Control of breathing Flashcards
Describe central regulation of breathing
Controller
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Medullary Respiratory Center, which is comprised of:
- VRG/DRG: Ventral and Dorsal Respiratory Group.
- Pre-Botzinger Complex – The Pacemaker.
Central Regulation
The central pattern generator is located within the medulla.
It receives many sources of input, including:
- hypothalamus (limbic, related to emotion, triggers autonomic system response)
- pons
- cortex (voluntary control largely)
- chemoreceptors
- other reflexes
In turn, the central pattern generator outputs to either stimulate inspiration or expiration.
The CPG also sends signals to inspiratory and expiratory motor neuron pools.
- expiratory signal inhibits inspiratory motor neuron pool
Groups of nuclei include the dorsal respiratory group, which is associated with inspiration, and the ventral group, which is mixed with inspiratory and expiratory signalling. It is associated with the timing of the respiratory cycle.
Recall from [[Physiology B2 - Lecture 19]] there are multiple nuclei associated with stages of respiration, and fire at different frequencies:
- early inspiratory
- augmenting etc
- in hypoventilation: PAO2 decreases, while PCO2 increases
- the reverse occurs in hyperventilation
- minute ventilation increases PAO2 up to a point – oxygen cascade means that it saturates
- this is not the case with CO2: it will drop, and patient will pass out ^[e.g. anxiety, or compensating for acidosis]
List the sensors responsible for detecting changes in CO2, O2 and pH
- central chemoreceptors
- peripheral chemoreceptors
- ## mechanoreceptors
Describe cenral chemoreceptors
Central Chemoreceptors
- located within the medulla
- as they are CNS structures, they are enveloped by meninges
- in other words, there is a blood-brain barrier
- H+ cannot diffuse across
- CO2 can
- it reacts with water to form H2CO3, which dissociates to form HCO3- and H+
- H+ then interacts with chemoreceptors
- if there is high pCO2 in the blood, more H+ is detected, which increases firing and stimulates the CPG to increase respiratory rate
Note: the chemoreceptors have a low tolerance to pH changes in CSF. It is buffered bicarbonate shift to normalise pH and reset chemoreceptor sensitivity.
Note 2: mechanism of bicarbonate shift debated
Note 3: ventilation changes with PaCO2 - reflects differing sensitivities of chemoreceptors.
If left shifted, the threshold is changed. Earlier response, steeper slope. Fast respiratory rate.
When right shifted, slower response, and less steep slope.
Slower respiratory rate.
Note that PaCO2 increases with minute ventilation.
Hypoxaemia produces a steep slope.
High PaO2, decreases response to CO2
True or false: paCO2 increases with minute ventilation
FALSE: The higher the minute ventilation, the more exchange and loss of PCO2 will occur inversely.
Describe peripheral chemoreceptors
- responds to more i.e. H+, CO2, O2
- note: it responds to dissolved O2 NOT O2-Hb
- peripheral chemoreceptors are the first to respond to pCO2 changes, although central chemoreceptors do most of the heavy lifting (80%)
- peripheral chemoreceptors are heavily perfused, which means changes to cardiac output affect detection
- three cells present at peripheral chemoreceptors
- type I Glmous cells: have oxygen sensitive potassium channels, which close if pO2 decreases, thus increasing pCO2 sensitivity
- CO2 sensitivity increased by hypoxia < 60mmHg
- type II: maintain homeostasis
- type I Glmous cells: have oxygen sensitive potassium channels, which close if pO2 decreases, thus increasing pCO2 sensitivity
Note: peripheral chemoreceptors are sensitive to acid. Decreasing pH increases minute ventilation and vice versa.
Describe the role of pulmonary mechanoreceptors
Pulmonary Mechanoreceptors:
- Essentially stretch receptors in trachea and bronchi
- Inflation reflex, most present in neonates, prevents overinflation/overdistension and increases desire to breathe out
- Hering-Breuer reflex aka
What is the effect of opioids on respiration?
Note also the effect of opioids, which act via δ and μ receptors on pontine and CPG respectively to induce respiratory depression.
Describe the various effectors of respiration
- Diaphragm via Phrenic nerve (C3, C4, C5)
- External intercostals (bucket handle movement) via Intercostal nerves
- Accessory muscles: SCM and trapezius via Accessory nerve (CN 11) - recruited e.g. in asthma
- Expiration is passive at rest, but internal intercostals and abdominals are recruited for active expiration
- not always passive at tidal breathing e.g. some postures
Describe the effect of exercise on breathing, CO2 and O2
- CO2 does not change significantly, except at peak activity with a bit of hyperventilation, despite augmented metabolic conditions, and changes to respiratory rate
- O2 is also maintained
- Thought to be a mix:
- cortical control
- SNS activation
- muscle stretch and mechanoreceptors
All of these increase minute ventilation
Note: what does change is oxygen uptake, and venous oxygen content as a result.
Note 2: in heart disease, no VQ match- results in deadspace.
Describe the effects of altitude on breathing, CO2 and O2
- Everest: 8848m
- Atmospheric pressure: 33% of sea level (pO2 54 vs. 160 mmHg)
- Alveolar pCO2: 7 vs. 35
- Alveolar pO2: 35 vs. 100 - low even with compensation
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Acclimatization:
- Hb 15 g/dl
- EPO increased
- Hyperventilation and decreased CO2
- Acute alkalosis (pH 7.7)
- 2,3 DPG increased
- Peripheral chemoreceptors active
- Central chemoreceptors CO2 sensitivity increased
- O2-Hb Dissociation Curve shifts
- But, takes days to weeks
Side note on COPD:
- severe, always hypoxic - set point changed: supplementing with 100% o2 reduces drive and results in paradoxic hypoxia: so saturate with normal O2 (for patient)
- chemoreceptors are desensitised i.e. pick up at higher pCO2
- peripheral receptors are key drivers
Describe OSA
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Obstructive Sleep Apnea:
- e.g. to age, enlarged tonsils, obesity
- loss of muscle control of soft palate, tongue, pharyngeal dilator muscles
- falls into oropharynx to occlude breathing
- chemoreceptors shift at point in order to tolerate high pCO2 resulting in a loss of both voluntary and involuntary control, apnoea
n.b. respiratory paradox: chest is sucked in, abdomen out
Describe some other respiratory conditions
- Central Sleep Apnea: completely different, related to diaphragm ^[innervate to treat]
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Sudden Infant Death Syndrome (SIDS): Disorder of homeostasis where infants with brainstem abnormalities struggle with metabolic challenges during sleep.
- cant adjust to or defend against asphyxia or other challenges
- Ondine’s Curse: cannot breathe involuntarily but CAN voluntarily. Must be ventilated
- Cheyne-Stokes Respiration: cycles of erratic breathing and apnoea. Opioids can create this
- Kussmaul Breathing: i.e. in DKA, ketones results in acidosis. Patient compensates with hyperventilation. Rapid AND deep breathing. Minute ventilation is very high, and bicarbs low ^[mixed disorder]
