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Respiratory > Physiology > Flashcards

Physiology Flashcards

1
Q

what is internal respiration?

A

refers to the intracellular mechanisms which consume oxygen and produce carbon dioxide.

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2
Q

what is external respiration?

A

refers to the sequence of events that lead to the exchange of oxygen and carbon dioxide between the external environment and the cells of the body.

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3
Q

what are the four steps of external respiration?

A

1- ventilation (gas exchange between the atmosphere and alveoli)
2- exchange of 02 and C02 between air in alveoli and blood in pulmonary capillaries.
3-binding and transport of 02 and C02 in the circulating blood
4 - exchange of 02 and C02 between blood and tissues

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4
Q

what are the four systems involved in external respiration?

A
  • respiratory
  • cardiovascular
  • haematology
  • nervous
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5
Q

describe the anatomy of the respiratory system.

A

nasal passages and mouth > pharynx >larynx > trachea > right and left bronchus > bronchioles > terminal bronchiole > alveoli

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6
Q

what is boyle’s law?

A

At any constant temperature the pressure exerted by a gas varies inversely with the volume of the gas.

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7
Q

how does air move into the lungs during inspiration?

A

The intra-alveolar pressure must become less than atmospheric pressure for air to move into the lungs during inspiration. It does this by active contraction of inspiratory muscles. during inspiration the thorax and lungs expand reducing intra-alveolar pressure and allowing air to enter down its pressure gradient.

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8
Q

what two forces hold the thoracic wall and the lungs in close opposition?

A

1 - intrapleural fluid cohesiveness = the water molecules in the inrapleural fluid are attracted to each other and resist being pulled apart, hence the pleural membranes tend to stick together.
2 - The negative intrapleural pressure = the sub-atmospheric intrapleural pressure creates a transmural pressure gradient across the lung and chest walls. so the lungs are forced to expand outwards and the chest is forced to squeeze inwards.

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9
Q

what is atmospheric pressure?

A

the pressure caused by the weight of the gas in the atmosphere on the Earths surface - normally 760mm Hg at sea level.

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10
Q

what is intra-alveolar (intrapulmonary) pressure?

A

pressure within the lung alveoli. (760 mm Hg when equilibriated with atmospheric pressure)

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11
Q

what is intrapleural (intrathoracic) pressure?

A

pressure exerted outside the lungs within the pleural cavity, usually less than atmospheric pressure.

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12
Q

what is inspiration?

A

= an active process depending on muscle contraction

  • the volume of the thorax is increased vertically by contraction of the diaphragm flattening out its dome shape.
  • the external intercostal muscle contraction lifts the ribs and moves out the sternum (bucket handle mechanism).
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13
Q

what is expiration?

A

-normal expiration is a passive process brought on by the relaxation of inspiratory muscles. The chest wall and lungs resume their original size and the intra-alveolar pressure rises. The air then leaves down its pressure gradient until the intra-alveolar pressure equals the atmospheric pressure.

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14
Q

what is a pneumothorax?

A

= air in the pleural space

  • can be spontaneous, traumatic or iatrogenic and air can have entered from outside of from the lungs.
  • this can abolish transmembrane pressure leading to lung collapse.
  • small pneumothorax can be asymptomatic. larger pneumothorax may have symptoms such as shortness of breath and chest pain
  • physical signs = hyperressonant percussion note and decreased/ absent breath sounds.
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15
Q

what causes the lungs to recoil during expiration?

A
  • elastic connective tissue in the lungs

- alveolar surface tension (most important)

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16
Q

what is alveolar surface tension?

A
  • attraction between water molecules at liquid air interface
  • in the alveoli this produces a force which resists the stretching of the lungs
  • if the alveoli were lined with water alone the surface tension would be too strong so the alveoli would collapse.
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17
Q

what is LaPlace’s law?

A

the smaller the alveoli, the higher the tendency to collapse

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18
Q

what is pulmonary surfactant?

A

= a complex mixture of lipids and proteins secreted by type 2 alveoli

  • it lowers alveolar surface tension by interspersing between the water molecules lining the alveoli.
  • it lowers the surface tension of smaller alveoli more than larger alveoli, preventing collapse.
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19
Q

what can cause respiratory distress of a new born?

A

developing foetal lungs are unable top produce surfactant until late pregnancy so premature babies may not have enough surfactant. This may lead to the baby making very strenuous inspiratory efforts in an attempt to overcome the high surface tension and inflate the lungs.

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20
Q

what is alveolar interdependence?

A

if an alveolus starts to collapse the surrounding alveoli are stretched and then recoil exerting expanding forces in the collapsing alveolus to open it.

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21
Q

what are the major inspiratory muscles?

A

diaphragm and external intercostal muscles

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22
Q

what are the accessory muscles of inspiration?

A

(contracts only during forceful inspiration) sternocleidomastoid, scalenus and pectoral

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23
Q

what are the muscles of active expiration?

A

abdominal muscles and internal intercostal muscles.

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24
Q

what is tidal volume?

A

volume of air entering or leaving lungs during a single breath (average 0.5L)

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25
Q

what is inspiratory reserve volume?

A

Extra volume of air that can be maximally inspired over and above the typical resting tidal volume (3.0L average)

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26
Q

what is expiratory reserve volume?

A

Extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume. (average 1L)

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27
Q

what is residual volume?

A

minimal volume of air remaining in the lungs even after maximal expiration (1.2L)

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28
Q

what is inspiratory capacity?

A

= inspiratory reserve volume + tidal volume

maximum volume of air that can be inspired at the end of a normal quiet expiration = 3.5L average

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29
Q

what is functional residual capacity?

A

= Expiratory reserve volume + reserve volume

volume of air in lungs at the end of normal passive expiration - 2.2L average

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30
Q

what is vital capacity?

A

maximum volume of air that can be moved out during a single breath following maximal inspiration.
= inspiratory reserve volume + tidal volume + expiratory reserve volume. (4.5L average)

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31
Q

what is total lung capacity?

A

vital capacity + residual volume

-(5.7L average)

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32
Q

why might residual volume increase?

A

when elastic recoil of the lungs is lost e.g. in emphysema

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33
Q

what can volume time curves/ dynamic lung volumes tell you?

A

FVC = forced vital capacity (maximum volume that can be forcibly expelled from the lungs following a maximum inspiration)
FEV1 = Forced expiratory volume in one second. Volume of air that can be expired during the first second of expiration in an FVC determination.
FEV1/FVC ratio = the proportion of the FVC that can be expired in the first second (normally more than 70%)

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34
Q

what does a low/ normal FVC, a low FEV1 and a low FEV1/FVC ratio suggest?

A

airway obstruction

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35
Q

what does a low FVC, a low FEV1 and a normal FEV1/FVC ratio suggest?

A

lung restriction

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36
Q

what does a low FVC, a low FEV1 and a low FEV1/FVC ratio suggest?

A

a combination of obstruction and restriction.

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37
Q

what is the primary determinant of airway resistance?

A

the radius of the conducting airway.

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38
Q

what do parasympathetic and sympathetic stimulation cause in the airway?

A 
parasympathetic = bronchochonstriction
sympathetic = bronchodialation
39
Q

describe how dynamic airway compression makes active expiration more difficult in patients with an airway obstruction.

A
  • the rising pleural pressure during active expiration compresses the alveoli and airway.
  • if there is an obstruction, the driving pressure between the alveolus and airway is lost over the obstructed segment, causing a fall in airway pressure. this results in an increased likelihood of collapse.
40
Q

what is pulmonary compliance?

A

= a measure of effort that has to go into stretching or distending the lungs. it is the volume change per unit of pressure change across the lungs. the less compliant the lungs are, the more work is required to produce a given degree of inflation.

41
Q

what does decreased pulmonary compliance mean for a patient?

A
  • decreased by factors such as pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia, absence of surfactant.
  • decreased pulmonary compliance can cause shortness of breath on exertion and a restrictive pattern of lung volumes in spirometry.
42
Q

what does increased pulmonary compliance mean for a patient?

A
  • compliance can become abnormally increased if the elastic recoil of the lungs is lost.
  • increased compliance occurs in emphysema. patients have to work harder to get the ait out of lungs (hyperinflation)
  • dynamic airway obstruction will also be aggravated in patients with COPD
  • compliance increased with increasing age.
43
Q

when is the work of breathing increased?

A

(normally around 3% of energy)

  • when pulmonary compliance is decreased- when elastic recoil is increased
  • when elastic recoil is decreased
  • when there is a need for increased ventilation.
44
Q

what is pulmonary ventilation?

A

= tidal volume X respiratory rate (the volume of air breathed in and out per minute)

45
Q

what is alveolar ventilation?

A

the ventilation takin into account the anatomical dead space (not available for gas exchange due to inadequate perfusion)
= (tidal volume - dead space volume) X respiratory rate
(the volume of air exchanged between atmosphere and alveoli per minute)

46
Q

why is it more advantageous to increase depth of breathing?

A

due to alveolar dead space.

47
Q

how do perfusion and ventilation vary from the bottom to the top of the lung?

A 
perfusion = greatest at the bottom and less nearer the top.
ventilation = less significant decrease but still higher at the bottom than the top.
48
Q

how do local controls act on smooth muscles of the airways and arterioles?

A
  • they match airflow and blood flow
  • accumulation of CO2 in alveoli due to increased perfusion, decreases airway resistance leading to increased airflow.
  • increase in alveolar 02 concentration as a result of increased ventilation causes pulmonary vasodilation which increases blood flow to match larger airflow.
49
Q

what happens to pulmonary arterioles with increased and decreased 02?

A 
increased = vasodilation
decreased = vasoconstriction
50
Q

what happens to systemic arterioles with increased and decreased 02?

A

increased = vasoconstriction

decreased = vasodilation

51
Q

what are the factors influencing the rate of gas exchange across alveolar membrane?

A
  • partial pressure gradient of 02 and C02
  • diffusion coefficient for 02 and C02
  • surface area of alveolar membrane
  • thickness of alveolar membrane
52
Q

what is partial pressure ?

A

= the pressure that one gas in a mixture of gases would exert if it were the only gas present in the whole volume occupied by the mixture at a given temperature.

53
Q

what are PAO2, PiO2 and PaCO2?

A 
PA02 = partial pressure of 02 in alveolar air
Pi02 = partial pressure of 02 in inspired air
PaC02 = partial pressure of CO2 in arterial blood.
54
Q

what is the 02 partial pressure gradient across pulmonary and systemic capillaries?

A

pulmonary = 60 mm Hg
systemic = > 60mm Hg
(C02 more soluble in membranes = diffusion coefficient)

55
Q

what is the C02 partial pressure gradient across pulmonary and systemic capillaries?

A

pulmonary = 6 mm Hg

systemic > 6 mm Hg

56
Q

what does a big gradient between PA02 (alveolar 02) and Pa02 (arterial 02) suggest?

A

-problems with gas exchange in the lungs or a right to left shunt in the heart.

57
Q

what is fick’s law of diffusion?

A

the amount of gas the moves across a sheet of tissue in unit time is proportional to the area of the sheet but inversely proportional to its thickness.

58
Q

Describe alveoli.

A
  • thin walled inflatable sacs which function in gas exchange
  • walls consist of a single layer of flattened type 1 alveolar cells.
  • pulmonary capillaries encircle each alveolus
59
Q

what factors affect the rate of gas exchange across the alveolar membrane?

A
  • partial pressure gradient of 02 and C02
  • diffusion coefficient
  • surface area of alveolar membrane
  • thickness of alveolar membrane.
60
Q

what are non-respiratory function of the respiratory system?

A
  • route for water loss and heat elimination
  • enhances venous return
  • helps maintain normal acid-base balance
  • enables speech, singing, and other vocalisations
  • defends against inhaled foreign matter
  • removes, modifies, activates or inactivates various material passing through the pulmonary circulation.
  • nose serves as the organ of smell.
61
Q

what is henry’s law?

A

The amount of a given gas dissolve in a given type and volume of liquid (e.g blood) at a constant temperature is proportional to the partial pressure of the gas in equilibrium with the liquid.

62
Q

what is normal 02 concentration in the blood?

A

around 200 ml per litre (at a normal arterial p02 of 13.3kPa and haemoglobin of 150 grams per litre)

63
Q

what percentage of 02 carried is bound to haemoglobin?

A

98.5%

64
Q

describe haemoglobin.

A
  • haemoglobin can reversibly bind with 02
  • each Hb molecule contains 4 haem groups which bind to 1 02 molecule
  • Hb is is fully saturated when all Hb present is carrying its maximum 02 load
  • the p02 is the primary factor determining the percentage saturation of haemoglobin with 02.
65
Q

describe 02 haemoglobin dissociation curve.

A

see diagram

66
Q

how do you work out the 02 delivery index?

A 
D02I = CaO2 X Cl
(= oxygen content of arterial blood X cardiac index)
67
Q

How do you work out the 02 content of arterial blood?

A

Ca02 = 1.34 X [Hb] X Sa02 (%Hb satirated with 02)

68
Q

how can 02 delivery to the tissues be impaired?

A

respiratory diseases - decreased partial pressure of inspired 02
Heart failure - decreases cardiac output
Anaemia - decreases Hb conc. and hence the 02 content of blood

69
Q

what happens to the shape of Hb when all sites become occupied?

A

it flattens

70
Q

how does foetal haemoglobin differ from adult haemoglobin?

A
  • foetal Hb has a structure of 2 alpha units and 2 gamma units (adult has 2 alpha and beta).
  • foetal interacts less with 2,3-biphosphoglycerate in rbc
  • HbF has a higher affinity for 02 which allows 02 transfer from mother to foetus even if P02 is low
71
Q

Describe myoglobin.

A
  • present in skeletal and cardiac muscles
  • only one haem group per molecule
    -no co-operative binding of 02
  • dissociation curve is hyperbolic
    releases 02 at very low P02
    -provides short-term storage of 02 in anaerobic conditions
  • presence in blood indicates muscle damage
72
Q

how is C02 transported in the blood?

A
  • solution (10%) (C02 20X more soluble than 02)
  • as Bicarbonate (60%)
  • As carbamino compounds (30%)
73
Q

how is bicarbonate formed in the blood?

A

C02 +H20 > H2C03 > H+ AND HC0-3

Occurs in red blood cells

74
Q

how are carbamino compounds formed?

A

by combining C03 with terminal amine groups in blood proteins

  • especially globin of haemoglobin to gives carbine-haemoglobin
  • reduced Hb binds more C02 than Hb02
  • rapid without enzyme
75
Q

what is the Haldane effect?

A

removing 02 from Hb increases the ability of Hb to pick up C02 and C02 generated H+
(works with bohr effect)

76
Q

how does the bohr effect facilitate the removal of 02 from haemoglobin at tissue level?

A

by shifting the 02-Hb dissociation curve to the right.

77
Q

what does oxygen do to the C02 dissociation curve?

A

shifts it right - the Haldane effect

78
Q

Describe C02 transport in the blood

A

C02 picked up in 1 of 3 ways > haemoglobin is present in rbcs as carbonic anhydrase, the enzyme that catalyses the production of HC03- > H+ generated during this also binds to Hb > bicarbonate moves by facilitated diffusion down its conc. gradient out of rbc into plasma> Cl- moves by same passive carrier into rbc down electrical gradient.
the reactions occurring at tissue level are reversed at pulmonary level where C02 diffuses out the blood to enter the alveoli.

79
Q

what is the major rhythm generator of respiration?

A

The medulla

- network of neurons called pre-botzinger complex. (located bear upper end of medullary respiratory centre)

80
Q

what gives rise to inspiration (and rhythm?)

A
  • rhythym generated by pre-borzinger complex
  • excutes dorsal respiratory group neurones
  • fires in bursts leading to contraction of inspiratory muscles
  • when firing stops, passing expiration occurs
81
Q

what gives rise to ‘active’ expiration?

A
  • increased firing of dorsal neurone excites a second group
  • ventral respiratory group neurones
  • excite internal intercostals, abdominals etc.
  • this leads to forcefull expansion (doesn’t normally occur)
82
Q

how is rhythm generated in the medulla modified by neurones in the pons (PC)?

A
  • pneumotaxic centre stimulates termination of inspiration
  • PC is stimulated when dorsal respiratory neurones fire (inhibiting inspiration)
  • without PC, breathing is prolonged inspiratory gasps with brief expiration = APNEUSIS
83
Q

How is rhythm generated in the medulla modified by the apneustic centre?

A
  • impulses from these neurones excite inspiratory area of the medulla
  • this prolongs inspiration
  • rhythm is generated in the medulla an can be modified by inputs from pons
84
Q

where do stimuli that influence the respiratory centre come from?

A
  • higher brain centres
  • stretch receptors
  • juxtapulmonary (J) receptors (stimulated by pulmonary capillary congestion and oedema)
  • joint receptors
  • baroreceptors
  • central/peripheral chemoreceptors
85
Q

what are examples of involuntary modifications of breathing?

A

-Pulmonary Stretch Receptors Hering-Breuer Reflex
-Joint Receptors Reflex in Exercise
-Stimulation of Respiratory Centre by Temperature,
Adrenaline, or Impulses from Cerebral Cortex
-Cough Reflex

86
Q

what are joint receptors?

A
  • impulses from moving limbs reflexly increase breathing

- probably contributes to the increased ventilation during exercise.

87
Q

what factors may increase ventilation during exercise?

A
  • reflexes originating from body movement
  • adrenaline release
  • impulses from cerebral cortex
  • increase in body temp
    later: accumulation of C02 and H+
88
Q

Describe the cough reflex.

A
  • vital part of body defences mechanism, helps to clear airways of dust, dirt or excessive secretions
  • activated by irritation of airways or tight airways
  • centre in the medulla
  • afferent discharge stimulates intake of breath, closure of larynx, contraction of abdominal muscles (increases alveolar pressure) and finally opening of larynx and expulsion of air at a high speed
89
Q

Describe chemical control of respiration.

A
  • example of negative feedback control system
  • the controlled variables are the blood gas tensions, especially C02
  • chemoreceptors sense the values of gas tensions
90
Q

what do peripheral chemoreceptors do?

A

sense tension of 02 and C02 and [H+] in blood.

  • stimulated when p02 is less than 8kPa
  • play a major role in adjusting for acidosis caused by addition of non-carbonic acid H+ to blood (e.g. lactic acid)
  • causes hyperventilation and increasesco2 elimination
  • important in acid base balance
91
Q

what do central chemoreceptors do?

A
  • situated near the surface of medulla of brainstem
  • respond to the [H+] of cerebrospinal fluid (CSF)
  • CSF is separated from the body by the blood-brain barrier (relatively impermeable to H+ and HC03-, C02 diffuses readily
  • CSF contains less protein than blood and hence is less buffered than blood.
92
Q

what happens to ventilation when hypoxia occurs?

A
  • initially it increases rapidly to try and increase blood flow
  • but if severe hypoxia continues eventually it platos and then decreases.
93
Q

what is hypoxia at high altitudes caused by?

A

decreased partial pressure of inspired oxygen

acute response = hyperventilation and increased cardiac output

94
Q

what are chronic adaptations due to high altitude hypoxia?

A
  • increase in RBC production
  • increase in 2.3 BPG produced in RBCs
  • increased no. of capillaries
  • increased no. of mitochondria
  • kidneys conserve acid

Respiratory (17 decks)

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