Control of breathing Flashcards
Central control of breathing: explain the central organisation of breathing, and recall the principle inputs and outputs, including sensitivity to carbon dioxide and hypoxia Sleep: explain the effect of sleep on breathing and blood gases; explain the apnoeic threshold and how this may lead to central sleep apnoea; explain the influences of sleep on the upper airway and how this may lead to obstructive sleep apnoea; explain how cardiorespiratory disease may be exacerbated by changes in breathing
What are the functions of the respiratory muscles? (x5)
- Maintenance of arterial PO2, PCO2 and pH – pH most important. NON-VOLUNTARY. 2. Defence of airways and lung through sneeze, cough, yawn. 3. Fight or flight. 4. Speech, blow, cry… THIS AND THE REST IS VOLUNTARY. 5. Control of intrathoracic and intra-abdominal pressures e.g. defecation, vomiting.
How is a tidal breath drawn and annotated on a graph?
Photo graphs a typical breath. Honestly don’t think this is necessary!
VT = tidal volume. TTOT = duration of breath. 1/TToT = number of breaths per second – it is a measure of respiratory frequency. 60/TTOT = number of breaths per minute. VE (minute ventilation) = VT x frequency: measure of volume in exhalation as a product of tidal volume and frequency. We measure exhalation usually for convenience.
TI = time spent on inspiration. TE = time on expiration. VT/TI (volume over time) = mean respiratory flow – describes inspiration i.e. how rapidly and strongly the diaphragm – in particular – is contracting. We can re-express VE by giving an actual formula for frequency: VE = VT x 60/TTOT. Multiply both sides by TI/TI, then you get: VE (minute ventilation) = VT/TI (mean inspiratory flow) x TI/TTOT (proportion of the breath you spend inspiring).
What happens to TI/TTOT with a healthy and diseased individual?
Stays the same always – because it is a measure of the proportion of the breath spent inspiring.
What happens to the annotated values during exercise?
Increased metabolic demand, so there’s increased mean inspiratory flow (VT/TI) and VE. TI/TTT does not change.
What regions of the CNS control breathing? (x2 – 3 parts of the voluntary control)
INVOLUNTARY: metabolic centre in the brainstem. Responds to metabolic demands via autonomic control in response to pH levels. VOLUNTARY: behavioural centre in the motor area of the cerebral cortex controls holding breath and singing; limbic system controls emotional responses and the frontal cortex (?) controls survival responses (e.g. suffocation) – both can influence the metabolic centre. Metabolic will always override behavioural.
What are the two parts of the metabolic centre?
MEDULLA (muscles): primary respiratory control centre with a ventral respiratory group that stimulates expiration (innervates accessory muscles), and a dorsal respiratory group to stimulate inspiration (innervates diaphragm and external intercostal muscles).
PONS (VT): other respiratory centre located above the medulla that controls RATE of breathing – stimulates long, deep breathing (larger tidal volume), and can inhibit inspiration by limiting phrenic nerve activity to lower tidal volume.
What inputs does the metabolic centre receive? (x3)
INPUTS: Sensory receptors that transduce chemical signals to action potentials; respiratory chemoreceptors sense pH of environment because most CO2 converted to carbonic acid so pH proportional to CO2. 1. Metabolic controller H+ receptor on the medulla, which detects H+ in the extracellular fluid surrounding the metabolic centre – uses H+ because it is in very close equilibrium with CO2 (so when CO2 levels drop in expiration, H+ rapidly responds). 2. Carotid bodies – called peripheral chemoreceptors. Found in the junction of internal and external carotid arteries, supplied by the glossopharyngeal nerve and well vascularised to detect changes in arterial pH, PCO2 AND PO2 – rapid response system. Input into the metabolic centre with its H+ receptor. H+ responds more slowly in the ECF bathing the medulla; thus, fast and slow responses exist. 3. Aortic chemoreceptors – detect oxygen and CO2 – not pH.
What is the effect of PaCO2 on minute ventilation?
Increasing PaCO2 leads to increased minute rate = breathing rate and/or tidal volume.
What responses are delivered by the metabolic centre? (x2)
INPUTS LEAD TO: certain impulse frequencies to respiratory spinal motor neurones, and then the phrenic nerve which drives the diaphragm. Upper airway muscles are also stimulated: dilated on inspiration and narrowed on expiration to ensure SMOOTH AIR FLOW.
What feedback mechanisms act on the metabolic centre? (x3)
FEEDBACK CONTROL: lung has stretch receptors, respiratory muscles have muscle spindle, and blood receptors have chemoreceptors that signal back to the metabolic controller, leading to alteration of timing of control of breathing – if not constricted, expiration would result in sudden outwards air movement because expiration is a passive process.
What are the neural afferents involved in reflex actions of the respiratory system? (x3)
CNV: afferents from nose and face respond to irritants. CNIX: from pharynx and larynx respond to irritants. CNX: from bronchi and bronchioles responds to irritants and stretch (called the Hering-Breuer reflex – responds to pulmonary stretch receptors which sense lengthening and shortening to prevent overexpansion. Uses Vagus nerve and sends signals to the Pons). LEAD TO COUGHING, SNEEZINING… NB: there is no nervous control of the peripheries – alveoli.
What does the metabolic centre also respond to in the blood? (x2)
Acidosis and hypoxia (not enough oxygen).
What is sleep apnea and why does it occur?
When CO2 is low, you will stop breathing in sleep, causing CO2 to rise again and start breathing – does not happen when awake.
What is the nature of oxygen sensitivity on the metabolic centre?
Metabolic centre not as sensitive to oxygen as H+ (i.e. CO2). However, increased levels of PCO2 means that the metabolic centre is more sensitive to small changes in PO2. Only the carotid bodies are sensitive to oxygen.
How does feedback control of PCO2 on the metabolic centre work?
A fall in ventilation causes a fall in PaO2, and a rise in PaCO2. The fall in O2 increases sensitivity and signals from the carotid bodies from (PaCO2 and) H+, so ventilation and PaO2 increases and PaCO2 falls by negative feedback.
How does an EEG differ at sleep and awake?
Neurons fire at same time to produce high voltage, low frequency waves in sleep (delta activity), whereas when awake, neurons fire more RANDOMLY, so they are low voltage and high frequency.
What region of the motor cortex exercises voluntary control over breathing when awake?
The motor cortex – between the region that supplies the shoulder and trunk.
What neural pathways are used in voluntary and automatic breathing?
VOLUNTARY: uses the corticospinal pathway (from the motor cortex). Corticospinal tract – from motor cortex. AUTOMATIC: uses the bulbospinal pathway (from respiratory neurones in brainstem). Bulbospinal pathway – fibres emerge from the brainstem.
What happens to oxygen saturation in sleep?
Minute ventilation and tidal volume decrease, so PaO2 decreases, but does not lead to meaningful decrease in oxygen saturation because it changes on the flat region of the oxygen dissociation curve – look at photo.
What happens to oxygen saturation when sleeping if you have a cardiorespiratory disease?
Cardiorespiratory disease may be exacerbated by changes in breathing control during sleep. If you have respiratory disease and a lower baseline PaO2 as a result, then you will have a much larger decrease in sats for same decrease in PaO2, which results in NOCTURNAL RESPIRATORY FAILURE!
What is the pathophysiology of obstructive sleep apnoea? (x1 factor for intraluminal and x2 factors for extraluminal)
When you breathe in, intraluminal pressure (inside the airway) gets more negative, which is what causes air movement from the atmosphere and into the lungs. When asleep, upper airway muscles go floppy, so the negative pressure that is generated downstream causes the upper airways to be sucked close when air is breathed in. Positive extraluminal (outside the airways) pressure such as fat around the neck and gravity also pushes the airway closed (shown as white in the image).
What is the symptomatic difference between central and obstructive sleep apnoea?
CENTRAL: airflow, thoracic and abdominal effort stops when become apnoeic – no effort to breathe. OBSTRUCTIVE: airflow stops, but thoracic/abdominal effort does not stop, and instead REDUCES and becomes less frequent – effort to breath is present, but ineffective.
