9. Breathlessness and Control of Breathing - Awake Flashcards
What are the functions of the respiratory muscles?
- Maintenance of arterial PO2, PCO2 and pH (most important)
- Defence of airways and lungs
- Exercise
- Speech
- Blow
- Control of intrathoracic and infra-abdominal pressures
How do you calculate frequency in a volume-graph?
- 1/TTOT (duration of a single respiratory cycle)
* 60/TTOT - frequency per minute
What is the average TTOT and respiratory rate?
- TTOT - 4 seconds
* Respiratory rate - 15 breaths/min
What is V.E and how is it calculated?
- Minute ventilation - volume of gas inhaled or exhaled during one minute
- VT x 60/TTOT (tidal volume x frequency)
What can TTOT (duration of a single cycle) be split into?
- Inspiratory (TI)
- Expiratory (TE)
(both durations)
What is the mean inspiratory flow and how do you calculate it?
- How powerfully the muscles contract
- Neural drive
- VT/TI (tidal volume/inspiratory TTOT)
What is the inspiratory duty cycle and how do you calculate it?
- Proportion of the cycle spent actively ventilating (inspiring)
- Normally close to 40%
- TI/TTOT
What happens to the mean inspiratory flow, TTOT and frequency if metabolic demands increase?
- Mean inspiratory flow (VT/TI) - increases
- TTOT (duration) - decreases
- Increased frequency
What happens to the neural drive if more impulses are sent down the phrenic nerve to the diaphragm?
• Increases
- diaphragm contracts more frequently and stronger
What is the normal tidal volume?
0.5L
What changes occur when you wear a noseclip?
• Deeper breathing - VT increases • Slower breathing - decreased frequency • Ventilation remains around the same
What changes occur when you breath through a tube?
• Extra dead space
- increased VT
- increased V.E
- increased frequency
- increased neural drive (VT/TI)
- unaltered inspiratory duty cycle (TI/TTOT)
How does breathing change in chronic bronchitis and emphysema (i.e. COPD)?
• Intrathoracic airways are narrowed
- difficulty ventilating (worse for EXPIRING)
• Proportion of time for expiration (downward gradient) doesn’t change
• Higher residual volume
- increased stiffness and work required
• Shallower and faster breathing - shorter TTOT
(bronchitis has a shorter TTOT than emphysema)
• Don’t breathe any harder (VT/TI roughly the same)
- neural drive is still increased
• Diaphragm needs to work harder
- hyperinflation shortens diaphragm fibres - less efficient
How does exercising change the breathing values (in COPD)?
• Increase in neural drive (VT/TI)
- Frequency doubles
• Inspiratory duty cycle (TI/TTOT) decreases to give more time for expiration (normally increases to give more time for inspiration)
How does the CNS control breathing?
- Involuntary/metabolic centre - medulla
- Voluntary/behavioural centre - motor area of cerebral cortex
- Metabolic always overrides behabioural
- Other parts of the cortex (involuntarily) control the metabolic centre e.g. emotion
- Sleep influences the metabolic centre via the reticular formation
- Behavioural - breath holding and singing
What happens to the metabolic centre in sleep?
- Reset
- PCO2 rises a little bit
- Breathing becomes disorganised when dreaming
How does the limbic system, frontal cortex and sensory input influence the metabolic centre?
- Limbic system - survival responses
- Frontal cortex - emotions
- Sensory inputs - pain, startle
- all alter breathing
Where is the metabolic and behavioural centre located?
- Metabolic centre - bulbo-pontine region
* Behavioural centre - components scattered throughout the mid and upper parts of the brain
What changes occur in the behavioural centres when you voluntarily breath deeply?
- More active
- Can be seen using PET scans
- Site responsible for behavioural control of breathing is small
How does the metabolic controller H+ receptor work?
- Hydrogen ion receptor -detects [H+] in extracellular fluid
- Phrenic nerves switched on and off (in cervical region of the upper spinal cord)
- Respiratory muscles activated
- TI and TE affected
- Information from respiratory muscles and lungs feed back to metabolic controller (using stretch receptors)
Whats the most important feedback to the metabolic controller in breathing?
- Chemoreceptors (in carotid bodies) sensing H+ levels
- Metabolic controller has H+ receptors itself
(essentially pH)
How would the response to CO2 change if the carotid bodies were removed?
Acute response to CO2 reduced by 40%
What effect does the metabolic controller have on the upper airways?
- Dilate the pharynx and larynx on inspiration - reducing resistance
- Narrow them on expiration - brake => smooth flow
What is breathing like in non-REM sleep?
Normal
What is the carotid body and how does it work?
- Chemoreceptor
- Well vascularised bundle of cells
- At the junction of the internal and external carotid arteries
- Transmits a signal to the lower brain via the glossopharyngeal nerve
- Hypoxia amplifies the response to hydrogen ions
(PCO2 receptors in airways of birds’ lungs, CO2 and H+ receptors at origin of aorta in other animals)
Where is the pacemaker activity of the lungs located?
- Many pacemakers
- Close together in the brain stem
- Inaccessible
- 10 groups of neurones in the medulla, near the nuclei of cranial nerves IX and X (GP and vagus)
What is the pre-Botzinger complex and how does it work?
- One group of pacemaker activity
- Essential for generating respiratory rhythm
- ‘Gasping centre’ - gasping under low levels of oxygen
- Rare to find disease
What are the 6 groups of neurones in the brain stem involved in the generation of tidal breath?
- Early inspiratory - initiates inspiratory flow via the respiratory muscles
- Inspiratory augmenting - dilates pharynx, larynx and airways
- Late inspiratory - signals end of inspiration & brakes the start of expiration
- Expiratory decrementing - may brake passive expiration (adducting the larynx and pharynx)
- Expiratory augmenting - activate expiratory muscles when ventilation increases
- Late expiratory - sign end of expiration and onset of inspiration, may dilate the pharynx
(all discharge at different phases of the respiratory cycle)
What muscles are used to open and close the airways?
- Pharyngeal and laryngeal muscles
* Also act as a brake in breathing
What is obstructive sleep apnoea?
- Pharyngeal muscles lose tone (relax)
- Airway is blocked
- Snoring or stopped breathing
What are cranial nerves V, IX and X involved in?
• V - afferents from nose and face (irritant)
• IX - from pharynx and larynx (irritant)
• X - from bronchi and bronchioles (irritant and stretch)
- Hering-Breuer reflex: pulmonary stretch receptors => inhibit activity of the medullary inspiratory neurones => termination of inspiration/expiration
(all lead to coughing and sneezing - defensive)
What are the 2 parts of the metabolic controller?
- Central part in medulla
* Peripheral part in carotid bifurcation
What does a change in H+ reflect and how is it detected differently in the 2 parts of the metabolic controller?
- H+ changes mirror PCO2 changes
- Reflection of PCO2 changes occur slowly in ECF around medulla
- Reflection of PCO2 changes occur rapidly in (hyperperfused) carotid bodies
How can the sensitivity of the metabolic centre be tested?
• Carbon dioxide challenge
- ventilation is measured against changes in arterial PCO2
• Induced by patient breathing in and out of a 6L bag of oxygen primed with 7% CO2
• PCO2 rises 1 kPa per minute
• 30L/min rise in minute ventilation
Describe a minute ventilation-arterial PCO2 graph (with reference to changes during hypoxia, chronic metabolic acidosis and chronic metabolic alkalosis)
- Normal breathing (normoxia) - positive linear graph
- Hypoxia - increased gradient
- Acidosis - increased gradient + shift left
- Alkalosis - decreased gradient
What happens to ventilation when arterial PCO2 is goes below 5.3 kPa?
- Ventilation reaches a minimum limit - not 0, when awake
* Drops to 0 when sleeping - breathing only starts when PCO2 is above apnoeic point
How does a depressed ventilatory response to PCO2 change the ventilation-PCO2 graph?
- Flattened slope (decreased sensitivity)
- Rise in the set point (resting arterial PCO2)
(same changes in COPD due to mechanical limitation or airflow obstruction)
What can cause a depressed ventilatory response to PCO2?
- Disease affecting the metabolic centre
- Sedative drugs suppressing the metabolic centre
- Respiratory muscle weakness (peripheral)
What happens during hypoxia (alveolar PO2/arterial SaO2 - minute ventilation)
- Lower alveolar PO2 (high-altitude)
- Higher minute ventilation to counter this
- Graph shows this at fixed levels of PACO2 - higher PACO2, graph is further right and higher
- Minute ventilation decreases at a decreasing rate with increasing alveolar PO2
- Minute ventilation is higher at a lower arterial SaO2
- 30L/min increase in minute ventilation for a 7kPa decrease in PaO2 (SaO2 99% => 60%)
(system is more sensitive to PCO2)
What does ‘not isocapnic’ mean?
- PaCO2 not controlled
- Allowed to fall during hypoxic hyperventilation
- Reduces the stimulus
- Reduces the ventilatory response
What happens when there is a fall in ventilation (in relation to PaO2 and PaCO2)?
- Fall in PaO2
- Rise in PaCO2
- Fall in PaO2 increases sensitivity of carotid body to PaCO2 and H+
- Ventilation increases - PaO2 increases
- PaCO2 falls (negative feedback)
Which gas values are controlled more in breathing?
- PaCO2 and H+ controlled more tightly than PaO2
* arterial SaO2 better defended than arterial PaO2
Why are control systems not well equipped for a fall in PO2 caused by altitude?
- Hypoxic hyperventilation at a higher altitude => lower PCO2
- Inhibited ventilatory response
- Several days of acclimatisation required
What is the difference between PO2, PAO2, PaO2 and SaO2?
- PO2 - partial pressure of O2 in a given environment
- PAO2 - partial pressure of O2 in alveoli
- PaO2 - partial pressure of O2 dissolved in (arterial) blood
- SaO2 - amount of oxygen bound to haemoglobin in arterial blood (saturation)
What is metabolic acidosis and what causes it?
• Source of excess hydrogen ions comes from metabolism
• Not from inadequate ventilation
• Causes:
- diabetic ketoacidosis (lack of glucose in cells, starts to metabolise fatty acids)
- salicylate (aspirin) overdose
- renal tubular defects
What are the compensatory mechanisms for metabolic acidosis?
- Ventilatory stimulation lowers PaCO2 and H+
- Renal excretion of weak (lactate and keto) acids
- Renal retention of chloride (reduce strong ion difference)
What is respiratory acidosis and what is the response?
- Fall in ventilation
- Rise in PCO2 and H+
- Rapid response - stimulates the metabolic controller to increase breathing and return the system to normal
- Slow response - renal excretion and retention of weak acids (back up response if the lungs can’t compensate)
What determines the hydrogen ion concentration of the blood?
- PCO2:bicarbonate ratio
- PCO2 controlled by the lungs
- Bicarbonate controlled by the kidneys (and lungs)
What is metabolic alkalosis and what is the response?
• Loss of H+ leads to excess HCO3- • Causes: - vomiting - diuretics - dehydration
- Hypoventilation - raises PaCO2 and H+
- Renal retention of weak acids
- Renal excretion of chloride to increase strong ion difference
What can lead to central (acute and chronic) hypoventilation?
Acute
• metabolic centre poisoning (drugs)
Chronic
• vascular/neoplastic disease of metabolic centre
• congenital central hypoventilation syndrome
• obesity hypoventilation syndrome
• chronic mountain sickness
What leads to peripheral (acute and chronic) hypoventilation?
Acute • muscle relaxant drugs • Myasthenia gravis Chronic • Neuromuscular with respiratory muscle weakness
What are the hypoventilation conditions like in COPD?
- Mix of central (won’t breathe) and peripheral (cannot breathe)
- Could be due to difficulty of the controller in raising ventilation sufficiently or lung inefficiency
- Or, could be due to the metabolic controller becoming insensitive - allowing higher PCO2
What can hyperventilation be caused by?
- Chronic Hypoxaemia
- Excess H+ (metabolic)
- Pulmonary Vascular Disease
- Chronic Anxiety (psychogenic)
What is breathlessness (rest vs. exercise)?
- Like dyspnoea
- At rest - difficulty with inspiration or expiration
- On exercise - excessive breathing for the task
What are the 3 types of breathlessness?
- Tightness - difficulty inspiring
- Increased Work and Effort - breathing at a high lung volume or against a resistance
- Air hunger - sensation of a powerful urge to breath, mismatch between V.E demand and achieved
How does the cerebral cortex compare V.E demand and V.E achieved?
- Demand - efferent signal sent by metabolic controller to spinal motor neurones
- Achieved - afferents from lung, chest wall and chemoreceptors
How can breathlessness be scored?
10-point Borg Scale
How can you test the strength of behavioural versus metabolic controller?
- Breath holding time
- Break point - expression of air hunger
- Prolonged by increasing lung volume, lowering PaCO2 or isoxic/isocapnic breath near the break point
- Acute thoracic muscle paralysis with Curare (poison) does not prolong it
- BHT - stretch receptor drive x metabolic drive
