8 Breathlessness and Control of Breathing in the Awake State Flashcards

1
Q

Q: What are the main functions of respiratory muscles? (6) Most important?

A

A: -Maintenance of arterial PO2, PCO2 and pH (optimal biochemistry) -> ensure biochemcical processes (ENZYMES) work in most optimum way

  • Defence of airways and lung: cough, sneeze, yawn
  • Exercise: fight and flight - running
  • Speech/singing/blow
  • cry/laugh/emotions
  • Control of intrathoracic and intra-abdominal pressures

H+ concentration

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2
Q

Q: What does a spirogram show? Draw one. Describe (4).

A

A: one typical representative breath

time (s) = X and volume = Y

single line from origin goes up then down with point

  • total time of a single cycle is T (tot)= at rest= 4s
  • size of upstroke= inspiration= V (t)= tidal volume
  • TTOT can be split into two: Inspiratory (TI) and Expiratory (TE)
  • slope= VT/VI = MEAN INSPIRATORY FLOW (neural drive)
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3
Q

Q: What stands for minute ventilation? How is it calculated? Av value?

A

A: V.E = Minute ventilation (expired volume)

volume breathed per minute= sum of all inspiratory V(t)s in a minute (or expir V(t)s as are the same)

VE = Vt x f
minute vent = tidal volume x freq

where f = 60 / T(tot) = converts to respiratory frequency per minute

VE= 5.9L/min

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4
Q

Q: From a spirogram, what is flow? (how is it calculated). What does it show? also called? Av value?

A

A: take VE = Vt x 60 / T(tot)

multiply the minute ventilation equation by TI/TI then you get:

V.E = VT/TI x TI/TTOT

Where VT/TI = MEAN INSPIRATORY FLOW

This is how powerfully the muscles contract

This is called the neural drive

VT/TI = 0.26L/s

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5
Q

Q: From a spirogram, what is the inspiratory duty cycle? (how is it calculated). What does it show? also called? Av value?

A

A: take VE = Vt x 60 / T(tot)

multiply the minute ventilation equation by TI/TI then you get:

V.E = VT/TI x TI/TTOT

TI/TTOT = INSPIRATORY DUTY CYCLE

The proportion of the cycle spent actively ventilating (i.e. inspiring)

38%

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6
Q

Q: If metabolic demands increase and more ventilation is required, what happens? (explain with spirogram) (4)

A

A: -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

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7
Q

Q: How does the brain control the diaphragm? changes result in? (2)

A

A: Brain sends certain freq of impulses via phrenic nerve to diaphragm (more freq = it will shorten more strongly and faster)

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8
Q

Q: Summarise inspiration control. (4) Expiration? (3)

A

A: -at a certain moment inspiration is switched on,

  • another controller controls drive- how hard the muscles contract
  • third controller- stretch receptors detect chest has expanded sufficiently for metabolic requirements
  • 4th controlled stops inspiration
  • expiration is mostly passive
  • system returns to resting volume
  • lots of braking mechanisms ensure it is controlled and doesn’t occur too fast
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9
Q

Q: Normal. Vt? Freq? Inspiratory duty cycle? Mean inspiratory flow? Minute ventilation?

A
A: tidal volume= 0.4L
15/min
TI/TTOT = 38%
VT/TI = 0.26L/s
VE= 5.9L/min
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10
Q

Q: What happens when you have to breathe through a tube? What happens to VT, V.E, Frequency, VT/TI (neural drive)? Inspiratory duty cycle (TI/TOT)?

A

A: the tube will act as extra DEAD SPACE which has to be cleared

When artificial dead space is added, VT, V.E increases compared to the middle column

Frequency decreases to 14.8

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

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11
Q

Q: Draw 3 overlapping spirograms for normal, chronic bronchitis and emphysema. (what are they both?)

What happens with both conditions? How does this affect:

expiration and inspiration?
Residual volume?
TTOT?
VT/TI?
TE/TTOT?
TI/TTOT?
VT/TI?
downward slope?
A

A: COPD

REFER

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)

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

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

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12
Q

Q: What happens when exercising to:

VT/TI?
ventilation?
TTOT?
Frequency?

Those with COPD?

A

A: 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

same effects

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13
Q

Q: What is the main driver of breathing? What are the 3 controls? Where are the components? What will always override?

A

A: diaphragm

Involuntary or metabolic centre = MEDULLA (bulbo-pontine brain) ***

Voluntary or behavioural centre = motor area of CEREBRAL CORTEX -> Behavioural components are scattered throughout the mid and upper parts of the brain

Reflex control -> coughing, sneezing

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14
Q

Q: What does the involuntary control of breathing respond to? What does it determine? What can influence it? (4)

A

A: Responds to metabolic demands for/ production of CO2

determines, in part, “set point” for CO -> generally monitored as PaCO2

  • 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 (frontal cortex)
  • sensory inputs (pain, startle)
  • limbic system (survival responses (suffocation, hunger, thirst))
  • Sleep (absence of wakefullness) via the reticular formation (set of interconnected nuclei in the brain stem) also influences the metabolic centre
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15
Q

Q: What is the voluntary control of breathing responsible for?

A

A: controls acts such as breath holding, singing

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16
Q

Q: Draw a diagram representing the organisation of breathing control. Most important feedback?

A

A: REFER

carotid bodies

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17
Q

Q: What is the most important feedback involved in breathing control? Passed back to? via?

Compare H+ response.

A

A: Peripheral chemoreceptor:

  • Well perfused carotid body
  • At junction of internal and external carotid arteries in the neck
  • A rapid response system for detecting changes in arterial PCO2 and PO2

passed back to metabolic controller (medulla)
-glossopharyngeal nerve

rapid system when compared to response in brain to extracellular fluid (bathing metabolic centre)

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18
Q

Q: Compare the coordination of central breathing in brain to heart. Diseases of central breathing?

A

A: 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

-rare

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19
Q

Q: Name one group of neurons in the medulla controlling breathing. Where is it? Role? Relation to other controllers?

A

A: pre-Borzinger complex (ventro-cranial medulla near 4th ventricle)

essential for generating respiratory rhythm -> called the ‘gasping centre’

-> its coordination with other controllers may be needed to convert into an orderly and responsive respiratory rhythm

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20
Q

Q: Aside from prev example, what do 6 groups of neurons in medulla and brainstem have? When do they act?

A

A: distinct functions in the generation of a tidal breath - they discharge at different phases of the respiratory cycle

different points in inspiration and expiration

  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
  6. Late expiratory may sign the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration
21
Q

Q: What is the role of pharyngeal and laryngeal muscles? (2) Lack of tone in the pharyngeal muscles may play a part in?

A

A: 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

22
Q

Q: Which 3 nerves are part of reflex control of breathing? What do they respond to? (2) Involvement of defensive response?

A

A: 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

23
Q

Q: What’s the most well known reflex control of breathing nerve? What is the name of the reflex? from? senses? effect in humans?

Describe. Summarise.

A

A: 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

24
Q

Q: What are the 2 parts of metabolic breathing control?

A

A: Central part in the medulla responding to the hydrogen ion concentration in the extracellular fluid (SLOWER RESPONSE)

Peripheral part at the carotid bifurcation (carotid sinus) - there are hydrogen ion receptors here as well (feedback via glossopharyngeal nerve) (RAPID RESPONSE)

25
Q

Q: Relationship between H+ and CO2? In terms of metabolic breathing control?

A

A: 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

26
Q

Q: The sensitivity of the metabolic respiratory centre to hydrogen ions can be tested with? Graph axis? Describe experiment. 2 lines?

Shows?

A

A: carbon dioxide challenge - where ventilation is measured against changes in arterial PCO2

  • changes in arterial PCO2 are induced by asking the subject to breathe into and out of a bag, the arterial PCO2 rises at a constant rate due to the bodies continuing CO2 production
  • rise in arterial PCO2 causes a very pronounced rise in minute ventilation

In the graph, the GREEN lines were obtained during normoxia

The ORANGE lines were obtained during hypoxic breathing

Hypoxic breathing increases the sensitivity (gradient) of the acute CO2 response - this effect is mediated through the carotid body

massive sensitivity is seen- small changes in arterial CO2 result in large changes in minute ventilation

27
Q

Q: What can chronic metabolic acidosis and alkalosis do to the sensitivity of the metabolic respiratory centre to hydrogen ions?

A

A: Chronic Metabolic Acidosis (orange dotted line) increases the threshold (shifts the intercept with the x axis to the left around point B) but does NOT alter the sensitivity (gradient)

Chronic Metabolic Alkalosis (green dotted line) has the opposite effect and so shifts the intercept to the right

28
Q

Q: What happens if arterial PCO2 is reduced below the normal resting level (5.3 kPa)? During sleep? Apnoeic threshold?

A

A: ventilation does NOT drop to zero but to the horizontal black line

The minimal drive to breathe is attributed to wakefulness

In SLEEP, ventilation would drop to zero but continuing CO2 production (via metabolic processes) means that in 10-60 seconds, arterial PCO2 has risen sufficiently above the apnoeic point to restart breathing

apnoeic threshold-sensitive to acid base status but only operates when asleep

29
Q

Q: What amplifies ventilatory responses to hypoxia? Explain.

A

A: CO2

with hypoxia and increased levels of CO2, minute ventilation increases more so than if CO2 levels were lower

30
Q

Q: What is the relationship between VE and alveolar pO2? VE and arterial oxygen saturation? How does oxygen saturation and arterial pO2 compare?

A

A: curvilinear, linear

Oxygen SATURATION appears to be better defended than arterial PO2 (due to the nature of oxygen binding to haemoglobin and the oxygen dissociation curve)

31
Q

Q: What does not isocapnic mean?

A

A: 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

32
Q

Q: Compare the control of O2 and CO2 and H+?

A

A: PaO2 is NOT as tightly controlled as PaCO2 and H+

33
Q

Q: What does a fall in ventilation cause in terms of O2? Co2? How do they relate? (3) Effect of altitude? (3)

A

A: Usually, a fall in ventilation causes a fall in PaO2, and rise in PaCO2 = strong stimulus to breathe more

  1. The fall in PaO2 increases sensitivity of the carotid body to PaCO2 and H+
  2. This means that ventilation increases and so PaO2 increases
  3. PaCO2 falls by negative feedback

Control systems are not so well equipped for a fall in PO2 caused by altitude

Hypoxic hyperventilation on going to altitude lowers the PCO2 and inhibits the ventilatory response

Several days of acclimatisation is required before the metabolic centre adjusts to a lower PO2 set point

34
Q

Q: What are the compensatory mechanisms for too much acid or alkali? (2) What can happen if one has a problem?

What are the 2 pH related statuses we can have? 2 types from those?

A

A: -lungs (fast responder)
-kidneys (slow)

if lung has problem, rely on kidney to fix which takes days

  • acidosis (acidaemia is measured)
  • alkalosis

-metabolic or respiratory (in terms of cause)

35
Q

Q: What determines pH?

A

A: ratio of pCO2 : HCO3-

[H+] = pCO2 x HCO3- x constant

36
Q

Q: What is metabolic acidosis? Causes? (3) Compensatory mechanisms? (3)

A

A: Acidosis: excess production of H+

causes: diabetic ketoacidosis, salicylate overdose (aspirin poisoning), renal tubular defects (can’t excrete)

compensatory mechanisms:

  • Ventilatory stimulation lowers PaCO2 and H+ (overbreath)
  • Renal excretion of weak (lactate and keto) acids
  • Renal retention of chloride to reduce strong ion difference
37
Q

Q: What is metabolic alkalosis? Causes? (3) Compensatory mechanisms? (3)

A

A: 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
38
Q

Q: What is respiratory acidosis? What is it called if we can cope? how do we cope? What is it called if the lungs cannot cope? what happens? (3) How long does this take?

A

A: The lung fails to excrete the CO2 produced by metabolic processes (and failure to keep pO2 up)

Acute: hypoventilation causes decrease in PaO2, PaCO2 and H+ (^) which stimulates metabolic centre (and carotid body) to increase minute ventilation and restore blood gas and H+ levels.

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

-> takes long time

39
Q

Q: What does it mean to have a hypoventilation condition? 3 overarching causes?

A

A: high PaCO2

  • central (acute and chronic)
  • peripheral (a and c)
  • chronic obstructive pulmonary disease COPD
40
Q

Q: What are the central causes for hypoventilation? (5)

A

A: (high PaCO2)

Acute
-Metabolic centre poisoning (anaesthetics, drugs)

Chronic

  • Vascular/ neoplastic disease of metabolic centre
  • Congenital central hypoventilation syndrome (born with certain CO2 sensitivity)
  • Obesity hypoventilation syndrome (OHS) (ACQUIRED)
  • Chronic mountain sickness (ACQUIRED- if live with it from birth)
41
Q

Q: What are the peripheral causes for hypoventilation? (3) Other cause?

A

A: Acute

  • Muscle relaxant drugs
  • Myasthenia gravis

Chronic
-Neuromuscular with respiratory muscle weakness (motor neuron disease)

CHRONIC OBSTRUCTIVE PULMONARY DISEASE
-Mixture of central (won’t breathe) and peripheral (cannot breathe)

42
Q

Q: What is respiratory alkalosis? Mechanism? Causes? (4) How common is it?

A

A: low PaCO2

Mechanism: ventilation in excess of metabolic needs

Causes:

  • Chronic hypoxaemia
  • Excess H+ (metabolic causes) (overcompensate)
  • Pulmonary vascular disease
  • Chronic anxiety (psychogenic)

uncommon

43
Q

Q: What are the 2 types of breathlessness? Medical term?

A

A: “Breathless with excitement” “breathless with anticipation”
suspended breathing with an emotional cause (~ without breath)

“out of breath” (~ too much breathing)
normal experience when exercise exceeds a threshold of comfort

dysponea

44
Q

Q: What is dysponea? Question asked. 2 answers.

A

A: the medical term for breathlessness but with the connotation of discomfort or difficulty

“do you get breathless at rest/ on exercise”?

At rest, that usually implies difficulty with inspiration or expiration.

On exercise, it means excessive breathing for the task ± (with or without) difficulty

45
Q

Q: What are the 3 types of breathlessness? Worst type?

A

A: Tightness: difficulty in inspiring due to airway narrowing; a feeling that the chest is not expanding normally- connected with asthma

Increased work and effort: 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

**Air hunger: sensation of a powerful urge to breath, e.g a breath hold during exercise

46
Q

Q: What is air hunger? experimentally?

A

A: type of breathlessness

Experimentally, air hunger is produced by driving breathing with added CO2, while restricting tidal volume by breathing from a bag of fixed volume: very unpleasant.

47
Q

Q: What causes air hunger? Explain (2).

A

A: mismatch between V.E demand and V.E achieved

Cerebral cortex compares TWO different inputs

  • Demand - a copy (corollary) of signal sent by metabolic controller to spinal motor neurones
  • Afferents from lung, chest wall and chemoreceptors (carotid body) - output
48
Q

Q: How can breathlessness be measured? (3)

A

A: Scales for measuring breathlessness during an exercise test

Breathlessness can be scored on the 10-point BORG SCALE

Subjects score themselves during a task

49
Q

Q: What does breath hold time BHT test? What is breakpoint? How can it be altered? (3)

What doesn’t affect BHT?

Calculation?

A

A: tests strength of behavioural versus metabolic controller

“break point” is an expression of “air hunger”

prolonged by increasing lung volume, lowering PaCO2 or by taking an isoxic/isocapnic breath near the break point

acute thoracic muscle paralysis with curare does not prolong BHT

BHT ~ stretch receptor drive x metabolic drive