Breathlessness and control of breathing

Question 1

what contributes to respiration

Answer 1

Breathing in

Question 2

what is the equation to work out minute ventilation

Answer 2

VE= Vt x f

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

Question 3

what is minute ventilation

Answer 3

minute ventilation= tidal volume x frequency

Question 4

what can TTOT be split into?

Answer 4

-Inspiratory (TI)

Expiratory ( TE)

Question 5

Is tidal expiration an active or passive process?

Answer 5

Passive - due to the natural recoil of the lungs

Question 6

State the equation for minute ventilation.

Answer 6

VE = VT x Frequency 
Frequency = 60/TTOT (if you want it per minute)

Question 7

How can this equation be manipulated to include TI?

Answer 7

VE = VT/TI x TI/TTOT

Question 8

What does VT/TI represent?

Answer 8

Neural Drive - mean inspiratory flow. This is how powerfully the muscles contract

Question 9

What does TI/TTOT represent?

Answer 9

Inspiratory Duty Cycle

Proportion of the cycle spent actively ventilating (i.e. breathing in)

Question 10

How do these factors change when there is an increase in metabolic demand?

Answer 10

Increased metabolic demand —> increased ventilation
VT/TI = INCREASE
TTOT = DECREASE (increase frequency)
TTOT is decreased by a combination of reduction in TI and TE

Question 11

What is the normal tidal volume and normal minute ventilation?

Answer 11

Normal Tidal Volume = 0.5 L
Minute Ventilation = 6 L/min
Breathing Rate = 12 breaths per minute

Question 12

What changes take place if you use a noseclip?

Answer 12

Breathe more DEEPLY - increase in VT
Breathe SLOWER - decrease in frequency
Ventilation remains the SAME

Question 13

What changes take place when artificial dead space is added?

Answer 13

Compared to with mouthpiece only:
Minute ventilation = INCREASE
VT = INCREASE
Frequency = INCREASES
TTOT= DECREASES
VT/TI = INCREASE, to satisfy the need for more ventilation.
-the inspiratory duty cycle ( TI/TOT) is essentially unaltered.

Question 14

How is the breathing of someone with COPD different to a normal person?

Answer 14

Breathing is:

• shallower
• faster (shorter TTOT)
• However, breathing is not any harder (VT/TI is similar)
• People with COPD have expiratory airway obstruction but the proportion of time used for expiration in patients with COPD does not change
• Hence, the gradient of the downward slope is the same

Question 15

What changes when we exercise?

Answer 15

• Increases neural drive and hence ventilation
• Increases frequency (doubles since TTOT is halved)
• Inspiratory duty cycle (TI/TTOT) increases a little to give more time for inspiration
• In people with airway obstruction, TI/TTOT decreases a little to give more time for expiration as people with obstructive lung disease have difficulty expiring

Question 16

Where is the voluntary and involuntary control of breathing located?

Answer 16

Voluntary or behavioural = motor area of Cerebral Cortex

Involuntary or metabolic = Medulla

Question 17

How is the metabolic controller reset in sleep?

Answer 17

PCO2 rises

Question 18

Where, in the motor homunculus, is behavioural control of breathing located?

Answer 18

Between the hip and the trunk

Question 19

Which receptors are involved in regulating the involuntary control of breathing?

Answer 19

HYDROGEN ION RECEPTORS found in the carotid bodies and in the metabolic centre itself

Question 20

Where are the peripheral chemoreceptors located?

Answer 20

Carotid bodies (at the junction of the internal and external carotids)

Question 21

Where are the pacemakers for respiratory breathing located?

Answer 21

Medulla

Question 22

What is the main group of neurons that are involved in generating respiratory rhythm?

Answer 22

Pre-Botzinger Complex

Question 23

What are the 6 groups of neurons in the medulla and brainstem and what muscles do they affect?

Answer 23

1. Early inspiratory
   - initiates inspiratory flow via the respiratory muscles
2. Inspiratory augmenting
   - may also dilate pharynx, larynx, and airways
3. Late inspiratory
   - may signal the end of inspiration, and ‘brake’ the start of expiration
4. Expiratory decrementing
   - may ‘brake’ passive expiration by adducting the larynx and pharynx
5. Expiratory augmenting
   - may activate expiratory muscles when ventilation increases on exercise (internal intercostal and abdominal muscles)
6. Late expiratory
   - may sign the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration

Question 24

Describe the Hering-breuer reflex. Which nerve is involved?

Answer 24

Vagus Nerve (cranial nerve X)
Pulmonary stretch receptors are activated by large airway/lung inflation leading to a CUT OFF signal for inspiration
- Stretch receptors in the airways and intercostal muscles send afferent signals to the medulla via the vagus nerve.
- These signals dampen down respiratory centre activity.
- This leads to decreased firing of the phrenic nerve -> decreased respiratory rate.

IMPORTANT: changes in proton concentration mirrors changes in PCO2.

Question 25

Describe the carbon dioxide challenge and what it shows.

Answer 25

Changes in arterial PCO2 are induced by asking a subject to breathe in and out of a bag with a fixed volume of oxygen and primed with 7% CO2. Re-breathing means that arterial PCO2 rises at a constant rate The rise in PCO2 is accompanied by a pronounced rise in minute ventilation *There is a 30 L/min rise in minute ventilation for every 1 kPa rise in arterial PCO2

Question 26

How does hypoxia affect the acute CO2 response?

Answer 26

Hypoxia increases the sensitivity of the acute CO2 response. | With hypoxia, there is an even GREATER rise in minute ventilation per 1 kPa rise in PCO2.

Question 27

How does chronic metabolic acidosis affect the PCO2 threshold that gives a minimal drive to breathe?

Answer 27

Chronic metabolic acidosis shifts the line to the left - a lower PCO2 is needed to cause an increase in minute ventilation Chronic metabolic alkalosis does the opposite

Question 28

Is the minimal drive to breathe present when asleep?

Answer 28

No - in sleep, ventilation will drop down to the zero but then the arterial PCO2 will rise rapidly to exceed the apnoeic threshold and cause breathing.

Question 29

What can depress the ventilatory response to PCO2? Give a central and a peripheral example.

Answer 29

Central - disease affecting the metabolic centre or DRUGS (e.g. opioids and anaesthetics) Peripheral - respiratory muscle weakness

Question 30

Describe the ventilatory response to a hypoxic challenge.

Answer 30

You get a 30 L/min change in minute ventilation for every 7 kPa change in PO2 So the system is MUCHMORE SENSITIVE TO PO2

Question 31

How does a high PCO2 affect the ventilatory respone to hypoxia?

Answer 31

Increased PCO2 increases the sensitivity of the response to hypoxia. But usually it is the PCO2 that has a greater effect on control of ventilation.

Question 32

Why is this system bad at dealing with altitude where you experience hypoxic hyperventilation?

Answer 32

Hypoxic hyperventilation ---> fall in PCO2 ---> inhibits the ventilatory response (effect of PCO2 in increasing ventilation)

Question 33

How is neural drive different in people with COPD?

Answer 33

VT/TI seems to indicate that their neural drive is normal but, in fact, they have a MUCH HIGHER NEURAL DRIVE (if you measure diaphragm activity). They have to try much harder to maintain the same VT/TI as normal healthy people. This is partly because of the airway narrowing and because the hyperinflated lungs are pressing down on the diaphragm meaning that the diaphragm fibres are shorter and don't contract as efficiently.

Question 34

How do people with obstructive disease maintain a normal minute ventilation despite breathing more shallowly?

Answer 34

Increase frequency - breathe faster

Question 35

How is the PCO2 in someone with bronchitis different to someone with emphysema?

Answer 35

Bronchitis would cause V/Q mismatch because they are breathing SHALLOWER so their PCO2 will be HIGHER Emphysema - reduced efficiency of gas exchange - PCO2 is LOWER than bronchitis

Question 36

What are the rapid and slow responses to respiratory acidosis?

Answer 36

ACIDOSIS RAPID (lungs) - fall in ventilation will lead to a rise in PCO2 SLOW (kidneys) - renal compensation as the kidneys retain bicarbonate (compensatory metabolic alkalosis) ALKALOSIS (e.g. due to panic attacks, COPD, heart attack) RAPID - hyperventilation removes CO2 SLOW - excrete bicarbonate, retain acid

Question 37

How is metabolic acidosis different to respiratory acidosis?

Answer 37

Source of excess H+ comes from metabolism rather than from inadequate ventilation (not due to high PCO2)

Question 38

How is metabolic acidosis different to respiratory acidosis? Source of excess H+ comes from metabolism rather than from inadequate ventilation (not due to high PCO2) What are the mechanisms for dealing with metabolic acidosis and alkalosis?

Answer 38

ACIDOSIS (due to diabetic ketoacidosis= production of acid, kidney failure= kidney failure) Lungs - Acidic blood stimulates metabolic controller to increase breathing (compensatory respiratory alkalosis) Kidneys - increase in ventilation, renal excretion of weak acids, renal retention of Cl- to reduce the strong ion difference ALKALOSIS (due to vomitting= acid loss, excessive gaviscon= alkali gain) Lungs - alkaline blood reduces stimulation of metabolic centre, hypoventilation to raise PCO2, compensatory respiratory acidosis Kidneys: retain weak acids (e.g. lactate, ketones)

Question 39

Give some central and peripheral causes of hypoventilation.

Answer 39

Central Acute: metabolic centre poisoning e.g.drugs Chronic: vascular/neoplastic disease, congenital central hypoventilation syndrome, obesity hypoventilation syndrome, chronic mountain sickness Peripheral Acute: muscle relaxant drugs, myasthenia gravis Chronic: neuromuscular with respiratory muscle weakness

Question 40

What are the three types of breathlessness?

Answer 40

1. Air Hunger: a powerful urge to breathe e.g. breath holding during exercise or breathing hypoxic air 2. Increased Work and Effort: breathing against increased resistance or at higher lung volumes e.g. COPD or heart failure leading to pulmonary oedema 3. Tightness: difficulty in expanding the thorax, generally associated with airway narrowing

Question 41

What scale is used to measure breathlessness?

Answer 41

Modified Borg Scale - Breathlessness can be scored on the 10-point borg scale - Subjects score themselves during a task Breath holding time - Tests behavioral versus metabolic controller - Break point is an expression of air hunger - Can be prolonged by increasing lung volume, lowering PaCO2 - Acute thoracic muscle paralysis does not prolong BHT

Question 42

what effects the metabolic centre and how?

Answer 42

- there are other parts of the cortex that are not under voluntary control e.g. emotional responses - sleep via the reticular formation also influences the metabolic centre - Limbic system ( survival responses e.g. suffocation, hunger) and - frontal cortex ( emotions) and sensory inputs ( pain, startle) may influence the metabolic centre