respiratory viva style questions

Question 1

how to measure: total lung capacity?

Answer 1

Body plethysmograph P1V1=P2 (V1+change in V)

Question 2

how to measure: anatomical dead space?

Answer 2

Fowlers method- tracer washout

Question 3

how to measure: physiological dead space?

Answer 3

Bohr’s equation- measures the volume of lung that doesnt eliminate CO2. The normal ratio of dead space to total voume is 0.2-0.35 at rest. If larger then would indicate CLD and inequality in blood flow to ventilation.

Question 4

what affects diffusion of a gas?

Answer 4

Diffusion= A/T x D x (P1-P2)
Diffusion is propotional to area and to diffusion constant and the differences in partial pressure.
It is inversley properotional to thickness.
The diffusion constant = solublity/ sqR mol.wt
- mainly depeneds on the solubility of the gas; where CO2 is 20x more soluble

Question 5

What is diffusion limited gas transfer?

Answer 5

Where the gas transfer is not dependent on the amount of blood available, only on the diffusion properties of the gas.

Explains how CO rapidly crosses the alveolar wall and continues to do so as the difference in PP between the alveoli and blood remain high, therefore continues to rapidly cross. This would only change if the diffusing properties of the gas changes.

Question 6

When does O2 becomes diffusion limited?

Answer 6

In severe exercise–> diffusion of O2 should still be normal with severe exercise unless abnormally thick barrier

In high altitude –> diffusion impairment evident combined with exercise

Question 7

What is perfusion limited gas transfer?

Answer 7

The amount of gas taken up into blood is dependent on blood flow and not diffusion.
Because N2O doesnt combine with Hb, the PP in blood rises rapidly to match alveolar PP, therefore there is less transfer across the membrane, unless perfusion is increased.

Question 8

When does O2 become perfusion limited?

Answer 8

Normally O2 is in RC by 1/3 of the time blood is spent in the capillary. However if HR is increased, then RC would only just become oxygenated, therefore becoming perfusion limited.

Question 9

How is diffusing capacity of the lung measured?

Answer 9

Measured with carbon monoxide CO via the Single-Breath method.
This is because its transfer is soley limited by diffusion.
Diffusion= A/T x D (P1-p2)
Because A/T x D is hard to measure, the DC of lung (DL) replaces this. Also Difference in P1-P2 is neglegible with CO.
Therefore DL= diffusion/PaCO

The normal DL at rest is 25ml/min/mmHg
With exercise, this can increase 2-3 fold due to recruitment and distension of pulm capillaries.

Question 10

What factors affect pulmonary vascular resistance?

Answer 10

Pulm Resistance= (input - output pressure) / blood flow

Lung= gravity, lung volumes,
Vascular= venous and arterial pressure,
recruitment, distension, hypoxic pulmonary vasoconstricion, vascular endothelium and smooth muscle affectors (constrictors- hypoxia, serotonin, histamine, TXA2, endothelin) (dilators- NO, phosphodiecterase inhibitors, CCB, prostacyclin)

Question 11

Describe the differences in the distribution of blood flow throughout the lung

Answer 11

Low flow at the apex, high flow at the base. Is affected by posture and exercise. This can be explained by the hydrostatic pressure differences.
Zone 1: Apex: Alveolar P > Pa>Pv = ventilated but not perfused.
Zone 2: Midzone: pulmonary arterial pressure increases above alveolar pressure (Pa > alveolar P > Pv) therefore flow is determined by the difference between arterial and alveolar pressure
Zone 3: venous pressure now exceeds alveolar

Other causes of uneven blood flow= random vascular arrangement, peripheral parts of the lung

Question 12

What are the metabolic functions of the lung?

Answer 12

1. activation: ANG I to II via ACE
2. inactivation: bradykinin (via ACE), prostaglandins, NA, serotonin
3. metabolism: arachodonic acid to leukotrienes and PG via COX; carbohydates
4. Synthesis: surfactant, collagen, elastins, proteases

Question 13

What are the causes of hypoxaemia? What cannot be reversed by giving O2?

Answer 13

Hypoventilation, diffusion limitation, shunt, V/Q mismatch. Hypoxia is not corrected in SHUNT, as the shunted blood does not reach the area of the ventilated lung

Question 14

What are some causes of hypoventilation?

Answer 14

CNS: drugs, decreased central drive from damage
Airway: obstruction, increased BMI
MSK: chest wall damage, mscle paralysis

Question 15

What are some causes of diffusion limited hypoxia?

Answer 15

Thick barrier, low FiO2, exercise

Question 16

What is a shunt and some causes?

Answer 16

Shunt~ blood entering the systemic arterial system without being ventilated.
Physiological causes: bronchial artery, coronary venous blood vis thebesian veins
Pathological: AVM in small pulmonary A-V, heart disease (PDA, PFO, VSD)

Question 17

What is V/Q mismatch and how does it cause hypoxia?

Answer 17

The conc of O2 in lung unit is determined by the ratio of air getting into the alveolus (ventilation) and the blood flow through capillaries (perfusion).
V/Q mismatch results in hypoxaemia (Low ratio means lots of blood around, but poor ventilation; High ratio means lots of ventilation occuring but because of poor blood flow, O2 is not getting to the circulation), becuase of the nonlinear shape of the O2 dissociation curve, whcih means that although units with higher ventilation -perfusion ratios have a relatively high PAO2, this does not increase the oxygen concentration of the blood much, thus overall the mixed return has lower O2 concn than expected.

Question 18

In the upright lung, how does V/Q ratio change?

Answer 18

Apex: high ventilation, low perfusion
Base: high perfusion, low ventilation
Both blood flow and ventilation increases from apex to base, however blood flow increases faster to be more than ventilation by the time it gets to the base.
Because most of the blood comes from the base rather than the apex, the small amount of highly oxygenated blood from the apex does not increase the PaO2 dramatically therefore there is an overall depression of the PaO2.

Question 19

How can V/Q mismatch be measured?

Answer 19

A-a gradient, where normal difference is 5-10mmHg.

or with CTPA or v/q scan

Question 20

What conditions results in high V/q mismatch?

Answer 20

PE, pulmonary oedema, emphysema

Question 21

What conditions results in low V/Q mismatch?

Answer 21

chronic bronchitis

Question 22

What is the effect on CO2 and O2 if there is V/Q mismatch?

Answer 22

CO2 changes little: CO2 dissociation curve is linear, hence increasing ventilation (due to chemoreceptor activiation) causes CO2 to be blown off in both high and low areas of mismatch.

O2 is reduced due to the non-linear, S-shaped O2 dissociation curve; which means increasing ventilation has little effect on overall O2 conc due to having minimal volume compared to the base; and the base has poorer ventilation with greater volume, hence overall O2 level is decreased

Question 23

How is O2 transported in the blood?

Answer 23

dissolved (0.3ml of O2/ 100ml blood)

Combined with Hb (20ml/100ml blood)

Question 24

What are the standard points on O2 dissociation curve>

Answer 24

p50 or 50% HbSaturation= PaO2 27
pO2 40mmHg= 75% sats
pO2 56= 90% sats 
pO2 80= 95% sats
pO2 100= 97.5% sats

Question 25

What are the implications of the oxygen dissociation curve shape?

Answer 25

In arterial blood= Easy LOADING of O2 even as PO2 falls, up until sats 90% before loading is affected. And large pressure gradient between alveolar and blood maintained

Venous blood= easy unloading in the peripheries for small drops in PO2

Question 26

What causes the oxygen dissociation curve to shift?

Answer 26

R shift= decreased O2 affinity but better offloading in the peripheries; occurs in exercise
–> acidosis, H CO2, H Temp, high 2-3DPG (end product of RBC)

L shift= less offloading in the peripheries,
–>alkalosis, low CO2, hypothermia, low 2-3DPG, CO

Question 27

How is CO2 transported in the blood?

Answer 27

1. Dissolved= 24x more soluble than O2
2. As bicarbonate= where CO2+H20= H2CO2=H+HCO3. Where carbonic anyhydrase increases the speed of conversion of CO2 to bicarb.
3. As carbamino compounds= where CO2 combines with terminal amine in Hb forming carbaminoHb

Question 28

What is chloride shift?

Answer 28

To maintain electrical neutrality, as HCO3 can move out of RC easily but H+ can’t, therefore Cl- swaps in, and H+ gets exchaned out as H+Hb

Question 29

Draw and explain the CO2 dissociation curve and explain the difference with O2 dissociation curve with regards to PO2/PCO2 conc

Answer 29

y axis: [CO2]/100ml
x axis: PCO2 mmHg
Straight line, which is much steeper than the O2 curve. the curve is right shifted by increasing O2 concentration, therefore greater CO2 concentration for a given PCO2= Haldane Effect

Compared to O2 curve: per 100ml of blood, there is more CO2 than O2 therefore CO2 curve would be higher up.

CO2 curve is steeper, and for a given change in CO2 concentration, there is little change in PCO2 therefore minimal PCO2 difference between arterial and venous blood.
However for O2 curve, shallow, therefore change in PO2 is large for same change in O2 conc.

Question 30

how thick is the blood gas barrier between alveolar and capillary?

Answer 30

<0.5um

Question 31

How thick if the capillary-peripheral cell barrier?

Answer 31

50um

Question 32

What is pulmonary compliance?

Answer 32

compliance is the slope of the curve= change in V/P, normal value approx 200ml/cmH2O. It is greatest mid inspiration, and stiffer at higher expanding pressures where the curve is flat.

Question 33

What disease states causes increased compliance?

Answer 33

Age, emphysema due to alteration in elastic tissue

Question 34

What disease states cause decreased compliance?

Answer 34

increased fibrous tissue, alveolar oedema, atelectasis, increased pulmonary pressure

Question 35

How does surfactant help with compliance?

Answer 35

Decreases the surface tension of the alveolar lining fluid, therefore = increased compliance, therefore=

1. decreased WOB
2. increased stability of alveoli preventing collapse
3. keeps alveoli dry by decreasing hydrostatic pressure in alveoli

Question 36

Describe the different types of tissue hypoxia

Answer 36

1. hypoxic hypoxia: low PaO2 (altitude)
2. Anaemic hypoxia: decreased ability of O2 carriage (anaemia, CO)
3. circulatory hypoxia: decreased circulating blood (shock, local obstruction)
4. histotoxic hypoxia: impaired tissue utilisation of O2 (cyanide)

Question 37

What factors affect airway resistance?

Answer 37

airway resistance affects if flow is laminar or turbulent

Viscosity of gas- important for laminar flow
Density of gas- important for turbulant flow as higher density means higher pressure, therefore harder to breath due to increased resistance.
Length of tube
Radius of tube to the 4th power- affected by lung volume, bronchial smooth muscle (reflex from irritants, ANS from PNS, ACh, CO2 causing constriction; beta2 causing dilation) peak resistance at segmental brochails, least at terminal bronchials
Velocity= higher velocity, more turbulant

Question 38

Whats is dynamic airway compression? What exaggerates this mechanism?

Answer 38

Where intrapleural pressure is greater than the alveolar pressure therefore preventing expiration esp when forced.

Exaggerating factors: increased resistance, decreased lung volume (which decreases driving pressure between alveoli minus intrapleural P), diseased lungs such as emphysema

Question 39

What 2 factors determine the work of breathing? What variables affect each of these?

Answer 39

1. elastic forces- affected by compliance of lung tissue and chest wall, lung volume, surfactant,
2. airway resistance- rate of breathing which changes flow rate, radius, increased gas density

Question 40

What is the Haldane effect?

Answer 40

deoxyHb binds more H+ than oxyHb, and forms carbamino compounds more readily. However in the presence of O2 and Hb reduces the binding of CO2. This allows for enhanced elimination of CO2 from peripheries, and promotes the dissociation of CO2 from Hb in the presence of O2, which is vital for gas exchange.