72 - Physiological Consequences of Airway Obstruction Flashcards

1
Q
Sensation of airflow obstruction
1)
2)
3)
4)
A

1) Increased sensation of breathing
2) Increased respiratory muscle effort
3) Active exhalation
4) Longer time to inspire and expire

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2
Q
Things that can increase load on breathing 
1
2
3
4
A

Stiff lungs
Narrow airways
Chest wall
Diaphragm

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3
Q
Things that can increase the drive to breathe 
1
2
3
4
5
6
A
Higher centres (limbic system)
Mechanoreceptors
Irritant receptors
Chemoreceptors
Baroreceptors
Temperature
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4
Q

Factors contributing to the work required to breathe
1)
2)

A

1) Load on lungs.

2) Drive to breathe

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5
Q

When is difficulty breathing a sensation?

A

When appropriate

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6
Q

When is difficulty breathing a symptom?

A

When inappropriate

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7
Q

Nerve stimuli leading to inspiration

A

Stimulation of the diaphragm by phrenic nerves.

External intercostal stimulation by intercostal nerves.

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8
Q

Contraction of the diaphragm does what to thoracic dimensions?

A

Increases the longitudinal and lateral dimensions of the thorax

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9
Q

Amount of breathed oxygen that goes to respiratory muscles at rest

A

~3%

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10
Q

When does the intra-alveolar pressure equal atmospheric pressure?

A

At the end of inspiration and expiration

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11
Q

Intra-pleural pressure relative to intra-alveolar pressure

A

Intra-pleural is always lower than intra-alveolar, because of elastic recoil of lungs and chest wall (pleura held together by fluid tension, upon inspiration negative pressure within lungs pulls inwards on pleura. Fluid pressure resists this, leading to decreased pressure in pleural space).

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12
Q

Intrapleural pressure during inspiration

A

Decreases pressure in pleural cavity

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13
Q

Pleural cavity pressure during one inspiration/expiration cycle.

A

Decreases until change from inspiring to expiring, then increases in pressure again. Frequency is ~1/2 that of inspiration/expiration pressure.

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14
Q

Why is work of breathing increased when there is an airway obstruction

A

Inspiratory muscles need to generate higher pressures to overcome obstruction to airflow

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15
Q

Consequences of obstruction
1
2
3

A

1) Recruitment of accessory muscles of inspiration
2) Increased oxygen consumption by respiratory muscles
3) Risk of respiratory muscle fatigue (if obstruction is severe)

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16
Q

Effect of respiratory muscle fatigue

A

Too little O2 dissolved in blood

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17
Q

Ventilatory failure

A

When rate of O2 entry into body is below rate of CO2 expiration.

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18
Q

Arterial partial pressures considered to be ventilatory failure

A

PaO2 under 60mmHg, PaCO2 over 50mmHg

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19
Q

How is exhalation normally passive?

A

Elastic recoil of lungs generates positive intrapulmonary pressure, pushing air out.

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20
Q

Muscles involved in active exhalation

A

Abdominals, internal intercostals

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21
Q

TLC

A

Total lung capacity.

Greatest possible breath.

22
Q

Amount of time for a normal FVC

A

2-3 seconds

23
Q

Spirometric measurement of total lung capacity

A

FVC

24
Q

% of vital capacity in FEV1

A

~80%

25
Q

FEV1 percentage of FVC considered normal

A

Over 70% (if older)

~80% in a young person

26
Q

Appearance of a FVC graph for someone with airway obstruction

A

Flatter, increases less quickly than that of a healthy person (person able to expire less quickly)

27
Q

Flow-volume loop

A

Measurement of flow rate vs volume during a FVC, followed by a forced inspiratory manoeuvre.

FVC is on the upper part of y-axis, inspiratory pressure is on the lower part of y-axis

28
Q

WOB

A

Work of breathing

29
Q

Effect of obstruction leading to uneven ventilation

A

Leads to impaired gas exchange

30
Q

Examples of obstructions that can lead to uneven ventilation

A

COPD, asthma

31
Q

Ventilation/perfusion matching

A

Gas exchange is most efficient when ventilation and perfusion are matched (V/P=1) in all alveolar-capillary units.

32
Q

How can you image whether ventilation and perfusion match?

A

Ventilation and perfusion scans.
Ventilation - inhale radioactive particles, which are non-absorbable.
Perfusion - Inject radioactive particles into systemic vein which lodge in small pulmonary arterioles.

33
Q

Appearance of COPD on ventilation/perfusion scan

A

Non-homogenous ventilation and perfusion in lungs

34
Q

Effect of V/Q mismatch

A

O2 binding sites on Hb not filled.

Some blood returning to left atrium not fully oxygenated.

35
Q

Most clinically important cause of reduced PaO2

A

Low V/Q units

36
Q

Shunt

A

A unit of blood that goes through a non-ventilated area of lungs, so isn’t oxygenated.
An extreme form of low V/Q unit.

37
Q

Compensatory mechanism for regions of reduced ventilation (causing low V/Q)

A

Vasoconstriction occurs in areas of low ventiation to reduce the hypoxaemic effects of low V/Q units.

This is effective in reducing altered gas exchange, but not usually fully successful

38
Q

Potential downstream effect of compensatory mechanism for low V/Q units

A

Increased pulmonary arterial pressure

39
Q

Things that airflow obstruction can be due to
1)
2)

A

1) Spasm of bronchial smooth muscle

2) Airway inflammation

40
Q

Things that can be used to treat spasm of bronchial smooth muscle
1)
2)
3)

A

1) Beta agonists
2) Anti-cholinergics
3) Methyl-xanthines

41
Q

COPD

A

Smoking related disease
Causes inflammation of bronchial mucosa.
Inflammation is not steroid-responsive
Causes destruction of lung parenchyma

42
Q

Differences between asthma and COPD

A

COPD inflammation is not steroid responsive
COPD leads to destruction of airway parenchyma
Asthma is steroid responsive and doesn’t destroy airway parenchyma

43
Q

Effects of COPD
1)
2)
3)

A

1) Collapse of small airways (destruction of elastic tissue in airways), particularly in inspiration
2) Impaired gas exchange from V/Q mismatch, loss of alveolar-capillary membrane
3) Reduced capillary bed, from pulmonary hypertension

44
Q

What are asthma inflamed airways responsive to?

A

Corticosteroids

Leukotriene antagonists

45
Q

Alveolar-arterial gradient for oxygen

A

Measure of the overall efficiency of gas exchange across all alveolar-capillary units

46
Q

How is alveolar pressure calculated for A-a gradient of O2?

A

Estimated using the ideal gas equation:
PAO2 = PiO2 - PACO2/RQ

R=~0.8
PiO2 = Partial pressure of inspired oxygen
PACO2 = Alveolar CO2

47
Q

Effect of hypoventilation on O2 and CO2

A

Decrease O2, increase CO2

48
Q

How to tell if someone is hypoxic from hypoventilation, so something more.

A

Calculate the amount of hypoxia from alveolar-arterial gradient for O2, see if there is more in a patient than is expected.

49
Q

RQ

A

0.8

50
Q

PiO2 at sea level

A

150

51
Q

Normal A-a gradient

A

15-30

52
Q

How can cellular O2 consumption be calculated?

A

Fick equation

QO2 (cellular use of O2) = Cardiac output x (arterial O2 content - venous O2 content)