Breathlessness and control of breathing

Question 1

VT?

Answer 1

Tidal volume

Question 2

TTOR?

Answer 2

duration of a single respiratory cycle

Question 3

VE?

Answer 3

Minute ventilation

Question 4

Frequency = ?

Answer 4

1/TTOT

Question 5

60/TTOT ?

Answer 5

converts to respiratory frequency per minute

Question 6

What are the separate controllers in the brain?

Answer 6

Automatic bulbopontine controller (Brainstem)

Behavioural Suprapontine control (widely distributed)

Question 7

Involuntary centre is in the?

Answer 7

Involuntary or “metabolic” centre, in the medulla (bulbo–pontine brain)

Question 8

Voluntary centre is in the?

Answer 8

Voluntary or “behavioural” centre, in motor area of cerebral cortex

Question 9

Metabolic will always override the ?

Answer 9

Metabolic will always override the behavioural

Question 10

Other parts of cortex, not under voluntary control, influence the metabolic centre, such as ?
What influences the metabolic centre?

Answer 10

Other parts of cortex, not under voluntary control, influence the metabolic centre, such as emotional responses.
Sleep via reticular formation influences the metabolic centre

Question 11

Metabolic centre responds to ?

Answer 11

Metabolic centre responds to metabolic demands for and production of CO2 (V´CO2) and determines, in part, the “set point” for CO2, generally monitored as PaCO2.

Question 12

Behavioural centre controls acts such as ?

What 3 things influence metabolic centre?

Answer 12

Behavioural centre controls acts such as breath holding, singing
Metabolic will always override the behavioural
The limbic system (survival responses [suffocation, hunger, thirst]), and frontal cortex (emotions) and sensory inputs (pain, startle) may influence the metabolic centre.

Question 13

Where is the peripheral chemoreceptor?

Answer 13

The well perfused carotid body “tastes” arterial blood
It lies at the junction of the internal and external carotid arteries in the neck
It is a rapid response system for detecting changes in arterial PCO2 and PO2

Question 14

Group pacemake activity comes from?

Answer 14

“group pacemaker” activity coming from about 10 groups of neurons in the medulla near nuclei of IX and X cranial nerves
One group, the pre–Botzinger complex, in ventro–cranial medulla, near 4th ventricle, seems essential for generating the respiratory rhythm, and has been called the “gasping centre”.
Coordination of pre–Botzinger complex with the other “controllers” may be needed to convert “gasping” into an orderly and responsive respiratory rhythm.
Cellular mechanisms and neurotransmitters are a complex and specialised subject

Question 15

Discrete groups of neurons in the medulla discharge at different phases of the respiratory cycle and have different functions
Early inspiratory initiates ?
Inspiratory augmenting may also ?
Late inspiratory may signal ?
Expiratory decrementing may “brake” ?Expiratory augmenting may activate ?
Late expiratory may signal ?

Answer 15

Discrete groups of neurons in the medulla discharge at different phases of the respiratory cycle and have different functions
Early inspiratory initiates inspiratory flow via 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 larynx and pharynx.
Expiratory augmenting may activate expiratory muscles when ventilation increases on exercise.
Late expiratory may signal the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration.

Question 16

Reflex control
Vth nerve:
IXth nerve:
Xth nerve:

Answer 16

Vth nerve: afferents from nose and face (irritant)
IXth nerve: from pharynx and larynx (irritant)
Xth nerve: from bronchi and bronchioles (irritant and stretch)

irritant receptors leading to cough, sneezing etc are “defensive”

Question 17

Hering–Breuer reflex is?

Answer 17

Hering–Breuer reflex from pulmonary stretch receptors senses lengthening and shortening and terminates inspiration and expiration, but weak in humans (ventilatory responses in denervated lungs post–transplantation are normal).

Question 18

Thoracic spinal cord: from ?

Answer 18

Thoracic spinal cord: from chest wall and respiratory muscles (spindles ~ “stretch”)

Question 19

What are the 2 parts of the metabolic controller?

Answer 19

Metabolic controller has two parts:
A) central part in medulla responding to H+ ion of ECF
B) peripheral part at carotid bifurcation, the H+ receptors
of the carotid body
CO2 is very diffusible, and H+ changes mirror PCO2 changes, very rapidly for the hyperperfused carotid body, but more slowly in the ECF bathing the medulla. Thus, fast and slow responses exist.

Question 20

PaO2 is not as tightly controlled as PaCO2 and H+
SaO2 rather than PaO2 appears to be defended.
What happens in a fall in ventilation ?

Answer 20

PaO2 is not as tightly controlled as PaCO2 and H+
SaO2 rather than PaO2 appears to be defended.
Usually, a fall in ventilation causes a fall in PaO2 and a rise in PaCO2, and the fall in PaO2 increases sensitivity of carotid body to PaCO2 and H+ , so ventilation and PaO2 increases, and PaCO2 falls by negative feedback

Question 21

Compensatory mechanisms for too much acid or alkali are ?

Answer 21

the lung (fast responder) and kidney (slow responder).
If the lung is the problem, the response will be slow (hours, days)
The causes of acidosis (acidaemia is what is measured) and alkalosis are twofold   a) metabolic,  b) respiratory

Question 22

What determines [H+] ?

Answer 22

[H+] = constant x PaCO2/HCO3–

Strong ion difference: [Na+ + H+] – Cl-

Question 23

What is acidosis: excess production of H+
causes: ?
compensatory mechanisms:?

Answer 23

Acidosis: excess production of H+
causes: diabetic ketoacidosis, salicylate overdose, renal tubular defects
compensatory mechanisms:

Ventilatory stimulation lowers PaCO2 and H+
Renal excretion of weak (lactate and keto) acids
Renal retention of chloride to reduce strong ion difference

Question 24

What is alkalosis: excess production of H+
causes: ?
compensatory mechanisms:?

Answer 24

Alkalosis: loss of H+ leads to excess HCO3–
causes: vomiting, diuretics, dehydration
compensatory mechanisms
Hypoventilation raises PaCO2 and H+
Renal retention of weak (lactate and keto) acids
Renal excretion of chloride to increase strong ion difference

Question 25

``` Respiratory acidosis The lung fails to excrete the CO2 produced by metabolic processes Acute: What happens if the lung cannot cope? Chronic: ```

Answer 25

The lung fails to excrete the CO2 produced by metabolic processes Acute: hypoventilation causes PaO2 ↓, PaCO2 and H+ ↑ which stimulates metabolic centre (and carotid body) to increase minute ventilation and restore blood gas and H+ levels. What happens if the lung cannot cope? Chronic: ventilatory compensation may be inadequate for PaCO2 homeostasis but a) renal excretion of weak acids (lactate and keto), b) renal retention of chloride to reduce strong ion difference, returns H+ to normal, even though PaCO2 remains high and PaO2 low.

Question 26

Hypoventilation conditions | both acute and chronic examples

Answer 26

acute: metabolic centre poisoning (drugs and anaesthetics) chronic: vascular/neoplastic disease of metabolic centre cogential central hypoventilation syndrome obesity hypoventilation syndrome (OHS) chronic mountain sickness

Question 27

Hypoventilation conditions | peripheral and chronic obstructive pulmonary disease

Answer 27

peripheral - acute: muscle relaxant drugs, myasthenia gravis - chronic: neuromuscular with respiratory muscle weakness chronic obstructive pulmonary disease -mixture of central (won't breathe) and peripheral (cannot breathe)

Question 28

respiratory alkalosis

Answer 28

mechanism: ventilation in excess of metabolic needs causes: chronic hypoxaemia excess H+ pulmonary vascular disease chronic anxiety

Question 29

what is breathlessness

Answer 29

breathless with excitement/ anticipation suspended breathing with an emotional cause out of breath normal experience when exercise exceeds a threshold of comfort

Question 30

dyspnea

Answer 30

medical term for breathlessness but with the connotation of discomfort or difficulty at rest that usually implies difficulty with inspiration or expiration on exercise it means excessive breathing for the task +- difficulty

Question 31

what are the 3 types of breathlessness?

Answer 31

tightness air hunger increased work and effort

Question 32

what is tightness

Answer 32

difficulty in inspiring due to airway narrowing, a feeling that the chest is not expanding normally

Question 33

what is air hunger

Answer 33

sensation of a powerful urge to breath, eg a breath hold during exercise mismatch between VEdemanded / VEachieved a) demand: a copy of signal sent by metabolic controller to spinal motorneurones b) afferents from lung, chest wall and chemoreceptors (carotid body)- output

Question 34

what is increases work and effort

Answer 34

breathing at a high minute ventilation, or at a normal minute ventilation but at a high lung volume or against an inspiratory or expiratory resistance

Question 35

scales for measuring breathlessness during an exercise test

Answer 35

borg CR- 10 scale | visual analogue scale

Question 36

breath holding time (BHT)

Answer 36

tests strength of behavioural versus metabolic controller break point: prolonged by increases lung volume, lowering PaCo2 or by taking an isoxic/isocapnic breath near the break point breakpoint is an expression of air hunger

Question 37

Vt/Ti is?

Answer 37

mean inspiratory flow - indicator of how fast the diaphragm is contracting how hard the muscles are being driven

Question 38

2 equations for VE?

Answer 38

VE = Vt * 60/Ttot VE= Vt/Ti * Ti/Ttot

Question 39

determinants of a tidal breath in disease? | -chronic and emphysema

Answer 39

see graph

Question 40

how does the metabolic centre work?

Answer 40

Metabolic centre: has an H+ controller, detecting ECF H+ and carotid bodies H+ as H+ in equilibrium with CO2 - leading to certain impulse frequency to respiratory spinal motor neurones and then to phrenic nerve to drive diaphragm Upper airway muscles: dilated on inspiration and narrowed on expiration to ensure smooth air flow - controlled by metabolic controller Feedback: lung has stretch receptors, respiratory muscles have muscle spindle and blood receptors have chemoreceptors that all signal back to the metabolic concentration to lead to alteration of timing to control breathing