Breathlessness and control of breathing (awake) Flashcards
What are the main functions of the respiratory muscles?
- Maintaining arterial PO2, PCO2 and pH -
- Defence of airways and lungs when coughing etc
- Exercise
- Speech
- Sing, blow
- Expressing emotions
- Control of intrathoracic and infra-abdominal pressures e.g. defecation, belching, vomiting
How does arterial PO2 differ in neonates/elderly and during the years in between?
It is lower in neonates/elderly
What are the two main voluntary and involuntary controls of breathing and which is more important?
Involuntary or metabolic centre = medulla (bulbo-pontine region)
Voluntary or behavioural centre = motor area of cerebral cortex
Metabolic will always override behavioural
What can influence the metabolic centre?
There are other parts of the cortex that are not under voluntary control and have an influence on the metabolic centre such as emotional responses. The limbic system and sensory inputs may influence the metabolic centre.
Sleep via the reticular formation (set of interconnected nuclei in the brain stem) also influences the metabolic centre.
What is the main driver of breathing and what happens to breathing when we dream?
The main driver of breathing is the diaphragm
Breathing becomes quite disorganised when we’re dreaming
What happens to the behavioural controller site when taking deep breaths (voluntarily)?
PET scans show that its becomes more active when you voluntarily take deep breaths.
The control of breathing - how is H+ conc detected and how is breathing organised?
- There are on and off switches for the phrenic nerves in the cervical region of the upper spinal cord - this activates the muscles that will move the chest wall and, hence, the lungs.
- Information from the respiratory muscles and the lungs is fed back to the metabolic controller.
- Chemoreceptors in the carotid bodies in the neck sense the hydrogen ion levels in the blood.
- The metabolic controller also has hydrogen ion receptors.
- The metabolic controller activates the upper airway muscles in the neck to dilate the pharynx and the larynx on inspiration and narrow them on expiration.
The peripheral chemoreceptor
- The carotid body chemoreceptor is a well vascularised bundle of cells at the junction of the internal and external carotid arteries.
- It tastes arterial blood
- It is a rapid response system for detecting changes in arterial pCO2 and pO2
Pacemakers in breathing
- Breathing has many pacemakers that are close together in the brain stem and are inaccessible
- The group pacemaker activity of breathing comes from around 10 groups of neurons in the medulla near the nuclei of cranial nerves IX and X
Give an example of a group pacemaker
Location?
How is it coordinated?
- The pre-Botzinger complex (found in the ventro-cranial medulla near the 4th ventricle) seems essential for generating the respiratory rhythm and is called the ‘gasping centre’
- Coordination of the pre-Botzinger complex with the other controllers may be needed to convert gasping into an orderly and responsive respiratory rhythm.
How many groups of neurons in the medulla and brain stem are important in tidal breath generation/
Six groups of neurons in the medulla and brain stem have distinct functions in the generation of a tidal breath - they discharge at different phases of the respiratory cycle
What are the 6 groups of neurones controlling the phases of the respiratory cycle?
- Early inspiratory initiates inspiratory flow via the respiratory muscles
- Inspiratory augmenting may also dilate pharynx, larynx and airways
- Late inspiratory may signal the end of inspiration, and ‘brake’ the start of expiration
- Expiratory decrementing may ‘brake’ passive expiration by adducting the larynx and pharynx
- Expiratory augmenting may activate expiratory muscles when ventilation increases on exercise
- Late expiratory may sign the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration
What is the importance of the laryngeal and pharyngeal muscles?
In opening up the airways or acting as a ‘brake’ in breathing
A lack of tone in the pharyngeal muscles may play a part in the breathing that occurs at night - obstructive sleep apnoea syndrome
Reflex control of breathing and nerves involved
- 5th nerve: afferents from nose and face (irritant)
- 9th nerve: from pharynx and larynx (irritant)
- 10th nerve: from bronchi and bronchioles (irritant and stretch)
What do irritant receptors do?
They make you cough and sneeze
Hering Breuer Reflex (most well known reflex in lung)
Hering-Breuer reflex from pulmonary stretch receptors senses lengthening and shortening and terminates inspiration and expiration, but weak in humans
What are the two parts of the metabolic controller?
Central part in the medulla responding to the hydrogen ion concentration in the extracellular fluid
Peripheral part at the carotid bifurcation (carotid sinus) - there are hydrogen ion receptors here as well
What are slow and fast responses?
The change in H+ reflecting changes in PCO2 occur very rapidly in the hyperperfused carotid bodies but more slowly in the ECF bathing medulla - so fast and slow responses exist.
Metabolic acidosis
what is it, causes and compensatory mechanisms?
Excess production of H+
Causes: diabetic ketoacidosis, salicylate overdose, renal tubular defects
Compensatory mechanisms:
Ventilatory stimulation to lower PaCO2 and H+,
renal excretion of weak acids (lactate and keto), renal retention of chloride to reduce strong ion difference
Metabolic alkalosis
what is it, causes and compensatory mechanisms?
Loss of H+ leads to excess HCO3–
Causes: vomiting, diuretics, dehydration
Compensatory mechanisms:
Hypoventilation raises PaCO2 and H+, renal retention of weak acids and renal excretion of chloride to increase strong ion difference
Respiratory acidosis: acute and chronic
The lung fails to excrete the CO2 produced by metabolic processes
Acute: hypoventilation causes PaO2 ↓, PaCO2 and H+ ↑ which stimulates metabolic centre (and carotid body) to increase minute ventilation and restore blood gas and H+ levels.
If the lung cannot cope then:
Chronic: ventilatory compensation may be inadequate for PaCO2 homeostasis but
a) renal excretion of weak acids (lactate and keto)
b) renal retention of chloride to reduce strong ion difference
returns H+ to normal, even though PaCO2 remains high and PaO2 low.
Hypoventilation Conditions
Central - acute and chronic
Acute:
- Metabolic centre poisoning (anaesthetics, drugs)
Chronic:
- Vascular/ neoplastic disease of metabolic centre
- Congenital central hypoventilation syndrome
- Obesity hypoventilation syndrome (OHS)
- Chronic mountain sickness
Hypoventilation Conditions
Peripheral - acute and chronic
Acute:
- Muscle relaxant drugs
- Myasthenia gravis
Chronic:
- Neuromuscular with respiratory muscle weakness
Chronic obstructive pulmonary disease
Mixture of central (won’t breathe) and peripheral (cannot breathe)
Could be due to lung inefficiency and difficulty of the controller in raising ventilation sufficiently
Or could be due to the metabolic controller becoming insensitive and allowing higher PCO2
Respiratory alkalosis - mechanism and causes
also same as hyperventilation conditions
Mechanism: ventilation in excess of metabolic needs
Causes:
- Chronic hypoxaemia
- Excess H+ (metabolic causes)
- Pulmonary vascular disease
- Chronic anxiety
What is breathelessness?
- It is hard to define and is a perception so is subjective
- Breathlessness at rest - implies difficulty with inspiration of expiration (e.g. due to acute bronchospasm of an asthma attack)
- Excessive breathlessness for the task (can be associated with many cardiac or respiratory diseases)
What is dyspnoea?
The medical term for breathlessness but with the connotation of discomfort or difficulty
What are the three types of breathlessness?
- tightness
- increased work and effort
- air hunger
Tightness (breathlessness)
Difficulty in inspiring due to airway narrowing; a feeling that the chest is not expanding normally
Increased work and effort (breathlessness)
Breathing at a high or normal minute ventilation but at a high lung volume, or against an inspiratory or expiratory resistance
In other words, breathing against an abnormal mechanical load or breathing a lot
Air hunger (breathlessness)
Sensation of a powerful urge to breathe
- May well occur in acute asthmatic attacks where you just can’t get enough air because you haven’t been able to exhale the previous breath.
- Air hunger is similar to suffocation
- It is a mismatch between V.E demand and V.E achieved
- Cerebral cortex compares two different inputs
Demand - a copy of signal sent by metabolic controller to spinal motor neurones
Afferents from lung, chest wall and chemoreceptors (carotid body) - output
Scales for measuring breathlessness during an exercise test
- Breathlessness can be scored on the 10-point Borg scale
- 10 is very severe and 1 is nothing
- Subjects score themselves during a task
Breath Holding Time (BHT) : what does it test and what is the breakpoint affected by?
- Tests the strength of behavioural versus metabolic controller
- Break point prolonged by increasing lung volume, lowering PaCO2 or by taking an isoxic/isocapnic breath near the break point
- Acute thoracic muscle paralysis with curare does not prolong BHT
What is tightly controlled by the body?
PaCO2 and H+
What does a fall in VE lead to?
fall in PaO2 and rise in PaCO2 -> fall in PaO2 raises sensitivity of carotid body to PaCO2 and H+ -> VE increases so PaO2 increases
Ventilatory responses to hypoxia are amplified by CO2 (the body system is much more sensitive to CO2)
What is the equation for VE?
VE = VT * 60/TTOT
VE = minute ventilation, volume exchanged in a minute TTOT = total time for respiratory cycle 60/TTOT = resp frequency per min
Equation for VE including TI
VE = VT/TI * TI/TTOT
This equation represents the gradient of inspiration multiplied by the proportion of time spent on inspiration.
VT/TI = Mean inspiratory flow – i.e. how powerfully the muscles contract
This is known as the neural drive.
What does TI/TTOT tell us?
Inspiratory duty cycle – the proportion of time spent actively ventilating.
What is normal VE and tidal volume and TI/TTOT
Normal VE = ~6Lmin-1
Normal Tidal Volume = 0.5L
Inspiratory duty cycle = 40%
What happens to minute ventilation parameters during experiments?
- Use of a nose clip reduces breathing rate while VE remains roughly the same but VT increases as breathing is deeper.
- Breathing through a tube increases dead space which increases VE, VT and frequency to clear dead space.
- The neural drive (VT/TI) also increases to satisfy more ventilation.
What happens to tidal breathing in diseases like Chronic Bronchitis, Emphysema and COPD?
- Intrathoracic airways are narrowed so difficulty ventilating lungs more on expiration.
- Lower TV as less air can fill the lungs but compensated by a faster breathing rate (equal TI/TTOT).
- People with COPD breathe much shallower and faster but not harder.
