Mechanisms and Regulation of Breathing Flashcards

1
Q

What are the pressures at the end of a normal breath?

A

Atmospheric pressure= alveolar pressure

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2
Q

What is elastic recoil?

A
  • Having the property of returning to the original shape after being distorted
  • To spring back
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3
Q

What happens as you breathe out?

A
  • Elastic recoil in the lung pulls inwards

- Chest wall resists inward distortion from resting position

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4
Q

What does equilibrium result in?

A

Negative pleural pressure

Lung elastic recoil inward= chest wall elastic recoil outward

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5
Q

How does gas get into the lungs?

A

Expand chest wall creates differences in pressure- pressure gradient as atmospheric greater than alveolar

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6
Q

Describe the mechanism of inspiration

A

Expansion of chest wall, movement of ribs via external intercostal muscles
Inspiratory neural activity from brain via phrenic nerve

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7
Q

What happens at the end of a breath in?

A

Lung recoil is increased
Elastic forces act inward
No inspiratory neural activity

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8
Q

What is the difference between inspiration and expiration in terms of energy and time?

A
Inspiration= active, shorter
Expiration= passive, longer
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9
Q

Why is forced expiration active?

A

Internal intercostals and abdominal muscles contract

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10
Q

What is Minute Ventilation?

A

Vt x fR (litres/min)
Vt- tidal volume, depth of breath
fR= respiratory frequency (breaths per minute)

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11
Q

What happens when central neural control is removed?

A
  • Cortex and upper pons= slow gasping breaths
  • Pons= return to rhythmic breathing
  • Medulla= breathing stops
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12
Q

Which part of the brain is controlling voluntary/ involuntary respiratory?

A
Voluntary= cortex
Automatic= pons, medulla, spinal cord
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13
Q

What are the groups in the brainstem?

A

Pontine Respiratory Group
Ventral Respiratory Group
Dorsal Respiratory Group

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14
Q

How is the basic rhythm of breathing generated?

A
Inspiratory neurones activate expiratory neurones 
Expiratory neurones (medullary neurones- VRG, DRG) inhibit respiratory neurones
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15
Q

What is the effect of large inspiration?

A

Large activation of expiratory neurones, expiratory neurones cause contraction of expiratory muscles

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16
Q

What things change the basic breathing pattern?

A

-Inhaled noxious substances
-Speech/ volition
-Sleep (pons neurones 15% drop to sleep)
Exercise

17
Q

What are the feedback inputs to the respiratory rhythm generator?

A

Lung receptors= Slowly Adapting Receptors, Rapidly Adapting Receptors, C-fibre endings (afferent nerve fibres carried in vagus)
Chemoreceptors= central, peripheral (report to medulla)

18
Q

How does lung receptor activity affect pattern of breathing?

A

Vagal nerves cut= slower

Vagal nerves stimulated= faster

19
Q

Describe Slowly Adapting Receptors

A
  • Stretch receptors
  • Mechanoreceptors situated close to airway smooth muscle
  • Stimulated by stretching of airway walls during inspiration
  • Help initiate expiration and prevent over inflation of the lungs
  • Initiate Hering-Breuer inflation reflex (prolonged inspiration produces prolonged expiration)
  • Afferent fibres= myelinated
20
Q

Describe Rapidly Adapting Receptors

A
  • Irritant receptors
  • Located in airway epithelium
  • Primarily a mechanoreceptor so respond to rapid lung inflation
  • Respond to chemicals (e.g. histamine), smoke, dust
  • RARs in trachea and large bronchi initiate cough, mucus production, bronchoconstriction
  • Afferent fibres= myelinated
21
Q

Describe bronchial C-fibres Endings

A
  • In airway epithelium
  • Unmyelinated nerve fibres
  • Stimulated by increased interstitial fluid (oedema) and various inflammatory mediators (histamine, prostaglandins, bradykinins)
22
Q

Describe Pulmonary C-fibres

A

Juxtapulmonary capillary receptors, J-receptors

Endings close to pulmonary capillaries

23
Q

How do chemoreceptors respond to arterial O2 and CO2?

A

Peripheral- fast response to arterial pO2, pCO2, (H+)

Central- slow response to arterial pCO2

24
Q

What is the terminology for different oxygen levels?

A

Above normal= hyperoxia
Normal= normoxia
Below normal= hypoxia (in blood= hypoxaemia)

25
Q

What is the terminology for different CO2 levels?

A

Above normal= hypercapnia
Normal= normocapnia
Below normal= hypocapnia

26
Q

How do central chemoreceptors work?

A

pCO2 in arterial blood crosses blood-brain barrier
pCO2 + H2O= (H+) + HC03-
Central chemoreceptors on surface of medulla send signals to medullary rhythm generator

27
Q

What happens in severe chronic obstructive pulmonary disease?

A

Hypoxia and CO2 build up= chronic hypercapnia= loss of sensitivity of central chemoreceptors
Drive to breathing =hypoxia, drive abolished if patient given high inspired O2= further hypoventilation= further increase in arterial pCO2= CO2 narcosis, acidosis= death

28
Q

How is neural activity involved in sleep?

A
Midbrain neural activity stimulates breathing during wakefulness ("wakefulness drive to breathe"
Neural activity (cortex, pons, medulla) also regulates muscles in the upper airway (above the trachea)
29
Q

What occurs during sleep?

A

Respiratory drive increases (loss of wakefulness drive)- reduction in metabolic rate, reduced input from higher centres such as pons and cortex
Loss of tonic neural drive to upper airway muscles

30
Q

What are the consequences of loss of wakefulness drive?

A

Patients with impaired ventilation (e.g. muscle weakness, severe lung disease, neuropathy or spinal deformity) first develop respiratory failure (raised arterial CO2) during sleep

31
Q

What are the types of upper airway muscle activity?

A

Phasic

Tonic

32
Q

Describe phasic activity

A

Contraction of upper airway muscles
Opening of upper airway
Facilitates inward airflow
Similar activity in diaphragm/ external intercostals which generate inspiration

33
Q

Describe tonic activity

A

Continuous background activity
Tends to maintain patent airway
Varies with state of alertness
Similar to activity in skeletal muscles which maintain posture

34
Q

How does phasic ad tonic activity relate during sleep?

A
Loss of tonic activity to upper airways
Airways collapse (obstruct) to give cessation of breathing (apnoea)
35
Q

Describe Obstructive Sleep Apnoea

A

Common
Fragments sleep causing daytime sleepiness
Important cause of traffic accidents
Risk factors: obesity, alcohol, nasal obstruction, anatomical abnormalities

36
Q

What drugs in respiration are depressants?

A
  • Anaesthetics= almost all
  • Analgesics= opioids (morphine and its analogues)
  • Sedatives (anti-anxiolytics, sleeping tablets)= benzodiazepines (diazepam, temazepam)
37
Q

What drugs in respiration are stimulants?

A

Primary action= doxapram

Secondary action= beta 2 agonists (bronchodilators)

38
Q

How can breathing control be disrupted?

A
  • Airflow obstruction (lower or upper)
  • Weakness or deformity of respiratory muscles
  • Sedative drugs