Physiology (Respiratory) Flashcards

1
Q

What are the 4 stages in external respiration?

A

Ventilation, exchange between alveoli and blood, transport and exchange at tissue level.

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2
Q

What is Boyle’s law?

A

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

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3
Q

What forces hold the thoracic wall and lungs together?

A

Intrapleural fluid cohesiveness (attraction between water molecules means pleural membranes stick together) and negative intrapleural pressure (creates transmural pressure gradient across lung and chest wall).

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4
Q

What muscles are involved in inspiration and how do they cause this?

A

Diaphragm - increases volume of thorax by flattening out. External intercostal muscles - lifts the ribs and moves the sternum stretching chest wall (known as bucket handle mechanism).

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5
Q

What makes the chest wall and lungs recoil in expiration and what does this cause?

A

Their elastic properties and it makes intra-alveolar pressure rise.

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6
Q

What is a pneumothorax, what are the symptoms and physical signs of it?

A

Air in the pleural space. Symptoms: shortness of breath and chest pain. Signs: hyperressonant percussive note and decreased/absent breath sounds.

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7
Q

What gives lungs their elastic behaviour?

A
  1. Elastic connective tissue. 2. Alveolar surface tension (more important).
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8
Q

What causes alveolar surface tension and what reduces it?

A

Attraction between water molecules at liquid air interface. Surfactant (complex mixture of lipids and proteins).

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9
Q

What is surfactant secreted by and what does it prevent?

A

Types II alveoli. Lowers surface tension of smaller alveoli more than larger ones so prevents smaller alveoli from collapsing and emptying air into larger ones.

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10
Q

What is respiratory distress syndrome of the newborn?

A

Where developing foetal lungs are unable to synthesise surfactant until late in pregnancy so premature babies may not have enough. They makes strenuous inspiratory effort to try and overcome high surface tension and inflate the lungs.

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11
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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12
Q

List the forces keeping the alveoli open and the forces promoting collapse.

A

Open: transmural pressure gradient, pulmonary surfactant and alveolar interdependence. Collapse: elasticity of stretch lung connective tissue and alveolar surface tension.

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13
Q

What are the accessory muscles of inspiration?

A

sternocleidomastoid, scalenus and pectoral.

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14
Q

What are the muscles of active expiration?

A

Abdominal muscles and internal intercostal muscles.

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15
Q

Describe the tidal volume and inspiratory reserve volume and give their average values.

A

TV: volume of air entering or leaving lungs during single breath (0.5L). IRV: extra volume of air that can be maximally inspired over and above the typical resting tidal volume (3.0L).

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16
Q

Describe the expiratory reserve volume and the residual volume.

A

ERV: extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume. (1.0L). RV: minimum volume of air remaining in the lungs even after a maximal expiration (1.2L).

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17
Q

Describe the inspiratory capacity and the functional residual capacity.

A

IC: max volume of air that can be inspired at the end of a quiet expiration (IRV+TV, 3.5L). FRC: Volume of air in lungs at end of normal passive expiration (ERV+RV, 2.2L).

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18
Q

Describe the vital capacity and the total lung capacity.

A

VC: max volume of air that can be moved out during a single breath following a maximal inspiration (IRV+TV+ERV, 4.5L). TLC: total volume of air the lungs can hold (VC+RV, 5.7L).

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19
Q

Why can we not measure total lung capacity by spirometry?

A

Because residual volume cannot be measured by spirometry.

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20
Q

What are dynamic lung volumes useful for the diagnosis of?

A

Obstructive and restrictive lung diseases.

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21
Q

What does a volume time curve allow you to determine?

A

FVC (forced vital capacity), FEV1 (forced expiratory volume in 1 second) and the FEV1/FVC ratio (proportion of forced vital capacity that can be expired in the first second).

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22
Q

What will the effect of obstructive and restrictive lung diseases be on the dynamic lung volumes?

A

Obstructive: same FVC but lower FEV1/FVC ratio (<70%). Restrictive: lower FVC but FEV1/FVC will remain the same.

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23
Q

What makes active expiration more difficult in patients with airway obstruction?

A

Dynamic airway compression (where rising pleural pressure compresses the alveoli and airway).

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24
Q

Why does dynamic airway compression cause a problem in people with obstructed airways?

A

Driving pressure between alveolus and airway is lost over obstructed segment, causing a fall in airway pressure downstream resulting in airway compression by rising pleural pressure during active expiration. Problem worsened if decreased elastic recoil of lungs.

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25
Q

What is pulmonary compliance?

A

Measure of the effort required to stretch or distend the lungs. Volume change per unit of pressure change across the lungs.

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26
Q

What is pulmonary compliance decreased by and what does this mean?

A

Pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia and absence of surfactant. Means greater change in pressure is required to produce a given change in volume (shortness of breath).

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27
Q

What may cause a restrictive pattern of lung volumes in spirometry?

A

Decreased pulmonary compliance.

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28
Q

What abnormally increases pulmonary compliance and what does it occur with?

A

If elastic recoil of lungs is lost, occurs in emphysema

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29
Q

What will cause the work of breathing to increase?

A

If pulmonary compliance is decreased, airway resistance is decreased, elastic recoil is decreased and if there is a need for increased ventilation.

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30
Q

Why is aveolar ventilation less than pulmonary ventilation and how would you calculate this?

A

Because of anatomical dead space. Alveolar ventilation (L/min) = (tidal volume - dead space volume) x resp rate

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31
Q

Why is it more advantageous to increase depth of breathing instead of rate?

A

Due to dead space more air will reach alveoli.

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32
Q

Define alveolar ventilation.

A

Volume of air exchanged between atmosphere and alveoli per minute.

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33
Q

What is the difference between the ventilation and perfusion between the bottom and top of lungs?

A

Blood flow better at bottom of lungs, air flow also better at bottom of lungs but less pronounced. Ventilation/perfusion ratio higher at top of lungs.

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34
Q

What is the difference between anatomical dead space and alveolar dead space?

A

Anatomical: space in the respiratory tract where gas transfer cannot occur. Alveolar: ventilated alveoli that are not adequately perfused with blood.

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35
Q

What is the alveolar dead space like in healthy and diseased people?

A

Healthy: very small and of little importance. Disease: can increase significantly.

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36
Q

What is the physiological dead space?

A

The anatomical dead space + the alveolar dead space.

37
Q

What occurs in an area with greater perfusion than ventilation?

A

CO2 increases in area, O2 decreases, causes dilation of local airways and constriction of local blood vessels, airflow increases and blood flow decreases.

38
Q

What happens in an area with greater ventilation than perfusion?

A

CO2 decreases in area, O2 increases, constriction of local airways, dilation of blood vessels, airflow increases and blood flow decreases.

39
Q

Define partial pressure.

A

The pressure that one gas in a mix of gases would exert if it were the only gas present in the whole volume occupied by the mixture.

40
Q

How do we calculate the partial pressure of alveolar oxygen?

A

PAO2 = PiO2-[PaCO2/0.8]

41
Q

Why does CO2 diffuse across the alveolar membrane when its partial pressure gradient is much lower than that of oxygen?

A

The diffusion coefficient is 20 times that of O2.

42
Q

List some non-respiratory functions of the respiratory system.

A

Route for water loss and heat elimination, enhances venous return, helps maintain normal acid-base balance, enables speech and vocalisations, defends against inhaled foreign matter. Also removes, modifies, activates or inactivates various materials passing through the pulmonary circulation.

43
Q

What is the effect of partial pressure on gas solubility?

A

The amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in equilibrium with the liquid.

44
Q

What percentage of oxygen in blood is bound to haemoglobin?

A

98.5%.

45
Q

What is the primary factor which determines the percentage saturation of haemoglobin?

A

The PO2.

46
Q

How does the concentration of haemoglobin affect the partial pressure required to saturate it?

A

It has no effect, a higher concentration will be saturated at the same partial pressure as a lower concentration.

47
Q

What is the oxygen delivery index (DO2I) and how is it calculated?

A

A function of oxygen content of arterial blood and the cardiac output, DO2I=CaO2xCI (cardiac index relates cardiac output to the body surface area).

48
Q

What can oxygen delivery to the tissues be impaired by?

A

Decreased partial pressure of inspired oxygen, respiratory disease, anaemia and heart failure.

49
Q

What does the flat upper portion of the oxygen haemoglobin dissociation curve mean?

A

Moderate fall in alveolar PO2 will not much affect oxygen loading.

50
Q

What does the steep lower part of the oxygen haemoglobin dissociation curve mean?

A

The peripheral tissues get a lot of oxygen for a small drop in capillary PO2.

51
Q

What is the Bohr effect and what causes it?

A

A shift of the oxygen haemoglobin curve to the right. Increased PCO2, [H+], temp, [2,3-biphosphogylcerate].

52
Q

What is a beneficial aspect of the Bohr effect?

A

There is an increased release of O2 by conditions at the tissues.

53
Q

What is the structure of foetal haemoglobin (HbF)?

A

Has 2 alpha and 2 gamma subunits.

54
Q

What aspect of foetal haemoglobin (HbF) allows oxygen transfer from mother to foetus?

A

HbF interacts less with 2,3-biphosphoglycerate so has higher affinity for oxygen (curve shifted to left).

55
Q

Where is myoglobin present and when does it release O2?

A

Skeletal and cardiac muscles, very low PO2.

56
Q

What does myoglobin supply and how can it indicate muscle damage?

A

A short-term storage f O2 for anaerobic conditions. If it is present in blood.

57
Q

How is CO2 transported in the blood?

A

10% in solution, 60% as bicarbonate, 30% as carbamino compounds.

58
Q

What are the reactions that form bicarbonate, what facilitates this reaction and where does it occur?

A

CO2 + H2O H2CO3 H+ + HCO3-, carbonic anhydrase (CA) and in red blood cells.

59
Q

How is bicarbonate formed?

A

CO2 diffuses into RBS and reacts with water in presence of CA. Bicarbonate moves into blood plasma in exchange for Cl-. H+ ion produced reacts with Hb to produce HbH (buffered).

60
Q

Give an example of a carbamino compound and is an enzyme needed for this to form?

A

carbamino-haemoglobin and no (reaction rapid even without enzyme).

61
Q

What can bind more CO2: reduced Hb or HbO2?

A

Reduced Hb.

62
Q

What is the Haldane effect?

A

Removing O2 from Hb increases the ability of Hb to pick up CO2 and CO2 generated H+.

63
Q

How do the Bohr and Haldane effect work in synchrony?

A

Bohr effect means Hb releases more O2 at tissue levels which means that more CO2 and H+ can bind to haemoglobin at tissue level.

64
Q

How does oxygen shift the CO2 dissociation curve?

A

To the right (Haldane effect).

65
Q

How does the Pre-Botzinger complex on the medulla give rise to inspiration (generate rhythm)?

A

Excites dorsal respiratory group neurones, fire in bursts, leads to contraction of inspiratory muscles, passive expiration when firing stops.

66
Q

What groups of neurones cause inspiration and active expiration?

A

Inspiration: dorsal respiratory group neurones. Active expiration: ventral respiratory group neurones.

67
Q

Where is the pneumotaxic centre located, when is it stimulated and what does it do?

A

The pons, when dorsal respiratory neurones fire, causes inhibition of inspiration.

68
Q

Where is the apneustic centre located and what does it do?

A

The pons, excited inspiratory area of medulla leading to prolonged inspiration.

69
Q

Where is respiratory rhythm generated in the brain and what can this be modified by?

A

The medulla, inputs from the pons.

70
Q

What produces stimuli that influences the respiratory receptors?

A

Higher brain centres, stretch receptors in walls of bronchi and bronchioles, juxstaposition (J) receptors, joint receptors, baroreceptors, central and peripheral chemoreceptors.

71
Q

What are J receptors stimulated by?

A

Pulmonary capillary congestion, pulmonary oedema and pulmonary emboli (leads to rapid shallow breathing)

72
Q

What is the Hering-Bruer reflex?

A

When pulmonary stretch receptors are activated during inspiration. Their afferent discharge inhibits inspiration. Not during normal resp cycle by may be important in newborns or when doing hard exercise.

73
Q

What are the factors that may increase ventilation during exercise?

A

Reflexes originating from body movement, adrenaline release, impulses from cerebral cortex, increase in body temp, accumulation of CO2 and H+ generated by active muscles.

74
Q

What is the ventilatory response to exercise?

A
  1. Rapid increase in ventilation (due mainly to neural changes). 2. Gradual increase in ventilation (due mainly to chemical changes). 3. Increases until it reaches steady state. 4. Gradual decrease when exercise stops due to removal of chemical changes.
75
Q

Where is the cough reflex centre?

A

The medulla.

76
Q

Describe the stages of the cough reflex.

A

Afferent discharge stimulates short intake of breath -> closure of larynx -> contraction of abdominal muscles -> opening of larynx and expulsion of air at high speed.

77
Q

What do chemoreceptors sense?

A

Values of blood gas tensions.

78
Q

Where are the peripheral chemoreceptors and what do they sense?

A

Aortic and carotid bodies. Sense tension of oxygen, carbon dioxide and H+ conc in the blood.

79
Q

Where are the central chemoreceptors and what do they sense?

A

Near surface of the medulla of the brainstem. The [H+] conc of the cerebrospinal fluid.

80
Q

How does H+ from the blood get past the blood-brain barrier?

A

It doesn’t (it is impermeable to H+). CO2 diffuses across, CSF contains less protein then blood so CO2 is less buffered and forms H+ more easily which is then detected by central chemoreceptors.

81
Q

What does an increase in PCO2 cause and how?

A

A sharp increase in ventilation (due to CO2 generated H+ going through central chemoreceptors).

82
Q

What happens to ventilation in hypoxia?

A

If arterial PO2 drops significantly (8kPa) peripheral chemoreceptors activated. If it decreases further it will depress the neurones and ventilation will decrease again.

83
Q

What causes the hypoxic drive of respiration?

A

The peripheral chemoreceptors.

84
Q

What are the symptoms of acute mountain sickness?

A

headache, fatigue, nausea, tachycarida, dizziness, sleep disturbance, exhaustion, shortness of breath, unconsiousness.

85
Q

What are the chronic adaptations to high altitude hypoxia?

A

Increased RBC production (polycythaemia), increased 2,3-biphophoglycerate produce within RBC, increased number of capillaries and mitochondria, kidneys conserve acid.

86
Q

What plays a major role in adjusting for acidosis caused by the addition of non-carbonic acid H+ to the blood?

A

The peripheral chemoreceptors (not central as H+ does not readily cross the blood-brain barrier).

87
Q

What does the stimulation of peripheral chemoreceptors by H+ cause?

A

Hyperventilation and increases elimination of CO2 from the body.

88
Q

What has the main effect on central and peripheral chemoreceptors?

A

Arterial PCO2 on central, arterial PO2 and H+ conc on peripheral.