Respiratory Physiology Flashcards

1
Q

What are the functions of the respiratory system

A

Gas exchanged
Acid base balance
Protect from infection
Communication

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2
Q

What happens in systemic circulation

A

02 rich blood from L side of heart to tissue

CO2 rich blood from tissue taken to R side

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3
Q

What happens in pulmonary circulation

A

C02 rich blood from R rich goes to lungs for gas exchange

Returns O2 rich blood to L side

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4
Q

What is the pulmonary circulation compared to systemic

A

High flow but low pressure as 5l takes same time as it does to go through systemic

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5
Q

How does actual lung tissue get its blood supply

A

From systemic

Part of bronchial circulation

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6
Q

What is the conducting zone of the respiratory system

A

Trachea
Primary bronchi
Bronchioles
Resistance decreases as go down as less molecules and more anatomical dead space

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7
Q

What is the respiratory zone / exchange

A

Alveoli surrounded by pulmonary capillaries

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8
Q

What makes alveoli good for gas exchange

A

Single layer of epithelium

Elastic fibres that stretch when you breath in creating a recoil

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9
Q

What are type 1 alveoli for

A

Gas exchange

Simple sqaumous

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10
Q

What are type 2 alveoli for

A

Producing surfactant - decreased tension, prevent collapse and increase compliance

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11
Q

What are the lungs enveloped in

A

Visceral (outer surface of lungs) and parietal (inner surface of ribs) pleura

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12
Q

What is the space between lungs and thoracic wall called

A

Pleural space

Filled with pleural fluid (30ml) which creates a seal holding lungs to thoracic wall to move with breathing

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13
Q

What content state are the lungs in

A

Wanting to recoil due to inspiration
Elastic recoil pushes chest out when inspire
Creates a negative pressure in the pleural cavity

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14
Q

What are muscles of inspiration

A

Diaphragm = most important
External intercostal

Accessory
Scalene
SCM

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15
Q

What are muscles of expiration

A

Passive at rest
Internal intercostal
Abdominal

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16
Q

What is Boyle’s law

A

Pressure is inversely proportional to volume

As pressure increases volume decreases

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17
Q

What happens in inspiration

A

Diaphragm contracts pushes abdominal cavity down
External intercostal and scalene pull ribs out
Leads to increase in volume of thoracic cavity
Intrapleural pressure decreases
Alveolar pressure becomes < than atmosphere and air drawn in

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18
Q

What happens in passive expiration

A

Muscles relax
Elastic recoil of stretched lungs allow them to recoil back to original volume
Decreased volume so increased P and air drawn out

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19
Q

What happens in forced expiration

A

Contraction of abdominal muscles push thoracic cavity up
Internal intercostal pull ribs in
Alveolar pressure increases pushing air out
Reduces duration of breathing cycle

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20
Q

What happens in forced inspiration

A

Similar to normal
Requires accessory muscles
SCM, scalene, pec majro and minor, lattismus dorsi, serratura anterior

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21
Q

What is the alveolar pressure

A

Pressure inside thoracic cavity

Equal to atmosphere

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22
Q

What is intrapleural pressure

A

Pressur inside pleural cavity

Always -ve due to state of wanting to recoil

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23
Q

What is transpulmonary pressure

A
Difference between alveolar and intrapleural
Always +ve
Opposes elastic recoil
Dpeendent on volume of lung
Larger lung = larger pressure
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24
Q

What happens between breaths at the end of an unforced expiration

A

No air I flowing
Lungs stretched and attempting to recoil
Chest wall attempting to move out
Creates sub atmospheric intrapleural pressure
Transpulmonary pressure opposes this recoil

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25
Q

What part of brains is involved in subconscious ventilation

A

Pons

Medulla

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26
Q

What nerves

A
Phrenic = diaphragm
Intercostal = external intercostal
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27
Q

What part of medulla set breathing pattern

A

DRG - control muscles of inspiration through phrenic and intercostal, receive sensory from vagus

VRG - control muscles of larynx / pharynx

PRG - receive sensory info from DRG, speak with higher brain to initiate and terminate inspiration

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28
Q

How do you change respiratory drive

A
Emotion via limbic
Voluntary 
Mechano-sensory
Swalloing inhibits 
Drugs 
Chemical composition detected by chemoreceptors
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29
Q

What is the primary stimulus for changes in ventilation

A

CO2
Detected by central chemoreceptors in medulla
More sensitive to small changes in PCo2

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30
Q

How do central chemoreceptors work

A

Detect changes in H+ in CSF which are related to CO2

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31
Q

What happens when there is an increase in CO2

A

Rate and depth of breathing increases to remove CO2

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32
Q

Where are peripheral receptors located

A

Carotid and aortic bodies

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33
Q

What do peripheral receptors detect

A

Change in arterial Po2 NOT CONTENT

Relatively insensitive and require a significant fall in Po2 or rise in H

34
Q

Can you override peripheral

A
No
Effects are instantaneous 
Increased RR and TV 
Blood flow directed to kidney and brain 
INceased CO
35
Q

When are peripheral chemoreceptor important

A

If chronic elevation of PCO2
Central response is blunted
Patients go into hypoxic drive and rely on peripheral receptors to detect O2 falling

36
Q

Why do you have to be careful in patients who rely on peripheral

A

Careful when giving O2 to patients with chronic lung disease e.g. COPD
They will have elevated PCO2
Rely only on O2 levels for their breathing

37
Q

What does hypoventilation cause

A

Increased CO2
Blood = acidic
COPD / neuro / chest wall

38
Q

What does hyperventilation cause

A

Decreased CO2 and alkaline blood
Decreases free Ca = paraesthesia / cramps
Anxiety / HF / PE

39
Q

What drugs affect ventilation

A

Opiods / barbiturates = depress
Anasthetic = increase RR but decrease TV
NO = blunts peripheral chemo so if chronic lung = no way to control ventilation

40
Q

What happens at altitude

A

Peripheral detect fall in O2 = hyperventilation
Resulting hypocapnia and alkalosis stop any increase in RR due to central chemoreceptors
After a few days kidney works to remove alkalosis so peripheral takes over again
Rise in DPG
Polycythaemia - physiological as erythropoietin produced from kidney but can cause hypervisocotyi

41
Q

If an anaemic patient has o2 content 1/2 normal what happens to RR + depth

A

No change
Receptors respond to partial pressure
Amount of O2 in plasma is normal but just decreased RBC to hold O2 so content reduced
Haem saturation will be the same

42
Q

What is more uncomfortable
1- a high PCo2 and low Po2
2- a low o2 and no CO2

A

1

PACO2 increased and impairs the gradient so will stay in blood

43
Q

What is the pressure of O2 and CO2 in artery PA

A
O2 = 100
CO2 = 40
44
Q

What is the pressure of O2 and CO2 in alveoli Pa

A
O2 = 100
CO2 = 40
45
Q

What is the pressure of O2 and CO2 in venous Pv

A
O2 = 40
CO2 = 46
46
Q

What is the difference between partial pressure and o2 content

A
Content = all 02 in solution 
Partial = solubility
47
Q

How does gas exchange work

A

Gas moves across permeable membrane down pressure gradient until equilibrium reached

48
Q

What is the rate of diffusion affected by

A
Directly proportional to gradient 
Solubility - more soluble = faster
SA - larger = faster (alveoli destroyed in emphysema so decreased SA) 
Distance - smaller = faster 
Molecular weight - smaller = faster
49
Q

What diffuses faster CO2 or O2

A

CO2

Although O2 is smaller but CO2 is much more soluble

50
Q

Once O2 is in the blood what happens

A

Binds to haemoglobin = oxyhaemoglobin
Only 3ml O2 dissolves per L plasma so Hg greater increases capacity of O2
Hg = high affinity for O2 so will pull until saturated

51
Q

Does exercise affect gas exchange

A

No as only takes 0.25s

52
Q

What type of molecules does haemoglobin bind

A
92% = HbA (2 alpha and 2 beta) 
8%. = HbF (gamma chains replace beta)
53
Q

What determines degree of saturation

A

Partial pressure of O2

54
Q

When does partial pressure of O2 begin to affect saturation

A

Almost 100% saturated at normal PaO2 100mHg
90% if PaO2 60
When PaO2 = 40 very difficult to saturate Hg and deliver O2 to cell

55
Q

If two individuals with partial pressure of 100 and 80 who has most O2

A

No diff in saturation

Individual with most haemoglobin

56
Q
What are variables in oxyhemoglobin dissociation curve 
Acidic 
PCO2
Hyperventilation
Asthma
Temp 
DPG
A

More acidic = more Co2 and less O2 and curve shifts to right (less saturated)
Increase pCo2 = shifts to R
Voluntary hyperventilation = shifts to the L
Asthma = shifts to R as constricted so decreased ventilation
Temp = shifts to R as want oxygen available for exercise
DPG added = shifts to R as produced when No o2 so want o2 to be available

57
Q

What type of haem molecules have highest affinity for oxygen

A

Myoglobin - as muscles need most
Fetal - 2nd most as want to extract from maternal vblood
HbA has least affinity

58
Q

Can you have a low partial pressure and normal O2 content

A

No
Partial pressure is what pushes O2 onto haemoglobin
If o2 content low but partial pressure normal then haemoglobin would still be saturated

59
Q

What happens in anaemia

A

Partial pressure is normal
O2 content reduced as not enough RBC to carry O2
Ventilatory drive is normal as PaO2 is normal

60
Q

What happens in CO poisoning

A

CO binds to haemoglobin

Affinity much greater than O2 and dissociates more slowly

61
Q

What are the symptoms of CO poisoning

A
Hypoxia
Anaemia
Headache
Cherry red skin
Nausea
RR unaffected as PCo2 is normal
62
Q

How is Co2 transported in the blood

A

Only 7% dissolves in plasma
93% diffuse into RBC
Converted to H2CO3 with H20 -> HCO3 + H
Products removed to keep reaction going

63
Q

What enzyme catalyses

A

Carbonic anhydrase

64
Q

What are products exchanged for

A

HCO3 for Cl = chloride shift
H binds to deoxyhaemoglobin to bufer
If CO2 increases not enough Hg = acidosis

65
Q

How does CO2 go back to alveoli

A
Pco2 alveoli < venous blood 
CO2 diffuses out of RBC
Disturbes Co2-HCO3
H leaves Hg 
CL shift reverses 
Co2 diffuses into alveoli
66
Q

What needs to be matched adequately

A

Ventilation
Perfusion
Usually both 5l/ minute
Ideally ratio would be 1

67
Q

What affects ventilation / perfusion

A

Disruption of blood flow - influenced by Pa (hydrostatic) and PA (alveolar)
Resistance

68
Q

What happens as you move from the apex to base of the lung

A

Ventilation and perfusion rise
Perfusion increases at a greater rate
Pleural pressure greater at base = more compliant and greater ventilation
Hydrostatic pressure is decreased at apex = decreased blood flow and perfusion

69
Q

What happens at the base of the lung

A
Blood flow high as Pa is higher 
Pa > PA
Low resistance 
Blood flow > ventilation 
V/Q = 0.8
70
Q

What happens at the apex of the lung

A
Blood flow low as Pa < PA
Alveoli compressed and more compliant
Higher resistance 
Ventilation > blood flow 
V/Q = 3.3
71
Q

What happens when perfusion > ventilation

V/Q <1

A

Po2 falls in the alveoli and Pco2 will rise
Less O2 in alveoli than is being pulled out
Decrease in partial pressure of O2
Increase in partial pressure CO2
Lose gradient so can’t get ri dog CO2 in blood
Shunt form as blood goes from R-L without getting O2

72
Q

What could cause V/Q <1

A
Low O2 in air 
Poor alveolar ventilation as decreased compliance 
Increased resistance
Drug overdose 
COPD / asthma / pneumonia / IRDS
73
Q

What happens to deal with this

A

Hyperventilation
Blood vessels in lung constrict
Mild bronchial relaxation
Causes hypoxia as reduced ventilation, CO2 can still get out as rest of lung takes over so no hypercapnia = type 1

74
Q

What happens when ventilation > perfusion

V/Q >1

A

Increase in alveolar O2

75
Q

What causes V/Q >1

A

Blood clot / PE

76
Q

What happens to deal with this

A

Pulmonary vasodilatation to well perfused areas so V/Q in this is <1
Bronchial constriction if decrease in PCo2

77
Q

What is type 1 respiratory failure

A

PaO2 <8kPa
PaCO2 normal or low
Problem is with diffusion or exchange so cannot oxygenate haemoglobin
Unaffected part of lung will keep CO2 out

78
Q

What is type 2 respiratory failure

A

PaCO2 >6.5kPA
Respiratory mechanism fails
Not usually primary

79
Q

What is hypoxia

A

Insufficient O2 supply

80
Q

What is hyperaemia

A

O2 arterial supply low

81
Q

What causes hypoxaemia in type 1

A

V/Q mismatch = most common and responds well to increase FIO2
Shunt = no ventilation so respond poorly to FIo2
Alveolar hypoventilation due to reduced res drive - will respond to increase in FIo2
Diffusion impairment if loss of alveoli