Resp 8 - Breathlessness and control of breathing Flashcards
Is tidal expiration an active or passive process?
Passive - due to the natural recoil of the lungs
State the equation for minute ventilation (VE)
VE = VT x Frequency Frequency = 60/TTOT (if you want it per minute) or 1/TTOT for frequency TTOT = duration of one inspiration VT = tidal volume
How can this equation be manipulated to include TI?
VE = VT/TI x TI/TTOT TI is the Inspiratory time TE is the expiratory time TTOT = TE + TI VT/TI mean inspiratory flow
What does VT/TI represent?
Neural Drive - mean inspiratory flow (volume over time gives flow)
How powerfully the muscles contract. It is the slope of the upstroke.
What does TI/TTOT represent?
Inspiratory Duty Cycle
Proportion of the cycle spent actively ventilating (i.e. breathing in)
How do these factors change when there is an increase in metabolic demand?
Increased metabolic demand —> increased ventilation
VT/TI = INCREASE
TTOT = DECREASE (increase frequency)
TTOT is decreased by a combination of reduction in TI and TE
What is the normal tidal volume, normal minute ventilation, breathing rate, TI/TTOT?
Tidal Volume = 0.5 L
Minute Ventilation = 6 L/min
Breathing Rate = 12 breaths per minute
TI/TTOT = 40%
What changes take place if you use a noseclip?
Breathe more DEEPLY - increase in VT
Breathe SLOWER - decrease in frequency
Ventilation remains the SAME
What changes take place when artificial dead space is added?
Compared to with mouthpiece only: Minute ventilation = INCREASE VT = INCREASE Frequency = INCREASE VT/TI (neural drive)= INCREASE - to satisfy need for more ventilation TI/TOTT UNALTERED
How is the breathing of someone with COPD different to a normal person?
Breathing is SHALLOWER and FASTER
Difficulty more on expiration
Neural drive is the same - do not breathe harder
What changes when we exercise?
Increases neural drive and hence ventilation Increases frequency (halving TTOT)
Where is the voluntary and involuntary control of breathing located?
Voluntary = Cerebral Cortex Involuntary = Medulla
How is the metabolic controller reset in sleep?
PCO2 rises
Where, in the motor homunculus, is behavioural control of breathing located?
Between the hip and the trunk
Which receptors are involved in regulating the involuntary control of breathing?
HYDROGEN ION RECEPTORS found in the carotid bodies and in the metabolic centre itself
Where are the peripheral chemoreceptors located?
Carotid bodies (at the junction of the internal and external carotids, supplied by pharyngeal nerve)
Where are the pacemakers for respiratory breathing located?
Many pacemakers close together in the brain stem. Inaccessible.
10 groups of neurons in medulla
What is the main group of neurons that are involved in generating respiratory rhythm?
The pre-Botzinger complex situated near 4th ventricle
called the ‘gasping centre’
Describe the Hering-breuer reflex. Which nerve is involved?
10th nerve
Pulmonary stretch receptors sense lengthening and shortening and terminates inspiration and expiration.
Basically feedback from lung helps terminate inspiration.
What are the two parts of the metabolic controller?
- central part in the medullla responding to [H+] in the EC fluid -> SLOW response
- peripheral part at the carotid bifurcation (carotid sinus) - H receptors -> FAST
Fast and slow responses due to the fact that change of H+ is rapidly sensed in hyperperfused carotid bodies but not in EC fluid
Describe the carbon dioxide challenge and what it shows.
Testes the sensitivity of the metabolic respiratory centre to H ions.
Ventilation measured against PCO2.
Changes in PCO2 induced by breathing in and out of 6L bag with 7% CO2.
The slope of the curves obtained indicate the chemosensitivity. Arterial PCO2 rises at a constant rate of about 1 pKa per minute. This causes a rise in minute per ventilation - 30L/min per pKa.
How does hypoxia affect the acute CO2 response?
Hypoxia increases the sensitivity (so the slope is greater) of the acute CO2 response. mediated through carotid bodies
How does chronic metabolic acidosis affect the PCO2 threshold that gives a minimal drive to breathe?
Increases the threshold (shifts the intercept with the x on the left) but does not alter sensitivity (gradient is the same as in hypoxia). Chronic metabolic alkalosis has the opposite effect.
Is the minimal drive to breathe present when asleep?
No it is attributed to wakefulness. In sleep, ventilation would drop to 0 but continuing CO2 production means that in 10-60 seconds, arterial PCO2 has risen sufficiently above the apnoeic point to restant breathing.
What can depress the ventilatory response to PCO2? Give a central and a peripheral example.
Depress ventilatory response to CO2 means a flattening of the slope and rised set point.
This is caused by disease affecting metabolic control (tumour, congenital) but more commonly suppressed by drugs - opioid/anaesthetics
Peripheral cause - respiratory muscle weakness
COPD
Describe the ventilatory response to a hypoxic challenge.
It increases when alveolar PO2 decreases - the relationship is hyperbolic.
And increases when oxygen saturation decreases - a linear relationship.
There is a 30L/min increase in minute ventilation for a 7kPa change in arterial PO2 –> a similar change of 30L/min would be brought about by 1kPa change in arterial PCO2.
Why is this system bad at dealing with altitude where you experience hypoxic hyperventilation?
Altitude = a fall in PaO2 and PaCO2 together.
System is good at dealing like this: fall in ventilation –> fall in PaO2 and rise in PaCO2
The fall in PaCO2 increases sensitivity of carotid bodies to PaCO2 and H+ therefore ventilation is increased and PaO2 increased.
Altitude lowers PCO2 and inhibits the ventilatory response because no rise in PaCO2 but a fall.
So the body needs several days of acclimatisation before metabolic centres adjust.
How is neural drive different in people with COPD?
It is the same
How do people with obstructive disease maintain a normal minute ventilation despite breathing more shallowly?
Their frequency increases
What are the rapid and slow responses to respiratory acidosis?
Rapid - fall in ventilation leads to rise in PCO2 and H+ which stimulates metabolic controls to increase breathing
Slow - renal excretion and retention of weak acids as an important backup if the lungs can’t compensate fully
How is metabolic acidosis different to respiratory acidosis?
When the excess H+ comes from metabolism rather than inadequate ventilation.
Example of ause: diabetic ketoacidosis
What are the mechanisms for dealing with metabolic acidosis?
Compensatory mechanisms: ventilatory stimulation - hyperventilation, renal excretion of weak acids, renal retention of chloride to reduce strong ion difference
Metabolic alkalosis would be the opposite.
Give some central and peripheral causes of hypoventilation.
Central
Anaesthetics, drugs - acute - metabolic centre poisoning
chronic:
Disease of metabolic centre, congenital central hypoventilation syndrome, obesity hypoventilation syndrome, chronic mountain sickness
Peripheral Acute Muscle relaxant drugs, myasthenia gravis Chronic Neuromuscular with respiratory muscle weakness
What are the three types of breathlessness?
- tightness
- increased work and effort
- air hunger
What scale is used to measure breathlessness?
Borg scale
