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