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 |
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