Week 6: Control of Breathing Flashcards
What are the two types of respiratory centres in the medulla and what are they mainly used for?
Dorsal respiratory group (DRG) which is predominately concerned with inspiration and the ventral respiratory group (VRG) which is predominately concerned with active inspiration and expiration
How does DRG work?
- They produce an impulse from the medullar respiratory centre which sends a signal down the spinal cord
- This then goes to the phrenic and intercostal nerves
- Which innervate the diaphragm and intercostal muscles
- This causes an inspiration
- When the DRG then pauses (when it doesn’t fire), it will cause relaxation of the muscles causing a passive expiration
What are the DRG signals known as?
ramp signals
What are ramp signals
Firing of the signals from the DRG
- Their ability to be controlled and altered, that is you can increase the rate of the ramp signal (increasing lung volume more rapidly, controlling tidal volume [make the triangle taller]) and you can alter the termination point (used to control breathing frequency, [make the triangle longer])
- The combination of these two advantages means we only need 1 signal to control inspiration. Not one for tidal volume or one for frequency, the ramp signal allows us to control both with one signal
What controls the inherent respiratory rhythm of DRG?
Pre-Botzinger complex
What are the 3 areas of the VRG
- Caudal VRG
- peachy colour
- is home to expiratory neurons - Rostral VRG
- Blue area
- Mostly inspiratory neurons - Botzinger complex (not to be confused with the pre-botzinger complex)
- Pink area
- Mostly expiratory neurons
What is responsible for active inspiration and active expiration?
Ventral respiratory group (VRG)
What controls the ‘off’ switch for the DRG inspiratory ramp signal?
Pneumotaxic centre of the PONS
What prolongs the inspiratory ramp, increasing the tidal volume and decreasing breathing frequency?
Apneustic centre of the PONS
What is the function of the PONS
- Is concerned with the fine control of breathing and is known as the pontine respiratory group (PRG) which simply put, plays with the ramp signal put forward by the DRG
- Not essential for the generation of respiratory rhythm – fine control
What are the two groups that make up the PONS?
- Pneumotaxic centre
- Controls the ‘off’ switch for the DRG inspiratory ramp signal
- This will decrease tidal volume and increase breathing frequency
- ‘shortens the ramp’ - Apneustic centre
- This centre prolongs the inspiratory ramp, increasing the tidal volume and decreasing breathing frequency
- ‘The ramps get longer and higher’
What other 3 areas of the brain that the PONS acts as a relay station for?
- Cortical control (which provides you with voluntary control over breathing)
- Peripheral sensory information (temperature, odour etc.) which may affect breathing
- Visceral and cardiovascular inputs (pain, changes in blood pressure)
What provides you with voluntary control over breathing?
Cortical control
What happens when you hold your breath to the DRG and pre-botzinger complex
- When you want to hold your breath, you temporarily ignore the DRG and pre-botzinger group (you don’t turn it off) and instead act directly on the respiratory muscles motor neurons
What is odines curse?
- Now known as primary alveolar hypoventilation syndrome, this is a breathing disorder caused by a defect in the automatic respiratory control
have lost automic breathing but can breath on command easily
What are the two types of pulmonary stretch receptors?
- Slowly adapting stretch receptors (SARs)
- Are found predominately in the smooth muscle of the tracheobronchial tree (the airways)
- These are believed to detect the state of lung inflation
- They are a lung volume sensor - Rapidly adapting stretch receptors (RARs)
- Are located in the superficial mucosa layer
- Are much more sensitive to finer changes to tidal volume
- These also play a role in detection of lung compliance
- These are also weakly sensitive to CO2 (makes up 20% of their function, a minor role)
Describe the hering-breur reflex
- The inflation reflex turns off the inspiratory ramp (which limits lung inflation when lung volume gets too big)
- The deflation reflex triggers an inspiration when lung volume gets really low (preventing lung volume from getting excessively low)
What is the reflex that prevents the lungs from overinflating?
Herin-breur reflex
What gases/ions are the peripheral chemoreceptors sensitve to?
Directly by low arterial O2, high arterial H+ and weakly by CO2
What are the gases the central chemoreceptors are sensitive to?
High arterial CO2 indirectly via CSF H+
What are the sensors which detech change in H+ cerebral spinal fluid called?
TASK-2 and GPR4
How do the central chemoreceptors (TASK-2, GPR4 and RTN) work?
- high levels of CO2 increase cerebral spinal fluid levels of CO2, this increases CSF hydrogen ion concentration which will stimulate TASK-2, GPR4. THese signal the RTN neurons, these then take the information to the pre-botzinger complex of the brain, which signals signal the DRG to increase ventilation (dropping CO2 levels)
What is cheyne stokes respiration
- A Cheyne-stokes breathing pattern looks like increases, then decreases, then increases, and then a pause (hyperventilation, hypoventilation then an apnoea)
This is because the central chemoreceptors are playing catchup to the peripheral receptors as they are much faster.
What is owles point and what triggers it?
- It is at owles point that we begin to produce lactic acid, and so as a consequence we begin to breath more to get rid of some hydrogen ions (breathing to get rid of the acidosis)
Why do we go into anaerobic metabolism?
Because not supplying enough O2 to the mitochondria
Why is constant neural input required for normal breathing? How does this differ to the continuous beating of the heart? What impact may quadriplegia have on the constant neural input required for normal breathing?
To breath involuntarily
WE can choose to voluntarily control it through cortical control. Heart have own pacemaker cell.
C3 -C5 if affected around this will lose diaphragm ability. Lower than C5 will have weaker breathing, lose intercostal
Higher than C3 will need assisted ventilation
Compare and contrasta the functions of dorsal respiratory group and the ventral respiratory group of the medulla oblongata?
DRG - receive from pulmonary stretch receptors, passive expiration, constantly on
VRG - active breathing, only activated for increase respiratory demand –> matches metabolic demand, from chemoreceptors and higher brain command
What is meant by cortical control of breathing?
When you hold breath you ignore DRG and pre-botzinger complex and act directly on respiratory muscles motor neurons.
What happens if you hold your breath for too long?
Will ass out and DRG will take over inherent breathing
or CO2 will build up and have to breath
or decrease O2 will trigger breathing
Whichr receptors indirectly detect increase CO2 and indirectly CO2?
Indirectly via the central chemoreceptors and directly via peripheral chemoreceptors
CO2 concentration has a potent acute effect on controlling respiratory drive but only weak chronic effect after a few days of adaption. Why?
This isbecause increase CO2 in first day but after couple of days renal mechanisms have kicked in and buffered.
Rick hyperventilates for several minutes before diving into a swwimming pool. He sprint swims a short distance underwater and blacks out. Why?
Hyperventilating results in excess removal of CO2. It doesn’t increase O2 as Hb saturation already high.
High intensity swimming will decrease O2 and increase CO2. Due to hyperventilation, there will be an increased period of time before arterial Co2 increase is detected by chemoreceptors to stimulate ventilation.
Therefore, will have decrease O2 which will cause a blackout before he has the reflex to breath.
Do changes in the rate of ventilation have greater effect of O2 or CO2?
More effect on Co2 as Hb is usually close to complete saturation at 98% sat.
Are central or perihperal chemoreceptors more sensitve to arterial blood gas changes?
Central but peripheral respond more rapidly
Mr Dave had advanced COPD for 15 years. While hospitalised with respiratory infection, she goes into respiratory distress. Without thinking the nurse adminsters 100% O2 which causes him to stop breathing. Why?
uncontrolled O2 adminsteration –> hypercapnia
Chronic hypercapnia in a servere COPD patient causes CO2 chemorecptors to reset (triggering at higher levels CO2.) Therefore, hypercapnia is no longer the main trigger to breath. Hypoxia is the main trigger. With adminstering 100% brain thinks it has high O2 however cells are getting no O2.
The increase O2 will increase O2 to poorly ventilated alveoli –> decreases hypoxic pulmonary vasoconstriction and therefore lead to V’Q mismatch –> leads to decrease arterial O2 and increase CO2
How is increased ventilatory activity though to be initiated with exercise?
PaO2, PaCO2 and H+ show little change with exercise. Therefore once we cross anaerobic threshold will increase lactic acid and trigger increase breathing
Why are some cases that may lead to cheyne stokes breathing pattern?
Cardiac failure, preterm babies and high altitude
How does cheyne-stokes occur at high altitudes?
Decrease in arterial O2 –> hypoxia
hypoxia stimulates peripheral chemoreceptors and increase ventilation which triggers hyperventilation
Hyperventilation decrease Arterial Co2 which depresseses central chemoreceptors and results in hypoventilation.
