| 508317467 | How many branches is the airway divided into? | 24
(trachea = 0 + 23 airway branches) | | 0 |
| 616314922 | Which sections make up the conducting zone? | Trachea + first 16 airway branches | | 1 |
| 111579359 | What are the roles of the conducting zone? | 1) *Warm + humidify* air
2) *Distribute* air to depth of lungs
3) *Defence* - against bacteria/dust | | 2 |
| 410606029 | What anatomical area do the areas in the conducting zone constitute?
What is the size of this (ml)? | anatomical dead space
150ml | | 3 |
| 635721413 | What is the vascular system of the conducting zone called? | Bronchial circulation | | 4 |
| 287988947 | Which sections make up the respiratory zone? | Last 7 airway branches (17-23) | | 5 |
| 109124221 | What is the volume of the respiratory zone? | 2.5-3L | | 6 |
| 1017204128 | What is Fick's law of diffusion? | [C1]-[C2] = *pressure gradient* |  | 7 |
| 1013653939 | What is the thickness for diffusion from alveoli to blood? | 0.5µm | | 8 |
| 11922957 | How do alveoli number and size change with age? | Alveoli number and surface area ↑ from birth → adolescence
After adolescence numbers say the same but size ↑ | | 9 |
| 55876675 | What are the three transmural pressures? | *Transpulmonary pressure* = alveolar pressure - pleural pressure
*Trans chest wall pressure* = pleural pressure - atmospheric pressure
*Trans total system* = alveolar pressure - atmospheric pressure | | 10 |
| 918577366 | What is Tidal Volume? | The volume of inspiration and expiration at normal quiet breathing
~500ml | | 11 |
| 109163710 | What is Inspiratory reserve volume (IRV)? | Additional volume of inspiration on maximal inspiration
~3000ml | | 12 |
| 109163711 | What is Expiratory reserve volume (ERV)? | Additional volume of expiration on maximal expiration
~1200ml | | 13 |
| 109163713 | What is Residual volume (RV)? | Volume of gas remaining after maximal forced expiration
~1200ml | | 14 |
| 803069951 | What is Inspiratory capacity (IC)? | Tidal volume + inspiratory reserve volume
~3500ml | | 15 |
| 803069952 | What is Functional residual capacity (FRC)? | Expiratory reserve volume + residual volume
~2400ml | | 16 |
| 309380982 | What is Vital capacity (VC)? | Inspiratory capacity + expiratory reserve volume
~4700ml | | 17 |
| 309380983 | What is Total lung capacity (TLC)? | All the lung volumes | | 18 |
| 198860723 | What is the STPD? | *Standard Temperature and Pressure Dry*
0°C (273K)
1 atmosphere (760mmHg/101kilopascals)
Dry | | 19 |
| 550244542 | What is BTPS | *Body Temperature and Pressure Saturated (BTPS)*
Physiological conditions within the body
37°C (310K)
713mmHg
Saturated | | 20 |
| 2395980467 | What is the formula for working out the partial pressure exerted by an individual gas in a gas mixture? | Fraction of mixture occupied by gas A x Total pressure exerted by mixture (mmHg) | | 21 |
| 2396020529 | How can we measure Residual Volume and Functional Residual Capacity? | RV and FRC cannot be measured by spirometry
Need to be measured using dilution techniques | | 22 |
| 2396039951 | What makes up the physiological dead space? | *1) Anatomical Dead Space*
150ml (conducting zone)
*2) Alveolar dead space*
Alveoli that do not participate in gas exchange:
a) Alveoli with no blood flow
b) Alveoli with reduced blood flow such that ventilation > perfusion | | 23 |
| 2396041653 | What is the dead space of a seated individual? | It is equal to their weight (170lb person has a dead space of 170ml) | | 24 |
| 2396047281 | What is the total inspired ventilation rate? | Tidal volume x Breathing frequency
500 x 12 = *6L/min* | | 25 |
| 2396048932 | What is the expired minute volume? | Tidal volume x Breathing frequency
500 x 12 = *6L/min*
This is based on the assumption that volume inspired = volume expired (not quite true because more O₂ is consumed than CO₂ is produced) | | 26 |
| 2396077312 | What is alveolar ventilation? | Volume of fresh air reaching alveoli
*Simple equation*
(Tidal volume - dead space volume) x frequency | | 27 |
| 2396086061 | How can we directly measure alveolar ventilation? | Volume of CO₂ expired per minute can be worked out using a spirometer (measure to total expired volume and the fraction conc. of expired CO₂)
The fractional concentration of alveolar CO₂ can be worked out by sampling the last portion of tidal volume |  | 28 |
| 2396097164 | How can the alveolar ventilation formula be re-written to account for conversion of STPD to BTPS? | |  | 29 |
| 2396115449 | What is the relationship between alveolar ventilation and alveolar PCO2? | They are inversely proportional.
Also because PACO₂ is in equilibrium with PCO₂ - alveolar ventilation has the same relationship with PCO₂
Doubling alveolar ventilation → 1/2 PCO₂
1/2 alveolar ventilation → double PCO₂ | | 30 |
| 2396130654 | What is the relationship between alveolar ventilation and alveolar PAO2? | ↑ Avleolar ventilation → ↑ Alveolar PAO₂
*Doubling alveolar ventilation does not double alveolar PAO₂*
This is because:
1) Inspired PO₂ is not zero
2) More O₂ is removed from gas than CO₂ is added | | 31 |
| 2396141154 | What is the alveolar gas equation for working out PAO2? | R = 0.82 (sea level)
PACO₂ = 40mmHg
PIO₂ = 149mmHg |  | 32 |
| 2396151979 | What is the normal alveolar values for P02 and Pco2? | PAO₂ = 100mmHg
PACO₂ = 40mmHg | | 33 |
| 2396383297 | What two conclusions can be drawn from a pressure-volume loop? | 1) *Hysteresis* - Lung volume at any given pressure is higher during expiration
2) With no transpulmonary pressure, the lung volume is never zero |  | 34 |
| 2396400940 | What is lung compliance? | The volume change per unit change in transpulmonary pressure | | 35 |
| 2396419094 | What are the factors that affect lung compliance? | *1) Lung volume*
↑ volume → ↓ compliance
*2) Elastic properties of the lung*
*3) Lung size*
↑ size → ↑ compliance
*4) Surface forces inside alveoli*
↓ surface tension → ↑ compliance
Pulmonary surfactant ↓ surface tension
*5) Regional lung compliance*
in normal conditions, base of lung is more compliant than apex | | 36 |
| 2396492399 | What pathologies cause loss or increase in compliance?
What are their functional consequences? | |  | 37 |
| 2396515279 | How is compliance measured on pressure-volume curves? | The gradient of the slope | | 38 |
| 2396577460 | Draw total pressure-volume relationship:
What are the points to take away from this? | 1. At zero transmural pressure, lungs are at volume < residual volume but chest wall is at a volume ~75% of vital capacity
2. At FRC the transmural pressure of the chest wall is negative (opposes the tendency of the chest wall to spring out as a result of its elastic recoil forces)
In contrast at FRC the transmural pressure of the lungs is positive (opposes the tendency of the lungs to recoil inwards as a result of their elastic recoil forces)
The opposing pressures are exactly equal at FRC |  | 39 |
| 2396593162 | What determines chest wall compliance? | *1) Rigidity of thoracic cage*
*2) Shape of thoracic cage*
Therefore compliance can ↓ if chest wall is deformed with obesity
*3) Diaphragm and abdominal structures*
Therefore compliance can ↓ in abdominal conditions that push the diaphragm up or in muscular conditions that lead to rigidity of thoracic and abdominal muscles | | 40 |
| 2396626910 | What is Laplace's Law?
How is it different in the alveolus | Pressure = (4x Surface tension)/radius
Because the alveolus only has a single air-liquid interface, the numerator 4 is replaced with 2 | | 41 |
| 2396756868 | What cells produce pulmonary surfactant? | Alveolar Type II cells | | 42 |
| 2396759411 | What is the main agent in surfactant that reduces surface tension?
What is this produced from? | DPPC (Dipalmitoyl phosphatidyl choline)
Produced from glucose, choline and palmitate (provided by pulmonary circulation) | | 43 |
| 2396763556 | What is the role of surfactant? | *1) Increases compliance* (by reducing surface tension)
This reduces work effort needed for breathing
*2) Allows the coexistence of different sized alveoli*
Reduces surface tension in smaller alveoli more
*3) Keeps alveoli dry*
Atelectaisa → -ve interstitial fluid that draws in liquid from capillaries | | 44 |
| 2396772029 | How does surfactant reduce surface tension? | DPPC is hydrophobic on one end and hydrophilic the other. This therefore resists the normal attractive forces between surface water molecules | | 45 |
| 2396990584 | What is Poiseuille's law? | |  | 46 |
| 2397003983 | What is the major site of resistance in airways? | Medium sized bronchi | | 47 |
| 2397043390 | What affect airway resistance? | *1) Lung volume*
↑ volume → ↓resistance
As lung expands parenchyma opens up airways
*2) Contraction of bronchial smooth muscle*
Dilation: Beta-2 agonists + ↑PCO₂ in conducting airways
Constriction: Chemicals, Dust, Smoke, ↓PCO₂ in conducting airways
*3) Viscosity and density of gas* | | 48 |
| 2397119799 | What is the Equal Pressure Point (EPP)? | The point along the airway in maximal expiration where transairway pressure = 0 | | 49 |
| 2397145109 | What conclusions can we draw from EPP? | 1) Peak flow rate cannot be increased (regardless of how forceful the expiratory effort is)
2) Maximal flow rates are determined mainly by *elastic recoil of the lung* | | 50 |
| 2397164385 | What sets the EPP? | Compliance of the lung | | 51 |
| 2397217533 | What is the normal:
FVC
FEV1
FEV1/FVC | FVC = 5L
FEV1 = 4L
FEV₁/FVC = 80% | | 52 |
| 2397220130 | What do we see on the spirometry of obstructive disease?
(Asthma/COPD) | FEV₁ reduces more than FVC
Therefore FEV₁/FVC reduces (usually below 75%) | | 53 |
| 2397225957 | What do we see on the spirometry of restrictive disease?
(Fibrosis) | FVC reduces
Therefore FEV₁/FVC stays the same or increases | | 54 |
| 2397886646 | What is the formula when we add Henry's law to Fick's law? | ΔP = partial pressure gradient
d = diffusion constant (Made up of solubility coefficient [s] and diffusion coefficient [D]) |  | 55 |
| 2397912960 | What is the formula for the diffusion constant? | Therefore smaller and more soluble particles will diffuse at a faster rate |  | 56 |
| 2397925064 | What is the solubility coefficient for O2 in plasma? | 0.03ml O₂/litre plasma/mmHg | | 57 |
| 2397928536 | What is the solubility coefficient for CO2 in plasma | 0.7ml CO₂/litre plasma/mmHg
*23 times more soluble than O₂*
But overal CO₂ is 20 times faster at diffusion (because due to its larger size cf. O₂ it brings it down from 23 to 20) | | 58 |
| 2397961029 | What maintains the diffusion gradient for gas exchange at the alveoli? | 1) Alveolar ventilation
2) Pulmonary circulation | | 59 |
| 2397965154 | What is the *transit time*? | Time for blood to flow from beginning to end of pulmonary circulation
<1sec | | 60 |
| 2397966895 | What is the *Diffusion reserve*? | Gas exchange between the alveoli and the pulmonary capillaries happen in a way such that the gas equilibrium is reached with room to spare (compared to the transit time) | | 61 |
| 2398064228 | What is the bound O2 capacity of blood? | 1 gram Hb contains 1.39ml O₂
Blood has 15ml Hb/100ml
Therefore blood can carry 20.8ml O₂/100ml | | 62 |
| 2398124966 | Why is the O2 dissociation curve sigmoidal? | This reflects the cooperative nature of O₂ binding to Hb | | 63 |
| 2398128152 | What is the loading plateau? | Above Po₂ 60mmHg the Hb saturation is high and starts to level off
Below this, curve is steep and significant loss of O₂ | | 64 |
| 2398133489 | What pushes O2 dissociation curve to the right? | 1) CO₂
2) ↓pH
3) 2,3 DPG
4) Temperature
5) Exercise
CADET face right
(CO₂, Acid, DPG, Exercise, Temperature) | | 65 |
| 2398139466 | What is the Bohr effect? | Right shift of dissociation curve due to CO₂ and ↓pH | | 66 |
| 2398223303 | What is the formula for total concentration of O2 in blood? | |  | 67 |
| 2398234561 | What are the different types of hypoxia?
What is hyperoxia, hypercapnia and hypocapnia? | |  | 68 |
| 2398250775 | Why is CO poisoning so dangerous? | *1) High Hb affinity*
~240 times more than O₂
*2) Left shift to O₂ dissociation curve*
Thus, little O₂ bound can't unload in tissues
*3) No physical signs of hypoxia*
COHb is bright red too
*4) PO₂ remains normal*
Total O₂ content plummets but PO₂ is normal
*5) Colourless, odourless and non-irritant* | | 69 |
| 2398545443 | How is CO2 transported in the blood? | 1) Dissolved CO₂
5-10%
2) As bicarbonate (HCO₃⁻)
Majority (90%)
3) Carbamino compounds
5% | | 70 |
| 2398548940 | What is the Haldane effect? | • Amount of CO₂ carried by blood depends on PO₂ (and ∴ saturation of Hb)
• More CO₂ is carried in deoxygenated blood over oxygenated blood
• Mechanism of this:
*1. Dynamic proton dissociation constant for Hb*
• Deoxygenated Hb is a weaker acid ∴ retains more protons
• This retaining of more protons means that the chemical gradient favours the formation of HCO3-
*2. Deoxygenated blood forms more carbamino compounds*
∴ overall, change in PO₂ → change in CO₂ | | 71 |
| 2398561485 | What buffers the protons produced by carbonic anhydrase in the RBCs? | *imidazole groups* on the *histidine* amino acid residues of the alpha and beta polypeptide chains of Hb | | 72 |
| 2398567862 | What is Hamburger's Phenomena? | Most of the HCO₃⁻ produced in RBCs (for CO₂ transport) leaves the RBC down its concentration gradient
This charge movement is compensated by influx of Cl⁻ ∴ the RBCs accumulate Cl⁻ in exchange for HCO₃⁻ This is referred to as the *Cl⁻ shift* or *Hamburger's phenomena*
This exchange occurs very rapidly in the capillary beds as a result of the high anion permeability of the RBC membrane
The extra intracellular HCO³⁻ and Cl⁻ increase the intracellular osmolarity and osmotic pressure resulting in *water influx and cell swelling* | | 73 |
| 2410348395 | What are the functions of the pulmonary circulatory system? | 1) Gas exchange
2) Blood reservoir
3) Filtration
4) Metabolism of vasoactive hormones | | 74 |
| 2410349164 | What hormones are metabolised by pulmonary circulation? | *Angiotensin I*
*Hormones inactivated*
Noradrenaline
Bradykinin
Prostaglandins
*Hormones unaffected*
Histamine
Adrenaline
Vasopressin | | 75 |
| 2410358246 | What catheter can be used to measure both pulmonary arterial and venues pressure? | *Swan-Ganz catheter*
Wedge-pressure = venous pressure | | 76 |
| 2410360572 | What is the pressure gradient across the pulmonary circulation?
What is the pressure gradient across the systemic circulation? | Pulmonary circulation = ~10mmHg
Systemic circulation = ~85-90mmHg
Pulmonary circulation must have very low resistance for flow to occur | | 77 |
| 2410383185 | How is pulmonary circulation resistance kept low? | 1) Large number of vessels
2) Vessels are dilated (NO CONTROL FROM AUTONOMICS) | | 78 |
| 2410383890 | How does the following effect pulmonary vascular resistance?
a) Cardiac output
b) Lung volume
c) Hypoxia | *a) Cardiac output*
↑CO → ↓ resistance
This is because of capillary recruitment and distension
*b) Lung volume*
Effect on alveolar and extra alveolar vessels.
Extra-alveolar (affected by intracellular pressure. ↑volume → ↓resistance)
Alveolar (affected by alveolar volume. ↑volume→↑resistance)
*c) Hypoxia*
↑Hypoxia → ↑resistance
Regional hypoxia → little effect on pulmonary arterial pressure
General hypoxia → ↑ pulmonary arterial pressure (could lead to pulmonary hypertension and oedema) | | 79 |
| 2410406689 | What can cause oedema in the lung? | *1) ↑ pulmonary capillary pressure*
Left heart failure / general hypoxia
*2) ↑ capillary permeability*
Oxidant damage (O₂ therapy/ozone)
Endotoxins
*3) ↓ capillary colloid osmotic pressure*
Loss of capillary proteins (starvation)
*4) ↑ Surface tension*
Surfactant loss → ↑interstitial hydrostatic pressure
*5) Lymphatic blockage* | | 80 |
| 2410417391 | What are the different zones that explain the interaction of blood flow and alveolar pressure? | *Zone 1 (Upper zone)*
Alveolar pressure > arterial pressure
∴ pulmonary capillaries = collapsed and there is no flow
*Zone 2 (Middle zone)*
Arterial pressure > alveolar pressure
This is ∵ of ↑hydrostatic influence due to moving closer to the level of the heart
But alveolar pressure > venous pressure
∴ blood flow in this region is determined by the different between the arterial and alveolar pressure
Venous pressure has no influence on flow until it exceeds alveolar pressure
*Zone 3 (Lower zone)*
Arterial pressure > venous pressure > alveolar pressure
Flow is determine by the arterial-venous pressure difference
In healthy individuals, zone 1 conditions do not exist ∵ arterial pressure in upper lung is usually sufficient to overcome small alveolar pressures. This condition can however exist if pulmonary arterial pressure ↓(e.g. severe haemorrhage) or if alveolar pressure ↑ (e.g. forced ventilation) | | 81 |
| 2410440138 | What is alveolar ventilation at rest? | ~4L/min | | 82 |
| 2410440265 | What is blood flow at rest? | ~5L/min | | 83 |
| 2410440986 | What is the average ventilation:perfusion ratio? | 0.8 | | 84 |
| 2410444292 | What happens to ventilation and perfusion as we move down the lung? How does this affect ventilation:perfusion ratios? | Ventilation ↑ (2x more at base)
Perfusion ↑ (5x more at base)
V:Q ratio ↓ |  | 85 |
| 2410450510 | What effect does increasing V:Q ratio have on the gas complex found in the alveoli? | ↑V:Q ratio → ↑PO₂ and ↓PCO₂
therefore TB tends to localise at apex of lung (↑PO₂ is favourable for Mycobacterium tuberculosis) | | 86 |
| 2410454599 | What is venous admixture? | Mixing of oxygenated blood with non-oxygenated blood | | 87 |
| 2410461235 | What are the causes of venous admixture? | *1) Shunting*
a) Right to left shunting (septal defects/bronchial circulation [20% of admixture])
b) Alveolar shunting (blood reaching the alveoli but no access to oxygen - oedema, pneumonia, atelectasis)
*2) Low V:Q ratio* (causes 80% of admixture)
Normal differences at base | | 88 |
| 2410528705 | What is the function of the pneumotaxic centre? | Limits inspiration | | 89 |
| 2410546253 | What is the function of the apneustic centre? | Prolongs inspiration | | 90 |
| 2410547691 | What is the function of the medullary centre? | Central pattern generator | | 91 |
| 2410547961 | What is the function of the vagi with regards to breathing? | Terminates inspiration | | 92 |
| 2410563609 | What are the different groups in the medullary centre? | *1) Dorsal respiratory group (DRG)*
- inspiratory neurons
*2) Ventral respiratory group (VRG)*
- inspiratory and expiratory neurons | | 93 |
| 2410564836 | What is the group in the pneumotaxic centre called? | *Pontine Respiratory Group (PRG)*
Send inhibitory signals to the inspiratory ramp | | 94 |
| 2410568841 | What variable is under closest control by the respiratory system? | *Arterial PCO₂*
Usually 40mmHg | | 95 |
| 2410572139 | What is the average respiratory drive? | Respiratory drive is the increase in ventilation rate per increase in PCO₂
It is usually:
*2-3L/min/mmHg increase in PCO₂* | | 96 |
| 2410852088 | Where are central chemoreceptors found? | Ventral surface of medulla
In chemosensitive areas (CSA)
CNVIII → CNXI
and CN XII | | 97 |
| 2410823551 | Where is CSF formed? | Choroid plexuses | | 98 |
| 2410829931 | Compared to plasma, what is low/high in CSF? | Low = Protein, HCO₃⁻, Ca²⁺, K⁺
High = Na⁺, Cl⁻ | | 99 |
| 2410844312 | What changes in CSF do central chemoreceptors respond to? | H⁺ ions (pH)
Not PCO₂ | | 100 |
| 2410861255 | Where are peripheral chemoreceptors found? | Carotid and aortic bodies
Type I Glomus cells | | 101 |
| 2410862447 | What do peripheral chemoreceptors respond to? | 1) PCO₂ (↑)
2) PO₂ (↓)
3) pH (↓) | | 102 |
| 2410881408 | When do peripheral chemoreceptors respond to reduced PO2? | ↓PO₂ is exclusively picked up by carotid bodies
When PCO₂ is normal, PO₂ must be below 60mmHg to elicit a response
When PCO₂ is ↑, PO₂ below 100mmHg elicits a response | | 103 |
| 2411401024 | What are the respiratory systems responses to high altitude? | 1) Hyperventilation
2) Polycythemia
3) Alveolar hypoxia induced pulmonary hypertension
4) ↑ 2,3 DPG (therefore right shift in dissociation curve) | | 104 |
