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Respiratory System Module > L23 Control of Breathing > Flashcards

L23 Control of Breathing Flashcards

1
Q

Why do you breathe?

A

You breath because you are responding to a need (or a load)
-most obesity is genetic
All action needs an integrate response

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2
Q

Normal, quiet breathing overview

A

Inspiratory area

  • -> 2 seconds on : Contraction of diaphragm–> normal inspiration
  • -> 3 seconds off: Relaxation of diaphragm –> normal expiration
  • diaphragm does the work and nothing else has to work. Humans are more efficient animals at breathing by far.
  • can go for longer and run faster
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3
Q

Heavy breathing overview

A

Inspiratory area

1) Contraction of diaphragm and external intercostals –> forced inspiration
- have to get alot of air in quickly
- have to work hard at that
2) Inspiratory area activates Expiratory area –> Contraction of internal intercostal and abdominals –> forced expiration
- have to get the air out
- have to keep inspiration and expiration in balance, (no point in breathing out while youre breathing in)

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4
Q

The feedback Loop *

A
  1. Central integration (medulla, pons)
  2. Efferent Output (ventilation, Bronchial muscle, Secretory glands)
    - send messages to your breathing muscles + bronchi and mucous glands to do things as your breathing
  3. Feedback (gas exchange, mechanics)
    - monitor breathing
  4. Afferent input
    - higher CNS centre (behaviour)
    - Lung receptors (mechanics)
    - Chemoreceptors (arterial blood)
    - response to decide what to do with next breath
    * *each breath is individually modulated to fit the task
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5
Q

4x Main aims of control of breathing

A
  1. To maintain the “interior” milieu: (normal PaO2, PaCO2, pH) (blood gases and pH)
  2. To meet the oxygen requirement of tissues during exercise, or stress (e.g. sepsis or other disease state) (CO2 production comes with O2)
  3. Protect arterial Po2 by minimising A-aDO2- gas exchange crucial (minimum load on respiratory muscles, spare energy to do kill)
  4. Minimise work of respiratory muscles - respiratory mechanics crucial to efficiency (decrease work by maintaining gas exchange incredibly efficient)
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6
Q

Potential problems with breathing

A

No feedback/afferents? (to brain to tell her to breath)
No efferents (doesnt know how to breath, muscles dont do anything)
No central integration (doesnt have correct messages to know what to do)
No drive to breath?

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7
Q

Ondine’s curse

A

-exceptionally rare
-good illustration of control of breathing going wrong
Uneventful delivery- resuscitation call to post delivery unit as baby apnoeic following feed
18 months later- well but tracheostomy since birth & respiratory supports (when asleep)
Crawls and moves normally without breathing support
Stops breathing if sleeps

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8
Q

Odine’s curse possible efferent output problem

A

Efferent output: Ventilation, Bronchial muscles, Secretory glands

  • this toddles ventilates appropriately when awake
  • this implies normal responses to efferent output of the respiratory control centres (can other normal activities like everyone else breathing fine)
  • i.e. the breathing muscles and lungs work normally
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9
Q

Odine’s curse possible feedback/afferent problem

A

(does she get any messages)
Appropriate breathing pattern when active (not fast or slow) so must be getting feedback form lungs and chest wall (normal central feedback/integration when awake)
Coughs if chokes so intact receptors
Yawns and sighs normally
Capable of maintaining normal oxygen and CO2 (normal blood gases) awake so must be sensing blood gases (not let them drift)

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10
Q

Odine’s curse possible central integration problem

A

Odine’s curse has No central drive/control to breathe? (tell ourselves to breath)

  • What stimulates breathing: medulla, pons
  • How is breathing controlled
  • How is it modulates to produce the most efficient breathing pattern
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11
Q

Rhythm and pattern generation

A

Rhythm generation =/= pattern generation

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12
Q

Rhythm generation

A

Reliable but highly liable
Up to 10^9 breaths in life (billions breaths moving 1/2 billion L of air)
Robust system that does not fail (cannot fail!) (cannot stop, system must be able to cope with health, sickness, exercise, because if stops=dead)
Flexible:
-up to magnitude of change in volume so rhythm is involved as frequency has to alter as does inspiratory and expiratory ratio (4-5L per min –> 20-25Lper min with exercise, change needs to occur 2-3 sec to maintain adequate O2 delivery to exercising muscles)
-very rapid and precise response to maintain gases during exercise, fever or sepsis (complex)

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13
Q

Pons and Medulla Simplified

A

Pons and medulla is where most of breathing happens
-involving multiple groups of neurons/Networks of neurons/centres
-lots of things feeding into the complex of centres
*NTS-nucleus tractus solitarius - feeds in
BC - Bottinger complex
preBotC- preBottinger complex - stimulus to breathe
VRG- ventral respiratory group
*RTN/pFRG- Retro-trapezoid nucleus/parafacial group - control expiration
*LC- Locus Ceruleus
Nuclei w. * thought to be responsive to pH and CO2 + some evidence lateral hypothalamus also responds

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14
Q

Current view of rhythmogenesis

A

Rhythm Generator=

  1. preBotC(stimulus to breathe/inspiration):
    - Not a simple pacemaker - inspiratory oscillator (rhythm and amplitude) (amplitude must be varied b/w inspiration and expiration in some expirated fashion) - inputs modulate output triggering inspiration (constantly changing balance b/w inspiration and expiration dependant on what you’re doing. Less time to breath in and out when doing exercise and moving alot of air)
  2. RTN/pFRG (active expiration) (also osscilator)
    - there has to be 1. an inspiratory “off” switch to allow expiration (so two remain integrated) and 2. ability to switch on active expiration (runs expiration during heavier exercise)
    - off switch must be very accurate as have to switch inspiration off abruptly and accurately to match the breathing pattern
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15
Q

Summary on oscillators for rhythmogenesis/rhythm generator

A

Oscillator= Rhythm (pacemaker) + Amplitude
-how it talks back to each other isnt clear cut
-but must talk b/w each other in or to make a balanced system
+ (cannot tell pacemaker in heart to stop (can stop breathing voluntarily))

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16
Q

Suprapontine stations after rhythm generator

A
  1. Voltional
    -phonation (changing breathing depending on talking and breathing in long or short sentence) (constantly interfering in the control of breathing as talk)
    -breath holding (cannot tell pacemaker in heart to stop (can stop breathing voluntarily))
    -hyperventilation
  2. Emotional
    -laughing, sighing, crying (interferes with breathing)
    Overall: alot of interference from above. some of which can control, others of which are built in)
17
Q

Neuromodulatory input for breathing

A

Neuromodulators e.g. adrenergic, peptides; cytokines

  1. Raphe (detecting CO2)
  2. Locus coerulus (stimulated by neurotransmitters)
  3. Dorsolateral pons (stimulated indirectly by hypoxia)
  4. Hypothalamus (Orexia substance: controls appetite, REM sleep and controls breathing) (only 200-200000 neurons) (falling asleep and still breathing)
18
Q

Sensory input for breathing

A

Sensory modulators (e.g. lung volume)

  1. Airways (cough, sneeze, gag) (respond to noxious substances, so doesnt damage lungs)
  2. Lung (stretch + irritant receptors)
  3. Muscle (stretch receptors, exercise, diaphragm)
  4. Hypothalamus (temperature)
19
Q

What are the overall diagram titles for current view of rhythmogenesis

A 
Inputs: 
1. Suprapontine modulators
2. Neuromodulators e.g. adrenergic peptides ; cytokines
3. Sensory Modulators (e.g. lung volume)
-->
Rhythm Generator
--> 
Central Pattern Generator (generating a pattern of ventilation appropriate to the situation)
20
Q

Current view of “patternogenesis”

A

Aim: mechanically most efficient pattern for task in hand i.e. least work of breathing
Pattern consisting of:
1. Frequency
2. Depth (tidal volume)
-1 and 2 sufficently meeting requirements (Enough O2 and removing CO2)
3. Inspiratory/ Expiratory timing (I/E ratio) (most efficient for your breathing muscles, so not wasting energy)
-breathing is “clean and green” using the least amount of CO2 is can

21
Q

Why is sleeping bad for the girl with Odine’s curse?

A

Rhythm generator centre:
RTN/pFRG: Active expiration:
-She has a single mutation in the Phox2b gene in the RTN
-Phox2b involved in responding to increasing CO2
-mutated: doesnt respond to CO2
–>awake: stimulating breathing in multiple ways (no problem)
–> asleep: using majority of things stimulating the osscilator (oscillator amplitude drops when sleeping) (normal sleep apnoeic)
–> asleep + mutation: CO2 drive very low, CO2 threshold changes, CO2 does not stimulate her to breath again, essentially doesnt bother breathing –> hypoxic
-will breath unless her brain is so hypoxic that it is in the process of shutting down and dying of hypoxia (fatal condition)

22
Q

Sleep Apnoea

A
  • everyone is apnoeic (stopped breathing) when sleeping. Normal. 2-5 sec.
  • reset threshold for CO2 from 3.8-3.9kPA –> 4.3-4.4 (increase 0.5 kPa)
  • CO2 rise stimulates you to breathe, so sleep breathing returns to normal
  • sometimes also occurs when moving b/w sleep stages as changing sensitivity
23
Q

Ondine’s Curse- CCHS

A

CCHS= Congenital Central Hypoventilation Syndrome
-At sleep onset: reset CO2 response threshold so brief apnoea results (seconds) till CO2 rises above new threshold
-Phox 1 gene mutation results in very damped response to CO2 so when asleep (& no other stimulus to breathe) inadequate drive to breathe till hypoxic (i.e. asphyxiating)- can be too late and respiratory arrest
NB: this is not the cause of Sudden infant death syndrome! (thought to be loss of serotonin response in infant brain(stem) + positioning)
-Serotonin is involved in the control of breathing
- women with SSRI serotonin inhibitor have a slightly higher incidence of Sudden infant death

24
Q

Hypoxia complicating pneumonia

A

Breathless
-Hypoxic,
-Hypocapnic (CO2 low as working so hard is blowing off CO2)
and acidotic (metabolic) (HCO3- bicarbonate levels off.
-Lactate levels: 1. Hypoxic as low BP so not delivering enough O2 to muscles 2. Respiratory muscles produce lactate when working overload
-Resp rate 34/min (Temp 38.9 C) (pyrexial)
-Saturation SpO2 80% (should be 95-98%)
-Lobar pneumonia

25
Q

Hypoxia - impact on breathing

A

How is hypoxia sensed?
-complex and still poorly understood (cellular (cell wall) sensing of hypoxia)
-Hypoxia inducible factor (HIFa) in cells is 95% recognised
-sensing hypoxia and feeding to its brainstem
Where is it sensed? (chemoreceptors- arterial blood)
-carotid bodies (+ aortic bodies to an extent)
-exclusively? (may have some central hypoxia sensing in our brain stems)

26
Q

Sensors of Hypoxia

A

Peripheral Chemoreceptors

  • Aortic Bodies
  • Carotid Bodies
27
Q

Aortic Bodies

A

Transmit via vagus
-Aortic bodies: aortic arch, sense pO2, pCO2 and pH - augmented response if both pO2 and pCO2 change (increase breathing)
-stretch receptors detecting blood pressure (there mostly for controlling cardiovascular responses)
-weak chemoreceptors compared to carotid bodies
NB: crucial role in control of BP involved in integrating cardiovascular & respiratory responses to exercise, stress and disease (physiologically intertwined) (applies to control of breathing + autonomic responses)

28
Q

Carotid Body

A

Sit at bifurcation of the carotid arteries
Account for all the hypoxic drive (?), but only 20% of the hypercapnic drive (?)
Feed via glossopharyngeal (9th cranial nerve) nerve to brainstem respiratory centres at level of RTN (retro-trapezoid nucleus. v involved in control of/switching of inspiration)

29
Q

Carotid Chemoreceptors

A

-carotid bodies glomus cell is awash in arterial blood
(blood leaving the carotid body is arterial level- sees so much O2 cannot take enough O2 out to make a difference to PO2)
-doesnt detect O2 Content in blood, but measures the arterial pressure of O2 in the plasma going past it
-triggers reaction in glomus cell, triggers depolarisation, sends stimulus up glossopharyngeal nerve to brain stem to breath harder
Low [O2), high [CO2] & high [H+] (low pH) lead to increased ventilation
-1. Rapid and 2. slow response - different transmitters
-2x frequencies response depending on the rate at which you become hypoxic (possibly through different transmitters)
-Hypoxic drive varies- at what level? (last used hypoxic drive/last time you were significantly hypoxic was when going through birth canal) - first breath of life (shoudnt happen)

30
Q

Carotid body- PaO2, PaCO2, pH sensor

A

Senses PaO2, not CaO2 (pressure not content) - due to very high blood flow and response - hyperbolic (Vt»f)
Powerful PaCO2 sensor if not supressed by normal PaO2 (threshold)
Prone to surgical trauma - carotid endarterectomy
-only need one cartoid body for adequate control of ventilation
-divers are cartoid as dont use hypoxic drive much
-used to remove both
? Dont think capable of breath by breath control of breathing (dont believe it can respond that fast and that accurately)

31
Q

Ventilatory response to hypoxia

A

Normally breathing 4-5L per min
Hyperbolic response to hypoxia= if stable CO2
PaO2 = 6.6 mmHg/8kPA= respiratory failure= not much response= 90-91% saturation carrying lots of O2
Non-isocapnic= PAco2= 37 = not as brathless as expect as have blown off CO2 so having a slumped hypoxic response
Normocapnic = breathing v hard= PAco2= 42.blowing off CO2 changing response to hypoxia
Hypercapnic= PAco2= 48

32
Q

Integrated response to hypoxia (Oxygen)

A
  • Hyperbolic response
  • Much less ventilatory response than pCO2
  • Resulting hyperventilation causes pCO2 to fall, thus decreasing overall response
  • Very little role in normal subjects (very variable hypoxic drives) but resting VE falls with carotid body resection (resting PaCO2 rises as result)
  • Very important in patients with severe lung disease or normal subjects at altitude
33
Q

When does the hypoxic response occur?

A
  • Sick
  • hypoxic with lung/heart disease
  • important if you want to climb everest (altitude- need to have a strong enough hypoxic drive to climb everest without oxygen)
  • -> Reason for altitude sickness
34
Q

Correcting hypoxia

A

-in ED shoving in O2 at 12Lmin-1 to increase O2. still not normal as some blood is being shunted in the lobar pneumonia (some blood will never be oxygenated no matter how much O2 is in the other alveoli)
-improve blood gas (increase CO2 + less acidotic, but still not normal)
With high flow oxygen
-Hypoxia improved but still some shunting through consolidated lung
-still breathless (low PaCO2) as other stimuli to breathing persist: (corrected hypoxia but other things stimulating breathing)
-fever
-inflamatory cytokines
-stress response so raised catecholamines (near death experience)
-C & J receptor stimulation
Direct and Indirect stimulation of respiratory control centres altering pattern and causing dyspnoea
-still feel breathless, and still breathing hard, but less hard than would have been when hypoxic

35
Q

65 year old man with COPD in ED

A

COPD= Chronic obstructive pulmonary disease
-3 day increasing breathlessness
-cyanosed (blue), respiratory rate 42/min, using accessory breathing muscles (neck, lifting shoulders up)- sweaty, distressed and very anxious
Arterial blood gas on air:
-PO2 better than pneumonia
-breathing faster
Hypoxic, hypercapnic (Increased CO2) and acidotic (respiratory acidosis)

36
Q

Ventilatory responses to hypoxia in COPD

A

PaO2= 7.4
Non-isocapnic=37
Normocapnic= PAco2=42
Hypercapnic= PAco2=48
-responding to hypoxia. but is more breathless than the patient with pneumonia as CO2 levels are higher, even though has a lower PO2 (has hypercapnia + bad lungs(feedback)
PaCO2= 8.4kPa (63mmHg)
Bircabonate HCO3- increased: illustrates chronic hypercapnia (for a long time) as has bad lungs
-but has had an acute increase as as become acidotic

37
Q

Regulation of Ventilation: Chemoreceptors

A

s

Respiratory System Module (25 decks)

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