Respiratory System Flashcards

1
Q

Explain mechanics of inspiration in the mammal

A
  1. Diaphragm contracts, moves caudally and flatters, expands size of thorax
  2. external intercostal muscles that run caudoventrally from rib in front to rib behind pull back rib forwards and out
  3. increases thorax size resulting in a drop in pressure in alveoli so breath in
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2
Q

Describe the mechanisms of active expiration

A

internal intercostal muscles that pull ribs back and in and abdominal wall muscles

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3
Q

What is the respiratory rate and what is it in most domestic species and horses

A

number of breaths in 1 min.
DS = 20-30 bpm
Horses = slower resting resp rate of about 10-12bpm

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4
Q

What is:

  1. Normal resting breathing
  2. Increases resp rate
  3. Increases resp depth
  4. Laboured brething
  5. Absence of breath
A
  1. Eupnoea
  2. tachypnoea
  3. Hyperpnoea
  4. Dyspnoea
  5. apnoea
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5
Q

What direction do external intercostal muscles run and where do they lift ribs

A

caudoventrally. lift ribs out adn cranially

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6
Q

What occurs during active expiration

A
  1. abdominal muscles push abdominal contents cranially forcing relaxed diaphragm to dome up into thorax
  2. costal portions of intercostal muscles which slope cranioventrally oull ribs caudally and inwards
  3. overall reduces size of the thorax, increasing pressure in alveoli
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7
Q

what is compliance?

A

the degree to whihc a change in transpulmonary pressure causes a change in volume of lung

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8
Q

what is compliance dependent on?

A
  1. elasticity in lung tissue and thoracic cage

2. surface tension in alveoli

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9
Q

what is surface tension and what deos it do in alevoli

A
  1. the interface between fluid lining the respiratory bronchioles, alveolar ducts and alveolar sacs and air forms H bonds, creating surface tension.
  2. it tends to reduce surface area, thus ST in alveoli will resist expansion of the lung which reduces compliance of the lung.
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10
Q

how is surface tension resistance counteracted in the alveolus

A
  1. by type 2 alveolar cells producing surfactant- a mixture of phospholipids, proteins adn Ca2+ which reduces the formation of H bonds between water molecules and hence reduces ST inside alveolus
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11
Q

how does surfactant counteract the alveolar resistance

A
  1. reduces the formation of H bonds between water molecules as hydrophilic heads of phospholipids dissolce in liquid linign alveolus and philic tails remain on inside preventing H bonds
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12
Q

What is one of the reasons premature neonates struggle to survive. what can this lead to and what deos it present as?

A
  1. due to their inadequate production of surfactant

2. leads to respiratory distress syndrome, which presents with severe dyspnoea (laboured breathing)

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13
Q

Why is sighing important with surfactant production? What could occur during prolonged general anaesthesia if inadequate ventilation is provided

A
  1. signing can stimulate release of surfactant

2. develop atelectasis = collapse of alveoli

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14
Q

What is pressure in alveolus dependent on? Equation

A
  1. radius
  2. surface tension
    P = πŸπ“/r
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15
Q

If a smaller alveolus has a higher internal pressure than a larger why don’t they collapse as air moves down p gradient into larger alveoli

A

Amount of surfactant is the same in every alveoli so smaller alveoli have higher conc

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16
Q

What is airway resistance governed by?

A
  1. length and radius of the tube
  2. viscosity of the substance travelling through
  3. turbulence of the air in the airway
17
Q

How does turbulence change as air moves through respiratory system?

A
  1. declines with each division of the airway becuase the total cross sectional area of the airways increases with each division
18
Q

What is the smooth muscle in the walls of the airways innervated by?

A

autonomic nervous system

19
Q

What effect does activation of the sympathetic ANS on smooth muscle cells thus on ventilation?

A

relax due to stimulation of beta 2 adrenoreceptors, causing an increase in the radius of the airways, therefore a reduction in resistance to flow and increased lung ventilation to allow for an increases oxygen demand

20
Q

Definition of tidal volume. what is normal tidal volume in domestic species

A
  1. volume of air moved during a respiratory cycle (normal volume)
  2. normal = around 10-15 ml/kg
21
Q

how to calculate minute ventilation

A

multiplying tidal volume by number of breaths

22
Q

What is residual volume. What is it due to

A

volume of air that remains after a full expiration. Due to limitations in compressibility of the thoracic wall

23
Q

What is functional residual capacity

A

Expiratory reserve volume + residual volume = total amount of air left in lungs after normal expiration at rest

24
Q

What is FO2.

What is partial pressure

A
FO2 = 0.21 = proportion of gas mixture that is made up of O2
Pa = pressure exerted by an individual gas within a gas mixture
25
Q

DEscribe how gas exchange occurs at the alveolus

A
  1. blood entering lung caps from RV with have low pa O2 and high pa CO2
  2. so CO2 will diffuse into alveolar air and O2 with doffuse into blood until eq is reached
26
Q

Talk about ventilation:perfusion in the alveolus

A
  1. Ideal ventilation: perfustion are matched = enabled full equilibrium of gases to be achieved = correct transfer of gases
  2. In reality ratio mismatched. If low ventilation but normal perfusion
27
Q

What is dead space

A

areas which are ventilated but don’t aprticipate in gas exchange e.g. anatomical (airways) unperfused alveoli = functional dead space

28
Q
  1. what 2 factors deos alveolar compliance depend on
A
  1. Surface tension

2. Elasticity

29
Q

what effect will stimulation of beta 2 adrenoreceptors have on resistance to movement of air through the airways

A

decrease because causes relaxation and dilation of smooth muscle airway

30
Q

Why is alveolar paO2 lower than pO2 in room air

A
  1. constant exchange of oxygen at alveolus and not replacing all of that air every time
  2. water vapour in gas mixture so everything has reduced partial pressure