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Respiratory System > 9. Breathlessness and Control of Breathing - Awake > Flashcards

9. Breathlessness and Control of Breathing - Awake Flashcards

1
Q

What are the functions of the respiratory muscles?

A
  • Maintenance of arterial PO2, PCO2 and pH (most important)
  • Defence of airways and lungs
  • Exercise
  • Speech
  • Blow
  • Control of intrathoracic and infra-abdominal pressures
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2
Q

How do you calculate frequency in a volume-graph?

A
  • 1/TTOT (duration of a single respiratory cycle)

* 60/TTOT - frequency per minute

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3
Q

What is the average TTOT and respiratory rate?

A
  • TTOT - 4 seconds

* Respiratory rate - 15 breaths/min

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4
Q

What is V.E and how is it calculated?

A
  • Minute ventilation - volume of gas inhaled or exhaled during one minute
  • VT x 60/TTOT (tidal volume x frequency)
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5
Q

What can TTOT (duration of a single cycle) be split into?

A
  • Inspiratory (TI)
  • Expiratory (TE)

(both durations)

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6
Q

What is the mean inspiratory flow and how do you calculate it?

A
  • How powerfully the muscles contract
  • Neural drive
  • VT/TI (tidal volume/inspiratory TTOT)
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7
Q

What is the inspiratory duty cycle and how do you calculate it?

A
  • Proportion of the cycle spent actively ventilating (inspiring)
  • Normally close to 40%
  • TI/TTOT
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8
Q

What happens to the mean inspiratory flow, TTOT and frequency if metabolic demands increase?

A
  • Mean inspiratory flow (VT/TI) - increases
  • TTOT (duration) - decreases
  • Increased frequency
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9
Q

What happens to the neural drive if more impulses are sent down the phrenic nerve to the diaphragm?

A

• Increases

- diaphragm contracts more frequently and stronger

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10
Q

What is the normal tidal volume?

A

0.5L

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11
Q

What changes occur when you wear a noseclip?

A 
• Deeper breathing
- VT increases
• Slower breathing
- decreased frequency
• Ventilation remains around the same
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12
Q

What changes occur when you breath through a tube?

A

• Extra dead space

  • increased VT
  • increased V.E
  • increased frequency
  • increased neural drive (VT/TI)
  • unaltered inspiratory duty cycle (TI/TTOT)
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13
Q

How does breathing change in chronic bronchitis and emphysema (i.e. COPD)?

A

• Intrathoracic airways are narrowed
- difficulty ventilating (worse for EXPIRING)
• Proportion of time for expiration (downward gradient) doesn’t change
• Higher residual volume
- increased stiffness and work required
• Shallower and faster breathing - shorter TTOT
(bronchitis has a shorter TTOT than emphysema)
• Don’t breathe any harder (VT/TI roughly the same)
- neural drive is still increased
• Diaphragm needs to work harder
- hyperinflation shortens diaphragm fibres - less efficient

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14
Q

How does exercising change the breathing values (in COPD)?

A

• Increase in neural drive (VT/TI)
- Frequency doubles
• Inspiratory duty cycle (TI/TTOT) decreases to give more time for expiration (normally increases to give more time for inspiration)

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15
Q

How does the CNS control breathing?

A
  • Involuntary/metabolic centre - medulla
  • Voluntary/behavioural centre - motor area of cerebral cortex
  • Metabolic always overrides behabioural
  • Other parts of the cortex (involuntarily) control the metabolic centre e.g. emotion
  • Sleep influences the metabolic centre via the reticular formation
  • Behavioural - breath holding and singing
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16
Q

What happens to the metabolic centre in sleep?

A
  • Reset
  • PCO2 rises a little bit
  • Breathing becomes disorganised when dreaming
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17
Q

How does the limbic system, frontal cortex and sensory input influence the metabolic centre?

A
  • Limbic system - survival responses
  • Frontal cortex - emotions
  • Sensory inputs - pain, startle
  • all alter breathing
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18
Q

Where is the metabolic and behavioural centre located?

A
  • Metabolic centre - bulbo-pontine region

* Behavioural centre - components scattered throughout the mid and upper parts of the brain

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19
Q

What changes occur in the behavioural centres when you voluntarily breath deeply?

A
  • More active
  • Can be seen using PET scans
  • Site responsible for behavioural control of breathing is small
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20
Q

How does the metabolic controller H+ receptor work?

A
  • Hydrogen ion receptor -detects [H+] in extracellular fluid
  • Phrenic nerves switched on and off (in cervical region of the upper spinal cord)
  • Respiratory muscles activated
  • TI and TE affected
  • Information from respiratory muscles and lungs feed back to metabolic controller (using stretch receptors)
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21
Q

Whats the most important feedback to the metabolic controller in breathing?

A
  • Chemoreceptors (in carotid bodies) sensing H+ levels
  • Metabolic controller has H+ receptors itself

(essentially pH)

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22
Q

How would the response to CO2 change if the carotid bodies were removed?

A

Acute response to CO2 reduced by 40%

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23
Q

What effect does the metabolic controller have on the upper airways?

A
  • Dilate the pharynx and larynx on inspiration - reducing resistance
  • Narrow them on expiration - brake => smooth flow
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24
Q

What is breathing like in non-REM sleep?

A

Normal

25
Q

What is the carotid body and how does it work?

A
  • Chemoreceptor
  • Well vascularised bundle of cells
  • At the junction of the internal and external carotid arteries
  • Transmits a signal to the lower brain via the glossopharyngeal nerve
  • Hypoxia amplifies the response to hydrogen ions

(PCO2 receptors in airways of birds’ lungs, CO2 and H+ receptors at origin of aorta in other animals)

26
Q

Where is the pacemaker activity of the lungs located?

A
  • Many pacemakers
  • Close together in the brain stem
  • Inaccessible
  • 10 groups of neurones in the medulla, near the nuclei of cranial nerves IX and X (GP and vagus)
27
Q

What is the pre-Botzinger complex and how does it work?

A
  • One group of pacemaker activity
  • Essential for generating respiratory rhythm
  • ‘Gasping centre’ - gasping under low levels of oxygen
  • Rare to find disease
28
Q

What are the 6 groups of neurones in the brain stem involved in the generation of tidal breath?

A
  • Early inspiratory - initiates inspiratory flow via the respiratory muscles
  • Inspiratory augmenting - dilates pharynx, larynx and airways
  • Late inspiratory - signals end of inspiration & brakes the start of expiration
  • Expiratory decrementing - may brake passive expiration (adducting the larynx and pharynx)
  • Expiratory augmenting - activate expiratory muscles when ventilation increases
  • Late expiratory - sign end of expiration and onset of inspiration, may dilate the pharynx

(all discharge at different phases of the respiratory cycle)

29
Q

What muscles are used to open and close the airways?

A
  • Pharyngeal and laryngeal muscles

* Also act as a brake in breathing

30
Q

What is obstructive sleep apnoea?

A
  • Pharyngeal muscles lose tone (relax)
  • Airway is blocked
  • Snoring or stopped breathing
31
Q

What are cranial nerves V, IX and X involved in?

A

• V - afferents from nose and face (irritant)
• IX - from pharynx and larynx (irritant)
• X - from bronchi and bronchioles (irritant and stretch)
- Hering-Breuer reflex: pulmonary stretch receptors => inhibit activity of the medullary inspiratory neurones => termination of inspiration/expiration

(all lead to coughing and sneezing - defensive)

32
Q

What are the 2 parts of the metabolic controller?

A
  • Central part in medulla

* Peripheral part in carotid bifurcation

33
Q

What does a change in H+ reflect and how is it detected differently in the 2 parts of the metabolic controller?

A
  • H+ changes mirror PCO2 changes
  • Reflection of PCO2 changes occur slowly in ECF around medulla
  • Reflection of PCO2 changes occur rapidly in (hyperperfused) carotid bodies
34
Q

How can the sensitivity of the metabolic centre be tested?

A

• Carbon dioxide challenge
- ventilation is measured against changes in arterial PCO2
• Induced by patient breathing in and out of a 6L bag of oxygen primed with 7% CO2
• PCO2 rises 1 kPa per minute
• 30L/min rise in minute ventilation

35
Q

Describe a minute ventilation-arterial PCO2 graph (with reference to changes during hypoxia, chronic metabolic acidosis and chronic metabolic alkalosis)

A
  • Normal breathing (normoxia) - positive linear graph
  • Hypoxia - increased gradient
  • Acidosis - increased gradient + shift left
  • Alkalosis - decreased gradient
36
Q

What happens to ventilation when arterial PCO2 is goes below 5.3 kPa?

A
  • Ventilation reaches a minimum limit - not 0, when awake

* Drops to 0 when sleeping - breathing only starts when PCO2 is above apnoeic point

37
Q

How does a depressed ventilatory response to PCO2 change the ventilation-PCO2 graph?

A
  • Flattened slope (decreased sensitivity)
  • Rise in the set point (resting arterial PCO2)

(same changes in COPD due to mechanical limitation or airflow obstruction)

38
Q

What can cause a depressed ventilatory response to PCO2?

A
  • Disease affecting the metabolic centre
  • Sedative drugs suppressing the metabolic centre
  • Respiratory muscle weakness (peripheral)
39
Q

What happens during hypoxia (alveolar PO2/arterial SaO2 - minute ventilation)

A
  • Lower alveolar PO2 (high-altitude)
  • Higher minute ventilation to counter this
  • Graph shows this at fixed levels of PACO2 - higher PACO2, graph is further right and higher
  • Minute ventilation decreases at a decreasing rate with increasing alveolar PO2
  • Minute ventilation is higher at a lower arterial SaO2
  • 30L/min increase in minute ventilation for a 7kPa decrease in PaO2 (SaO2 99% => 60%)

(system is more sensitive to PCO2)

40
Q

What does ‘not isocapnic’ mean?

A
  • PaCO2 not controlled
  • Allowed to fall during hypoxic hyperventilation
  • Reduces the stimulus
  • Reduces the ventilatory response
41
Q

What happens when there is a fall in ventilation (in relation to PaO2 and PaCO2)?

A
  • Fall in PaO2
  • Rise in PaCO2
  • Fall in PaO2 increases sensitivity of carotid body to PaCO2 and H+
  • Ventilation increases - PaO2 increases
  • PaCO2 falls (negative feedback)
42
Q

Which gas values are controlled more in breathing?

A
  • PaCO2 and H+ controlled more tightly than PaO2

* arterial SaO2 better defended than arterial PaO2

43
Q

Why are control systems not well equipped for a fall in PO2 caused by altitude?

A
  • Hypoxic hyperventilation at a higher altitude => lower PCO2
  • Inhibited ventilatory response
  • Several days of acclimatisation required
44
Q

What is the difference between PO2, PAO2, PaO2 and SaO2?

A
  • PO2 - partial pressure of O2 in a given environment
  • PAO2 - partial pressure of O2 in alveoli
  • PaO2 - partial pressure of O2 dissolved in (arterial) blood
  • SaO2 - amount of oxygen bound to haemoglobin in arterial blood (saturation)
45
Q

What is metabolic acidosis and what causes it?

A

• Source of excess hydrogen ions comes from metabolism
• Not from inadequate ventilation
• Causes:
- diabetic ketoacidosis (lack of glucose in cells, starts to metabolise fatty acids)
- salicylate (aspirin) overdose
- renal tubular defects

46
Q

What are the compensatory mechanisms for metabolic acidosis?

A
  • Ventilatory stimulation lowers PaCO2 and H+
  • Renal excretion of weak (lactate and keto) acids
  • Renal retention of chloride (reduce strong ion difference)
47
Q

What is respiratory acidosis and what is the response?

A
  • Fall in ventilation
  • Rise in PCO2 and H+
  • Rapid response - stimulates the metabolic controller to increase breathing and return the system to normal
  • Slow response - renal excretion and retention of weak acids (back up response if the lungs can’t compensate)
48
Q

What determines the hydrogen ion concentration of the blood?

A
  • PCO2:bicarbonate ratio
  • PCO2 controlled by the lungs
  • Bicarbonate controlled by the kidneys (and lungs)
49
Q

What is metabolic alkalosis and what is the response?

A 
• Loss of H+ leads to excess HCO3-
• Causes:
- vomiting
- diuretics
- dehydration
  • Hypoventilation - raises PaCO2 and H+
  • Renal retention of weak acids
  • Renal excretion of chloride to increase strong ion difference
50
Q

What can lead to central (acute and chronic) hypoventilation?

A

Acute
• metabolic centre poisoning (drugs)
Chronic
• vascular/neoplastic disease of metabolic centre
• congenital central hypoventilation syndrome
• obesity hypoventilation syndrome
• chronic mountain sickness

51
Q

What leads to peripheral (acute and chronic) hypoventilation?

A 
Acute
• muscle relaxant drugs
• Myasthenia gravis
Chronic
• Neuromuscular with respiratory muscle weakness
52
Q

What are the hypoventilation conditions like in COPD?

A
  • Mix of central (won’t breathe) and peripheral (cannot breathe)
  • Could be due to difficulty of the controller in raising ventilation sufficiently or lung inefficiency
  • Or, could be due to the metabolic controller becoming insensitive - allowing higher PCO2
53
Q

What can hyperventilation be caused by?

A
  • Chronic Hypoxaemia
  • Excess H+ (metabolic)
  • Pulmonary Vascular Disease
  • Chronic Anxiety (psychogenic)
54
Q

What is breathlessness (rest vs. exercise)?

A
  • Like dyspnoea
  • At rest - difficulty with inspiration or expiration
  • On exercise - excessive breathing for the task
55
Q

What are the 3 types of breathlessness?

A
  • Tightness - difficulty inspiring
  • Increased Work and Effort - breathing at a high lung volume or against a resistance
  • Air hunger - sensation of a powerful urge to breath, mismatch between V.E demand and achieved
56
Q

How does the cerebral cortex compare V.E demand and V.E achieved?

A
  • Demand - efferent signal sent by metabolic controller to spinal motor neurones
  • Achieved - afferents from lung, chest wall and chemoreceptors
57
Q

How can breathlessness be scored?

A

10-point Borg Scale

58
Q

How can you test the strength of behavioural versus metabolic controller?

A
  • Breath holding time
  • Break point - expression of air hunger
  • Prolonged by increasing lung volume, lowering PaCO2 or isoxic/isocapnic breath near the break point
  • Acute thoracic muscle paralysis with Curare (poison) does not prolong it
  • BHT - stretch receptor drive x metabolic drive

Respiratory System (18 decks)

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