Applied Respiratory Physiology

Question 1

Summarize the functions of the lungs

Answer 1

1. Gas exchange
2. Phospholipid production (surfactant)
3. Metabolism and de-activation of certain compounds (Angiotensin)
4. Synthesis of prostaglandins and histamine
5. Intrinsic component of the immune system
6. Reservoir for blood 500 - 900 ml

Question 2

Compare the VO2 in adults versus infants

Answer 2

Adults: 3 - 4 ml/kg
Infants: 7 - 9 ml/kg

Question 3

Define and classify respiratory failure

Answer 3

Type 1: PaO2 < 8 kPa | PaCO2 N or low

Type 2: PaO2 < 8kPa | PaCO2 > 6.5

Question 4

How many mmHg, cmH20, hPa are in 1 kPa

Answer 4

1 kPa = 7.5 mmHg = 10 cmH2O = 10 hPa

Question 5

Where is the respiratory center

Answer 5

In the Medulla oblongata

Question 6

Where are chemoreceptors found and what are the different chemoreceptors sensitive to?

Answer 6

PERIPHERAL CHEMORECEPTORS
Carotid bodies (@ bifurcation of common carotid a)
- Afferents carried by glossopharyngeal n.

Aortic bodies (aortic arch)
 - Afferents carried by vagus n.

STIMULATED BY

1. Low PaO2 (tension NOT content)
2. High PaCO2 (20% of hypercapnic response)
3. Acidaemia (pH<7.35 - carotid bodies only)
4. Hypotension

CENTRAL CHEMORECEPTORS
Ventral surface of the Medulla
1. CSF pH only caused by increased CO2 in CSF as H+ and HCO3 ions can’t diffuse in or out

Question 7

Explain why chronic CO2 retention (COPD) leads to reduced sensitivity to PaCO2

Answer 7

Kidneys reabsorb and regenerate HCO3 –> compensatory metabolic acidosis –> reduced stimulation of peripheral chemoreceptors

HCO3 is actively secreted into the CSF to buffer the change in pH –> pH returns to normal and the central chemoreceptors are no longer stimulated.

Therefore these patients are largely dependent on hypoxic drive (peripheral chemoreceptors)

Question 8

How do opioids and general anaesthetics affect the ventilatory response to PaCO2

Answer 8

Decreased response

Question 9

What is the formula for minute ventilation and what is normal minute ventilation. What is the effect of opioids and anaesthetic agents on MV

Answer 9

MV = RR x Vt
100 ml/kg/min
± 6 - 8 L/min

Opioids and anaesthetic agents all reduce VT and hence MV

Question 10

Define anatomical dead space and alveolar volume

Answer 10

Alveolar volume - the volume of air which reaches perfused alveoli

Dead Space - The volume of inspired air that plays no part in gas exchange

Question 11

What are the different types of dead space and how do they relate

Answer 11

Anatomical dead space - the volume of the first 16 generations of the tracheobronchial tree which form the conducting airways

Alveolar dead space - The total volume of ventilated alveoli that are unable to take part in gas exchange due to impaired perfusion (V/Q mismatch).

Physiological dead space - The total dead space that is the sum of the anatomical dead space and the alveolar dead space

DSphys = DSanat + DSalv

Question 12

Define alveolar ventilation

Answer 12

This is the alveolar minute ventilation:

Alveolar MV = (tidal vol - phys. dead space) x RR

Question 13

Define residual volume

Answer 13

The volume of air left in the lungs after a maximal forced expiration

Question 14

Define functional residual capacity

Answer 14

Functional residual capacity is the volume of air that remains in the lungs after a normal tidal exhalation and is comprised of the residual volume (RV) and the expiratory reserve volume (ERV)

Question 15

List the lungs volumes and capacities and there approximate normal values in a 70 kg adult.

Draw the spirometry trace with the lung volumes included

Answer 15

VT - 500 mL
IRV - 2500 mL
ERV - 1500
RV - 1500

IC = VT + IRV = 3000 mL
VC = IRV + VT + ERV = 4500 mL
FRC = RV + ERV = 3000 mL
TLC = VT + IRV + ERV + RV = 6000 mL

Trace axes: Lung volume versus time

Question 16

Why is FRC so important in anaesthesia

Answer 16

Pre-oxygenation denitrogenates the FRC which replaces the nitrogen with 80 - 100% O2. Theoretically this provides a ± 3 L O2 reservoir which can prevent desaturation in apnoea for up to 10 minutes ( depending on VO2 of patient which would be increased in kids/pregnancy/sepsis/pain/SIRS etc)

Question 17

List factors that reduce the FRC

Answer 17

Position: Supine, Lithotomy, Trendelenburg
Muscle relaxation: (NDMR/Volatiles)
Intra-abdo pain/pressure: Preg/obese/ascites/lapscope
Decreasing age
Lung disease (fibrosis/oedema/atelectasis/ARDS)

Question 18

List factors that increase FRC

Answer 18

PEEP
Emphysema
Asthma
Increasing age

Question 19

What is the difference between static and dynamic compliance

Answer 19

The measurement technique

Static compliance

• simultaneous pressure and volume measurements are taken at a steady state (when there is no gas flow) and plotted)
• the patient inspires in 500 ml increments and then pauses and the pressure and volume are measured.

Dynamic compliance
- Continuous measurements of P and V are taken during the respiratory cycle. There are two points where flow ceases: end expiration and end inspiration. These points are plotted and a straight line connects them = the gradient of this line = dynamic compliance

Question 20

Why is dynamic compliance always less than static compliance?

Answer 20

This is due to airway resistance only incurred during the measurement of dynamic compliance.

Question 21

Draw the pressure volume loops to illustrate static compliance during a vital capacity breath and a tidal volume breath.

Answer 21

Chambers - page 84

Question 22

Define Oxygen Consumption, Oxygen Delivery and the Oxygen Extraction Ratio

Answer 22

VO2 - the volume of O2 consumed by the body per minute
DO2- the volume of O2 delivered to the tissues from the lungs per minute

OER - the ratio of oxygen consumption to oxygen delivery

Question 23

What is VO2 max and how is it calculated

Answer 23

As exercise intensity increases the oxygen consumption exceeds oxygen delivery. At this point, anaerobic metabolism ensues. This point is called VO2 max i.e the point where the tissues switch over to anaerobic metabolism.

Question 24

Which principle is used to calculate oxygen consumption and what is the formula for this calculation

Answer 24

Reverse fick principle

VO2 = CO (CaO2- CvO2) x 10

CaO2 = (1.34 x Hb x SaO2/100%) + (0.003 x PaO2)

CaO2 = (O2 on Hb) + (O2 in plasma)

Question 25

What is Hufner’s constant

Answer 25

Each Hb molecule can bind 1.34 mL of O2. 1.34 is Hufner’s constant.

This is used in the Content of blood oxygen equation to calculate how much O2 is bound to Hb.

Question 26

What is the formula for Oxygen delivery DO2

Answer 26

DO2 = CO x CaO2

Dimensional analysis
CO units: L blood/min
CaO2 units: mL O2/ L blood

DO2 units: ml O2 / minute

Question 27

What is the formula for OER and how does this differ in different tissues

Answer 27

OER = VO2/DO2

Heart = 0.6 (higher O2 consumption –> less buffer for reduced delivery)

Other tissues = 0.25

Question 28

Draw the oxygen HB dissociation curve

Answer 28

Chambers page 30

Question 29

How does stored blood bank blood affect the OHDC

Answer 29

Depletion of 2.3 DPG –> Leftward shift P50 OHDC –> reduced ability of Hb to release O2 to tissues.

After a few hours the 2.3 DPG starts to recover and takes 1 - 3 days to fully recover.

Question 30

Define Hypoxia

Answer 30

An intracellular (mitochondrial) O2 tension below the critical level to sustain oxidative phosphorylation.

This is between 0.15 kPa and 0.3 kPa and is known as Pasteur point and is the point at which anaerobic metabolism begins.

Question 31

Define hypoxaemia

Answer 31

PaO2 < 8 kPa (60 mmHg)

Question 32

Classify and define the different causes of hypoxia

Answer 32

Hypoxaemic - Low PaO2
Anaemic - Low Hb or incapacitated Hb (anaemia | CO )
Stagnant - Low DO2 (circulatory failure)
Histotoxic - Mitochondria fail to use O2 (sepsis | Cyanide)

Question 33

List the causes of hypoxaemic hypoxia

Answer 33

1. Low FiO2
2. Low V
3. V/Q mismatch
4. Pathological shunt (refractory to FiO2)
5. Diffusion problem

Question 34

Describe the causes of increased and decreased SvO2

Answer 34

Increased SvO2

• Increased O2 delivery: High FiO2
• Decreased O2 demand (hypothermia | anaesthesia | NMB)
• High flow states: sepsis | liver dx | hyperthyroid

Decreased SvO2

• Decreased DO2 (anaemia/shock/hypoxia)
• Increased VO2 (hyperthermia/shiver/pain/seizure)

High SvO2 despite evidence of end-organ hypoxia

• microvasc shunting (sepsis)
• histotoxic hypoxia (cyanide)
• abN distribution of blood flow