clinical evaluation of respiratory function

Question 1

What is spirometry?

Answer 1

Spirometry is a common method of quantifying vital capacity, airflow, and the level of airway obstruction present during breathing.

Question 2

How does spirometry work?

how to interpret results?

Answer 2

Spirometry involves the patients producing a maximum forced expiration into a spirometer, which measures the volume of air passing through over time. This is then plotted on a graph from which calculations and interpretations can be made:

Question 3

What is FEV1?

what does it correspond to?

Answer 3

FEV1 (forced expiratory volume in one second) is a term used to describe the maximum volume that can be expired during the first second of a maximum forced expiration.

It corresponds to how quickly air can pass through the airways and reflects airway function and health.

Question 4

What is FVC?

what does this reflect?

Answer 4

FVC (forced vital capacity) measures the maximum volume of an individual can exhale in one breath (after inspiring as much air as possible) and reflects the volume of the lungs that the individual can utilise when breathing.

Question 5

fev1/fvc

what is indicative of obstructive airways disease?

Answer 5

total lung capacity an individual can exhale in the first second (<80% is indicative of obstructive airways disease)

Question 6

why fev1/fvc ratio?

what are fvc values compared to?

Answer 6

FEV1 values are normalised by expressing as FEV1/FVC ratio (expressed as a decimal or percentage) to take account of the fact that different individuals have varying rates of healthy airflow depending on their vital capacity (an individual with larger lungs and airways will naturally expire air faster).

Similarly, FVC values are compared to expected healthy values for a person of similar age, height and sex

Question 7

Obstructive airway diseases

what diseases are these usually?
what indicates this?
what is normally unchnaged and why?
what is the net effect?

Answer 7

Obstructive airway diseases, such as asthma and chronic bronchitis, are indicated by a reduction in FEV1/FVC ratio (<70%). FVC is typically unchanged as lung function is unaffected.

FEV1/FVC <70%
FVC >80%
E.g. Asthma
↑Resistance

hence slower airflow but overal airway capacity is the same (just longer to expire)

Question 8

Restrictive lung diseases

what diseases are these usually?
what indicates this?
what is normally unchnaged and why?
what is the net effect?

Answer 8

Restrictive lung diseases, such as pulmonary fibrosis, are indicated by a reduction in FEV1 and FVC (<80% expected value), with a relatively normal FEV1/FVC ratio (>70%, i.e. the decrease in FEV1 reflects an overall decrease in lung volume rather than airway obstruction).

FVC < 80%
FEV1/FVC > 70%
E.g. Fibrosis
↓Compliance

ratio of fev1/fvc is the same if no obstruction

Question 9

Basic interpretation of spirometry

what will indicate obstructive? restrictive? a mix?

Answer 9

FEV1/FVC <70%, FVC = Normal → Obstructive respiratory disease

FVC <80% of predicted volume, FEV1/FVC = Normal → Restrictive respiratory disease

FEV1/FVC <70% and FVC<80% → Mixed obstructive and restrictive respiratory disease

Question 10

Q: What sort of respiratory disease is indicated by the spirometry readings?

FEV1 = 2.4L (predicted = 3.9L)
FVC = 4.3L (predicted = 4.7L)

Answer 10

fev1/fvc = 0.56 therfore airway obstruction
fvc = 0.91 hence vital capacity is healthy

spirometry indicates that the patient has obstructive respiratory disease (asthma, bronchititis, cystic fibrosis)

Question 11

Q: What sort of respiratory disease is indicated by the spirometry readings?

FEV1 = 2.7L (predicted = 4.2L)
FVC = 3.0L (predicted = 5.0L)

Answer 11

fev1/fvc = 0.9 therefore healthy airway
fvc = 0.6 therefore restrictive lung

restrictive lung disease -> pulmonary firbrosis, emphysema)

Question 12

Lung compliance

what is the relationship between?

Answer 12

This relationship between the change in lung volume produced by a particular changed in transpulmonary pressure is termed ‘lung compliance’, and essentially describes how easily the lungs can be distended .

Question 13

What does it mean when lung compliance increases/decreases?

Answer 13

when increased, easier to expand but less recoil

when decreased, it is harder to expand

Question 14

What respiratory diseases are associated with increased/decreased compliance?

Answer 14

increased = degeneration of elastic fibres hence emphysema
decreased = pulmonary fibrosis

Question 15

Static compliance

what part of the graph is used?
when are lung measurements taken?
when airflow is 0, what is the pressure is equal and what is different?

Answer 15

For static compliance (measurements taken whilst airflow = 0), the steepest part of the curve is used

Lung measurments to determine static compliance are taken at specific lung volumes where the patient pauses inspiration at certain point (therefore airflow falls to zero)

when airflow is 0, pressure of atmosphere is equal to that in the alveoli (only difference in pressure is air in lungs/volume hence gradient)

Question 16

dynamic compliance

how do you determine this?
what do you measure now and why?

Answer 16

To determine dynamic compliance a patient breaths normally at tidal volume – dynamic complaince respresents the gradient of the line from the end of expiration to the end of inspiration.

as the alveoli pressure is changing all the time, you measure intrapleural pressure now

Question 17

dynamic compliance - graph

what is the size/fatness of the loop proportional to?
what does airway resistance increase with?

Answer 17

The size of the internal area or ‘fatness’ of the loop is proportional to the level of airway resistance. (how much it deviates from the straight line hence how much force is exerted during breathing)

Airway resistance increases with ↑airway obstruction and ↑speed of airflow therfore more force

Question 18

Obstructive airway disease e.g. asthma
dynamic compliance graphs

what will have chnaged and what will not have chnaged?
why?

Answer 18

gradient may have not changed but the graph will have got fatter due to airway obstruction hence more forced expiratory breathing

the area contained within the loop (the “fatness” of the loop) is proportional to the level of airway resistance generated (for example it would increase with a forced inspiration/expiration and airway obstruction, and would decrease with a very slow inspiration with low flow rate in the absence of airway obstruction.

Question 19

Change in gradient for dynamic compliance graphs

what does decreased gradient mean? disease?
increased gradient? disease?

Answer 19

Low compliance (stiff) (e.g. pulomnary fibrosis)
A greater pressure change change is required to produce the same change in volume (decreased gradient)

High compliance (floppy) (e.g. emphysema)
A smaller pressure change is required to produce the same change in volume (increased gradient)

Question 20

How do the respiratory system and kidneys function together to regulate and maintain blood pH?

what does the kidney regulate? timeframe?
what does the resp system regulate? timeframe?

Answer 20

ph = log (hco3-)/paco2

Renal regulation of HCO3-
E.g. regulating reabsorbtion/ excretion in glomerular filtrate (timeframe = hours to days)

Respiratory regulation of PaCO2
E.g. regulating ventilation (timeframe = minutes)

Question 21

The lungs & kidneys maintain blood pH homeostasis by regulating PaCO2 & [HCO3-], respectively

how does lungs regulate? what does it do to change pH?
kidneys? what does it change to regulate pH?

Answer 21

↑Ventilation = ↓PaCO2= ↑ pH
↓Ventilation = ↑PaCO2= ↓ pH
↓ HCO3 excretion = ↑[HCO3-] =↑ pH
↑ HCO3 excretion = ↓[HCO3-] =↓pH
(unless PaCO2 or HCO3 changes proportionally, in the opposite direction)

Question 22

Compensation and mixed disorders

what is compensation?
how is it identified?

Answer 22

The respiratory and metabolic systems can (and do) compensate for disruptions in pH caused by each other. Metabolic acidosis and alkalosis can be compensated by respiratory alkalosis and acidosis, respectively. When compensation occurs, it can be identified by a change in PaCO2 or [HCO3-] that takes place in the presence of a pH disruption that runs counter to the expected change:

Question 23

respiratory compensation

how is it identified?

Answer 23

Increased PaCO2 in the presence of high pH, or decreased PaCO2 in the presence of low pH = respiratory compensation

Question 24

metabolic compensation

how is it identified?

Answer 24

Increased [HCO3-] in the presence of low pH, or decreased [HCO3-] in the presence of high pH = metabolic compensation

Question 25

'full' or 'partial' compensation

Answer 25

Whether the degree of compensation is termed 'full' or 'partial', depends on whether the level of compensation has restored pH to its normal range (if pH = 7.35 - 7.45 = full compensation)

Question 26

mixed acidosis or mixed alkalosis how is it identified?

Answer 26

dysfunction in both respiratory and metabolic systems can and often doses occur simultaneously in patients, this is termed mixed acidosis or mixed alkalosis (depending on the direction of pH disturbance) and can be identified by simultaneous high PaCO2 + low [HCO3-], or low PaCO2 + high [HCO3-], respectively

Question 27

simple way of determining the nature of an acid-base disorder where both CO2 and HCO3- are abnormal 2 main ways to work it out

Answer 27

1. Understanding that the respiratory system is responsible for controlling PCO2 and the metabolic system responsible for controlling HCO3- 2. Thinking of CO2 as acidic and HCO3- as basic. Therefore: more CO2 = more acidic, more HCO3- = more basic. Abnormal changes in arterial pH can then be viewed in respect of whether the changes in CO2 and HCO3- explain or are consistent with the direction of pH change. For example, in the case of an acidosis (decreased pH), an increase in PaCO2 would explain why pH had fallen as CO2 is acidic and excessive level would cause an acidosis. In contrast a decrease in PaCO2 would not explain why pH had fallen – therefore the decrease in PaCO2 observed must be compensatory

Question 28

ABG results: patient 1 pH = 7.30 (7.35 – 7.45) PaCO2 = 7.1 (4.9 – 6.1) [HCO3-] = 25 (22 – 30)

Answer 28

pH = low = acidosis Which out of PaCO2 and [HCO3-] is abnormal? PaCO2 = high, therefore respiration is abnormal (hypoventilation). High PaCO2 can cause acidosis. Therefore answer = respiratory acidosis

Question 29

``` pH = 7.30 (7.35 – 7.45) PaCO2 = 4.0 (4.9 – 6.1) [HCO3-] = 18 (22 – 30) ```

Answer 29

pH = low = acidosis PaCO2 = low = hyperventilation, which doesn’t produce acidosis, therefore indicates respiratory compensation [HCO3-] = low. Low [HCO3-] does produce acidosis, therefore indicates metabolic acidosis Metabolic acidosis with respiratory compensation

Question 30

``` pH = 7.48 (7.35 – 7.45) PaCO2 = 3.0 (4.9 – 6.1) [HCO3-] = 18 (22 – 30) ```

Answer 30

pH = high = alkalosis PaCO2 = low = hyperventilating, which causes alkalosis. Therefore indicates reparatory alkalosis [HCO3-] = low. Low HCO3- causes acidosis, not alkalosis. Therefore indicates metabolic compensation Respiratory alkalosis with metabolic compensation (e.g. Response to altitude - because of decrease in o2 in atmosphere, breathing rate must increase to get more o2 which means more co2 is expelled leading to hypercania + alkalosis but kidneys try to compensate for this by increasing HCO3- excretion)

Question 31

``` pH = 7.10 (7.35 – 7.45) PaCO2 = 8.0 (4.9 – 6.1) [HCO3-] = 18 (22 – 30) ```

Answer 31

pH = low = acidosis PaCO2 = high = hypoventilating (fits with acidosis) = resp. acidosis [HCO3-] = low (fits with acidosis) = metabolic acidosis Mixed metabolic and respiratory acidosis

Question 32

In the broadest terms possible, what the two reasons why a patient might have low PaO2?

Answer 32

1) hypoventilation | 2) poor gas exchnage

Question 33

How can we determine the cause of hypoxaemia? Is the level of ventilation or oxygenation to blame? how can PAO2 be calculated? equation?

Answer 33

Alveolar content = O2 inspired - O2 consumed It is not practical in such situations to sample gas directly from alveoli, however PAO2 can be easily calculated from other measurements: 𝑃𝐴 𝑂2 = 𝐹𝐼𝑂2 × (𝑃b − 𝑃𝐻2𝑂) − (𝑃𝑎 𝐶𝑂2)/𝑅𝐸𝑅 alevolar pressure = fraction of o2 in inspired gas x (barometric pressure - H2o vapour pressure) - arterial co2 pressure/ respiratory exchange ratio

Question 34

respiratory exchange ratio | what is the realtionship?

Answer 34

The respiratory exchange ratio = the relationship between CO2 elimination & O2 consumption 𝑅𝐸𝑅=(𝑉𝐶𝑂2 𝑝𝑟𝑜𝑑𝑢𝑐𝑒𝑑)/ (𝑉𝑂2 𝑐𝑜𝑛𝑠𝑢𝑚𝑒𝑑)

Question 35

RER for modern diet? oxidation of carbs? fats?

Answer 35

RER for modern diet ≈ 0.8 Oxidation of Carbohydrates: 𝐶6𝐻12𝑂6 + 6𝑂2 → 6𝐶𝑂2 + 6𝐻2𝑂 𝑅𝐸𝑅= 6 𝐶𝑂2/ 6𝑂2 = 1 Oxidation of fatty acids: 𝐶16𝐻32𝑂2 + 23𝑂2 → 16𝐶𝑂2 + 16𝐻2𝑂 𝑅𝐸𝑅 = 16 𝐶𝑂2/ 23𝑂2 =0.7

Question 36

The alveolar gas equation and alveolar-arterial oxygen gradient are used to investigate hypoxaemia

Answer 36

𝑃𝐴 𝑂2 = 𝐹𝐼𝑂2 × (𝑃b − 𝑃𝐻2𝑂) − (𝑃𝑎 𝐶𝑂2)/𝑅𝐸𝑅 Alveolar 02 content = O2 inspired - O2 consumed Reading Value used FIO2 oxygen content of inspired air (e.g. 0.21 if breathing ambient air, 0.4 if breathing 40% oxygen) PB 100 kPa (at sea level) PH2O 6 kPa (if air = humidified) PaCO2 Measured in patient (e.g. 5 kPa) RER assume 0.8, unless otherwise indicated PAO2 Calculated in formula (e.g. 14 kPa)

Question 37

Using the AGE to evaluate respiratory problems | Is hypoventilation contributing to hypoxaemia? what value is used to determine this?

Answer 37

Hypoxaemia can be caused by hypoventilation and/or reduced oxygenation (i.e. oxygen reaches alveoli but gas exchange is limited). The PaCO2 value also helps to interpret this: if hypoventilation is the problem, then PaCO2 will be excessive. Conversely, PaCO2 will be lower if hypoxaemia is being caused V/Q inequality or deficits in oxygenation (but where there is sufficient overall ventilation to remove the excess PaCO2).

Question 38

Using the AGE to evaluate respiratory problems Is the oxygen that reaches the alveoli being exchanged into the blood adequately? what to look at to detemrine this? what can be done to remdy this?

Answer 38

If PAO2 is much greater than PaO2 (i.e. there is an excessive pressure gradient) this indicates issues with the level of gas exchange and blood oxygenation taking place (e.g. due to V/Q mismatch or diffusion defects such as excessive pulmonary fluid or increased basement membrane thickness). In healthy individuals, the difference between PAO2 and PaO2 should be small, on average less than approximately 2kPa (1.5 to 3kPa, depending on age, with older patients naturally having a greater A-a gradient). If A-a gradient much greater than 2kPa, this means that the volume of oxygen that reaches the alveoli isn’t getting diffusing into the blood efficiently. Again, depending on the nature of the defect (i.e. the extent of shunt effect), supplemental O2 therapy may be able to compensate by resolving V/Q mismatch or increasing the alveolar O2 pressure sufficiently so that an adequate quantity of O2 reaches the blood.

Question 39

A-a o2 gradient what is this and what is the value normally?

Answer 39

A-a O2 gradient is the difference between alveolar and arterial pressure: = PAO2 – PaO2. Normally ≈ <2kPa