Respiratory Physiology 2

Question 1

What is compliance?

Answer 1

The volume change per unit change in pressure.

(C = V/P)

(units: ml/cmH2O or L/kPa)

It’s measured on the pressure-volume graph, with the gradient of the line representing the degree of compliance. The steeper the gradient, the greater the compliance.

Question 2

What is the lung compliance value?

Answer 2

1.5 - 2 L/kPa

OR

200 ml/cm H2O

Question 3

What is the compliance of the chest wall normally?

Answer 3

1.5 -2 L/kPa

Question 4

What is the total thoracic compliance?

Answer 4

0.75 - 1 L/kPa

(it’s calculated by adding the reciprocals of lung compliance and chest wall compliance)

Question 5

Is static compliance or dynamic compliance usually higher?

Answer 5

Normally higher for static compliance as there is time for pressure and volume to equilibrate.

Question 6

What part of the lung is more compliant?

Answer 6

The lower part, because this will distend most (like a coiled spring).

At the apex of the lung the alveoli are held open as gravity pulls the lung down. As they commence inspiration (e.g. become inflated) they are closer to their elastic limit and therefore less compliant.

Question 7

What is Laplace’s Law?

Answer 7

P = 2T /R

(P - pressure, T - tension, R - radius)

It’s to do with surface tension, which is caused by forces of attraction between molecules of water at the gas/fluid interface. It acts to collapse down alveoli. The smaller the radius - the greater the pressure collapsing the sphere.

Question 8

Why would smaller alveoli collapse according to Laplace’s Law?

Answer 8

If surface tension (T) was equal for both small and large alveoli, the larger radius alveoli would have a smaller pressure and the gas would flow down the pressure gradient - collapsing the smaller alveoli.

Question 9

Why would a saline-filled lung have greater compliance?

Answer 9

Because the air-fluid interface (therefore surface tension) is removed.

Question 10

What is surfactant?

Answer 10

Phospholipid dipalmitoylphosphatidylcholine (DPPC), protein and carbohydrate.

Question 11

Where is surfactant produced from?

Answer 11

Type II pneumocytes from free fatty acids extracted from blood, production can be affected by lack of blood flow.

Question 12

What are the effects of surfactant?

Answer 12

• increases compliance by profoundly reducing surface tension and disrupting attractive forces
• prevents transudation of fluid into alveoli (pulmonary oedema)
• stabilizes alveoli - prevents collapse

Question 13

Does surfactant reduce surface tension to a greater extent in smaller or larger alveoli?

Answer 13

Smaller alveoli with low volume, because the DPPC molecules squash together and the repulsive forces between them increase, keeping the alveolus from collapsing.

This means that there’s equal pressures in smaller and larger alveoli - prevents collapse.

Question 14

Why does decreased FRC reduce compliance?

Answer 14

Because a drop in FRC moves the lung down the compliance curve to a less favourable gradient.

Question 15

How does work of breathing relate to compliance?

Answer 15

WOB is inversely proportional to compliance

Question 16

How can work of breathing be calculated?

Answer 16

By integrating the pressure-volume curve.

Work done = change in pressure x change in volume

• work done = force x distance*
• force = pressure x area*
• distance = volume/area*
• work done = (P x A) x (V/A)*
• = P x V*

Question 17

What is work of breathing?

Answer 17

• elastic forces in the lung (energy used for this is stored as potential enrgy during inspiration and used during expiration)
• the resistance from air flow and the viscous resistance of tissue moving over tissue (energy dissipated as heat)

Question 18

How is the total work done in inspiration spent?

Answer 18

• 65% is overcoming elastic forces (the energy is stored in elastic tissues)
• 35% is overcoming resistance forces (viscous forces ie tissue rubbing on tissue = 7% of this, and airway resistance accounts for 28%)
• energy generated is lost as heat

Question 19

What work of breathing is necessary for expiration?

Answer 19

• the only work needed is that required to overcome resistance
• during quiet breathing, this is less than energy stored in elastic tissues
• all of the energy of expiration is provided by elastic recoil -so it’s passive
• remaining energy is lost as heat

Question 20

How does RR and tidal volume affect work of breathing?

Answer 20

Increased RR increases WOB, because work against resistance forces (W_R) increases.

As V_T increases, work against elastic tissues (W_E) increases.

For a given minute volume, there’s an optimal RR to V_T ratio to minimize total work (W_t), usually 14-16 bpm.

In obstructive defects: higher V_T and lower RR minimize work.

In restrictive defects: lower V_T and higher RR minimizes work.

Question 21

What will cause an increase in work of breathing?

Answer 21

Anything that increases the area under the pressure-volume curve:

• larger tidal volumes
• reduction in compliance
• obstructive defects (at extremes expiration requires extra work - becoming an active process)
• exercise: this increases both VT and RR and again expiration becomes active

Question 22

What effects does general anaesthesia have on the work of breathing?

Answer 22

• reduced FRC, moving lung compliance down the compliance curve
• increased resistance to airflow through narrow ET tubes, valves and circuits
• all of this can increase WOB in the spontaneously breathing patient - in susceptible patients this can lead to respiratory failure

Question 23

Why does Heliox reduce the work of breathing?

Answer 23

Because Heliox is less dense than air, reducing the Reynolds number and promoting laminar flow, therefore reducing the resistive forces of airflow.

Question 24

Why does decreasing FRC increase the WOB?

Answer 24

Because this reduces compliance therefore increasing WOB.

Question 25

What is hypoxia?

Answer 25

Deficiency of oxygen for tissue respiration

Question 26

What is hypoxaemia?

Answer 26

Arterial PO2 less than 12 kPa.

Question 27

What are the classifications of hypoxia?

Answer 27

• hypoxic hypoxia
• anaemic hypoxia
• circulatory (stagnant) hypoxia
• cytotoxic (histotoxic) hypoxia

Question 28

What is the oxygen delivery equation, and where does hypoxic, anaemic and circulatory hypoxia affect this?

Answer 28

DO2 = CO x (1.34 x [Hb] x O2 sats) + (0.0003 x PaO2)

circulatory anaemic hypoxic

Question 29

Where does cytotoxic hypoxia occur?

Answer 29

At the cellular level (eg cyanide poisoning) with no deficit in O2 delivery.

Question 30

Where in the O2 cascade does Low FiO2 affect? What can cause a low FiO2?

Answer 30

It affects it at the “AIR” level.

Causes of Low FiO2:

• inadvertant hypoxic gas mix
• high altitude
• diffusion hypoxia following N2O administration

Question 31

What are the causes of hypoxic hypoxia?

Answer 31

• low FiO2
• hypoventilation
• diffusion defect
• V/Q mismatch/shunt

Question 32

Where does hypoventilation affect on the oxygen cascade?

Answer 32

Question 33

Where does a diffusion defect affect on the O2 cascade?

Answer 33

Question 34

Where does a V/Q mismatch affect on the O2 cascade?

Answer 34

Question 35

What is typical O2 consumption in an adult?

Answer 35

250 ml/min

Question 36

What is the alveolar gas equation?

Answer 36

P_AO2 = [Fi_O2 x (P_ATM - P_H2O)] - (P_ACO2/R)

P_AO2 is the alveolar O2 partial pressure

P_{<strong>ACO2</strong>} is the alveolar CO2 partial pressure

P_{<strong>ATM</strong>} is the atmospheric pressure

Fi_{<strong>O2</strong>} is the fraction of inspired O2

P_{<strong>H2O</strong>} is the standard vapour pressure of H2O at 37C

R is the respiratory quotient

Question 37

What is the value of the respiratory quotient?

Answer 37

R = 0.8 on a mixed diet

R = 1.0 on a pure carbohydrate diet

Question 38

Why is hypoxia usually secondary to an associated hypercarbia?

Answer 38

From the alveolar gas equation, as P_ACO2 increases, P_AO2 decreases.

Increasing the FiO2 can increase O2 sats and treat the hypoxia but doesn’t address the underlying problem

Question 39

What are potential causes of hypoventilation?

Answer 39

• reduced central respiratory drive
• impaired peripheral mechanisms of breathing
• increased dead space

Question 40

What are potential causes of reduced respiratory drive?

Answer 40

• drugs (eg opiates, benzos)
• metabolic alkalosis
• intracranial pathology
• alveolar hypoventilation syndrome
• hypothermia

Question 41

What are possible causes of impaired peripheral mechanisms of breathing?

Answer 41

• airway obstruction
• restriction (pain/obesity/ascites)
• chest disease (COPD/asthma/flail chest)
• muscular weakness (eg dystrophies, dystrophia myotonica, electrolyte abnormalities, critical illness neuropathies)
• neuromuscular junction impairment (eg muscle relaxants, MG)
• nerve lesions (polio, guillian barre, phrenic nerve/spinal cord injury)

Question 42

What is a diffusion defect and what can cause it?

Answer 42

Normally - O2 diffuses rapidly into the RBCs as it passes along the capillary, transfer is complete 1/3 of the way along the capillary (0.25s).

In diseases such as pulmonary fibrosis or oedema diffusion becomes abnormal.

Question 43

What values of PO2 and PCO2 should end capillary blood have in healthy lungs?

Answer 43

The same as in the alveolus:
PO2 = 14 kPa

PCO2 = 5.3 kPa

Question 44

What is no perfusion with normal ventilation called?

Answer 44

Dead space. The V/Q ratio = ∞

Question 45

What is no ventilation with normal perfusion called?

Answer 45

Shunt. V/Q ratio = 0

Question 46

What happens to capillary PcO2 in a shunt?

Answer 46

PcO2 is identical to PvO2 (ie low) because there is no gas exchange happening. The capillary blood mixes with oxygenated blood from ventilated areas of the lung

Question 47

Which part of the lung is best ventilated and perfused? How does this change with anaesthesia?

Answer 47

The bottom is better ventilated and perfused.

Under GA, FRC is decreased and the lung moves down the compliance curve so ventilation is now better at the top but perfusion is still best at the bottom. Ie a shunt has developed.

Question 48

What is closing capacity?

Answer 48

The lung volume above residual volume at which airway closure occurs

CC = closing volume + residual volume

If FRC decreases, or CC increases then eventually CC encroaches on FRC and airways close during quiet breathing. The lower (dependent) parts of the lung tend to collapse first, they’re at lower volume than the upper parts. This leads to shunting then hypoxaemia.

Question 49

What increases closing capacity?

Answer 49

• age, CC = FRC in
  
  • neonates/infants
  • supine 45yr old
  • upright 65yr old
• increased intrathoracic pressure (eg asthma)
• smoking

Question 50

What decreases closing capacity?

Answer 50

PEEP and CPAP

Question 51

What reduces FRC?

Answer 51

• body position (head down > supine)
• obesity/intra abdominal mass including pregnancy
• GA (esp with paralysis)
• restrictive lung disease (pulmonary fibrosis)
• female gender (10% less than men)
• youth

Question 52

What is Fowler’s method?

Answer 52

• single breath nitrogen washout
• at the end of tidal expiration a vital capacity breath of 100% O2 is taken
• exhaled N2 measured during a slow maximumal exhalation with N2 plotted against volume expired
• after the plateau phase, EtN2 rises again - this stage represents the closing volume
• the residual volume needs to be calculated (helium dilution/body plethysomography) and added to the CV to obtain the CC

Question 53

Why does Fowlers method graph have a 2nd N2 rise?

Answer 53

Because the ventilation is better at the bottom of the lung - so these lower alveoli will contain a greater proportion of O2.

The upper alveoli have poorer ventilation/expand less so contain a smaller proportion of O2 and higher N2 concentration.

Airway collapse occurs in the lower lung first - they’re at a lower volume then the expired gas increasingly comes from the N2 rich upper alveoli.

Question 54

Why is end tidal CO2 generally 0.7kPa below PaCo2 in healthy adults?

Answer 54

Because there is always some amount of dead space.

Question 55

Does a shunt affect the PaCO2 - Et CO2 gradient?

Answer 55

No, only dead space increases this.

Question 56

In an awake individual in the lateral position, which lung has better ventilation and perfusion? What will the P_AO2 and P_ACO2 be in the lower lung?

Answer 56

The dependent lung has better perfusion and better ventilation due to gravity.

The upper lung will tend towards dead space and so the P_AO2 will be higher in the lower lung.

The P_ACO2 will also be higher in the lower lung because perfusion is good, and so alveolar P_ACO2 will tend towards mixed venous (5.3kPa) whereas in the upper lung dead space P_ACO2 tends towards P_ICO2 (0 kPa).

Question 57

When the ventilation/perfusion ratio of a lung unit increases, what happens to the alveolar PO2, PCO2, end capillary PO2 and arterial PO2?

Answer 57

Alveolar PO2 rises

Alveolar CO2 decreases

End capillary PO2 increases

Arterial PO2 increases

Question 58

Where does hypoxic pulmonary vasoconstriction occur?

Answer 58

HPV occurs where P_AO2 is low (areas of shunt *not dead space*)

It only provides a small degree of compensation.

Question 59

In dead space, why can you compensate for this with increased minute ventilation?

Answer 59

To compensate for the increased PaCO2 (clinically, this may not seem an intuitive reaction to a low EtCO2).

If EtCO2 is low due to hyperventilation PaCO2 is also low.