Physiology of the respiratory system Flashcards

1
Q

What are the 2 major functions of nasal breathing?

A
  • To heat and moisten the air
  • To remove particulate matter
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2
Q

What is lung compliance?

A

Is a measure of the relationshup between retractive force and lung volume.

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3
Q

What is the functional residual capacity?

A
  • The volume of air remaining in the lung after a quiet expiration.
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4
Q

What are the accessory muscles of ventilation?

A

Sternomastid and scalene muscles

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5
Q

What can contribute to resporatory failure in patients with severe chronic airflow limitation and in those with primary neurologial and muscle disorders?

A

Inspiratory muscle fatigue (n.b. respiratory muscles are less prone to fatigue than skeletal muscles)

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6
Q

Provide the normal values for respiratory physiology

A
  • Pulmonary blood flow = 5L/min
  • 11 mmol/min of O2 to tissues
  • Ventilation = 6 L/min
  • CO2 removal from body = 9mmol/min
  • Arterial O2 pressure = 11-13 kPa
  • Arterial `CO2 pressure = 4.8-6.0 kPa
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7
Q

What innervates the respiratory musculature and where do the nerves orignate?

A

Rhythmical discharges arise from neurones in the reticular substane of the brainstem, known as the respiratory centre. Signals travel to the respiratory musculature via the phrenic and intercostal nerves.

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8
Q

What is the main driver for ventilation and when can this be compromised?

A
  • A rise in PaC02 which increases [H+] (Arterial pH) (Hypercapnic drive. Oxygen levels in arterial blood are usually above the level that triggers respiratory drive)
  • Sensitivity to hypercapnic drive may be lost in COPD patients where hypoxaemia is the chief stimulus to respiratory drive.
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9
Q

Roughly what is the difference in time required to remove particles from the nasal mucosa and the alveoli?

A
  • Nasla mucosa = 15 minutes
  • Alveoli = 60-120 days
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10
Q

What cells does nasal secretion contain? (3)

A
  • Immunoglobulin A (IgA) antibodies
  • Lysozyme
  • Interferons
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11
Q

Is mucocillary protection less effective against bacteria or virus and why?

A
  • Less effective against viruses
  • Viruses bind to receptors on epithelial cells
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12
Q

What does the majority of rhinoviruses bind to and on what cells (2) are this found?

A
  • Intercellular adhesion molecule 1 (ICAM-1)
  • Neuotrophils / eosinophils
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13
Q

What is the natural tendenacy of the lungs?

A
  • The lungs have an inherent elastic property that causes them to tend to collapse away from the thoracic wall, creating negative pressure within the pleural space.
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14
Q

Describe the mechanisms of inspiration and expiration. (Intraplueral pressure, alveolar pressure….)

A

….

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15
Q

In what patients can inspiratory muscle fatigue contribute to respiratory failure? (2)

A
  • Severe chronic airflow limitation (COPD??)
  • Primary neurological and muscle disorders
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16
Q

What three sources is the sensation of breathless derived from?

A
  • Changes in lung volume - sensed by receptors in thoracis wall muscles signalling changes in their length.
  • Tension developed by contracting muscles - sensed by Golgi tendon organs
  • Central perception of the sense of effort
17
Q

List the neurogenic factors controlling ventilation.

A
  • Pulmonary receptors - sensitive to stretch and bronchial irritation - stimulated in asthma / pulmonary embolism / pneumonia
  • Juxtacapillary (J) receptors - stumulated by asthma / pulmonary congestion (heart failure)
  • Muscle and joint receptors - stimulated by exercise
18
Q

List the chemical factors controlling ventilation.

A
  • Respiratory centre - stimulated by an increase in PaC02 and [H+]
  • Carotid and aortic bodies - stimulated by Pa02 < 8kPa
19
Q

What other than neurogenic and chemical factors can alter ventillation?

A

Voluntary control - anxiety / hysteria

20
Q

Why do you need to be careful when treating COPD patients with respiratory failure?

A
  • Normal pure oxygen is given to patients with respiratory failure. However, in patients with COPD giving oxygen may reduces respiratory drive and lead to a further rise in PaCO2.
21
Q

What happens to ventilation in patients with metabolic acidosis (i.e. diabetic ketoacidosis)?

A
  • The increase in [H+] will cause ventilation to increase to reduce PaCO2 - this causes deep sighing (Kussmaul) respiration.
22
Q

What can caused the respiratory centre to be depressed? (2)

A
  • Severe hypoxaemia (why??)
  • Sedatives (e.g. opiates)
23
Q

Where is airflow greatest?

A
  • In the trachea - it slows progressively towards the periphery - since the velocity of airflow depends on the corss-sectional area)
24
Q

How is the narrowing of the small airways in patients with COPD partially compensated?

A
  • Breathing closer to total lung capacity (TLC)
  • (At full inspiration (TLC) the airways are 30-40% larger in calibre than at full expiration (residual volume)).
25
Q

How is bronchomotor tone maintained?

A
  • By vagal efferent nerves that can be reduced by atropine or Beta-adrenoreceptor agonists.
  • Adrenoreceptors on the surface of broncial muscles respond to circulating catecholamines; there is no direct sympathetic innervation.
26
Q

Airway tone shows a circadian rhythm. When is this tone greatest and lowest?

A
  • Greatest = 04:00
  • Lowest = mid-afternoon
27
Q

What can transiently increase airway tone and what is the mechanism? When can this response be increased?

A
  • Inhaled stimuli acting on epithelial nerve endings trigger reflec bronchoconstriction via the vagus.
  • Stimuli - cigarette smoke / solvents / inert dust / cold air
  • Following respiratory tract infections
28
Q

Why are asthmatic symptoms usually worse in the mornings?

A
  • Because of the circadian rhythm that airway tone shows - greatest tone at 04:00
29
Q

What is alveolar pressure?

A
  • Alveolar pressure = pleural pressure + elastic recoil pressure of the lung
30
Q

During quiet breathing does the pleural pressure stay negative throughout? When may this change?

A
  • Yes
  • With vigourous expiratory efforts, e.g. cough
31
Q

What stops the lungs from collapsing when there is no airflow?

A
  • The positive recoil pressure is exactly balanced by an equivalent negative pleural pressure.
32
Q

What happens to to air pressure as air flows from the alveoli towards the mouth? Why does this happen?

A
  • It drops
  • There is low flow resistance
33
Q

Explain dynamic collapse of the airways in health individuals.

A
  • In forced expiration, the driving pressure raises both the alveolar pressure and the intrapleural pressure.
  • Betwen the alveolus and the mouth, there is apoint where the airway pressure equals the intrapleural pressure, and the airways collapse.
  • The collapse is temporary, as the transient occlusion of the airway results in an increase in pressure upstream, and this raises the intra-airway pressure so that the airways open and flow is restored.
34
Q
  • Why can dynamic collapse be a problem in patients with COPD?
  • What is a useful clinical index of this phenomenon?
  • How do COPD patients compensate for this problem?
  • Why is dynamic collapse only a problem during expiration?
A
  • The pathological loss of recoil pressure causes the collapse point to be further upstream and causes expiratory flow limitation.
  • Forced expiratory volume in 1 second (FEV1)
  • Purse their lips - to increase airway pressure
  • During inspiration, the intrapleural pressure is always less than the intraluminal pressure within the intrathoracic airways.
35
Q
A