Session 6

Question 1

What is ‘Spirometry’

Answer 1

• ‘Spirometry’ (Latin) = the measuring of breath
• The spirometer records the volume of air that is breathed in and out
• and generates tracings of air flow (i.e. pneumotachographs)
• Tracings used to calculate: – vital capacity, tidal volume – the flow rate of air movement

Question 2

Reasons for Pulmonary Function Tests

Answer 2

• Diagnosis -Tests are rarely diagnostic on their own – Results taken together with history and examination
• Patient assessment -Most usual reason for tests – Serial changes – Response to therapy – Assessment for compensation – Pre-surgical assessment
• Research purposes – Epidemiology – Study of growth and development – Investigation of disease processes

Question 3

Do we take spirometry readings standing or seated?

Answer 3

• FVC standing> FVC seated

– BUT high intrathoracic pressure can result in reduced cardiac output and cerebral blood flow

Question 4

3 types of graph produced using spirometry?

Answer 4

Tracings, Graphs Flow, Volume Loops

insert slide 6 lec 1

Question 5

Movements of the TRACE

Answer 5

• The classic presentation of the traces from these recordings is therefore:
• INSPIRATION as an upward deflection
• EXPIRATION as a downward deflection

Question 6

Draw a spirogram trace and label it. How are the values calculated?

Answer 6

insert slide 10 lec 1

• Lung Capacities – Inspiratory capacity =
• VT + IRV – FRC – VT – VC
• Inspirational capacity = – VT + IRV
• Functional Residual Capacity = – ERV + RV

Question 7

How do we get from a spirogram (volume-time trace) to a volume-time graph?

Answer 7

panopto

Question 8

Forced flow-volume measurements show us?

Answer 8

• How much air can the subject blow out? – can be reduced in restrictive disorders, – or if there is airway narrowing precipitating early airway closure (e.g. asthma or CF) • How fast is the air expelled? – can be reduced with airway narrowing. • Pattern of change in flow-volume curve (insp& exp) can indicate site of obstruction • Response to treatment (e.g. β2agonist) • Change with age or growth • Progression of disease

Question 9

What is FVC, FEV1, PEF and why is FEV1 useful

Answer 9

FVC: Maximal amount of air that the patient can forcibly exhale after taking a maximal inhalation

FEV1: Volume exhaled in the first second

Peak expiratory flow (PEF): Maximal speed of airflow as the patient exhales

FEV1 is the most reproducible flow parameter and is especially useful in diagnosing and monitoring patients with obstructive pulmonary disorders (eg, asthma, COPD).

picture from slide 14

Question 10

Nomogram for predicting FVC

Answer 10

Forced vital capacity (FVC) – The measured value is compared to that of healthy people of the same • gender, • age and • height slide 15 lec 1

Question 11

The time- volume graph

Answer 11

Patient inspires to vital capacity Rapid forced expiration • Convention shows expiration as a downward defection on a spirometry trace: • This is a graph volume (L) expired against time • Follows normal graph conventions inser pic from slide 16 lec 1

Question 12

Volume-time plot of maximal forced expiration

Answer 12

ue panopto slide 17 lec 1

Question 13

Volume-Time graphs in obstructive disease (Asthma, COPD)

Answer 13

• FVC is not markedly reduced
• (if given sufficient time to completely breathe out)
• Narrowed airways reduces the speed at which air can be breathed out.
• Fraction of air expelled during 1st second (FEV1 /FVC) is markedly reduced.
• Typical pattern in obstructive airways disease: – FVC nearly normal – FEV1 markedly reduced – The FEV1 /FVC ratio < 70%

slide 18 lec 1

Question 14

Volume-Time graphs in restrictive disease (lung fibrosis)

Answer 14

Volume-Time graphs in restrictive disease (lung fibrosis) • FVC is markedly reduced (lungs stiff, cannot be expanded adequately) • However, the speed at which air can be breathed out is normal (because no narrowing of airways) • the fraction of air expelled during 1st second is normal or even greater than normal • The typical pattern in restrictive airways disease: – A Low FVC – Low FEV1 – But FEV1 /FVC ratio ≥ 70% slide 19 lec 1

Question 15

How do we get from a spirogram (volume-time trace) to a flow-volume loop?

Answer 15

use panopto slide 21 lec 1

Question 16

Ho might the flow volume look normally compared to COPD, Fixed-extra thoracic obstruction, during a cough, restrictive lung disease and upper airway obstruction? and why?

Answer 16

slide 23 lec 1

Question 17

How do obstructive diseases differ on a flow volume loop compared to restrictive disease and then mixed disease

Answer 17

slide 30 lec 1

Question 18

What is bronchiectasis?

Answer 18

DEFINITION: Chronic IRREVERSIBLE dilatation of one or more bronchi – it is a pathological condition that can be caused by many diseases or be idiopathic- resulting in abnormally enlarged bronchi – These deformed bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

• AETIOLOGY: variety of underlying causes, with a common underlying mechanism of of chronic inflammation • Inflammation causes destruction of the elastic and muscular components of the bronchial wall and peribronchial fibrosis
• RADIOLOGICAL FINDINGS • CXR - usually abnormal but inadequate in the diagnosis or quantification of bronchiectasis/ bronchial dilatation – Gold standard diagnostic investigation = CT - specifically High Resolution CT
• We find -bronchial dilatation bigger than the adjacent blood vessel, bronchial wall thickening

Question 19

How is bronchiectasis signified on a CT?

Answer 19

Signet Ring Signdilated bronchus and accompanying pulmonary artery branch are seen in cross-section. healthy lung bronchus slightly Smaller than artery whereas in bronchiectasis, the bronchus is markedly dilated > artery slide 3 lec 2

Question 20

What do you notice about this pitients lungs insert diagram from slide 4 lec 2

Answer 20

Gross pathologic lung specimen from a patient with bronchiectasis. Notice the small pulmonary artery abutting the much larger dilated bronchus (arrow), both of which are seen on cross- section

Question 21

Clinical symptoms of bronchiectasis?

Answer 21

Very Common: • Chronic cough • Daily sputum production – can vary in quantity, colour and consistency Common: • Breathlessness on exertion • Intermittent haemoptysis • Nasal symptoms • Chest Pain • Fatigue Less Common: • Wheeze Symptoms not very specific – history and risk factors key to Dx

Question 22

Bronchiectasis – what are the clinical signs?

Answer 22

• Pulse oximetry may reveal hypoxaemia in advanced cases of bronchiectasis • Fever relatively common - More than half of patients with bronchiectasis will have recurrent episodes of fever • Haemoptysis - present in about 50% of patients - usually mild • Fine crackles (rales) • High-pitched inspiratory squeaks • Rhonchi • Sometimes can hear both crackles & wheezing - Lungs sounds from CF patient w/ bronchiectasis • Systemic signs - a history of weight loss common • Clubbing of the digits is less common

Question 23

Causes of bronchiectasis?

Answer 23

• Post infective– whooping cough (pertussis), TB • Immune deficiency– Hypogammaglobulinaemia • Mucociliaryclearance defects– Cystic fibrosis, primary ciliary dyskinesia, Young’s syndrome (triad of bronchiectasis, sinusitis, and reduced fertility), Kartagener syndrome (triad of bronchiectasis, sinusitits, and situs inversus) • Idiopathic • Alpha-1-antitrypsin deficiency • Obstruction – foreign body, tumour, extrinsic lymph node • Toxic insult – gastric aspiration (particularly post lung transplant), inhalation of toxic chemicals/gases • Allergic bronchopulmonary aspergillosis • Secondary immune deficiency – HIV, malignancy • Rheumatoid arthritis • Associations – inflammatory bowel disease; yellow nail syndrome

Question 24

Bronchiectasis Common Organisms - How is it a vicious cycle?

Answer 24

• Haemophilus influenzae • Pseudomonas aeruginosa • Moraxella catarrhalis • Stenotrophomonas maltophilia • Streptococcus pneumoniae • Fungi – aspergillus, candida • Mycobacteria tuberculosis • Nontuberculous mycobacteria (NTM) • Less common - Staphylococcus aureus Bronchial dilation leads to mucous accumulation, impaired ciliary function and increased risk infection; Infection leads to inflammation and loss bronchial elastic fibres and smooth muscle –leads to more dilatation!

Question 25

How might a patient with possible bronchiectasis present?

Answer 25

• History of “asthma” (particularly lifelong )without any great objective evidence – such as reversible airway obstruction on spirometry– also in asthma no inspiratory squeaks and crackles • History of “COPD” but diminished breath sounds, characterising COPD, are not found & different risk factors • BUTif they do have a history of – Severe chest infection earlier in life (bacterial, viral or atypical) – Lifelong chest infections ? genetic cause – Recurrent chest infections ?immunodeficiency – Recurrent sinus infections since childhood? ? Ciliary dysfunc, • Sputum culture positive for common organisms such as haemophilus or pseudomonas or atypical mycobacterium • Inflammatory bowel disease, rheumatoid arthritis – also associated with bronchiectasis

Question 26

Why is early diagnosis of bronchiectasis important?

Answer 26

early diagnosis and treatment of predisposing underlying disorders may impede disease progression

Question 27

How are Pulmonary function tests used to diagnose bronchiectasis?

Answer 27

• Initial and follow up spirometry is recommended with most surgery visits – diagnosis and follow up lung function • Obstructive airways disease component may be evidenced by reduced forced expiratory volume (FEV1) or an FEV1/forced vital capacity (FVC) ratio of <70% • Full pulmonary function testing may show an elevation of RV/TLC ratio consistent with air trapping. • Diffusing capacity for carbon monoxide (DLCO) may be reduced in severe disease • Question: We all remember diffusing capacity is inversely related to the distance the gas has to travel – so, since there is marked thickening of the bronchial walls why isn’t diffusing capacity reduced in early disease?

Question 28

Make a table showing the differences between chronic bronchitis, bronchiectasis, asthma, emphysema and bronchiolitis

Answer 28

slide 8

Question 29

Bronchiectasis Management

Answer 29

• PHYSIO / AIRWAYS CLEARANCE –Daily airway clearance is essential for treatment success • Sputum sampling –routine culture and NTM • Exclude immunodeficiency / treat identifiable causes • Consider long-term therapies at future visits • Annual Flu & routine vaccinations against Haemophilus influenzae and Streptococcus pneumoniae • An established MDT is key • Management plan for infective exacerbation

Question 30

Defining an exacerbation n bronchiectasis

Answer 30

• How do we define “exacerbation” in bronchiectasis? • Recent international expert consensus……….. A person with bronchiectasis with a deterioration in 3 or more key symptoms for at least 48 hours: • Cough • Sputum volume and / or consistency • Sputum purulence • Breathlessness and / or exercise tolerance • Fatigue • Haemoptysis

Question 31

What is the most common identifiable cause of bronchiectasis? how has survival rates for this condition changed?

Answer 31

Cystic Fibrosis • In the 1950s, median life expectancy for patients with cystic fibrosis was a few months • In the 1990’s median life expectancy was late teens • Today ~𝟒𝟎𝐲/𝐨! Tremendous improvement in life expectancy have been achieved by understanding the importance of –Augmenting airway clearance – 2-3x/day –Aggressively treating infection, –Correcting nutrition deficits –New drug treatments targeting underlying molecular defect?

Question 32

What cystic fibrosis?

Answer 32

• Autosomal recessive disorder • 1 in 2,500 in the UK are born with CF – CF mutations most common in populations with northern European ancestry where the predominant mutation is Phe508del (also known as F508del) – deletion of Phenylalanine at position 508 of the polypeptide chain • CF caused by mutations of gene located on long arm chromosome 7 that lead to abnormal function of an epithelial chloride channel the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) –which has a key role in maintaining lung epithelial function • Also important in normal epithelial function other body organs; important comorbidities caused by epithelial cell dysfunction occur in the pancreas (malabsorption), liver (biliary cirrhosis), sweat glands (heat shock), and vas deferens (infertility)) • Cystic Fibrosis Cellular Defect 1/3 • Cystic Fibrosis Cellular Defect 2/3 • Cystic Fibrosis Cellular Defect 3/3 Molecular basis Cystic Fibrosis I • CFTR is a transmembrane protein that transports chloride and bicarbonate & also regulates the Epithelial Sodium Chanel (ENAC) • CFTR enables Cl to be transported out of cells into airways - the transport of chloride ions helps control the movement of water • CFTR also regulates sodium reabsorption into cells • Therefore CFTR plays a critical role in the hydration of the mucus at the surface of the airway track • Defective ion transport mediated by CFTR reduces airway surface liquid hydration, which leads to thick & sticky mucous & impairs muco-ciliary clearance • Over 2000 mutations related to CTFR gene (though not all pathogenic) • Mutations have different effects on the – Manufacture of CFTR protein, – Transportation of CFTR – CFTR processing function, – CFTR stability at the cell membrane (More on mutations to follow later in lecture)

Question 33

How is cystic fibrosis diagnosed?

Answer 33

One or more of the characteristic phenotypic features • Or a history of CF in a sibling • Or a positive newbornscreening test result And • An increased sweat chloride concentration (> 60 mmol/l) –SWEAT TEST • Or identification of two CF mutations –genotyping – may need EXTENDED GENOTYPING

Question 34

Main CF Clinical Presentations (“classic” CF)

Answer 34

1. Meconium ileus • In 15-20% of newborn CF infants the bowel is blocked by the sticky secretions. There are signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium. 2. Intestinal malabsorption • Over 90% of CF individuals have intestinal malabsorption. In most this is evident in infancy. The main cause is a severe deficiency of pancreatic enzymes. 3. Recurrent chest infections 4. Newborn screening

Question 35

Late Diagnosis of cystic fibrosis?

Answer 35

• Cystic fibrosis is usually identified following newborn screening or during the first few years of life - people diagnosed after 20 years of age usually have a mutation associated with residual CFTR function – Or heterozygous CFTR mutations – one severe + one mild • Increasingly recognized that some variants of CF may present in adults – classified as “Atypical CF” • Need a high index of suspicion to diagnose • Consider in cases of recurrent “idiopathic pancreatitis” , recurrent sinusitis & lung infections, infertility, allergic bronchopulmonary aspergillosis (IgE hypersensitivity reaction to Aspergillus species)

Question 36

CF Complications

Answer 36

LUNGS • Bronchiectasis • Pneumothorax • ABPA • Haemoptysis • Respiratory failure NASAL / UPPER RESP TRACT • Chronic sinusitis • Nasal polyposis PANCREAS • DM - CFRD • Pancreatic insufficiency GUT • Distal Intestinal Obstruction Syndrome (DIOS) • oesophageal reflux / oesophagitis LIVER • Chronic liver disease • Portal Hypertension BILIARY TREE • Gallstones HEART • Cardiac failure JOINTS & BONES • Arthritis • Osteoporosis REPRODUCTIVE TRACT • Male infertility • Congenital bilateral absence of vas deferens (CBAVD) Pseudomonas aeruginosa colonisation and infection particularly virulent pathogen in CF

Question 37

CF Lifestyle advice

Answer 37

•No smoking •Avoid other CF patients •Avoid friends / relatives with colds / infections •Avoid jacuzzis (pseudomonas) •Clean and dry nebulisers thoroughly •Avoid stables, compost or rotting vegetation – risk of aspergillus fumigatus inhalation •Annual influenza immunisation •Sodium chloride tablets in hot weather / vigorous exercise

Question 38

CF Clinical Management

Answer 38

• Complex - led by CF Specialist Centres / MDT’s • Holistic care / Multisystem (organ) focus • Up to date pneumococcal and haemophilus influenza vaccinations and annual influenza • Key is maintaining lung health (chest physio, infection management) • Optimal nutritional state – pancreatic status, vitamin status, weight / BMI

Question 39

Role of nutrition in cystic fibrosis

Answer 39

• CF mostly recognized for its pulmonary morbidity, but earliest manifestations disease related to gastrointestinal and nutritional derangements • Several factors contribute to impaired nutritional status in cystic fibrosis – Pancreatic insufficiency, – Chronic malabsorption, – Chronic inflammation leading to increased energy expenditure – Increased energy requirements of breathing – Suboptimal nutrient intake related to impaired taste (sinuses), fatigue,I nflammatorymediated anorexia • Interestingly, nutritional status plays an important role in the progression of the pulmonary disease –better nutritional status associated with better lung function • In one study nocturnal gastrostomy tube supplementation was associated with improved FEV1 –this appeared to be related to preservation of muscle mass • In several intervention trials in children, prolonged nutritional therapy led to improvements in – pulmonary function parameters, – measures of respiratory muscle strength, – hospitalisation rates, – gains in exercise capacity Suggestion that nutritional therapy supports lung growth and development

Question 40

Molecular basis underlying Cystic Fibrosis II –categorisation of defects

Answer 40

CFTR mutations can be divided into six classes according to their effects on protein function • Range of mutation effects from • No protein production, • Protein made but never gets to the cell membrane, • Protein gets to the membrane but doesn’t work at all • Protein made but only partially active • Protein expressed at gene level but substantial reduction in mRNA or protein, or both, synthesis • Protein gets to membrane but partially unstable • Medications now being developed that target underlying disease mechanisms –not just complications

Question 41

What is Orkambi

Answer 41

• Trade name for two drugs • lumacaftor and ivacaftor • Lumacaftor – CFTR chaperone during protein folding increases the number of CFTR proteins that are trafficked to the cell surface – helps in people with Phe508del-most common mutation • Ivacaftor - CFTRpotentiator, improves the transport of chloride through the ion channel by binding to the channels directly and increasing the probability that the channel is open- helps in people with G551D mutation4–5% cases of cystic fibrosis • Interestingly – combining these two drugs synergistically helps people with the Phe50del mutation

Question 42

What is an X-ray

Answer 42

An electromagnetic wave of high energy and very short wavelength, which is able to pass through many materials opaque to light  A photographic or digital image of the internal composition of the body, produced by X-rays being passed through the body part and being absorbed to different degrees by different tissues  This is displayed as levels of contrast on a grey scale (black to white)

Question 43

What is the radiation dose of a chest x-ray?

Answer 43

What does this mean?  Ave UK background dose = 2.7 mSv/year  Thus x3 days worth of background radiation  But if living in Cornwall = 7.8 mSV  1 in a million lifetime additional risk of fatal cancer  IRR allows workers upto 20 mSV/year  Ave nuclear worker = 0.18 mSV  Transatlantic flight = 0.08 mSv  100g bag of brazil nuts = 0.01 mSv

Question 44

X-ray projection – why is it important?

Answer 44

use panopto slide 8

Question 45

What needs to be seen on a chest x ray

Answer 45

 1st rib  Lateral margin of ribs  Costophrenic angle  Alignment of:  Spinous process and  Clavicles

Question 46

How are lung volumes seen on a chest x-ray?

Answer 46

 Inspiratory phase  Normal  5th to 7th anterior ribs at MCL  Problems with incomplete inspiration:  Big heart  Increased lung markings  Exaggerated expansion  Obstructive airways disease use panopto

Question 47

What is penetration (X-rays)

Answer 47

 Degree to which the x-rays have passed through the body  Adequate penetration  Vertebrae just visible through heart  Complete left hemidiaphragm is visible  Digital manipulation often negates this

Question 48

What is an artefact (X-rays)

Answer 48

 External/iatrogenic material which obstructs view  Clothes  Buttons – beware!  Hair  Surgical/vascular lines  Pacemaker

Question 49

Label the: 1. Trachea 2. Hila 3. Lungs 4. Diaphragm 5. Heart 6. Aortic knuckle 7. Ribs 8. Scapulae 9. Breasts 10. Bowel gas

Answer 49

insert mage from slide 18 lec 3

Question 50

Describethe lobes of the lungs

Answer 50

slide 21 lec 3

Question 51

Where are the costophrenic angles and costophrenic recesses?

Answer 51

slide 24

Question 52

how might a stomach buble be seen on a chest X-ray

Answer 52

slide 25

Question 53

Mediastinal contours on chest x-ray

Answer 53

slide 27

Question 54

How to evaluate a chest X-ray

Answer 54

 Systematic ABC approach  Patient demographics  Projection  Adequacy  Airway  Breathing  Circulation  Diaphragm / Dem bones  Review areas

Question 55

Define Pulmonary ventilation

Answer 55

The movement of air into (inhalation) and out of the lungs (exhalation) – the total amount of air moving in and out of the lungs

Question 56

Define Pulmonary gas exchange

Answer 56

the diffusion of oxygen from the lungs into the blood, and the diffusion of carbon dioxide from the blood into the lungs

Question 57

Define Pulmonary perfusion

Answer 57

the flow of blood through the pulmonary capillaries surrounding the alveoli – typically expressed as Q ml/min

Question 58

Define ALVEOLAR ventilation

Answer 58

ALVEOLARventilation is the amount of air reaching alveoli in a given amount of time– function of the tidal volume, the amount of air in the anatomical dead space, and the respiratory rate –typically expressed as V – Example: someone breathing 14 times a minute, with a tidal volume of 500 ml, and anatomical dead space of 150 ml will have an – alveolar ventilation- of 14 /minute ×(500 ml air -150 ml air) = 4900 ml air/minute = V

Question 59

What is V/Q

Answer 59

When discussing ventilation/perfusion often referred to as V/Q

Question 60

Normal physiology of lung ventilation and perfusion

Answer 60

slide 4 lec 4

Question 61

Ventilation and perfusion has to be matched throughout the lung. How is this achieved?

Answer 61

Gas exchange optimal when: – V/Q ratio of individual alveolar units ≈ 1 • 300 million alveoli - may have widely differing amounts of ventilation and of perfusion. • Ideally, – Alveoli with ventilation should have perfusion – Alveoli with ventilation should have perfusion • When pulmonary capillary PaO2 is low, hypoxic vasoconstriction of pulmonary arterioles occurs - this diverts blood to better ventilated alveoli • When alveolar PA CO2 is low, bronchoconstriction occurs – This diverts air to better perfused lung • BUT • This process is not 100% efficient, so in some disease states, poorly ventilated alveoli still have significant perfusion – this is what is meant by ventilation-perfusion MISMatch

Question 62

Gas composition in a normal alveolus

Answer 62

Alveolar gas composition is steady at: PAO2= 13.3 kPa PACO2= 5.3 kPa Alveolar gas composition is steady because amount of O2 (ml/min) brought in by ventilation= amount of O2 (ml/min) diffusing into the blood and amount of CO2 removed by ventilation = amount of CO2 diffusing from blood into the alveolus There is equilibrium between the partial pressures of gas in the air and gas in the liquid (blood) slide 7 lec 4

Question 63

Consequences of Inadequate Ventilation of an alveolar unit

Answer 63

Inadequate ventilation for perfusion (V/Q <1) – PACO2 rises – PAO2 falls, – A new steady state established – diffusion continue at this new level – Blood equilibrates to the new alveolar PAO2 &PACO2

Question 64

V/Q mismatch with V/Q ratio <1

Answer 64

Some causes: – Asthma (airway narrowing – not uniform throughout lungs – COPD early stages – not uniform throughout lungs – Pneumonia -acute inflammatory exudate in affected alveoli – RDS in newborn -some alveoli not expanded and not uniform – Pulmonary oedema -fluid in alveoli - not uniform throughout lungs V/Q mismatch is the commonest mechanism causing hypoxia.

Question 65

What will be the PO2 in the mixed blood? Will it be normal? Lower than normal? Or higher than normal? By how much? slide 10 lec 4

Answer 65

•Need to consider more than just the PO2 values. •Determined by interaction of O2 with Hb as well. •Need to consider the Oxy-Hb dissociation curve . •So let’s review Oxy-Hb dissociation curve If a gas reacts with a substance within a liquid e.g. O2 binding to haemoglobin (Hb) -in addition to dissolving then this reaction must complete before equilibrium is reached and partial pressure is established – the oxygen binding to Hb does NOT contribute to pO2 in the blood • O2 enters plasma & dissolves in plasma, • dissolved O2 enters RBC to bindto Hb • Process continues till Hb fully saturated (each Hb molecules binds 4 O2 molecules) • After Hb is fully saturated, O2 continues to dissolve till equilibrium is reached • Total CONTENT O2 = Σ(sum) of dissolved and Hb bound oxygen • Necessary to have carrier because O2 not highly soluble BUT-once carrier is fully saturated –CAN’T carry any more no matter how much O2 is present! Corresponding O2 content in blood (in ml/L) –NB- most O2 content in blood associated with Hb Graph demonstrates how changes in the partial pressure of oxygen (PO2) influence oxygen (O2) binding to, and dissociation from, haemoglobin (Hb). PO2 on X axis represents value of PO2 in the alveoli of the lungs under resting conditions (resting respiratory rates) (red arrow) – converting to kPa 100 mmHg= 13.3 kPa NB:To convert mm Hg to kPa Multiple mmHg by 0.133322 As pO2 increases from 10.6 kPa (80 mmHg) to 13.3 kPa9 (100 mmHg) haemoglobin saturation markedly increases by greater than 20%

Question 66

Graph showing relationship between PCO2 and total CO2 content in blood

Answer 66

Ø Relatively straight line in the physiological range pCO2 i.e. there is a linear relationship between pCO2 and blood total content CO2 @ 4-6kPa Ø This is because CO2 Is highly soluble in blood Ø Unlike O2 it doesn’t require a carrier molecule – remember O2 carrier molecule is Hb Ø This explains why CO2 in blood is directly proportional to alveolar minute ventilation while O2 is NOT – after a certain point can’t load more haemoglobin with O2 no matter how high pO2

Question 67

What is the PO2 and PCO2 in the mixed blood –blood from poorly ventilated but still perfused lung combined with blood from well ventilated and perfused lung ? (Assume equal volumes of blood returning from the affected and unaffected areas)

Answer 67

slide 16 lec 4 17 too

Question 68

What is the effect of hyperventilation?

Answer 68

slide 18 lec 4 19 too