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ILA formatives > ILA4 - resp failure > Flashcards

ILA4 - resp failure Flashcards

1
Q

What is the order of air flow?

A

Nose, turbinates (sup., inf. and middle), pharynx, larynx, main bronchi, lobar bronchi, terminal bronchioles, respiratory bronchioles and alveoli

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2
Q

What is the function of the turbinates?

A

Increases surface area and slows down flow of air for more effective warming and humidifying

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3
Q

What are the three paired cartilages of the larynx?

A

arytenoid, corniculate, and cuneiform

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4
Q

What are the three single cartilages of the larynx

A

epiglottic, thyroid and cricoid

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5
Q

Where does the upper airway end?

A

Trachea

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6
Q

Where is the lower airway?

A

trachea onwards

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7
Q

Which part of the airway has the greatest resistance?

A

Trachea (long=increased resistance and less branching=decreased resistance)

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8
Q

Whats is the muscle covering the open posterior aspect of the c shaped cartilages in the trachea?

A

Trachealis muscle (smooth muscle)

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9
Q

What is the rough length of the left main bronchus?

A

5cm

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10
Q

What is the rough length of the right main bronchus?

A

1-2.5cm

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11
Q

Which main bronchus is more vertical?

A

Right

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12
Q

Name a cause of reduced perfusion to the pulmonary tisue?

A

Pulmonary embolism

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13
Q

What can cause reduced ventilation?

A

Blockage in airway
Chronic bronchitis: Blocks airways. Productive cough
(produces sputum)
Cystic fibrosis: Affects sodium channel resulting in thick
mucous secretions which block mucous ciliary
escalator

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14
Q

What is it when V/Q=0?

A

Shunt, no ventilation normal blood flow

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15
Q

What is it when V/Q=infinity?

A

Dead space, no perfusion normal ventilation

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16
Q

What does the respiratory centre do?

A

Control the pattern of breathing

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17
Q

Where is the respiratory centre located?

A

Medulla, it is a collection of neurons

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18
Q

Which neurons do the ventral lateral medulla contain?

A

Inspiratory and expiratory neurones

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19
Q

Which neurons do the dorsal medial medulla contain?

A

Inspiratory neurones

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20
Q

How does the primary centre work?

A

It consists of a collection of separately arranged neurones capable of altering their firing threshold so that activity oscillates between them during inspiration and expiration

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21
Q

Which areas of the pons stimulate the primary centre?

A

Apneustic (stimulates inspiration) and pneumotaxic (inhibits inspiration)

22
Q

What can inhibit the drive for ventilation by depressing the respiratory neuons in the lungs?

A

Hypoxia, a range of therapeutic drugs and inhibition of blood supply

23
Q

What do chemoreceptors do?

A

Detect changes in acidity of the blood and CSF

24
Q

Where do central chemoreceptors lie?

A

Just below the anterolateral surfaces of the medulla, close to the origins of IX and X nerves (pontomedullary junction)

25
Q

What do central chemorecpetors respond to?

A

Respond to change in pH in surrounding CSF

Rising pH inhibits ventilation and lowering pH stimulates it

26
Q

How does the pH fall in the CSF

A

Blood brain barrier is impermeable to H+ so H2CO3 beaks into CO2 and H2O, CO2 then diffuses through the barrier and form bicarb in the CSF. H+ is then released, dropping pH. Stimulates chemoreceptors, stimulates ventilation.

27
Q

Where are the peripheral chemoreceptors located?

A

Carotid bodies, found near the bifurcation of the common carotid artery on either side of the neck (glossopharyngeal afferents)
Aortic bodies in the aortic arch (vagus afferents)

28
Q

How do peripheral chemoreceptors work?

A
  • Surrounded by sinusoidal capillaries which allow cells within them to be bathed directly in blood
  • Glomus cells respond to hypoxia by releasing dopamine on to afferent nerve of the carotid sinus which run to the glossopharyngeal nerve and thence the medullary respiratory centres
  • Afferents of the aortic bodies run via aortic nerve to the vagus
  • Rapid response
  • Also baroreceptors
29
Q

What receptors are in the lungs?

A

Pulmonary stretch receptors and J-receptors

30
Q

Describe the pulmonary stretch receptors

A
  • Lie in the smooth muscle of the bronchi and trachea. Localised chiefly at points of branching where smooth muscle is thickest
  • Afferent fibres from receptors run in the vagus nerve to send impulses to the respiratory centre
  • Inflating the lungs stimulates these receptors.
  • Stimulation inhibits inspiration hence inspiration stimulates expiration
  • Deep breathing rather than small shallow breaths
31
Q

Describe J-receptors

A
  • Lie in the alveolar walls close to the capillaries
  • Impulses from these receptors travel along nerve fibres in vagus nerve
  • Stimulated by fluid in the alveoli and by histamine and other inflammatory mediators
  • Stimulation causes rapid, shallow breathing to clear lungs
32
Q

How do muscle stretch receptors control breathing rate?

A
  • Located in muscle spindles of diaphragm and intercostal muscles
  • As muscle is stretched too far the rate of fire increases
  • These receptors control the strength of muscle contraction to increase the depth of breathing
33
Q

How do baroreceptors control breathing rate?

A

Rise in BP detected by carotid or aortic sinus baroreceptors tends to depress respiration

34
Q

How is inspiration achieved?

A
  • Diaphragm contracts, flattens and moves downwards.
  • The diaphragm is attached to the parietal pleura and so movement downwards pulls the visceral pleura down so that airways and alveoli expand
  • This increases the volume and so decreases pressure
  • External intercostal muscles contract moving the ribcage upwards and outwards to increase lateral and anteroposterior diameter of the thorax
  • This further increases volume and so decreases pressure
  • If pressure in lungs is lower than that of the atmosphere then air is drawn into the lungs
35
Q

What is Boyle’s Law?

A

P1 X V1 = P2 X V2. So pressure is inversely proportional to volume. So if volume increases, pressure decreases (below atmospheric) bringing air into the lungs.

36
Q

Which way do external intercostals point?

A

Down and in (hands in pocket)

37
Q

Which way do internal intercostals point?

A

Up and in

38
Q

What is transpulmonary pressure?

A

The difference between the alveolar pressure and the intrapleural pressure in the pleural cavity

39
Q

How is expiration achieved?

A
  • Usually passive and results from the elastic recoil of the lungs and the chest wall and the inward pull of surface tension in the pleural space
  • Muscles of diaphragm and intercostals relax
  • Thoracic and intrapulmonary volumes decrease
  • Intrapulmonary pressure increases to above atmos pressure
  • Air is forced out of the lungs
40
Q

What muscles are involved in forced expiration?

A

Abdominals, internal intercostals and accessory muscles

41
Q

What is respiratory failure?

A

Inability of the respiratory system to adequately supply fresh O2 or remmove CO2. PaO2 falls below 8kPa, Pa CO2 can be normal or high depending on type

42
Q

What is normal PaO2?

A

10-13 kPa

43
Q

What is normal PaCO2

A

4.7-6 kPa

44
Q

What is Type 1 resp failure?

A 
Low O2 (<8kPa) (hypoxemia)
Normal - slightly low CO2
45
Q

What is the difference between restrictive and obstructive lung disease?

A

Obstructive lung disease is a narrowing of pulmonary airways, hindering a person’s ability to completely expel air from the lungs. Whereas restrictive causes increased difficukty fully expanding lungs during inhilation inhale.

46
Q

Causes of type 1 resp failure?

A

Lung can still expel CO2, just problems with oxygenating the blood (damage to the tissue).
Restrictive lung disease, V/Q mismatch, pneumonia (infection and inflammation of alveoli), pulmonary oedema (fluid in lungs), ARDS (acute resp distress syndrome) ,pneumothorax (air in pleural cavity causing lung collapse), fibrosing alveolitis (idiopathic pulmonary fibrosis, fibrosis= scarring)

47
Q

What is type 2 resp failure?

A 
PaO2 low (<8 kPa) (hypoxia)
PaCO2 high (>7 kPa) (hypercapnia)
48
Q

Causes of type 2 resp failure?

A

Problem is woth mechanisms of breathing
Obstructive lung diseases, COPD, emphysema, asthma, chest wall deformity, resp muscle weakness, central repression of resp centre (eg heroin od), obesity

49
Q

Clinical effects of hypoxia?

A
  • Interferes with aerobic metabolism so that cellular function is disrupted
  • Effects on brain lead to confusion and drowsiness, progressing to coma and death in severe cases
  • To compensate for reduced PaO2, renal tubular cells increase erythropoietin production so that RBC numbers increase and resultant polycythaemia increases the O2-carrying capacity of the blood
  • Pulmonary vasoconstriction to divert the blood from poorly ventilated parts of the lungs may lead to pulmonary hypertension and eventually cor pulmonade
50
Q

Clinical effects of hypercapnia?

A
  • Adds to the effects of hypoxia on the brain and also causes respiratory acidosis as a result of inadequate CO2 excretion
  • In COPD the respiratory centre becomes desensitised to hypocapnia so that the centre ventilatory drive for elevated PaCO2 no longer operates
  • Renal retention of bicarbonate can compensate for respiratory acidosis but is a slow process
  • Combo of hypoxia and hypercapnia induced-respiratory acidosis can be fatal

ILA formatives (10 decks)

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