Respiratory system Flashcards

1
Q

Whats the conducting zone?

A

The conducting zone extends from the trachea to the right and left stem bronchus then to the terminal bronchioles. The conducting zone contains no alveoli and therefore no gas exchange occurs here.

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2
Q

Whats the respiratory zone?

A

The respiratory zone extends from the respiratory bronchioles down and contains the alveoli - this is where gas exchange occurs.

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3
Q

Describe the anatomy of the lower respiratory tract.

A

The walls of the trachea and bronchi contain rings of cartilage which give them there cylindrical shape and support them. The first airway branches that no longer contain cartilage are termed bronchioles which branch into smaller, terminal bronchioles. Elveoli first begin to appear attached to the walls of the respiratory bronchioles.
The bronchioles are surrounded by smooth muscle which contracts/relaxes to alter the bronchiolar radius.

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4
Q

What is airway resistance?

A

Airway resistance = 1/conduction which is proportional to 1/radius^4.
Airway resistance is conduction summative, there are huge number of respiratory bronchioles, small airways make a small contribution to total resistance. Conducting zones have the largest influence.

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5
Q

In what ways can airway resistance be increased?

A

Obstruction with mucus, inflamed/thickened airway walls, structural changes in the conducting airways like smooth muscle growth and fibrosis.

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6
Q

The epithelium lines the cells in the airway. What variation is there in epithelium down the airway?

A

Bronchi - ciliated, goblet, glandular.
Bronchioles - ciliated and non ciliated, goblet and club cells.
Alveoli - squamous, cuboidal.

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7
Q

Whats the cellular structure (layers) of the conducting airways?

A

Cartaliginous layer, lamina propria, epithelium, mucus blanket.

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8
Q

What does the epithelial surface of the airways contain?

A

The epithelial surface contains cilia which constantly beat upwards towards the pharynx.
They also contain glands and individual endothelial cells which secrete mucous and macrophages which can phagocytize inhaled pathogens.
Particulate matter sticks to the mucucs which is continuously and slowly moved by the cilia to the pharynx and then swallowed.

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9
Q

What can negatively effect the cilia?

A

The ciliary activity and number can be decreased by many noxious agents - this is why smokers often cough up mucucs that would usually have been cleared by cilia.

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10
Q

What helps the mucus to ride freely?

A

The epithelium also secretes a watery fluid upon which the mucus can ride freely (production of this is impaired in cystic fibrosis).

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11
Q

Describe the innervation of the conducting airways.

A

Sensory (afferent) nerves from the airway epithelium and smooth muscles signal to the brain.
From the CNS there are autonomic fibres to glandular epithelium and smooth muscle:
- Parasympathetic branches off the vagus nerve having both inhibitory and excitatory functions.
- Sympathetic (postganglionic) have very little innervation - B-adrenoreceptors on airway smooth muscle are stimulated by circulating adrenaline.

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12
Q

What are the two types of alveolar epithelial cells?

A

Type I pneumocytes = these have a very large surface area (only 10% of cells yet take up 95% of alveolus), are squamous and the site of gas exchange.
Type II pneumocytes = the majority of cells are type 2, they are cuboidal and secretory (surfactant) and a precursor for type 1 cells.

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13
Q

What is surfactant?

A

Surfactant is a liquid consisting of 90% lipids (mainly phospholipids) and proteins, produced by type 2 alveolar epithelial cells.

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14
Q

Whats the role of surfactant?

A

Surfactant reduces surface tension and prevents alveolar collapse (atelectasis). It also has innate immunity function.

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15
Q

What happens to infants with respiratory distress syndrome?

Infants don’t have enough surfactant

A

The infact can have surfactant instilled in them - either beractant (bovine) or pumactant (a synthetic, lipid only liquid).

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16
Q

When do the lungs develop?

A

The epithelium of the lungs develops in the third trimester of pregnancy. Maturation can be stimulated by corticosteroids in premature babies.

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17
Q

As a foetus, the lung is filled with fluid - how is this rapidly emptied during birth?

A

There is a surge in corticosteroids and catecholamines, activation of absorptive channels (epithelial sodium channels) and pressure changes as the baby is squeezed through the birth canal.
In a C section, there is reduced drive for fluid absorption.

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18
Q

Explain how blood gets oxygenated.

A

The pulmonary artery carries deoxygenated blood directly from the right ventricle of the heart - there is low pressure but high flow. Blood then enters capillaries around the alveoli, oxygenating the blood to then return to the left atrium of the heart via the pulmonary vein.

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19
Q

The lungs also have a bronchial circulation - what is this?

A

Oxygenated blood from the left ventricle of the heart (via aorta) carries high pressure blood to the conducting airways, supplying oxygen and nutrients. This is only 2% of cardiac outflow and is not involved in systemic respiration processes.

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20
Q

Ventilation is the movement of air from the environment into the lungs. It is automatic but also under control of the CNS.
Explain the neuronal control of breathing.

A

The cerebral cortex sends signals to the respiratory center in the medulla - this sends nerve impulses to the spinal cord and from the spinal cord to the respiratory muscles. This causes movement of the lungs and chest wall (mechanoreceptors feedback this to the medulla) hence causing ventilation.
Diffusion occurs accross the alveolar-capillary barrier (chemoreceptors feedback the change in oxygen and carbon dioxide concentration to the medulla).

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21
Q

Explain the function of somatic motor nerves in the respiratory muscles.

A

Motor nerves innervate skeletal muscles in the thorax:

  • The phrenic nerve innervates the diaphragm - irritation causes hiccups.
  • There are multiple intercostal nerves which each innervate intercostal muscles.
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22
Q

Explain the function of autonomic nerves in the respiratory muscles.

A

Autonomic nerves work in the bronchials, supplying smooth muscle and secretory cells. There are both sympathetic (from CNS) and parasympathetic (branching from vagus nerve) that meet at the pulmonary plexus.
The autonomic nerves reflex bronchospasm and mucus secretion - they are important in asthma.

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23
Q

What happens to the respiratory muscles during inspiration?

A

The diaphragm contracts and the external intercostal muscles pull the ribs up and out. Upon maximal inspiration, the sternoclastimoid and scalenes elevate the sternum whilst the pectoralis minor elevates the ribs and the diaphragm contracts more.

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24
Q

What happens to the respiratory muscles during expiration?

A

The elasticity of the lungs recoils inward, the diaphragm is relaxed and the abdominal organs recoil and press diaphragm upwards. Upon maximal expiration, the internal intercostal muscles pull the ribs down and inwards whilst the abdominal wall muscles contract and compress abdominal organs, forcing the diaphragm higher.

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25
Q

There are myelinated sensory afferent pathways from the lungs sending impulses via the vagus nerve to medullary centres. These can be…

A

Slowly adapting - pathways are stimulated by stretch receptors in airway smooth muscle, eliciting shortened inflation and the Hering-Breur reflex, this is the promotion of expiration following steady inflation, preventing over inflation of the lungs.

Rapidly adapting - stretch receptors are stimulated by sudden, sustained inflation and by ‘irritant receptors’ among the epithelium. This elicits reflexes such as cough, bronchoconstriction and mucus secretion.

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26
Q

There are also unmyelinated sensory afferent pathways, what are these?

A

The unmyelinated sensory afferent pathways are pulmonary and bronchial C fibres located close to blood vessels (J receptors). They are activated by exogenous stimuli (noxious agents in air) and endogenous stimuli (inflammatory agents generated by the body) causing the reflex of bronchoconstriction and mucus secretion.

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27
Q

Explain the cough reflex.

A

The cough reflex begins by stimulation of irritant receptors, sending a signal via a sensory nerve to the medulla. Motor nerves then relay signals to skeletal muscles. The glottis closes and abdominal and internal intercostal muscles contract rapidly. Intrapulmonary pressure then rises and the glottis opens as you cough.

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28
Q

Whats the pleural membrane?

A

There is a double membrane surrounding the lungs with a pleural space in between containing pleural fluid which acts as a lubricant.
The left and right pleura are anatomically distinct hence a collapsed lung (pneumothorax) usually only affects one lung.

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29
Q

Explain the mechanisms of ventilation.

A

The fluid in the pleural sac helps the lung wall stick to the inside of the thorax.
Contraction of the diaphragm and external intercostal muscles increases the lung volume so internal pressure falls (Boyles law) hence air is drawn in.
Exhalation is passive at rest - elastic recoil.

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30
Q

Whats pulmonary compliance?

A

A measure of the elasticity of the lung. (calculated by change in volume, divided by change in pressure)

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31
Q

There are two forms of pulmonary comp-liance, what are they?

A
Static = the compliance at zero flow (end of inspiration/exhalation)
Dynamic = the compliance during active flow.
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32
Q

What factors affect pulmonary compliance?

A

Pulmonary compliance is:

  • Increased by surfactant.
  • Increased in emphysema (loss of elastic tissue so its easier to stretch).
  • Decreased in pulmonary fibrosis (scarring makes it harder to stretch).
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33
Q

What are the metabolic functions of the lungs?

A

Club cells detoxify inhaled substances using cytochrome P450.
Vascular cells inactivate some circulating hormones like prostaglandins.
Vascular cells activate angiotensin I to angiotensin II using angiotensin converting enzyme.
Fibrinolytic function.

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34
Q

How is ventilation controlled?

A

Chemical control occurs through cental and peripheral chemoreceptors.
Neural control occurs through central rhytm generator in medulla, controlled by nociceptors and receptors in the respiratory tract causing sneezing, coughing and hypernoea.

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35
Q

Breathing is automatically controlled by respiratory centres in the brainstem. Explain the anatomy of the repiratory centre of the brain.

A

Within the medulla of the brain is the respiratory centre - a group of neurons and pathways clustered together.
In the respiratory centre there is a dorsal group which sends signals through the vagus nerve and the glossopharyngeal nerve towards the respiratory muscles, causing inspiration.
Above the medulla is the pons, within the pons is the pneumotaxic center and the apneustic centre.

36
Q

What are the roles of the pneumotaxic centre and the apneustic centre within the pons?

A

The apneustic centre is an inhibitory centre, inhibiting inhalation. The apneustic centre prolongs medullary centre firing hence increasing the depth of breathing - therefore decreasing the rate of breathing.
The pneumotaxic centre inhibits the apneustic centre hence stimulating inhalation. It limits the duration of inspiration.
These two centres regulate the rate of breathing, fundamental rhythm is generated by the medulla.

37
Q

Whats the ventral respiratory group involved with?

A

Both inhalation and exhalation - but exhalation is not an active process - there is therefpre little activity in the expiratory centre at rest.

38
Q

Whats the innervation of the inspiratory and expiratory centre of the medulla?

A

They have effernt neurons to motor nerves and recieves afferent input from the pons and the periphery.

39
Q

Whats the pre-Botzinger complex?

A

The pre-Botzinger complex is a region of the ventral respiratory group in the medulla. It has a spontaneous rhythmic discharge, stimulating rhythmic discharge of motor nerves, resulting in contraction of the diaphragm.

40
Q

What happens when the pre-Botzinger complex is destroyed?

A

The breathing becomes much shallower and more rapid - this shows the complex is required for regulated, steady breathing.

41
Q

If you remove the brain cortex, what happens to respiration?

A

You can continue to breath steadily but not under voluntary/conscious control. E.g you cannot hold your breath.

42
Q

What happens if you section between the pons and medulla (pneumotaxic centre)?

A

You lose feedback, but you can continue to breath, but the rate will not be controlled.

Cutting below the medulla will stop all breathing.

43
Q

What controls voluntary control of breathing?

A

The cerebral cortex - it sends signals directly to respiratory motor neurons. This is sensitive to temperature and emotions.
Some people who have tumours/dysfunction of the hindbrain are unable to exhibit automatic control of breathing hence they require some sort of pacemaker.

44
Q

How does a lung transplant modify breathing?

A
  • Ventilation is maintained as motor nerves innervate skeletal muscles (ribs and diaphragm) hence they’re not damaged during a transplant.
  • The cough reflex is preserved from stimulation of larynx/trachea as the section is made below the larynx.
  • You lose cough stimuli from the lower airway as the original lung is removed hence we lose nervous connection back to the respiratory centres of the medulla so we lose automatic cough reflexes from the lower part of the airway.
  • You lose the Hering-Breuer reflex; when you distend the lung you no longer get a message to stop breathing in.
45
Q

What are the two types of chemoreceptors that control respiration?

A

Central chemoreceptors - this mainly occurs through carbon dioxide.
Peripheral chemoreceptors - carotid and aortic bodies, mainly detect changes in oxygen levels - there is also some input from H+ and CO2.

46
Q

How do the partial pressure of carbon dioxide and oxygen differ between the blood and the environment.

A

There is lower oxygen in the blood than the environment and higher carbon dioxide in the blood then the environment.

47
Q

Explain how central chemoreceptors control respiration.

A

The chemoreceptors are within the medulla -this is behind the blood brain barrier. It is difficult for charged ions to cross the BBB hence why changes in pH have a minor effect on alveolar ventilation. However carbon dioxide is uncharged and can therefore cross the BBB - once in the CSF it dissociates, producing hydrogen ions. The hydrogen ions then stimulate the medulla, increasing ventilation to reduce blood PCO2 as it is lost through exhalation.

48
Q

How are carbon dioxide levels of the blood regulated during excercise?

A

Anticipatory stimulation increases ventilation prior to a rise in blood CO2, hence arterial CO2 levels fall.
During excercise, equilibrium is reached in which the ventilation rate keeps PCO2 levels constant. At this point more carbon dioxide is being generated and released into venous blood from the muscles but this is matched by the increased rate of ventilation. When excercise stops, ventilation falls rapidly hence carbon dioxide will increase until it tails off.

49
Q

Peripheral control of respiration relies on aortic and carotid bodies being activated by oxygen levels. Where are these bodies located?

A

Aortic body is located in the aorta detecting the oxygen leaving the heart.
Carotid body is located in carotid arteries supplying the brain with oxygen hence its essential to regulate the concentration of oxygen in this blood supply.

50
Q

Explain how the peripheral control of respiration works.

A

Glomus cells located in the carotid and aortic bodies contain oxygen sensitive potassium channels and dopamine. A fall in oxygen levels stimulates the glomus cell, closing the O2 sensitive potassium channels hence causing depolarization. This triggers the release of dopamine from the glomus cell which stimulates afferent fibres via dopamine receptors on these nerves. The afferent fibres send a signal to the medulla to breath more.
Carotid bodies also respond to changes in pH, but oxygen is the main stimulus.

51
Q

How does the respiratory stimulant doxapram work?

A

Doxapram closes potassium channels on the glomus cell hence causing it to depolarise. This sends afferent signals to the medullary respiratory centre, increasing ventilation.
At high doses it also has a central action.

52
Q

How does caffeine act as a respiratory stimulant?

A

Caffeine and other xanthines causes non-specific CNS stimulation, including the respiratory centre. It can be used as a bronchodilator, in sleep apnoea and in premature babies.

53
Q

How does acetazolamide work as a respiratory stimulant?

A

Acetazolamide is a carbonic anhydrase inhibitor which stimulates respiration by creating mild metabolic acidosis. This occurs through decreased renal reabsorption of bicarbonate and hence reduced acid buffering. Carotid bodies then respond to the decreased pH, increasing ventilation.

54
Q

The majority of drugs with a depressant action on the CNS will be respiratory depressants as central chemoreceptors are very sensitive. Names some respiratory depressants.

A

Barbiturates, alcohol, narcotic analgesics.

Opiates affect sensitivity to carbon dioxide at low doses, directly suppressing the respiratory centre at high doses.

55
Q

Why do we need oxygen?

A

Aerobic respiration : krebs cycle cannot proceed without regeneration of NAD+, electron transport chain is dependent on O2.
Oxygen is required to pay oxygen debt after bursts of anaerobic metabolism.
ATP generated through respiration is required for all active processes e.g anabolic actions, muscle contraction, active transport etc.

56
Q

How can we calculate the amount of oxygen consumed?

A

In the body, oxygen is consumed and carbon dioxide produced during cellular respiration. O2 consumprion can be estimated by measuring the CO2 in arterial blood.

57
Q

Whats the respiratory quotient?

A

In a reaction, the CO2 produced divided by the O2 consumed is the respiratory quotient.

58
Q

Normally we have a combination of fuel sources - hence what is the respiratory quotient?

A

RQ = 0.8 - this means we consume 50ml of oxygen to produce 40 ml of CO2.

59
Q

How can the alveolar oxygen pressure be calculated?

A

O2 inspired - (CO2 produced/RQ)

60
Q

Explain how oxygen levels of the blood changes as it travels around the body.

A

In the systemic venous blood PO2 = 40.
Blood in the pulmonary capillaries increases in oxygen levels (as diffusion occurs through alveoli) reaching around PO2 = 104.
PO2 drops to around 100 in the systemic arterial blood as it is mixed with pulmonary shunt blood.
As blood enters the systemic capillaries, PO2 drops until it reaches around 40 in which it enters the systemic venous blood.

61
Q

How do oxygen levels change in the capillaries?

A

Blood entering the capillaries has a PO2 of about 95 whilst the PO2 of the tissues is about 23. Oxygen therefore diffuses accross the capillary into the tissues hence blood leaving the capillaries at the venous end has a PO2 of around 40.

62
Q

How is oxygen transported around the body?

A

Oxygen is transported in red blood cells bound to haemoglobin. Binding is cooperative- there are 4 molecules of oxygen per haemoglobin molecule.
At alveolar 104mmHg, haemoglobin is saturated. The total amount of oxygen in arterial blood is equal to the amount of oxygen bound to haemoglobin and the amount of O2 dissolved in blood.

63
Q

What is myoglobin?

A

Myoglobin is found in skeletal and cardiac muscle and has a role in the storage and transport of oxygen in metabolically active cells. It has a single oxygen binding site with a high affinity - this is not affected by pH or CO2.
So myoglobin is able to capture oxygen released by haemoglobin.

64
Q

How is carbon dioxide transported around the body?

A

70% as HCO3-.
7% dissolved as CO2.
23% as carbamino haemoglobin.
Carbon dioxide from the tissues diffuses into the plasma - most of this enters red blood cells and is converted to bicarbonate by carbonic anhydrase.

65
Q

What happens when CO2 production is increased (e.g. by excercise or disease)?

A

The fraction of CO2 increases relative to HCO3-.

More CO2 also passes into the CSF and is detected by central chemoreceptors of the medulla, increasing ventilation.

66
Q

How does the gas exchange occur in the lungs?

A

The high PO2 in the lungs causes the blood to release CO2.

67
Q

What affect does oxygen binding to haemoglobin have on carbon dioxide?

A

O2 binding to haemoglobin makes HB more acidic. This means there is less formation of HbCO2 and excess H+ ions bind bicarbonate to form carbonic acid, hence releasing CO2.

68
Q

Whats the ventilation-perfusion ratio?

A

For optimum gas exchange, ventilation of the alveoli must match the blood perfusion - this ratio is expressed as V/Q.
Normally ventilation = perfusion hence the ratio = 1. In disease this is mismatched - theres reduced blood PO2.

69
Q

What is hypoxaemia?

A

Hypoxaemia is when you have low oxygen levels. This can be caused by shunting meaning the alveoli of the lungs are perfused with blood as normal, but ventilation fails to supply the perfused region. This means the ventilation-perfusion ratio is zero.
It could also be caused by diffusion abnormalities like a thickened alveolar wall.

70
Q

Whats the response to hypoxaemia?

A

The response is hypoventilation - this can be drug induced or occurs when there’s an obstruction, or through a neuronal defect or muscle spasm.

71
Q

Whats hypercapnia?

A

Hypercapnia is when you have increased CO2 levels. It can be caused by increased dead space. The response is again hypoventilation.

72
Q

Whats the pulmonary response to low inspired oxygen?

A

Increased ventilation - an immediate response driven by peripheral chemosensors.
Pulmonary vasoconstriction - this is a rapid and homeostatic mechanism designed to shunt blood away from poorly ventilated areas.
Increased hematocrit:
- Hypoxia inducible factors (HIF) activation - this regulates oxygen-sensitive gene transcription
- Erythropoietin (produced by kidneys) stimulates the bone marrow to make red blood cells.

73
Q

Whats acute mountain sickness?

A

Rapidly going to a high altitude causes hypoxic pulmonary vasoconstriction and in some cases pulmonary and cerebral odema.

74
Q

Whats chronic mountain sickness?

A

When low PO2 cannot be matched by ventilation. There is increased erythropoietin production in the kidneys casuing the hematocrit to rise too high and blood turns viscous - this increases the load on the right heart.

75
Q

How can chronic mountain sickness be treated?

A

Acetazolamide (a carbonic anhydrase inhibitor) will inhibit kidney production of erythropoetin and increase ventilation.

76
Q

What does peak epiratory flow rate measure?

A

The instantaneous rate at which air is exhaled from the lungs as a measur of lung performance.
Peak flow rate varies with age gender and height.
We look at the best value - not average.

77
Q

What does a vitalograph show?

A

It displays the flow rate of exhalation against time in comparison with the predicted exhalation of someone with your criteria.
It also tells you the forced vital capacity.

78
Q

What does the FEV1/FVC ratio tell you?

A

The ratio represents the proportion of a persons vital capacity that they are able to expire in the first second of forced expiration.

79
Q

What does spirometry show?

A

Measures the lung volume over time.

80
Q

Whats the tidal volume?

A

The normal volume of air displaced between normal respiration.

81
Q

What value does the peak of forced inhalation give?

A

Total lung capacity

82
Q

Whats the residual volume?

A

The amount of air left in lungs after forced expiration.

83
Q

What does a pulse oximeter do?

A

Attaches to the index finger and tells us the oxygen saturation of the blood - we expect 98%, lower values indicate damage to lungs. This is a useful non-invasive procedure.

84
Q

How does the oximeter work?

A

Identifies the colour of the arterial blood as oxygenated blood is red (spectoral change of light as it goes through tissue).. However it can be affected by nail polish.
To make sure it measures erterial oxygen saturation rather than venous, it measures the blood which is stationary.

85
Q

Why cant the pulse oximeter identify anemia?

A

In aneamia, they have low haemoglobin levels (hence less oxygen can get transported) however all the haemoglobin still gets saturated with oxygen as normal and this is what it measures.

86
Q

Whats auscultation?

A

Auscultation involves using a stethoscope to listen to internal sounds.
If crackling is heard it suggests small airways and alveoli popping open or an infection.
If wheezing is heard it indicates asthma and COPD.

87
Q

Whats diffusion capacity and how is it measured?

A

Diffusion capacity imeasures gas transfer.
The patient empties their lungs, then fills with 0.3% carbon monoxide and holds their breath for 10 seconds. The carbon monoxide in the exhaled breath is then measured to estimate uptake.