Respiratory Flashcards
LO 1.1 Explain the broad functions of the respiratory system in health
The respiratory system works to ensure that all tissues receive the oxygen that they need and can dispose of the CO2 they produce.
Blood carries gases to and from tissues, where the lungs exchange them with the atmosphere.
LO 1.9 State Boyle’s law
If a given amount of gas is compressed into a smaller volume, the molecules will hit the wall more often. Therefore pressure will rise.
If temperature is constant, Pressure is Inversely Proportional to Volume
LO 1.9 State The Kinetic Theory of Gases
Kinetic Theory of Gases
Gases are a collection of molecules moving around a space, generating pressure by colliding with the walls of the space.
As collisions become more frequent, and harder, pressure goes up.
LO 1.9 State Charles’ Law
The kinetic energy of molecules Increases with Temperature.
As temperature increases, the molecules hit the walls more often, so pressure increases.
Pressure is Proportional to Absolute Temperature (scale starts at absolute zero)
LO 1.9 State the Universal Gas Law
The universal gas law allows the calculation of how volume will change as pressure and temperature changes.
Pressure x Volume = Gas Constant x Temperature (0K)
Describe partial pressure, vapour pressure, saturated vapour pressure and tension
Partial Pressure
In a mixture of gases molecules of each type behave independently. So each gas exerts its own pressure, which is a portion of the total pressure (a partial pressure).
It is calculated as the same fraction of the total pressure as the volume fraction of the gas in the mixture.
Vapour Pressure
In biological systems gas mixtures are always in contact with water.
So gas molecules dissolve, and water molecules evaporate, and then exert their own partial pressure. This partial pressure is known as vapour pressure.
Saturated Vapour Pressure
When the rate of molecules entering and leaving water at the same time is equal, this is the Saturated Vapour Pressure.
When gases enter our body, they are completely saturated with water vapour, so they don’t dry out our lungs.
Tension
Gas tension in liquids indicates how readily gas will leave the liquid, not (at least directly) how much gas is in the liquid.
At equilibrium (achieved very quickly in the body), Tension = Partial Pressure.
How to work out the Content of Gas in a Liquid
The amount of Gas that enters a liquid to establish a particular tension is determined by Solubility.
Content = Solubility x Tension
(How easily gas will dissolve x How readily it will leave)
If the gas reacts with a component of the liquid however, this reaction must be complete before tension, and therefore content can be established.
Total Content = Reacted Gas + Dissolved Gas
E.g.
Plasma just dissolves O2
A pO2 of 13.3kPa (ppO2 in the lungs), gives a blood content of 0.13 mmol/L of O2
Whole blood contains Haemoglobin, which reacts chemically with Oxygen.
At pO2 of 13.3kPa, Haemoglobin binds 8.8mmol/L of O2
Total Content = O2 Bound to Haemoglobin + O2 dissolved in Plasma
= 8.8 + 0.13
= 8.93 mmol/L
LO 1.10 Define the terms Tidal Volume, Respiratory Rate and Pulmonary Ventilation Rate
Tidal Volume
The lung volume that represents the amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied
Respiratory Rate/Pulmonary Ventilation Rate
The number of breaths taken in a set time, usually 60 seconds
Describe the Pulmonary Circulation and the pressure in the arteries, capillaries and veins of the pulmonary system.
The lungs have two circulations – pulmonary and bronchial.
The bronchial circulation is part of the systemic circulation, and meets the metabolic requirements of the lungs. The pulmonary circulation is the blood supply to the alveoli, required for gas exchange.
The pulmonary circulation must accept the entire cardiac output, and works with low resistance due to short, wide vessels, lots of capillaries connected in parallel (lower resistance) and arterioles with relatively little smooth muscle. This low resistance leads to the circulation operating under low pressure.
Pulmonary Artery - 15mmHG
Pulmonary Capillaries - 10mmHG
Pulmonary Vein - 5mmHG
Explain Ventilation/Perfusion Matching
For efficient oxygenation, ventilation of the alveoli needs to be matched with perfusion. The optimal Ventilation/Perfusion ratio is 0.8. Maintaining this means diverting blood from alveoli that are not well ventilated.
This is achieved by hypoxic pulmonary vasoconstriction. Alveolar hypoxia results in vasoconstriction of pulmonary vessels, and the increased resistance means less flow to the poorly ventilated areas and greater flow to well ventilated areas.
Chronic hypoxic vasoconstriction can lead to right ventricular failure. The chronic increase in vascular resistance puts a high afterload on the right ventricle, leading to its failure.
LO 1.2 Define the terms upper and lower respiratory tracts
LO 1.3 Describe the component parts of the upper and lower respiratory tract
Upper Respiratory Tract The parts of the respiratory system lying outside the thorax o Nasal Cavity o Pharynx o Larynx
Lower Respiratory Tract The parts of the respiratory system lying inside the thorax o Trachea o Main/Primary bronchi o Lobar Bronchi - Three on right - Two on left - Bronchi have cartilage in their walls o Segmental Bronchi o Sub-segmental Bronchi o Bronchioles - No Cartilage in the walls - More smooth muscle than Bronchi o Terminal Bronchioles - ~200,000 o Respiratory Bronchioles o Alveolar Ducts o Alveoli - ~300,000,000
LO 1.4 Outline the broad function of the different parts of the respiratory tract
The lungs are a means of getting air to one side, and blood to the other of a very thin membrane, with a large surface area.
The trachea and bronchi have cartilaginous rings in order to hold them open and provide a path for air to travel to the alveoli.
Bronchioles draw air into the lungs by increasing their volume, using the smooth muscle in their walls.
Alveoli provide the single cell thickness membrane for diffusion (Type I cells, Simple Squamous epithelia). They also produce surfactant (Type II cells) to reduce the surface tension of the alveoli.
LO 1.5 Describe the structure and function of the nose
Nose
The nose is part of the respiratory tract, superior to the hard palate. It is comprised of the external nose and nasal cavity, which is divided into the right and left cavities by the nasal septum.
The functions of the nose include smelling, respiration, filtration of dust, humidification of inspired air, and reception and elimination of secretions from the paranasal sinuses and nasolacrimal ducts.
Air passing over the respiratory area of the nose is warmed and moistened before it passes through the rest of the upper respiratory tract to the lungs.
The olfactory area contains the peripheral organ of smell
LO 1.5 Describe the structure and function of the Conchae (Terbinates)
The superior, middle and inferior Nasal Conchae (or terbinates) curve inferiormedially, hanging like short curtains from the lateral wall of the nasal cavity.
The conchae are scroll-like structures that offer a vast surface area for heat exchange.
The inferior concha is the longest and broadest and is formed by an independent bone (the Inferior Concha).
The middle and superior conchae are the medial processes of the Ethmoid Bone.
A recess or nasal meatus underlies each of the terbinates, diving the nasal cavity into five passages.
The Sphenoethmoidal Recess, lying superoposterior to the superior conca, receives the opening of the sphenoidal sinus
LO 1.5 Describe the structure and function of the Pharynx
The Pharynx is the superior, expanded part of the Alimentary System, posterior to the nasal and oral cavities and extending inferiorly past the larynx.
The Pharynx extends from the Cranial Base to the Inferior Border of the Cricoid Cartilage Anteriorly and the Inferior Border of C6 Vertebra Posteriorly.
It is widest (Approximately 5cm) opposite the hyoid and narrowest (approximately 1.5cm) at its inferior end, where it is continuous with the oesophagus.
The Pharynx is divided into Three Parts:
o Nasopharynx
Posterior to the nose and superior to the soft palate
Respiratory Function as it is the posterior extension of the nasal cavities
Lymphoid tissue forms a tonsillar ring around the superior part of the pharynx, which aggregates to form Tonsils
o Oropharynx
Posterior to the mouth
Extends from the soft plate to the superior border of the epiglottis
Digestive Function
Involved in swallowing (GI LO 2.7)
o Laryngopharynx
Posterior to the Larynx
Ends from the superior border of the epiglottis to the inferior border of the cricoid cartilage, where it becomes continuous with the oesophagus.
LO 1.5 Describe the structure and function of the Larynx
The Larynx connects the inferior Oropharynx to the Trachea. It also contains the complex organ of voice production (The ‘voice box’).
It extends from the Laryngeal Inlet, through which it communicates with the Laryngopharynx to the level of the inferior border of the cricoid cartilage. Here the laryngeal cavity is continuous with the Trachea.
The Larynx’s most vital function is to guard the air passages, especially during swallowing when it serves as the sphincter/valve of the lower respiratory tract, thus maintaining the airway.
The voice box controls sound production. It is composed of nine cartilages, connected by membranes and ligaments containing the vocal folds.
LO 1.5 Describe the structure and function of the Middle Ear
The cavity of the middle ear, or tympanic cavity is the narrow air-filled chamber in the petrous part of the temporal bone. The Tympanic cavity is connected with: o Nasopharynx - Anteromedially - Pharyngotympanic (Eustachian)Tube o Mastoid cells - Posterosuperiorly - Mastoid Antrum
LO 1.6 Describe the Histology of the Respiratory Tract and relate it to the functions and defence of the lungs
The respiratory system contains Mucous Membranes, which line the conducting portion of the respiratory tract, bearing mucus-secreting cells to varying degrees
Serious Membranes, which line the pleural sacs that envelop each lung
Pseudostratified Cilia with Goblet Cells Nasal Cavity Pharynx Larynx Trachea Primary / Secondary Bronchi
Simple Columnar Cilia with Clara Cells but NO Goblet cells
Bronchioles
Terminal Bronchioles
Simple Cuboidal with Clara Cells and Sparsely scattered Cilia
Respiratory Bronchioles
Alveolar Ducts
Simple Squamous Alveoli
LO 1.7 Describe the structure of the airways in the lung, distinguish bronchi from bronchioles and define what is meant by terminal bronchiole, alveolar duct and alveolus
The presence of lack of cartilage, glands and differing diameters distinguishes Bronchi from Bronchioles.
Terminal Bronchiole
o No alveolar openings
Respiratory bronchiole
o Bronchiole wall opens onto some alveoli
Alveolar Duct
o Duct wall has openings everywhere onto alveoli
Alveolus
o A single alveoli
Alveolar Sac
o Composite air space onto which many alveoli open
LO 1.8 Describe the structure of the Alveoli
o Abundant capillaries
o Supported by a basketwork of elastic and reticular fibres
o Covering composted chiefly of Type I pneumocytes
o Simple Squamous
o Cover 90% of surface area
o Permit gas exchange with capillaries
o Scattering of intervening Type II pneumocytes
o Simple Cuboidal
o Cover 10% of surface area
o Produce surfactant
o Macrophages line alveolar surface to phagocytose particles.
New alveoli continue to develop up to the age of 8 years, when there are approximately 300,000,000.
Alveoli can open into a respiratory bronchiole, an alveolar duct or sac or another alveolus (via an alveolar pore).
LO 2.10 Describe the properties of the mechanical system comprising the lungs, chest wall and diaphragm
Lungs
o Bronchioles dilate, increasing their volume and lowering the pressure inside the lungs, moving air in
Chest Wall
o Parietal pleura secretes fluid, the surface tension of which adheres the two pleural layers together
o So when the chest wall expands, the Parietal Pleura (attached to chest wall) moves with it, as does the Visceral Pleura, which is attached to the lung, causing it to expand
o External intercostals elevate the ribs in a ‘bucket handle’ type movement
o Accounts for 30% of chest expansion during quiet respiration
Diaphragm
o Contracts and descends
o Accounts for 70% of chest expansion during quiet respiration
LO 2.11 Describe the roles of the muscles involved in inspiration and expiration from the resting expiratory level
Quiet Breathing
o Inhalation
Diaphragm
External Intercostals
o Exhalation
None
LO 2.12 Describe the roles of the diaphragm and accessory respiratory muscles in different types of breathing
Forced Breathing
o Inhalation Diaphragm External Intercostals Scalene Pectoralis Minor Sternocleidomastoid Serratus Anterior
o Exhalation
Internal Intercostals
Innermost Intercostals
Abdominal Muscles
What are the lung volumes, define them
Measurement of Respiration
The movement of air during breathing can be measured with Spirometry.
Lung Volumes
Tidal Volume
The lung volume that represents the amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied
Inspiratory Reserve Volume
The extra volume that can be breathed in when extra effort is applied
Expiratory Reserve Volume
The extra volume that can be breathed out when extra effort is applied
Residual Volume
The volume left in the lungs at maximal expiration. This cannot be measured with a spirometer; it must be measured by helium dilution
What are the Lung Capacities, define them
Lung Capacities
Lung volumes change with breathing pattern. Capacities do not, as they are measured from fixed points in the breathing cycle.
Vital Capacity
The biggest breath that can be taken in, measured from the max inspiration to max expiration. It often changes in disease, and is about 5L in a typical adult.
Functional Residual Capacity
The volume of air in the lungs at resting expiratory level (Expiratory reserve volume + residual volume). It is typically about 2L.
Inspiratory Capacity
The biggest breath that can be taken from resting expiratory level (lung volume at the end of quiet expiration). It is typically about 3L.
What are the factors affecting diffusion in the lung
Blood flowing through alveolar capillaries picks up oxygen and loses carbon dioxide by diffusion of those gases across the alveolar wall. The rate at which gases exchange is determined by three factors:
Area
The area of the alveolar surface is large because there are a huge number of alveoli, generating in a normal lung an exchange area of around 80m2. In normal lungs, the area available is not a limiting factor on gas exchange.
Resistance to diffusion The diffusion pathway from alveolar gas to alveolar capillary blood is short, but there are several structures between the two. First gas must diffuse through the gas in the alveoli, then through: o The alveolar epithelial cell o Interstitial fluid o Capillary endothelial cell o Plasma o RBC membrane This means gases have to diffuse through 5 cell membranes, 3 layers of intra cellular fluid and 2 layers of extra cellular fluid. Despite this the overall barrier is less than 1 micron.
Two gases have to diffuse, oxygen into the blood and carbon dioxide out of it. The resistance is not the same for the two gases. For most of the barrier (the cells, membranes and fluid) the rate of diffusion is affected by the solubility of the gas in water, and carbon dioxide diffuses much faster, because it is more soluble.
Overall, Carbon Dioxide diffuses 21 times as fast as oxygen for a given gradient. This means that anything affecting diffusion will only change oxygen transport, as that is limiting (If there is a problem affecting the exchange of gases, O2 will be affected first)
Partial Pressure
The partial pressure of oxygen and carbon dioxide in the alveolar gas must therefore be kept very close to their normal values (O2 – 13.3kPa/CO2 – 5.3kPa) if the tissues of the body are to be properly supplied with oxygen and lose their carbon dioxide. This is achieved by exchange of gas between alveolar gas and atmospheric air brought close to it through the airways of the lung by the process of ventilation.
Air is driven through the airways of the lungs by the pressure changes produced by increases and decreases in the volume of the air spaces next to the alveoli. The movement of breathing lowers pressure in the terminal and respiratory bronchioles during inspiration, so air flows down the airways to them and then increased pressure during expiration so air flows back out again.
Fresh atmospheric air does not enter the alveoli, and exchange of oxygen and carbon dioxide occurs by diffusion between alveolar gas and atmospheric air in the terminal and respiratory bronchioles.
LO 2.14 Define the terms Serial Dead Space and Physiological Dead Space
Serial (Anatomical) Dead Space
Air enters and leaves the lungs by the same airways. So the last air in is the first air out, does not reach the alveoli and is therefore unavailable for gas exchange. The volume of the conducting airways is known as the Anatomical or Serial Dead Space and is normally about 150ml.
Physiological Dead Space
The air contained in the conducting airways is not the only air that fails to equilibrate with alveolar capillary blood. Some alveoli receive an insufficient blood supply; others are damaged by accident or disease, so that even in the air that reaches the alveolar boundary, there is a proportion that fails to exchange.
The volume of air in alveoli not taking part in gas exchange is known as the Alveolar (or Distributive) Dead Space.
Anatomical Dead Space + Alveolar Dead Space = Physiological Dead Space
How do you measure Serial Dead Space
Nitrogen Washout Test
o The patient takes a maximum inspiration of 100% oxygen.
o The oxygen that reaches the alveoli will mix with alveolar air, and the resulting mix will contain Nitrogen (there is 79% Nitrogen in air)
o However, the air in the conducting airways (dead space) will still be filed with pure oxygen.
o The person exhales through a one way vale that measures the percentage of Nitrogen in and volume of air expired
o Nitrogen concentration is initially zero as the patient exhales the dead space oxygen.
o As alveolar air begins to move out and mix with dead space air, nitrogen concentration gradually climbs, until it reaches a plateau where only alveolar gas is being expired
o A graph can be drawn to determine the dead space, plotting Nitrogen % against Expired Volume.
How do you measure Physiological Dead Space
Physiological Dead space is determined by measuring pCO2 (or pO2) of expired alveolar air. The alveolar air is diluted by dead space air to form the expired air, and the degree of dilution is a measurement of a physiological dead space.
LO 2.15 Calculate alveolar ventilation rate given pulmonary ventilation rate, dead space volume and respiratory rate
Alveolar Ventilation Rate
The amount of air that actually reaches the alveoli
Alveolar Ventilation Rate
= Pulmonary Ventilation Rate – Dead Space Ventilation Rate
or
= (Tidal Volume x RR) – (Dead Space Volume x RR)
LO 3.1 Describe the mechanical system of the lungs and thorax and what is a pneumothorax
Air is drawn into the lungs by expanding the volume of the thoracic cavity. Work is done during breathing to move the structures of the lungs and thorax and to overcome the resistance to flow of air through the airways.
The space between the lungs and thoracic wall, the pleural space, is normally filled with a few millilitres of fluid, the surface tension of which forms a pleural seal holding the outer surface of the lungs to the inner surface of the thoracic wall. Therefore the volume of the lungs changes with the volume of the thoracic cage.
Pneumothorax
If the integrity of the pleural seal is broken, the lungs will tend to collapse.
E.g. If air gets in between the two layers of the pleura, fluid surface tension is lost and the lungs collapse.
LO 3.2 Define the term ‘Compliance’ of the lungs and state how, in principle, it is measured
Lung Compliance
The ‘stretchiness’ of the lungs is known as compliance.
It is defined as volume change per unit pressure change.
High Compliance means that the Lungs are Easy to Stretch.
Compliance is measured by measuring the change in lung volume for a given pressure. The greater the lung volume the greater the compliance and vice versa. However, even with the constant elasticity of lung structures, compliance will also depend on the starting volume from which it is measured, so it is more usual to calculate Specific Compliance, which is:
Volume Change Per Unit Pressure Change / Starting Volume of Lungs
LO 3.3 Describe the factors which affect the compliance of the lungs, including the role of surfactant
The elastic properties of the lungs arise from two sources, Elastic Tissues in the lungs and Surface Tension forces of the fluid lining the alveoli.
Surface Tension
Surface tension is interactions between molecules at the surface of a liquid, making the surface resist stretching. The higher the surface tension, the harder the lungs are to stretch (lowers compliance).
Surfactant
At low lung volumes, the surface tension of the lungs is much lower than expected. This is due to the disruption of interactions between surface molecules by Surfactant, produced by Type 2 Alveolar Cells.
Surfactant is a complex mixture of phospholipids and proteins, with detergent properties. The hydrophilic ends of these molecules lies in the alveolar fluid and the hydrophobic end projects into the alveolar gas. As a result they float on the surface of the lining fluid, disrupting interaction between surface molecules.
Surfactant reduces surface tension when the lungs are deflated, but not when fully inflated. So little breaths are easy, and big breaths are hard, and it takes less force to expand small alveoli than it does large ones.
Bubbles in the Lung
Alveoli form an interconnecting set of bubbles. If Laplace’s law is applied (Pressure is inversely related to the radius of a bubble), large alveoli would ‘eat’ small ones.
As alveoli get bigger, the surface tension in their walls increases, as surfactant is less effective. So pressure stays high and stops them from ‘eating’ the smaller alveoli.
LO 3.4 Describe the factors which influence airway resistance in the normal lung and how airway resistance changes over the breathing cycle
Overall, work is done against:
o The elastic recoil of the lungs and thorax
o Elastic properties of the lungs
o Surface tension forces in the alveoli
o Resistance to flow through airways
o Of little significance in health, but often affected by disease
LO 3.5 Explain simple Spirometry
Spirometry
The patient fills their lungs from the atmosphere, and breathes out as far and fast as possible through a Spirometer.
Simple Spirometry allows measurement of many lung volumes and capacities. Vital capacity is particularly significant. Tables can be used to predict the vital capacity of an individual of known age, sex and height.
Vital Capacity may be less than normal because the lungs are not:
- Filled normally in inspiration
- Emptied normally in expiration
- Or Both
LO 3.6 Describe the measurement of forced vital capacity (FVC) and forced expiratory volume in one second (FEV1)
Forced Vital Capacity (FVC)
FVC is the maximum volume that can be expired from full lungs.
Forced Expiratory Volume in One Second (FEV1)
FEV1 is the volume expired in the first second of expiration from full lungs.
It is affected by how quickly air flow slows down, so is low if the airwards are narrowed (Obstructive deficit, see below).
LO 3.7 Explain obstructive and restrictive patterns of Spirometry
Vitalograph
Restrictive and obstructive deficits can be separated by asking patients to breathe out rapidly from maximal inspiration through a single breath spirometer, which plots volume expired against time.
Maximal filling of the lungs is determined by the balance between the maximum inspiratory effort and the force of recoil of the lungs. If the lungs are unusually stiff, or inspiratory effort is compromised by muscle weakness, injury or deformity, then a Restrictive Deficit is produced.
FVC Reduced
FEV1 >70% FVC
During expiration, particularly when forced, the small airways are compressed. This increases flow resistance, eventually to the point where no more air can be driven out of the alveoli.
If the airways are narrowed, then expiratory flow is compromised much earlier in expiration, producing an Obstructive Deficit.
FEV1 Reduced
FVC Relatively Normal
LO 3.8 Explain expiratory and inspiratory flow volume loops and how they are affected by upper and lower airway obstruction
Flow Volume Curves
Flow volume curves are a graph of Volume Expired against Flow Rate, derived from a Vitalograph trace.
A – When the lungs are full, the airways are stretched so resistance is at a minimum. Flow is therefore at maximum (Peak Expiratory Flow Rate PEFR)
B-D – As the lungs are compressed, more air is expired and the airways begin to narrow, so resistance increases and flow rate decreases.
In normal individuals, peak flow is affected most by the resistance of the large airways, but will also be affected by severe obstruction of the smaller airways (e.g. Asthma).
Mild obstruction of the airways produces a ‘scooped out’ expiratory curve. More severe obstruction will also reduce PEFR.
LO 3.9 Describe in principle the measurement of residual volume
Helium Dilution Test
The Helium Dilution Test is used to measure Functional Residual Capacity (FRC), which is used to calculate the residual volume. Helium is an inert, colourless, odourless, tasteless gas that is not toxic. It cannot transfer across the alveolar-capillary membrane and is therefore contained within the lungs.
o At the end of a normal tidal expiration the patient is connected to a circuit, which is connected to a contained containing a gas mixture with a known Helium Concentration (C1) and Volume (V1)
- End of Tidal Expiration:
- Lung Volume = FRC = ERV +RV
o The patient continues to rebreathe into the container until equilibrium occurs
- Usually takes 4 – 7 minutes
o The new concentration of Helium = C2
o C1 x V1 = C2 x V2
- V2 = V1 + FRC
o Since C1, V1 and C2 are all known, FRC can be calculated.
o Residual Volume = FRC – ERV
- ERV measured by Spirometry
LO 3.9 Describe in principle the measurement of transfer factor
Transfer Factor
The Carbon Monoxide Transfer Factor measures the rate of transfer of CO from the alveoli to the blood in ml per minute per kPa (ml/min/kPa). It is a way of measuring the diffusion capacity of the lung, because the amount transferred will depend on how well gas diffusion takes place.
Inhaled CO is used because of its very high affinity for Hb. Since almost all the CO entering the blood binds to Hb, very little remains in plasma so we can assume plasma ppCO is zero.
Therefore, the concentration gradient between alveolar ppCO and capillary ppCO is maintained. As a result the amount of CO transferred from alveoli to the blood is limited only by the diffusion capacity of the lung.
o The patient performs a full expiration, followed by a rapid maximum inspiration of a gas mixture composed of air, a tiny fraction of CO and a fraction of an inert gas such as helium.
Tiny fraction of CO as it is toxic
Fraction of inert gas to make an estimate of total lung volume
o The breath is held for 10 seconds.
o The patient exhales, and gas is collected mid-expiration, to gain an alveolar sample
o Concentration of CO and inert gas
o From these measurements, the Carbon Monoxide Transfer Factor is calculated
LO 3.10 Explain the nitrogen washout curve
Nitrogen Washout Test
Serial (Anatomical) Dead Space is measured by the Nitrogen Washout Test.
o The patient takes a maximum inspiration of 100% oxygen.
o The oxygen that reaches the alveoli will mix with alveolar air, and the resulting mix will contain Nitrogen (there is 79% Nitrogen in air)
o However, the air in the conducting airways (dead space) will still be filled with pure oxygen.
o The person exhales through a one way vale that measures the percentage of Nitrogen in and volume of air expired
o Nitrogen concentration is initially zero as the patient exhales the dead space oxygen.
o As alveolar air begins to move out and mix with dead space air, nitrogen concentration gradually climbs, until it reaches a plateau where only alveolar gas is being expired
o A graph can be drawn to determine the dead space, plotting Nitrogen % against Expired Volume.
LO 4.1 State the solubility of Oxygen in body fluids
Oxygen is not very soluble in water. At a partial pressure of 13.3kPa and a temperature of 370C, plasma contains 0.13mmol/L of dissolved oxygen.
At rest we need 12mmol of Oxygen per minute. The volume that would contain this amount is 92 Litres.
What is the typical pp02 in the tissues and lungs
Typical ppO2 in the lungs is 13.3kPa
Typical ppO2 in tissues is ~5kPa
LO 4.3 List the properties of the haemoglobin molecule that facilitate the transport of oxygen in the blood
Haemoglobin (Hb) reversibly binds to oxygen over a very narrow range of ppO2. It is a tetrameric protein (2xA, 2xB subunits) containing four Haem groups, allowing it to bind four molecules of oxygen.
Hb can exist in two states - a low affinity T-state (tense) and a high affinity R-state (relaxed). Transition between these two states gives Hb its sigmoidal binding curve, so Hb’s affinity to O2 increases as more O2 binds.
LO 4.4 Draw the effects on the haemoglobin oxygen dissociation curve of a fall in pH and a rise in temperature
H+, Increasing Temperature and CO2 and decrease the affinity of Hb for O2. At sites of low pH (high [H+]), and increased CO2, for example muscle tissue during exercise, more oxygen is required and will be released. This is called the Bohr effect.
The oxygen dissociation curve shifts to the RIGHT.
LO 4.5 Estimate the rate of delivery of oxygen to the tissues at different capillary pO2’s and pH’s
If the pO2 in the capillaries of tissues falls, pH falls and temperature rises so that Hb will give up more oxygen. Therefore the saturation of Hb leaving the capillaries will be greatly reduced.
If venous pO2 is known, a dissociation curve can be used to calculate the percentage of oxygen that has been given up to that tissue.
LO 4.6 State the factors influencing the diffusion of gases across the alveolar membrane
Blood flowing through alveolar capillaries picks up oxygen and loses carbon dioxide by diffusion of those gases across the alveolar wall. The rate at which gases exchange is determined by three factors:
o Area available for the exchange
o Resistance to diffusion
o Gradient of partial pressure
LO 4.8 List the Reactions of CO2 in the blood
o Dissolves in water
More soluble than O2
o Reacts with water
Forms H+ and HCO3-
Reversible reaction depending on concentrations of reactants
o Binds directly to proteins
Forms Carbamino compounds
LO 4.9 Write the Henderson-Hasselbach equation and be able to calculate the plasma pH, given the pCO2 and [HCO3-]
pHG = 6.1 + log (HCO3/[pCO2*0.23])
LO 4.10 State the factors influencing the Hydrogen Carbonate concentration of plasma
o In Plasma
CO2 dissolves in plasma and undergoes a slow reaction (little carbonic anhydrase) with water, creating HCO3-
o In RBCs
CO2 also reacts with water, rapidly (carbonic anhydrase is present) to form H+ and HCO3-.
H+ ions bind to Hb, drawing the reaction towards HCO3- production
The amount produced depends primarily upon the buffering effects of Hb
LO 4.11 Describe the buffering actions of Hb in RBCs
H+ ions bind to Haemoglobin, so it acts as a buffer by ‘mopping up’ H+ ions. This drives the reaction of CO2 with Water, producing more H+ ions and HCO3-.
LO 4.12 Describe the function of carbamino compounds
Carbamino Compounds
Carbamino compounds bind directly to proteins, contributing to CO2 transport, but not acid base balance.
There is slightly more formed in venous blood, as pCO2 is higher.
LO 4.13 State the normal content of CO2 in arterial and venous blood
Arterial Blood CO2 – 21.5 mmol/Litre
Venous Blood CO2 – 23.5 mmol/Litre
LO 4.14 Describe the process of transport of CO2 from tissues to lungs, and state the proportion of CO2 traveling in various forms
Venous Blood CO2 – Arterial Blood CO2 = Amount transported from tissues lungs
= 23.5 – 21.5
= 2mmol/Lire
o 80% travels as HCO3-
Depending on how much O2 Hb has lost, allowing it to bind H+
o 11% travels as carbamino compounds
o 8% travels as dissolved CO2
LO 5.1 Define the terms hypoxia, hypercapnia, hypocapnia, hyperventilation, hypoventilation
Hypoxia – A fall in alveolar, thus arterial pO2
Hypercapnia – A rise in alveolar, thus arterial, CO2
Hypocapnia – A fall in alveolar, thus arterial CO2
Hyperventilation – Ventilation increases with no change in metabolism
(Breathing more than you actually have to)
Hypoventilation – Ventilation decreases with no change in metabolism
(Breathing less than you actually have to)
LO 5.2 Describe the effects on plasma pH of hyper- and hypo-ventilation
pCO2 affects plasma pH (Henderson-Hasselbach)
o Hyperventilation
pCO2 down
pH up
o Hypoventilation
pCO2 up
pH down
LO 5.3 Describe the general effects of acute hypo- and hyper-ventilation
Hypoventilation
o Hypercapnia and Respiratory Acidosis
o pH falls bellows 7.0
o Enzymes become lethally denatured
Hyperventilation
o Hypocapnia and Respiratory Alkalosis
o pH rises above 7.6
o Free calcium concentration falls enough to produce fatal tetany
Ca2+ is only soluble in acid, so when pH rises, Ca2+ cannot stay in the blood. Nerves become hyper-excitable.
LO 5.4 Define the terms Respiratory Acidosis, Respiratory Alkalosis, Compensated Respiratory Acidosis and Compensated Metabolic Alkalosis
Respiratory Acidosis
CO2 is produced more rapidly than it is removed by the lungs (hypoventilation). Alveolar pCO2 rises, so [Dissolved CO2] rises more than [HCO3-], producing a fall in plasma pH.
Compensated Respiratory Acidosis
Respiratory Acidosis persists, and the kidneys respond to low pH by reducing the excretion of HCO3-, thus restoring to ratio of [Dissolved CO2] to [HCO3-], and therefore the pH.
Respiratory Alkalosis
CO2 is removed from alveoli more rapidly than it is produced (hyperventilation). Alveolar pCO2 falls, disturbing the ratio of [Dissolved CO2] to [HCO3-], producing a rise in plasma pH.
Compensated Respiratory Alkalosis
Respiratory Alkalosis persists, and the kidneys respond to the high pH by excreting HCO3-, thus restoring the ratio of [Dissolved CO2] to [HCO3-], and therefore the pH.
LO 5.5 Define the terms Metabolic Acidosis, Metabolic Alkalosis, Compensated Metabolic Acidosis, Compensated Metabolic Alkalosis
Metabolic Acidosis
Metabolic production of acid displaces HCO3- from plasma as the acid is buffered; therefore the pH of blood falls.
Compensated Metabolic Acidosis
The ratio of [Dissolved CO2] to [HCO3-] may be restored to near normal by lowering pCO2. The lungs increase ventilation to correct pH.
Metabolic Alkalosis
Plasma [HCO3-] rises, causing the pH of blood to rise (e.g. after vomiting).
Compensated Metabolic Alkalosis
The ratio of [Dissolved CO2] to [HCO3-] may be restored to near normal by raising pCO2. The lungs decrease ventilation to correct pH.
LO 5.6 Describe the acute effects upon ventilation of: falling inspired pO2, increase in inspired pCO2 and falls in arterial plasma pH
Falling Inspired pO2
The falling arterial pO2 is detected by Peripheral Chemoreceptors located in the Carotid and Aortic bodies.
The carotid and aortic bodies are stimulated by a decrease in oxygen supply relative to their own oxygen usage, which is small. They only respond to large drops in O2.
Stimulation of the receptors:
o Increases the tidal volume and rate of respiration
o Changes in circulation directing more blood to the brain and kidneys
o Increased pumping of blood by the heart
Increase in Inspired pCO2
The Peripheral Chemoreceptors in the Carotid and Aortic bodies also detect changes in pCO2, but are insensitive.
Central Chemoreceptors in the Medulla of the brain are much more sensitive, altering breathing on a second to second basis.
Central chemoreceptors detect changes in Arterial pCO2.
o Small rise in pCO2 -> Increase Ventilation
o Small falls in pCO2 -> Decrease Ventilation
o Are the basis of negative feedback control of breathing
LO 5.7 Describe the location and function of the Peripheral Chemoreceptors and their role in ventilator and other responses to Hypoxia
The arterial pO2 is detected by Peripheral Chemoreceptors located in the Carotid and Aortic bodies.
The carotid and aortic bodies are stimulated by a decrease in oxygen supply relative to their own oxygen usage, which is small. They only respond to large drops in O2.
Stimulation of the receptors:
o Increases the tidal volume and rate of respiration
o Changes in circulation directing more blood to the brain and kidneys
o Increased pumping of blood by the heart
LO 5.8 Describe the location and function of the central chemoreceptors, their role in the vetilatory respiratory to changes in arterial pCO2 and the roles of the cerebro-spinal fluid, blood brain barrier and choroid plexus in that response
Central Chemoreceptors in the Medulla of the brain are much more sensitive, altering breathing on a second to second basis.
Central chemoreceptors detect changes in Arterial pCO2.
o Small rise in pCO2 Increase Ventilation
o Small falls in pCO2 Decrease Ventilation
o Are the basis of negative feedback control of breathing
- If pCO2 rises, central chemoreceptors stimulate ventilation
- Which blows off CO2, returning pCO2 to normal
- Vice-versa
The central chemoreceptors actually respond to changes in the pH of cerebro-spinal fluid (CSF).
The CSF is separated from the blood by the blood-brain barrier. The pCO2 of the CSF is determined by arterial pCO2, but HCO3- and H+ cannot cross.
CSF [HCO3-] is controlled by Choroid Plexus Cells.
The pH of CSF is determined by the ratio of [HCO3-] to pCO2. In the short term, [HCO3-] is fixed (cannot cross BBB), so falls in pCO2 -> Inc. pH and rises in pCO2 -> Lower pH. Persisting changes compensated for via the Choroid Plexus Cells altering CSF [HCO3-].
LO 5.9 Define Hypoxia
Hypoxia – A fall in alveolar, thus arterial pO2
LO 5.10 What are the five factors necessary to maintain arterial pO2 in the normal range
There are five factors necessary to maintain arterial pO2 in the normal range, and problems with any of them may result in hypoxia
- Low pO2 in inspired air
Everything is normal, the air breathed in just has low pO2
People living at high altitudes - Hypoventilation
o Always associated with increased pCO2 (Type 2 Respiratory Failure)
o Neuromuscular Problems
Respiratory depression due to opiate overdose
Head injury
Muscle weakness (NMJ/Nerve/Muscle diseases)
o Chest wall problems (Mechanical)
Scoliosis/kyphosis
Morbid obesity
Trauma
Pneumothorax
o Hard to Ventilate lungs
Airway obstruction
COPD & Asthma when the airway narrowing is severe and widespread
Severe fibrosis - Diffusion Impairment
o O2 diffuses much less readily than CO2, so is always affected first
o pCO2 is therefore low/normal – Always Type 1 Respiratory Failure
o Structural Changes
Lung fibrosis causing thickening of alveolar capillary membrane
o Increased Path Length
Pulmonary Oedema
o Total area for diffusion reduced
Emphysema - Ventilation Perfusion Mismatch
o O2 diffuses much less readily than CO2, so is always affected first
o pCO2 is therefore low/normal – Always Type 1 Respiratory Failure
o Reduced Ventilation of some Alveoli
Lobar Pneumonia
o Reduced Perfusion of Some Alveoli
Pulmonary Embolism - Abnormal Right to Left Cardiac Shunts
o E.g. Cyanotic Heart Disease such as Tetralogy of Fallot (See CVS)
