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Respiratory > Week 1 > Flashcards

Week 1 Flashcards

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0
Q

Define external respiration.

A

The sequence of events that lead to the exchange of O2 and CO2 between the external environment and the cells in the body

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1
Q

What is internal respiration?

A

The intracellular mechanisms which consume O2 and produces CO2

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2
Q

What are the steps of external respiration?

A

Ventilation or gas exchange between the atmosphere and air sacs (alveoli) in the lungs
Exchange between alveoli and blood
Transport of O2 and CO2 round the body
Exchange between blood and tissues

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3
Q

What three systems are involved in external respiration?

A

Respirator
Cardiovascular
Haematology

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4
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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5
Q

How does air move into the alveoli?

A

The intra-alveolar pressure becomes less than atmospheric pressure creating a pressure gradient causing air to move in. This is done by the thorax and lungs expanding as a result of contraction of the respiratory muscles.

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6
Q

What links the lungs to the thoracic wall?

A

The intrapleural fluid cohesiveness:
- the water molecules in the fluid are attached and resist being pulled apart. Here the pleural membranes tend to stick together
Negative intrapleural pressure:
Sub atmospheric pressure create a transmural pressure gradient. Lungs are forced to expand and chest is forced to squeeze inwards

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7
Q

What muscles contract to cause inspiration and what do these do?

A

Diaphram contraction by phrenic nerve from C3,4 and 5 increasing the volume of the thorax
External intercostal muscle contraction lifting the ribs and sternum.
Both allow for lung expansion

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8
Q

How does expiration occur?

A

It is a passive process brought about by relaxation of the inspiration muscles causing the chest wall and lungs to recoil to normal size causing the intra-alveolar pressure to rise. The air then leaves the lungs down it’s pressure gradient.

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9
Q

What causes the lung to recoil during expiration?

A

Elastic connective tissue in the lungs
- whole structure bounces back into shape

Alveolar surface tension
- pressure caused by lining of alveoli with water and air causing

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10
Q

What is LaPlace’s law?

A

The fact that smaller alveoli (with smaller radius) have a higher tendency to collapse.

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11
Q

How is LaPlace’s law overcome?

A

The alveoli secrete pulmonary surfactant which lowers alveolar surface tension by interspersing between the water lining. The surfactant lowers surface tension of smaller alveoli more than large ones.

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12
Q

What is pulmonary surfactant?

A

A complex mixture of lipids and proteins

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13
Q

What is respiratory distress syndrome in new borns?

A

Developing fetal lungs are unable to synthesize surfactant until late in pregnancy. Premature babies may not have enough pulmonary surfactant so strenuous inspiratory efforts have to be made to overcome the high surface tension and inflate the lungs

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14
Q

What is the alveolar interdependence?

A

If one alveolus starts to collapse the surrounding alveoli are stretched and recoil exerting expanding forces in the collapsing alveolus (pushing air into it) to make it expand again

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15
Q

What forces keep alveoli open?

A

Transmural pressure gradient
Pulmonary surfactant
Alveolar interdependence

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16
Q

Define tidal volume and state it’s average volume

A

Volume of air entering or leaving lungs during a single breath.

500ml

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17
Q

Define Inspiratory reserve volume and state it’s average value.

A

Extra volume of air that can be maximally inspired over and above the typical resting tidal volume.

3000ml

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18
Q

Define inspiratory capacity and state it’s average value.

A

Maximum volume of air that can be inspired (IRV+TV)

3500ml

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19
Q

Define Expiratory reserve volume and state it’s average value.

A

Extra volume of air that can be actively by maximal contraction beyond the normal tidal volume.

1000ml

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20
Q

Define residual volume and state it’s normal value

A

Minimum volume of air remaining in the lungs even after a maximal expiration.

1200ml

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21
Q

Define functional residual capacity and state it’s average volume.

A

Volume of air in lungs at end of normal passive expiration (FRC = ERV + RV)

2200ml

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22
Q

Define vital capacity and state it’s average value.

A

Maximum volume of air that can be moved out during a single breath follow a maximum inspiration
(VC= IRV + TV + ERV)

4500ml

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23
Q

Define total lung capacity and state it’s average value

A

Maximum volume of air that the lungs can hold (TLC = VC + RV)

5700ml

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24
Define FEV1, how to calculate it and the normal result
Volume of air that can be expired during the first second of expiration in an FVC determination. FEV1% (FER) = FEV1/FVC x100 Normal > 75%
25
What is the primary determinant of airway resistance?
The radius
26
Define pulmonary compliance.
The measure of effort that has to go into stretching or distending the lungs
27
What can cause decreased pulmonary compliance?
Pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia and absence of surfactant
28
What effect does decreased pulmonary compliance have?
A greater change in pressure is needed to produce a given change in volume. This causes SOB especially on exertion. It may cause a restrictive pattern of lung volumes in spirometry (it is often caused by restricted disease - pulmonary fibrosis etc)
29
What causes increased pulmonary compliance?
The elastic recoil of the lungs is lost so less effort is required to expand them. This occurs in emphysema and patients have to work harder to get air out of their lungs.
30
What is alveolar ventilation and how is it calculated?
It is the | (tidal volume - dead space volume) x respiratory rate.
31
What is the difference between pulmonary and alveolar ventilation?
Pulmonary = volume of air breathed in and out per minute Alveolar = volume of air exchange between atmosphere and alveoli per minute. This is lower and represents new blood available for blood
32
What is most advantageous way of increasing alveolar ventilation?
Increasing the depth of breathing (not the rate)
33
What is physiological dead space?
Anatomical dead space (areas unable to pass oxygen to blood) + the alveolar dead space (areas not adequately perfused enough to pass oxygen to blood)
34
What is the result of increase perfusion of your alveoli?
Increased CO2 in alveoli (moved from blood to be exhaled) decreases airway resistance leading to increased airflow
35
What effect does increased O2 in the alveoli have on the pulmonary blood flow?
This causes pulmonary vasodilation which increases blood flow to match the large airflow. Allowing the extra O2 to pass into the blood to be distributed around the body
36
What are the four factors that influence the rate of gas exchange across the alveolar membrane?
Partial pressure gradient (O2 and CO2) Diffusion coefficient (O2 and CO2) Surface area of alveolar membrane Thickness of alveolar membrane
37
How does partial pressure gradient effect the transfer of O2 and CO2?
Rate of transfer increases as partial pressure gradient increases
38
How does diffusion coefficient influence rate of transfer of O2 and CO2?
Rate of transfer increases as diffusion coefficient increases
39
How does the surface area of the alveoli membrane influence the rate of gas transfer?
Rate of gas transfer increases as surface area increases
40
How does alveolar membrane thickness influence the rate of diffusion of gas?
The greater the thickness of the vessel the slower the rate of transfer of the gas
41
What is the total partial pressure in the lungs?
The pressure exerted by all the gases in a mixture
42
What effect does binding of O2 to haemoglobin have on the relationship between Hb and O2
It increases Hb affinity for O2 resulting in increased Hb saturation. This causes a sigmoid shaped curved as O2 rapidly binds to Hb after the first haem group is occupied
43
Why does the sigmoid curve created by oxygen binding affinity to haemoglobin flatten out?
As all the haem sites become filled it flattens as less new oxygen is able to bind to Hb
44
How can oxygen delivery to the tissues be impaired?
Respiratory disease Heart failure Anaemia
45
What does presence of myoglobin in the blood indicate?
Muscle damage (myoglobin is present in skeletal and cardiac muscle)
46
How is CO2 transported in the blood?
In solution As bicarbonate- HCO-3 As carbamino compounds
47
How is bicarbonate formed in the blood?
CO2 + H2O are acted upon by carbonic anhydrase (in red blood cells) to form H2CO3. This then dissociates to form H+ and (the bicarbonate that transfers CO2) HCO-3
48
What is the haldane effect?
Removing O2 from Hb increases the ability of Hb to pick up CO2 and CO2 generated H+
49
When does Hb have it's highest affinity for CO2?
When it is not carrying O2.
50
What parts of the brain are needed for rhythmic ventilation?
The medulla oblongata controls the rhythm but the section below is needed to pass this along (spinal cord). Fairly normal ventilation is maintained if section above the medulla (the pons) is removed
51
How is the breathing rhythm generated in the medulla?
A network of neurons called the pre-botzinger complex display pacemaker activity. These are located near the upper end of the medullary respiratory centre
52
What in the medulla gives rise to inspiration?
The pacemaker potential from the pre-boxinger neurones excite the dorsal respiratory group of neurones which fire in bursts leading to contraction of inspiratory muscles. When firing stops passive expiration takes place
53
How does active expiration happen and when?
During hyperventilation. Dorsal neurone firing increases and excited a second group - the ventral respiratory group neurones. These fire causing excitation of the internal intercostal a, abdominals etc with cause forceful expiration.
54
When are ventral neurones activated?
In hyperventilation by increased firing of dorsal neurones
55
What effect does the pons have on respiration control?
When the dorsal neurones fire the pneumotaxic centre (in pons) is stimulated. This sends signals to the dorsal neurones to cease firing inhibiting inspiration.
56
What would happen to respiration without the pons (and therefore the pneumotaxis centre)
Without PC breathing is prolonged: Inspiratory gasps with brief expirations known as apneusis
57
What is the hering-Breur reflex?
When stretch receptors in the walls of the bronchi and bronchioles are stimulated (by over inflation) that sends signals to the CNS that inhibit inspiration. Therefore helping to guard against hyperinflation
58
What effect do joint receptors have on breathing?
Afferent impulses from moving limbs are sent to increase breathing. Contributes to the increased ventilation during exercise
59
How is respiration controlled chemically?
It is a negative feedback control system. The controlled variables are the blood gas tensions, especially CO2. These tension values are controlled by chemoreceptors.
60
Where are peripheral chemoreceptors for respiration found and what do they sense?
In the carotid bodies and aortic bodies. They sense oxygen, CO2 and H+
61
Where are the central chemoreceptors found and what do they do?
Near the surface of the medulla of the brainstorm. CO2 diffuses into cerebrospinal fluid and forms bicarbonate and H+. H+ moves to chemoreceptors and stimulated it. These act to counteract change
62
What causes hypoxia at high altitude?
Decreased partial pressure of inspired oxygen so poor ventilation. This leads to hyperventilation and increased cardiac output.
63
What is the dominant neuronal control of bronchial smooth muscle tone?
Parasympathetic cholinergic system causing constriction
64
How does stimulation of parasympathetic system effect bronchi?
M3 causes bronchial smooth muscle contraction and increased mucus secretion collectively leading to increased airway resistance
65
What effect does the neuronal sympathetic division have on bronchi?
Barely any
66
How does the sympathetic system effect the bronchi smooth muscle?
The HORMONAL sympathetic division stimulates bronchi dilation. This is caused by sympathetic nerves supplying the adrenal medulla which when stimulated releases adrenaline which travels in the blood and acts on beta 2 adrenoceptors to cause bronchi dilation, decreased mucus secretion and increased mucociliary clearance, collectively reducing airway resistance
67
What is asthma?
Is a recurrent and reversible obstruction of the airways in response to a stimuli. Causes of attacks are numerous: Allergens, exercise, infections, smoke, dust, environment etc
68
What do asthma attacks cause?
Cough Expiratory wheezing Difficulty in breathing
69
What effect does chronic asthma have on bronchioles?
Result from long standing inflammation: Increased mass of smooth muscle (hyperplasia and hypertrophy) Accumulation of interstitial fluid (oedema) Increased secretion of mucus Epithelial damage (exposing sensory nerve endings)
70
How does hyper-responsive asthma occur?
Epithelial damage, exposing sensory nerve endings contributes to increased sensitivity of the airways to bronchoconstrictor influences. Two components: Hypersensitivity and hyper-reactivity
71
How do you test for hyper-responsiveness?
Provocation tests with inhaled bronchoconstrictors (spasmogens) such as histamine or methacholine. Much lower concentrations will be needed to induce a response in hyper-responsive asthma
72
What effect does asthma have on FEV1 and PEFR?
Lowers both!
73
How does asthma in an nonatopic individual occur?
Allergen stimulates phagocytosis by antigen presenting (dendritic) cell. Low level of Th1 response leads to cell-mediated immune response involving IgG and macrophages.
74
How does asthma in an atopic individual occur?
Allergen causes phagocytosis by antigen presenting (dendritic) cells stimulating a strong Th2 response, resulting in antibody-mediated immune response involving IgE.
75
What as the phases of an asthma attack?
Immediate Bronchospasm and then late phase in which inflammation occurs.

Respiratory (5 decks)

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