Breathlessness and Control of Breathing Flashcards
Functions of the Respiratory Muscles
Maintainence of arterial PO2, PCO2 and pH - pH is probably the most important
Defence of airways and lungs: cough, sneeze, yawn
Exercise: fight and flight
Speech
Sing, blow
Laugh, cry, express emotions
Control of intrathoracic and infra-abdominal pressures e.g. defecation, belching, vomiting
General Notes on Breathing
Only breathing in counts towards respiration
Breathing out is a passive process - the elasticity of the lungs and chest wall allow them to recoil back to the equilibrium position
The feedback loop involves CO2 and O2
What does the Upstroke, VT, TTOT, V.E mean?
How do you calculate the frequencey?
How do you convert to respiratory frequency per minute ?
Determinants of a Tidal Breath
This is a single respiratory cycle
Upstroke = Inspiration
VT = Tidal Volume
TTOT = Duration of a single respiratory cycle
V.E = Minute ventilation
Frequency = 1/TTOT
60/TTOT = converts to respiratory frequency per minute
V.E = VT x 60/TTOT
In other words, minute ventilation =………………….. ………………….. x …………………..
TTOT can be split into two: …………………….. (TI) and………………….. (TE)
If you multiply the minute ventilation equation mentioned earlier by TI/TI then you get the following equation:
……………………………………………………………………….
What is the equation to calculate mean inspiratory flow and what does it mean and what is it called?
What is the equation to calculate inspiratory duty cycle and what does it mean?
V.E = VT x 60/TTOT
In other words, minute ventilation = tidal volume x frequency
TTOT can be split into two: Inspiratory (TI) and Expiratory (TE)
If you multiply the minute ventilation equation mentioned earlier by TI/TI then you get the following equation:
V.E = VT/TI x TI/TTOT
VT/TI = MEAN INSPIRATORY FLOW
This is how powerfully the muscles contract
This is called the neural drive
TI/TTOT = INSPIRATORY DUTY CYCLE
The proportion of the cycle spent actively ventilating (i.e. inspiring)
If metabolic demands increase and more ventilation is required, you increase VT/TI and you decrease TTOT and hence INCREASE THE FREQUENCY
TTOT is decreased by a combination of reduction in TI and TE
DRAW THE TABLE BELOW IT WILL MAKE IT EASIER
Minute ventilation and breathing pattern in normal subjects
Left hand column is normal ventilation - around 6 L/min
Normal Tidal Volume = 0.5 L
Inspiratory Duty Cycle (TI/TTOT) is close to 40%
If you use a nose clip, your breathing becomes deeper and hence VT increases
Using a nose clip also means that breathing becomes slower (decrease in frequency) but ventilation remains around the same
If you have to breathe through a tube, the tube will act as extra DEAD SPACE which has to be cleared
When artificial dead space is added, VT, V.E and Frequency increases compared to the middle column
VT/TI (neural drive) also increases when there is extra dead space compared to the use of a nose clip - this change occurs to satisfy the need for more ventilation
The inspiratory duty cycle (TI/TOT) is essentially unaltered
Determinants of a tidal breath in disease
In both chronic bronchitis and emphysema, the intrathoracic airways are narrowed and so they have difficulty ventilating the lungs more on ……………….. than ………………..
As they have a higher ……………….. volume than normal people, this increases the stiffness of the chest and lungs and increases the work of breathing
Compared to controls, people with COPD breathe much shallower and faster (shorter ……………….. )
However, people with COPD DO NOT BREATHE ANY HARDER (……/ ….. is more or less the same)
Despite having an expiratory airflow obstruction, the proportion of time used for expiration in patients with COPD has ………….. been altered - the gradient of the downwards slope is the same
When exercising, there is an ……………….. in neural drive (…/…) and ventilation
Exercise will also bring about a halving of ……………….. and hence a doubling of frequency
Inspiratory duty cycle (……/…..) increases a little bit in normals to give more time for inspiration
In people with airway obstruction, …./………… decreases a bit in exercise to give more time for expiration
REMEMBER: people with obstructive lung disease have difficulty expiring
Determinants of a tidal breath in disease
In both chronic bronchitis and emphysema, the intrathoracic airways are narrowed and so they have difficulty ventilating the lungs more on EXPIRATION than inspiration
As they have a higher residual volume than normal people, this increases the stiffness of the chest and lungs and increases the work of breathing
Compared to controls, people with COPD breathe much shallower and faster (shorter TTOT)
However, people with COPD DO NOT BREATHE ANY HARDER (VT/TI is more or less the same)
Despite having an expiratory airflow obstruction, the proportion of time used for expiration in patients with COPD has NOT been altered - the gradient of the downwards slope is the same
When exercising, there is an increase in neural drive (VT/TI) and ventilation
Exercise will also bring about a halving of TTOT and hence a doubling of frequency
Inspiratory duty cycle (TI/TTOT) increases a little bit in normals to give more time for inspiration
In people with airway obstruction, TI/TTOT decreases a bit in exercise to give more time for expiration
REMEMBER: people with obstructive lung disease have difficulty expiring
CNS Control of Breathing
Involuntary or metabolic centre =……………… (bulbo-pontine brain)
Voluntary or behavioural centre = …………….. …………….. of…………….. ……………..
…………….. will always override ……………..
There are other parts of the cortex that are not under voluntary control and have an influence on the metabolic centre such as …………….. responses
Sleep via the …………….. …………….. (set of interconnected nuclei in the brain stem) also influences the …………….. centre
The main driver of breathing is the …………….. (striated muscle)
The metabolic controller is …………….. in sleep - PCO2 rises a little bit
Breathing becomes quite disorganised when we’re dreaming
Metabolic centre responds to metabolic demands for and production of CO2 (VCO2) and determines, in part, the ‘set point’ for CO2, generally monitored as PaCO2
The …………….. system (survival responses e.g. suffocation, hunger, thirst), and frontal cortex (emotions) and sensory inputs (pain, startle) may influence the metabolic centre
CNS Control of Breathing
Involuntary or metabolic centre = MEDULLA (bulbo-pontine brain)
Voluntary or behavioural centre = motor area of CEREBRAL CORTEX
Metabolic will always override behavioural
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
Sleep via the reticular formation (set of interconnected nuclei in the brain stem) also influences the metabolic centre
The main driver of breathing is the DIAPHRAGM (striated muscle)
The metabolic controller is RESET in sleep - PCO2 rises a little bit
Breathing becomes quite disorganised when we’re dreaming
Metabolic centre responds to metabolic demands for and production of CO2 (VCO2) and determines, in part, the ‘set point’ for CO2, generally monitored as PaCO2
The limbic system (survival responses e.g. suffocation, hunger, thirst), and frontal cortex (emotions) and sensory inputs (pain, startle) may influence the metabolic centre
Overview of Breathing Control
Metabolic centre is circled in TURQUOISE - in the brain stem in the bulbo-pontine region
Behavioural components are scattered throughout the mid and upper parts of the brain
Behavioural ‘Suprapontine’ Drives
PET scans show that the site of the behavioural controller becomes more active when you voluntarily take deep breaths
In the motor homunculus, the site responsible for behavioural control of breathing is between the hip and the trunk and is quite small compared to the trunk
The Organisation of Breathing Control
In the metabolic controller there is a …………… …………… ……………
There are on and off switches for the …………… nerves in the cervical region of the upper spinal cord - this activates the muscles that will move the chest wall and, hence, the lungs appropriately
Information from the respiratory muscles and the lungs is fed back to the …………… ……………
A much more important feedback is from the …………… in the carotid bodies in the neck - these sense the hydrogen ion levels in the blood
The other sensor is the …………… …………… itself, which has hydrogen ion receptors
If the …………… …………… are removed surgically, the acute response to carbon dioxide is reduced by 40%
Metabolic controller also activates the upper airway muscles in the neck to …………… the pharynx and the larynx on …………… and narrow them on …………… (to act as a brake on expiratory flow)
The Organisation of Breathing Control
In the metabolic controller there is a hydrogen ion receptor
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 appropriately
Information from the respiratory muscles and the lungs is fed back to the metabolic controller
A much more important feedback is from the chemoreceptors in the carotid bodies in the neck - these sense the hydrogen ion levels in the blood
The other sensor is the metabolic controller itself, which has hydrogen ion receptors
If the carotid bodies are removed surgically, the acute response to carbon dioxide is reduced by 40%
Metabolic controller also activates the upper airway muscles in the neck to dilate the pharynx and the larynx on inspiration and narrow them on expiration (to act as a brake on expiratory flow)
GREEN - breathing is normal in non-REM sleep
The Peripheral Chemoreceptor
The carotid body chemoreceptor is a well vascularised bundle of cells at the………………. of the internal and external ……………… arteries
…………….. in the blood reaching the chemoreceptors amplifies the response to the hydrogen ions
The Peripheral Chemoreceptor
The carotid body chemoreceptor is a well vascularised bundle of cells at the junction of the internal and external carotid arteries
Hypoxia in the blood reaching the chemoreceptors amplifies the response to the hydrogen ions
Central Coordination of Breathing
The heart has a single pacemaker in the ………. which is accessible to cardiologists for treating arrhythmias but breathing has many pacemakers that are close together in the ……………. …………… and are inaccessible
The group pacemaker activity of breathing comes from around ….. groups of neurons in the medulla near the nuclei of cranial nerves …… and ……
One group of pacemaker activity called the ……-………………. …………….. (found in the ventro-cranial medulla near the 4th ventricle) seems essential for generating the respiratory rhythm and is called the ‘……………… …………..’.
Coordination of the ……-………………. …………….. with the other ‘controllers’ may be needed to convert gasping into an orderly and responsive respiratory rhythm
Disease affecting these control centres in the brain are very rare
….. 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
Early inspiratory initiates ……………….. flow via the respiratory muscles
Inspiratory augmenting may also ………….. 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 ………….. and …………….
Expiratory augmenting may activate ………………….. muscles when ventilation increases on exercise
Late expiratory may sign the end of expiration and onset of inspiration, and may ………….. the pharynx in preparation for inspiration
There is an important role for the …………………. and ………………… muscles in opening up the airways or acting as a ‘brake’ in breathing
A lack of …………….. in the pharyngeal muscles may play a part in the breathing that occurs at night - obstructive sleep apnoea syndrome
Central Coordination of Breathing
The heart has a single pacemaker in the SAN which is accessible to cardiologists for treating arrhythmias but 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
One group of pacemaker activity called 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
Disease affecting these control centres in the brain are very rare
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
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
There is an important role for the pharyngeal and laryngeal 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
State if they are irratant aor stretch within the bracket or both
5th nerve: afferents from nose and face (……………….)
9th nerve: from …………….. and …………….. (……………..)
10th nerve: from …………….. and …………….. (……………)
Irritant receptors lead to coughing and sneezing and are ……………..
More on the 10th nerve: from bronchi and bronchioles (irritant and stretch)
What is the Hering-Breuer reflex?
Reflex Control
5th nerve: afferents from nose and face (irritant)
9th nerve: from pharynx and larynx (irritant)
10th nerve: from bronchi and bronchioles (irritant and stretch)
Irritant receptors lead to coughing and sneezing and are defensive
More on the 10th nerve: from bronchi and bronchioles (irritant and stretch)
Hering-Breuer reflex from pulmonary stretch receptors senses lengthening and shortening and terminates inspiration and expiration, but weak in humans
Notes from Vander’s (pg 474) about Hering-Breuer reflex:
Another cut off signal for inspiration comes from pulmonary stretch receptors which lie in the airway smooth muscle layer and are activated by large lung inflation
Action potentials in the afferent nerve fibres from the stretch-receptors travel to the brain and inhibit the activity of the medullary inspiratory neurons
This is the Hering-Breuer reflex
So, feedback from the lungs helps to terminate inspiration
What is being controlled?
The metabolic controller has TWO parts: name them?
What is being controlled?
The metabolic controller has TWO parts:
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
CO2 is very diffusible, and H+ changes mirror PCO2 changes
This 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
Look at laz notes
Ventilatory Responses to Hypoxia are Amplified by CO2
This is the response of ventilation to a hypoxic challenge
On the LEFT is a lowering of alveolar PO2 from 13 to 6 kPa, from 97.5 to 45 mm Hg at 2 fixed levels of PCO2 (because there is an interaction between O2 and CO2 as in the CO2 response)
Not isocapnic means that the PCO2 is not controlled and was allowed to fall during the hypoxic hyperventilation - this fall would reduce the stimulus and hence reduce the ventilatory response
The shapes of these curves are hyperbolic but when the x axis is changed from PO2 to oxygen saturation because of the shape of the oxygen dissociation curve
On the RIGHT, if you follow the PCO2 40 mm Hg line, there is a 30 L/min increase in minute ventilation for a 7 kPa change in arterial PO2 (saturation change of 99% to 60%)
IMPORTANT: a similar change of 30 L/min will be brought about by a 1 kPa change in arterial PCO2
THE SYSTEM IS MUCH MORE SENSITIVE TO PCO2
What is acidosis.
List 3 causes of Acidosis?
List 3 compensatory mechanisms?
What is alkalosis?
List 3 causes of alkolosis?
List 3 compensatory mechanisms for alkalosis?
