer inflation reflex mechanism
- over-inflation of lungs = stimulation of slowly adapting stretch receptors in smooth muscles of large and small airways
- activation of afferent vagal signals
- inhibits medullary and pontine inspiratory network
- terminates inspiration
Hering-Breuer inflation reflex- in who is this important
Important in neonates
Hering-Breuer deflation reflex mechanism
- deep expiration
- deflation of lungs
- decrease activity of slowly adapting stretch receptors or stimulation of other proprioreceptors in respiratory muscle
- decreased afferent vagal signals to respiratory centres
- increase in the activity of inspiratory neurons
- increased rate of breathing
J-receptor reflex
1) Pulmonary emboli or oedema or congestion
2) Stimulation of juxtapulmonary-capillary receptors
3) Sends impulses along vagal afferent to respiratory centre
4) Causes rapid shallow breathing (these receptors are responsible for the sensation of air hunger i.e. dyspnea or shortness of breath)
Cough, sneezing reflexes (rapidly adapting reflexors) mechanism
1) Dust, smoking, irritant substance -stimulates irritant receptors in upper airways (nose, larynx, bronchi)
2) Send afferent signals via vagus (larynx, cough) or trigeminal (nose, sneezing) which go to respiratory centre and cause deep inspiration followed by forced expiration against closed glottis
3) This opens glottis leading to forceful outlfow of air (to help remove irritants)
Other influences from higher centers (hypothalamus and limbic system) + what they do to respiratory rate
1) temperature - increases repiratory rate
2) pain -sudden - decreases respiraotry rate, prolonged - increases respiratory rate
3) alcohol - decreases rate
4) exercise - increases rate (through higher cortical centers)
Voluntary control of breathing - how
- through descending tracts from cerebral cortex to motor neurons of respiraotry muscles (dorsolateral corticospinal tracts)
- provide CNS the ability ot override the automatic regulation of respiration for a short time
ex: holding breath or deliberate hyperventillation - over time involuntary will take over
Adaptions to emphysema
- causes chronic hypercapnia and hypoxemia
- central chemoreceptors adapt to elevated PCO2 such that most chemical stimulus to breathe comes from low PO2
