17. Lung Mechanics Flashcards

1
Q

Define elasticity

A

The property of matter that causes it to return to its resting shape after deformation by an external force In the lung, the force is indicated by pressure exerted on the lung

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2
Q

Outline elastic resistance

A

Also known as elastance = change in pressure / unit of volume change

It is the reciprocal of compliance, therefore when elastic resistance is decreased, compliance increases:

o When a spring is easy to distend (spring open), it has low elastic resistance and high compliance (and vice versa)

Clinical correlate: Emphysema - lung elastic resistance is reduced, therefore compliance increases

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3
Q

Outline pleural pressure

A

The outer surface of the lungs are covered by visceral pleura, which is in close contact to the parietal pleura which lines the inner surface of the thoracic cage

The gap between the two pleura is called the pleural cavity The lungs tend to pull on the pleura inward away from the chest wall, therefore are more prone to collapse

This is due to the connective tissues, elastin and collagen in the lung, as well as the surface tension generated at the air-liquid interface in the alveoli If the thorax is opened, the chest wall volume will increase by 600-1000ml, thus increasing the outward pull of the chest wall and separating the two pleura

The tendency for the lungs to recoil inward (i.e. elastic recoil of the lungs) can be measured as the pleural pressure, i.e. it is the pressure between the pleural layers

During normal inspiration, the volume of the thorax increases, but the elastic recoils of the lungs and chest wall are cancelled out as they are equal therefore the lung does not collapse

There is normally a small amount of fluid present in the pleural cavity that allows the visceral and parietal pleura to slide over each other:

o If this cavity is filled with blood (haemothorax) or air (pneumothorax), the gap may expand increasing the pressure on the lung away from the chest wall, therefore increasing the risk of collapse

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4
Q

Define and outline compliance

A

Definition: the expression of the pressure-volume characteristic of the respiratory apparatus, i.e. the ability of the lung to stretch

Lung compliance = CL = Change in volume / change in pressure

→ i.e. the slope of a pressure volume curve

High compliance means less change in volume for a given change in pressure, i.e. less stretch

Non-compliant means that a larger pressure is required to achieve the same volume

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5
Q

Outline compliance in different conditions and draw a graph of volume/pressure to show this

A

Healthy lungs:

o 5cm water pressure → inspiration of 1 litre, therefore 1/5 = 0.20L/cm H2O

Emphysema (loss of elastic recoil):

o 5cm water pressure → inspiration of 2 litre, therefore 2/5 = 0.40L/cm H2O

Pulmonary fibrosis (increased elastic recoil):

o 5cm water pressure → inspiration of 0.5 litre, therefore 0.5/5 = 0.10L/cm H2O

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 34 for the graph]

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6
Q

How can pleural pressure be measured?

A

Directly - insert a needle

Indirectly - measure pressure in a thin-walled balloon introduced into the middle third of the oesophagus; the airway is anterior to the oesophagus and the surrogate pressure is reflective of the pleural pressure:

o This is because the oesophagus lies between the lungs and chest wall and because the walls of the oesophagus are thin and have little tone so exert little of their own pressure

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7
Q

Define and outline the concept of hysteresis

A

Definition: the phenomenon in which the value of a physical property lags behind changes in the effect causing it, as for instance when magnetic induction lags behind the magnetising force

In respiratory science, for any given pressure applied, the volume during deflation (expiration) is greater than the inflation (inspiration); this is known as hysteresis; without any pressure, there is always some volume in the lung due to the volume of air occupied by the airways

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8
Q

Outline the reasons for elastic recoil

A

Half of the elastic recoil of the lungs comes from the elastic properties of their tissues (think like elastic recoil of an inflated rubber balloon; there is always some air in the lungs therefore they are always slightly inflated)

The other half comes from their structure and surface; millions of alveoli filled with air, lined by liquid and connected to the atmosphere by bronchial tree; this creates an air-liquid surface tension:

o Filling the lung with fluid (like surfactant) reduces this air-liquid surface tension therefore reducing the elastic recoil making the lungs easier to inflate (this was shown by von Neergaard, 1929)

o Filling the lung with fluid also removes hysteresis as there is no air left in the lung

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9
Q

Outline hysteresis

A

Inflation of the lung follows a different pressure-volume relationship than deflation, i.e. it requires a greater pressure to reach a particular lung volume when inflating (inspiring requires a greater pressure; more active), than to hold is at that volume when deflating it (when expiring)

Saline inflation removes the effect of the elastic recoil of lung surface/structure, but just shows the recoil of the elastic properties of the lung tissues

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10
Q

Define and outline transpulmonary pressure

A

Definition: the pressure difference between the alveoli and pleural cavity, i.e. alveolar pressure - pleural pressure (Palv - Ppl)

NB: remember that the pleural pressure can be measured as the tendency of the lung to recoil away from the chest wall

The barometric pressure is the atmospheric pressure; this can be seen to be the same as in the mouth and trachea

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11
Q

Outline inspiration with regards to transpulmonary pressure

A

During inspiration, the chest expands and inspiratory muscles contract

This results in changes in the pressures affecting the respiratory system, which causes air to flow through the system

The respiratory apparatus (lungs, chest wall, diaphragm, abdominal contents, tracheobronchial tree) has an elastic force which offers resistance to this airflow; i.e. the respiratory apparatus does not want to distend, so offers a counter force which in turn offers resistance to the incoming airflow

o There is also resistance to airflow caused by the gas already present in the respiratory tract In order to overcome the resistance to airflow (which is the point of inspiration, to create airflow into the thorax), force is required:

o This force is the required pleural pressure

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12
Q

Outline the elastic forces during breathing

A

After quiet expiration, the outward recoil of the chest wall is equal to the inward recoil forces of the lungs; therefore there is no movement/change in pressures

However, a small volume of air still occupies the airways; this is FRC (functional residual capacity)

Relaxation pressure (RP) is the net balance between these two recoil forces and is derived by having a subject relax against a complete obstruction at different lung volumes:

o The relaxation pressure curve can be determined by considering the combined compliance of the chest wall and lung

  • At FRC, the recoil forces are equal but in opposite directions, therefore there is no movement of air and the RP is 0 or atmospheric
  • Below FRC, the recoil of the chest > inward recoil of lungs, therefore RP is negative and inspiration occurs
  • Above FRC, the inward recoil of lung > recoil of chest, therefore RP is positive and expiration occurs
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13
Q

Outline chest wall recoil

A

Assessed by measuring the pressure exerted by the relaxed respiratory system against an occluded airway over a range of voluntarily achieved vital capacity

This is unreliable and difficult to do The chest wall recoil increases as the chest wall stiffens, which occurs with age, obesity and deformities e.g. ankylosing spondylitis

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14
Q

Outline the measurement of residual volume (RV)

A

An increased residual volume leads to increased functional residual capacity

This suggests air trapping due to an airflow obstruction; result of possible asthma, COPD etc.

This air trapping means that the patient cannot expel as much air, resulting in an increased pressure which is uncomfortable for the patient In patients with COPD, the smaller the RV, i.e. the closer the inspiratory-to-total lung capacity is to 1, the lower the risk of mortality

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15
Q

Outline lung stabilisation

A

Factors which stabilise the lung:

  • Surfactant:

o Forms relatively late in gestation (approx. 25 weeks)

o Can be assessed in the amniotic fluid

o Glucocorticoids stimulate type II cells produce surfactant (can accelerate lung maturation)

o Respiratory distress syndrome (RDS) results from an inadequate amount of surfactant; replacement may improve condition Interdependence of lung units:

o Adjacent alveoli share a common wall, therefore tendency of one alveolus or lung unit to collapse is opposed by the support of surrounding units

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16
Q

Define and outline surface tension

A

Definition: the manifestation of attracting forces between atoms and molecules

Units of force/unit length (dynes/cm or N/m) May be lowered by certain substances when placed in a liquid (exert less attracting forces); surfactant or surface active molecules

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17
Q

Outline pulmonary surfactant

A

Present in the lungs of all air-breathing vertebrates

Formed in cuboidal type II alveolar epithelial cells (stored in osmiophillic lamellar bodies, secreted into the lumen)

Consists of phospholipids (90%) and specific apoproteins (10%) Without surfactant, smaller alveoli would empty into larger ones

Undergoes a continuous process of synthesis and degradation; its synthesis enhanced by glucocorticoids, cAMP, oestrogens, thyroid, and inhibited by beta receptor blockade:

o Fate - most recycled to Type II cells, phagocytosis and degradation by macrophages, intra-alveolar catabolism or removal by mucociliary escalatory

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18
Q

Outline the Law of Laplace

A

The Law of Laplace shows the relationship between wall tension (T) which tends to collapse, and distending pressure (P) necessary to hold the bubble open, therefore surfactant uses the law of Laplace to hold alveoli open during the ventilator cycle (P = 2T/r)

There is a tendency for the lung to collapse due to the elasticity of the lung parenchyma and the surface tension at the air-liquid interface

If surface tension remains constant, but the alveolar radius is reduced the pressure necessary to prevent collapse increases, therefore alveolar expansion requires a greater force In the lungs, the surface tension decreases with expiration (due to the decrease in alveolar radius), but increases with inspiration

If the surface tension changes, the alveolar pressure (P) must remain constant to prevent alveolar collapse throughout the ventilator cycle

This is the role of surfactant

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19
Q

Define parenchyma and stroma

A

Parenchyma/Stroma: The parenchyma of an organ consists of that tissue which conducts the specific function of the organ and which usually comprises the bulk of the organ

Stroma is everything else; connective tissue, blood vessels, nerves, ducts

The parenchyma/stroma distinction provides a convenient way to circumvent the listing of tissue types when discussing an organ

20
Q

State some applications of the Law of Laplace

A
  • May be applied in the alveoli of the lungs to explain their role in exhalation, the difficulty of the baby’s first breath and the unfortunate effects of Emphysema (COPD)
  • States that the wall tension increases with vessel radius
  • May be applied to the arterial wall and to the capillary walls and to clarify the danger of aneurysms
21
Q

Outline airflow resistance

A

During breathing, the respiratory muscles encounter a force as a result of the resistive properties of the lung and chest wall; the amount of force applied to breathe thus depends on this resistance

This resistance comes from:

  • Resistance of the air already present in the airways and upper-bronchial tree
  • Frictional resistance of tissues sliding over each other in lung parenchyma and chest wall
  • During inspiration, the force is provided by inspiratory muscles

During slow expiration, the elastic recoil of the lungs is sufficient to overcome the gas and tissue resistance until the level of FRC; to exhale down to RV, forced expiration is required, which uses the respiratory muscles

  • At end-inspiration/end-expiration, there is no air-flow, flow-resistance passes through 0, all pressure between airway opening and balloon (representing pleural pressure) is being applied to overcome the elastic resistance
22
Q

Define and outline transpulmonary pressure (Ptp), linking it to resistance, elasticity and distention

A

Transpulmonary pressure (Ptp) is the pressure across the respiratory system, and can be calculated by the alveolar pressure - pleural pressure (measure of the tendency of the lungs to recoil inwards)

The degree of stretch of the respiratory system during the ventilatory cycle is indicated by the change in volume (V), therefore compliance can be seen as = V/Ptp

During breathing, resistance must be overcome in order to move air through the respiratory system, whether in or out (inspiration/expiration)

This resistance is overcome by the generation of pressure in the pleural cavity by the respiratory muscles

This resistance comes from the elastic forces of the lungs, which resists distension; and the resistance to airflow e.g. turbulence at the back of the throat due to the change in angle of flow

23
Q

What are the 3 types of pressure which must be considered during breathing?

A

During breathing, there are 3 types of pressure which must be considered:

o The total pressure that must be applied to overcome resistance (Ptotal), which is the sum of:

o Pressure required to overcome elastic resistance (PEl)

o Pressure required to overcome flow resistance (PR)

At end-expiration/end-inspiration, there is no airflow, therefore PR = 0 and Ptotal= PEl

At any other point during the respiratory cycle, we can calculate PR, by using the equation PR = Ptotal - PEl

24
Q

Outline the 2 pressure-flow graphs [See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 38]

A

By measuring the rate of airflow and flow-resistive pressure at the same time, a pressure-flow plot can be derived (2nd graph)

1st graph - line to the right (next to red arrow) represents inspiration, as a higher pressure is required to overcome the resistive forces

2nd graph - the linear portion of the graph shows a linear relationship between pressure change and airflow; this is due to the laminar resistance of airflow through airways; the deviation from this straight line signifies a disproportionate increase in the pressure required to produce a further increase in airflow due to turbulent resistance in the airways

1st graph - flow resistance can be determined from the simultaneous relationship between volume and transpulmonary pressure during 1 breath; the elastic component of the transpulmonary pressure (PEl) is derived by joining the points of end-expiration & end-inspiration; the pressure necessary to overcome flow resistance (at any point) is the difference between Ptotal (transpulmonary) - PEI

2nd graph - when PR is plotted against the simultaneously measured rate of air flow, the flow resistance can be derived from the gradient of the linear portion of the curve

25
Q

Outline flow resistance

A

Flow resistance can be defined as the pressure required to produce a given rate of airflow (expressed in cmH2O/L/sec) = PR/ V (dot placed above V to indicate rate, also expressed as Q)

Continuous measurement of alveolar pressure is not necessary; pressure required to overcome flow resistance can be determined by simultaneous recordings of changes in:

o Lung volume

o Airflow

o Transpulmonary pressure In asthma or COPD, this pressure may be increased 10-15x

26
Q

Outline the process of getting air into the lungs

A

Air enters and leaves the lungs due to changes in the intrathoracic pressure

By increasing the size of the thorax, the inspiratory muscles lower the intrathoracic pressure relative to the atmospheric pressure; this causes bulk flow into the airways

Resistance to this flow is called flow resistance (R)

R = pressure (P) / Flow (V with dot/Q)

  • Once max flow has been achieved, the resistance is directly proportional to the driving pressure generated by the inspiratory muscle
27
Q

Outline expiration

A

Expiration is a passive process up to FRC; this involves passive recoil of the lungs

Expiration is an active process beyond FRC; this involves expiratory muscles (abdominal muscles)

Elastic forces at the end of a normal expiration (i.e. at FRC):

o No air moves into or out of the lungs

o A volume of air (equal to FRC) remains in the lungs

28
Q

Outline dynamic compression

A

Upon expiration, the intrapleural pressure becomes more positive than the alveolar pressure; therefore, pressure tending alveolar and airway collapse (occurs in non-cartillagenous small airways)

Upon forced expiration, dynamic compressionof the small airways causes an increase in airflow resistance (due to the relation of the inspiratory muscles leading to a reduction in thoracic volume)

When dynamic compression occurs, the alveoli exhibit elastic recoil to oppose the compression; this acts as a radial traction on the small airways - becoming the driving pressure for air out of the lung

The elastic recoil pressure of the alveoli can be derived by Palveoli - Ppleural

Along the airways, the pressure drops from alveolar pressure to atmospheric pressure in the mouth:

o At some point along the airways, the intramural and extramural pressures are equal, therefore there is no net transmural pressure; this is known as the equal pressure point (also ‘choke point’)

o Further towards the mouth, the intramural pressure may be less tham the extramural pressure, which creates a transmural pressure tending to narrow or close the airway (negative); at these points, flow limitation occurs and the airways may collapse

o Flow-limiting sites typically are in the 2nd and 3rd generations of airways

When dynamic compression occurs, the driving force for airflow becomes the difference between alveolar and intrapleural pressure, therefore the alveolar recoil pressure; this his is NOT determined by the respiratory muscle effort, but rather by the compliance and volume of the lung (a high lung volume means a high lung static recoil pressure)

In disease, the weakened airways can actually collapse causing air-trapping behind the blockade

Lip pursing moves the EPP to the mouth, a psychological relief to the patient

29
Q

Outline the main factors affecting dynamic compression

A

Airway resistance; increased airway resistance leads to a more rapid alveolar pressure drop, and thus earlier airway collapse

Compliance; increased compliance of the lung means reduced elastic recoil, leading to a reduced driving force for airflow

Lung volume; reduced lung volume means reduced stretch, which means reduced recoil, resulting in a reduced driving force:

o Reduced lung volume also increases airway resistance

o As lung volume decreases, the flow-limiting site moves peripherally (towards alveoli), therefore in late forced expiration the flow is increasingly determined by the properties of the small peripheral airways

30
Q

Outline isovolume pressure-flow curves

A

For any lung volume, maximum inspiratory flow is effort dependent

For high lung volumes,maximum expiratory flow is effort dependent

For low lung volumes: maximum expiratory flow is effort independent:

o I.e. maximum expiratory airflow increases to a maximum; further effort produces no further increase in flow due to airway compression

[See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 40]

31
Q

Outline asthma

A

Obstructive disorder, i.e. results in a narrowing of the airways.

The aperture of the small airways is completely different, resulting in changes to the FEV-1 (graph 2; is reduced)

The maximum expiratory flow is reduced, and the effort independent component of expiration (involving dynamic compression and the small airways)

32
Q

Outline the distribution of contribution to airway resistance of different sections of the respiratory system

A

Upper respiratory tract (nose → larynx) = 50%

Trachea → segmental bronchi = 35%

Distal to the bronchioles (airways <2mm) = 15%

33
Q

State some factors which affect airway resistance

A

Lung volume Airway calibre (diameter of the airway)

Airway generation

Airflow profile Phase of respiration

Vagal and sympathetic tone

Respiratory gases

34
Q

Outline airway generation as a factor affecting airway resistance

A

Regional airway resistance decreases as a function of airway generation

The highest regional resistance is at generation 4; these are medium-sized bronchi of short length and frequent branching, meaning highly non-laminar air flow with extreme turbulence

35
Q

Outline airflow profile as a factor affecting airway resistance

A

Airflow may be laminar, turbulent or transitional (at a branching)

Laminar flow occurs at low Reynolds numbers, where viscous forces are dominant, and is characterised by smooth, constant fluid motion:

  • Small airways (diameter <2mm) tend to show more laminar flow with Re <2000; turbulent flow occurs at high Reynolds numbers and is dominated by inertial forces, which tend to produce chaotic eddies, vortices and other flow instabilities
  • Large airways (diameter >2mm) tend to show more turbulent flow with Re > 2000 Reynolds number is used to assess the airflow profile, and is calculated by:

o Re = (airway diameter * velocity * density) / viscosity

o Reduced gas density such as helium will reduce the Reynolds number; helium may be of use in airway obstruction particularly

36
Q

Outline laminar flow and Poiseuille’s equation

A

V = (Pπ * r^4) / 8*η*L

Where:

P = Driving pressure

r = Radius η = viscosity

L = Length

I.e. for a given driving pressure under laminar conditions:

o Doubling the length of the airway will halve the flow rate

o Halving the tube diameter will decrease the flow 16x

Therefore, tube radius is the dominant factor in determining the resistance to flow (in small airways with diameter <2mm)

37
Q

Outline phase of respiration as a factor affecting airway resistance

A

Resistance is less in inspiration than in expiration

38
Q

Outline vagal and sympathetic tone (normally little if any) as a factor affecting airway resistance

A

Cholinergic blockade - decreases pulmonary resistance in both large and small airways

β2 receptor stimulation - produces bronchodilation and increased airway conductance in both large and small airways:

o NB: conductance is the reciprocal of resistance β-blockade - may increase airway resistance, i.e. reduce conductance

39
Q

Outline respiratory gases as a factor affecting airway resistance

A

Hypocapnia - may cause bronchoconstriction and an increase resistance, may also reduce ventilation due to poor perfusion

Hypercapnia - no effect on airway conductance

40
Q

Define viscosity and contrast dynamic, absolute and kinematic viscosity

A

Definition: resistance to flow; a physical property of a substance that is dependent on the friction of its component molecules as they slide by one another

Absolute viscosity is a measure of internal resistance, whereas dynamic viscosity is the tangential force per unit area required to move one horizontal plane with respect to another plane, at an unit velocity, when maintaining a unit distance apart in the fluid

Kinematic viscosity is the ratio of absolute (or dynamic) viscosity to density, a quantity in which no force is involved; kinematic viscosity can be obtained by dividing the absolute viscosity of a fluid with the fluid mass density

41
Q

Outline the work of breathing, referencing the following graphs: [See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 42]

A

Respiratory muscles must perform work in order to overcome the mechanical impedences to respiration offered by the lung and chest wall during breathing

In graph A, the mechanical work of breathing necessary to overcome elastic resistance is shown

In graph B, this is combined with the work required to overcome flow resistance

The expiratory portion of the flow resistance work loop falls within the triangle that represents elastic work:

o This indicates that expiration is passive and brought about by the elastic recoil of the lung, which was stretched during inspiration

The total work performed during inspiration is the sum of the elastic work and that required to overcome inspiratory flow resistance

In a healthy individual, the total mechanical work per quiet breath = work required to overcome elastic properties (2/3) and flow resistance (1/3)

NB: The product of pressure and volume also has the units of work

When the mechanical properties of the respiratory apparatus are altered by disease or during a forceful expiration, additional expiratory mechanical work is necessary, provided by expiratory respiratory muscles e.g. abdominals

42
Q

Define work

A

Definitions:

  1. Physical or mental effort to achieve a result
  2. The product of force acting against resistance to produce motion
43
Q

Outline increased flow-resistive work and increased elastic-resistance work

A

Increased flow-resistive work, e.g. asthma; elastic energy stored during inspiration is not enough to produce airflow during expiration, therefore the expiratory muscles must do extra work:

o NB: flow-resistive loop falls out of the elastic work area, thus additional work required to overcome flow resistance during expiration

Increased elastic-resistance work, e.g. pulmonary fibrosis; work required to overcome flow resistance is not altered, but much more work is required to overcome the high elastic resistance of the ‘stiff lungs’

44
Q

Outline alveolar ventilation

A

Work of breathing can affect the pattern of breathing and therefore the amount of ventilation taking part in gas exchange

For any given alveolar ventilation, there is an optimal respiratory rate and tidal volume at which the total mechanical work of breathing is minimal

When the respiratory rate is less than optimal, flow-resistive work is less but larger tidal volumes are required to achieve a given alveolar ventilation; this increases the work required to overcome the elastic resistance

When the respiratory rate is more than optimal, total ventilation must increase if the same alveolar ventilation is to be maintained; this is because more ventilation is wasted when the tidal volume is smaller

Therefore, the amount of work required to overcome the elastic resistance is less, but the flow-resistive work will increase roughly in proportion to the increase in respiratory rate In pulmonary fibrosis/kyphoscoliosis, the elastic resistance is increased, therefore the mechanical work required to overcome this increases; the graph is shifted upwards; the work is minimal at an increased frequency, meaning that respirations tend to become rapid and shallow In bronchial obstruction, the flow-resistance is increased, therefore the mechanical work required to overcome this increases; the graph is shifted upward; the work is minimal at a lower frequency means that respirations tend to become slower and deeper

45
Q

Label graphs A, B and C with their respective conditions [See http://www.icsmsu.com/exec/wp-content/uploads/2011/12/ABS-Respiratory_System.pdf Page 43]

A

A - Normal

B - Pulmonary fibrosis (increased elastic resistance)

C - Bronchial obstruction (increased flow resistance); the little arrows indicate respiratory rate at which total work is minimal

46
Q

Outline oxygen cost

A

In order to perform the work necessary to overcome the mechanical resistances encountered during breathing the respiratory muscles require oxygen

Oxygen consumption (VO2) increases by about 1ml/litre ventilation when ventilation in a healthy individual is increased to 60+ litres/min

At very high ventilations, oxygen consumption increases considerably and may become a significant proportion of the total body oxygen consumption In emphysema, oxygen cost (even at low ventilation rates) may be increased by 4-10x Respiratory insufficiency; oxygen consumption increases disproportionately even at very low ventilation, therefore anything that requires an increase in ventilation (e.g. exercise), leading to increased oxygen requirements; this needs to be considered when forming a management plan