Breathlessness and control of breathing Flashcards
Functions of Respiratory muscles
Maintainence of arterial PO2, PCO2 and pH
Defence of airways and lungs
Exercise: fight and flight
Speech
Control of intrathoracic and infra-abdominal pressures e.g. defecation, belching, vomiting
Breathing in vs out energy consumption
Breathing in requires respiration
Breathing out= passive
Minute ventilation equations
Graph of single respiratory cycle
slide 5, lecture 8
Graph explanation?
VE= VT x 60/T(TOT)
Multiplication of above by TI/TI:
VE= (VT/ T1) x (T1/T(TOT))
VE= minute ventilation
VT= Tidal Volume
T(TOT)= duration of single respiratory cycle
f= 1/ T(TOT)
60/ T(TOT)= respiratory frequency per minute
TI = Inspiratory
TE= Expiratory (TI+ TE= T(TOT))
VT/T1= Mean inspiratory flow, how powerfully muscles contract= called NEURAL DRIVE
T1/T(TOT)= Inspiratory Duty Cycle, proportion of cycle spent actively ventilating (inspiring)
Upstroke= inspiration
If metabolic demands increase?
More ventilation required
Increase VT/ T1 and decrease T(TOT) by decreasing TI and TE
Leads to increased frequency
Normal ventilation rate
6L/min
Normal Tidal Volume
0.5L
Normal inspiratory duty cycle
40%
Use of nose clip
Breathing=deeper= increase VT
Breathing= slower (decrease frequency) BUT ventilation= same
Inspiratory duty cycle= unaltered
Breathing through tube
Extra dead space
Increased VT, VE and frequency
Increased VT/TI (neural drive) compared to nose clip because need more ventilation
Inspiratory duty cycle= unaltered
Diagram of emphysema+ chronic bronchitis on tidal volume
(slide 7, lecture 8)
Cause of changes?
Intrathoracic airways = narrowed = difficulty ventilating the lungs more on EXPIRATION than inspiration
Higher residual volume = increases the stiffness of chest and lungs + increases the work of breathing
COPD?
COPD= breathe shallower and faster (shorter TTOT)
But DO NOT breathe any harder (VT/TI = same)
Proportion of time used for expiration NOT changed -gradient of the downwards slope is the same
Exercising?
Normal people?
Airway obstruction?
Increase in neural drive (VT/TI) + ventilation
Halves TTOT and hence doubling of frequency
Normal: Inspiratory duty cycle (TI/TTOT) increases a bit to give more time for inspiration
Airway obstruction:
TI/TTOT decreases to give more time for expiration
People with obstructive disease breathing change?
Difficulty expiring
CNS Control of Breathing Involuntary centre? Responds to? Influenced by? Voluntary centre? Affected by? Sleep? Driver of breathing?
Involuntary or metabolic centre = MEDULLA:
Responds to metabolic demands for and production of CO2 (VCO2) + determines, in part, the ‘set point’ for CO2, monitored as PaCO2
The limbic system (survival responses), frontal cortex (emotions) and sensory inputs (pain, startle) influences the metabolic centre
Voluntary or behavioural centre = motor area of CEREBRAL CORTEX
Voluntarily take deep breaths= more active
Metabolic will always override behavioural
Sleep via the reticular formation (interconnected nuclei in brain stem) influences the metabolic centre
The metabolic controller is RESET in sleep - PCO2 rises a little bit
Breathing = disorganised when we’re dreaming
Main driver of breathing =DIAPHRAGM (striated muscle)
Organisation of breathing control
Diagram
(slide 13, lecture 8)
Green?
- In metabolic controller =hydrogen ion receptor
- There are on and off switches for the phrenic nerves in cervical region of the upper spinal cord= activates muscles that will move chest wall and hence, lungs
- Information from the respiratory muscles and the lungs is fed back to the metabolic controller
- Feedback is from chemoreceptors in the carotid bodies in the neck - sense the hydrogen ion levels in the blood
- Other sensor = metabolic controller itself, has hydrogen ion receptors
- Metabolic controller also activates upper airway muscles in the neck to dilate the pharynx and the larynx on inspiration + narrow them on expiration (to act as a brake on expiratory flow)
Green= Behavioural controller can temporarily override
Peripheral Chemoreceptor
Location?
Responds to?
Carotid body chemoreceptor
Well vascularised bundle of cells at junction of the internal and external carotid arteries
Changes in arterial PCO2 and PO2 = amplifies response to the hydrogen ions
Central coordination of breathing
Location of breathing pacemakers?
Specific pacemaker activity for respiratory rhythm? Importance?
Location of neurones to do with tidal breath?
Stages of ventilation+ effects?
Importance of pharyngeal+ laryngeal nerves? Lack of tone in pharyngeal nerve?
Close together in the brain stem (inaccessible unlike heart pacemaker in SAN)
Group pacemaker activity of breathing comes from around 10 groups of neurons in the medulla near nuclei of cranial nerves IX and X
Pre-Botzinger complex (found in the ventro-cranial medulla near the 4th ventricle) = essential for generating the respiratory rhythm + called the ‘gasping centre’.
Coordination of pre-Botzinger complex with other ‘controllers’ needed to convert gasping into orderly + responsive respiratory rhythm
SIX groups of neurons in the medulla and brain stem have functions in generation of a tidal breath - discharge at different phases of respiratory cycle
- Early inspiratory initiates inspiratory flow via respiratory muscles
May also dilate pharynx, larynx and airways - Late inspiratory signals the end of inspiration, and ‘brake’ the start of expiration
- Expiratory decrementing ‘brake’ passive expiration by adducting (move towards midline) larynx +pharynx
- Expiratory augmenting activates expiratory muscles when ventilation increases on exercise
- Late expiratory signs the end of expiration + onset of inspiration, dilates the pharynx in preparation for inspiration
Opening up the airways or acting as a ‘brake’ in breathing
Lack of tone in pharyngeal muscles - obstructive sleep apnoea syndrome
Reflex control of breathing
Nerve numbers? Afferents?
Purpose of them?
5th nerve: afferents from nose and face (irritant)
9th nerve: from pharynx and larynx (irritant)
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
Irritant receptors = coughing + sneezing (defensive)
Metabolic controller 2 parts?
How does this relate to CO2?
Difference between the parts?
- Central part in medulla responding to the H+ concentration in extracellular fluid
- Peripheral part at the carotid bifurcation (carotid sinus) - there H+ receptors here as well
CO2 is very diffusible, and H+ changes mirror PCO2 changes
Change in H+ reflecting changes in PCO2 occur rapidly in the hyperperfused carotid bodies but more slowly in the ECF bathing medulla - so fast and slow responses exist
What are CO2 responses potentiated by? Draw graph (slide 20, lecture 8) S=? B=? B Measured by? Effect on VE? Green? Orange? Black? During sleep? How does a depressed ventilatory response to PCO2 affect the graph? Possible causes? Peripheral cause of reduction in sensitivity?
S= index of chemo-sensitivity.
B= apnoeic threshold, sensitive to acid-base status (only operates in sleep).
Measures sensitivity of metabolic respiratory centre to H+ by use of a carbon dioxide challenge – breathing into a CO2 primed bag. Respiration into closed bag maintains rising CO2 levels which raises the
minute ventilation in response.
30Lmin-1 rise in VE for every 1kPa rise in PaCO2.
Green = Normoxia:
Chronic Metabolic Alkalosis – decreases the threshold and again does not alter the gradient.
Orange = hypoxia (which increases sensitivity of
acute CO2 response – mediated by the carotid body):
Chronic Metabolic Acidosis – increases the threshold (x-axis intercept → left) but does NOT alter sensitivity (gradient).
Black line =the VE at which PCO2 is below normal resting level. During sleep, ventilation would drop to zero but due to continual CO2 production, after 10-60 seconds, PaCO2 has risen enough (threshold) to restart breathing.
Depressed ventilatory response to PCO2 = flattening of slope (decreased sensitivity) + rise in set point (resting PaCO2 threshold). Could be result of a disease affecting metabolic control or suppressive drugs (anaesthetics).
Peripheral cause of a reduction in sensitivity = respiratory muscle weakness which usually progresses to a raised PaCO2.
Response of ventilation to a hypoxic challenge? (slide 21, lecture 8) Left graph? Meaning of not isocapnic? Right graph? Implication? What is being controlled? Fall in VE=? At high altitude?
Lowering of alveolar PO2 from 13 → 6kPa at 2 fixed
levels of PCO2.
Not isocapnic= PCO2 is not controlled + allowed to fall
during hypoxic hyperventilation → reduces VE response.
Shows (on the 40mmHg) a 30Lmin-1
increase in VE for a 7kPa change in PaO2 (or saturation change of 99% to 60%).
HOWEVER, a 30Lmin-1 is also brought about by a 1kPa change in PaCO2 so the system is much more sensitive to changes in PaCO2
PaO2 is NOT as tightly controlled as PaCO2 and H+
Oxygen saturation better defended than PaCO2 (due to nature of oxygen binding).
Fall in VE → fall in PaO2 and rise in PaCO2 → fall in PaO2 raises sensitivity of carotid body to PaCO2 and H+ → VE increases so PaO2 increases.
At altitude, several days of acclimatisation are required to adjust for the lower PO2 set point.
Respiratory Acidosis
Rapid system response?
Slower system response?
H+ maintained by?
Rapid system response (acute hypoventilation) – fall in VE leads to a rise in PCO2 and [H+] which stimulates the
metabolic controllers to increase VE.
Slower system response (chronic hypoventilation) – renal excretion of weak acids to maintain homeostasis of
PaCO2 if the lungs are unable to cope (this takes a long time though).
[H+] is maintained by PCO2 (LUNGS): bicarbonate (KIDNEYS) ratio
Metabolic Acidosis meaning?
Compensatory mechanisms?
When the source of excess H+ comes from metabolism rather than inadequate ventilation.
VE stimulation.
Renal excretion of weak acids.
Renal retention of chloride to reduce strong ion difference.
Metabolic Alkalosis compensatory mechinisms
Hypoventilation = PaCO2 and H+
Renal retention of weak (lactate and keto) acids
Renal excretion of chloride to increase strong ion difference
(opposite of metabolic acidosis)
