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  • 1. The Respiratory System at a Glance
  • 2. The Respiratory System at a Glance Jeremy P.T. Ward Jane Ward Richard M. Leach With contributions from Charles M. Wiener Third edition A John Wiley & Sons, Ltd., Publication
  • 3. Library of Congress Cataloging-in-Publication Data
  • 4. Contents Structure and function History, examination and investigation Diseases and treatment Cases and self assessment Contents 5
  • 5. Preface to third edition The Respiratory System at a Glance At a Glance 6 Preface to third edition
  • 6. Units and symbols Units Pressure conversion: = · − = = = = = = = = ≈ = = = Contents − · − · − = · − = · − = = Standard symbols Primary symbols = = = P = = = = Q = Secondary symbols Gas = Blood = = = = = = = = = = = Tertiary symbols Examples = = = PAco = = Typical values Po Po Po Po Po < < > · − · − Pco Pco Pco · − · − + · − Po · − · − Pco · − · − − Units and symbols 7
  • 9. r1 Structure of the respiratory system: lungs, airways and dead space (a) Lung lobes Right lateral aspect Anterior aspect Left lateral aspect RU RM RL LU LL = Right upper = Right middle = Right lower = Left upper = Left lower Posterior aspect (c) Bohr equation for measuring dead space Anatomical dead space, Volume = VD Respiratory zone: Alveolar CO2 fraction = FACO2 End of inspiration End of expiration End-tidal = alveolar gas Anatomical dead space, Volume = VD In an expired breath none of the CO2 expired came from the dead space region ∴ Quantity of CO2 in mixed expired air = quantity of CO2 from alveolar region VT x = (VT –VD) x ∴ VD = VT ( – )/ Mixed expired gas: Volume = VT ; Mixed expired CO2 fraction = CO2-free gas CO2-containing gas RU RM RL LU LL RU RM RL LU LL LU LL RL RU T1 T12 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 C7 C6 (b) The airways Sternal angle (angle of Louis) Sternum Xiphoid process Diaphragm Nasal cavity Pharynx Epiglottis Larynx Cricoid Trachea (generation 0) Carina R and L main bronchi (generation 1) Bronchi (generations 2–11) Bronchioles (generations 12–16) Respiratory bronchioles (generations 17–19) Alveolar ducts and sacs (generations 20–23) Body Manubrium FECO2 FECO2 FECO2 FACO2 FACO2FACO2 10 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 10. Lungs lungs thoracic cage right lung transverse oblique fissures left lung oblique fissure hilum bronchopulmonary seg- ments pulmonary nerve plexus vagi ganglia sympathetic trunk β visceral pleura parietal pleura costodi- aphragmatic recess intercostal nerves phrenic nerve pleurisy Lymph channels bronchopulmonary nodes tracheobronchial nodes posterior mediastinal nodes upper respiratory tract lower respiratory tract cricoid cartilage right left main bronchi sternal angle Airways generation trachea main bronchi segmental bronchi Bronchioles terminal bronchioles respiratory bronchioles alveolar ducts alveolar sacs alveoli bronchial arteries pulmonary circulation ciliated columnar epithelial cells Goblet cells submucosal glands mucus mucociliary clearance type I alveolar pneumocytes squamous epithelium alveolar–capillary membrane type II pneumocytes surfactant Dead space conducting airways anatomical dead space pulmonary embolus alveolar dead space physiological dead space tidal volume respiratory frequency minute ventilation = × Alveolar ventilation = − × Bohr method ∼ ∼ Alveolar gas end-tidal gas Pco ideal alveoli Structure of the respiratory system: lungs, airways and dead space Structure and function 11
  • 11. r2 The thoracic cage and respiratory muscles c 1 2 3 4 5 6 7 8 9 10 (a) The sternum and ribs and their relationship to the lungs and pleural cavities Pleural Horizontal fissure Oblique fissure Costodiaphragmati recess Cardiac notch Oblique fissure Xiphoid process Body Manubrium Clavicle (b) Inferior aspect of a rib Sternum Articular facets of the head Head Neck Tubercle Articular facet of the tubercle Angle Costal groove Shaft Costal cartilage joins here (c) An intercostal space Intercostal: Vein Artery Nerve Innermost intercostal muscle To avoid the neurovascular bundle, needles being passed through the intercostal space (for example to drain a pleural effusion) should pass close to the top of the rib (d) Inferior aspect of the diaphragm Sternal part Xiphisternum Costal part Right phrenic nerve Inferior vena cava 12th rib Right crus Left crus Psoas major Quadratus lumborum Lateral arcuate ligament Medial arcuate ligament Median arcuate ligament Aorta Oesophagus Vagi Left phrenic nerve Central tendon of diaphragm External intercostal muscle Internal intercostal muscle Costal part L1 L2 L3 L4 T1 Lung lobes 12 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 12. Thoracic cage thoracic cage sternum ribs intercostal spaces thoracic vertebral column diaphragm The sternum sternum manubrium body of the sternum manubriosternal joint sternal angle (angle of Louis) xiphoid process The ribs and intercostal space true vertebrosternal vertebrochondral floating vertebral ribs head facets tubercle angle of the rib external intercostal muscles internal intercostal muscles innermost intercostal layer intercostal nerves thoracic nerves Intercostal veins arteries nerves The diaphragm diaphragm central tendon right crus left crus median arcuate ligament medial lateral arcuate ligaments psoas major quadratus lumborum phrenic nerves (C3, 4, 5) Muscles of respiration diaphragm intercostal muscles scalene muscles pump action bucket-handle action paradoxical breathing abdominal breathing thoracic breathing accessory inspiratory muscles scalene mus- cles sternomastoids serratus anterior pectoralis major abdominal muscles (rectus abdominis external internal oblique) The thoracic cage and respiratory muscles Structure and function 13
  • 13. r3 Pressures and volumes during normal breathing Total lung capacity (TLC) Functional residual capacity (FRC) Residual volume (RV) 7300 mL mL mL3500 1 800 mL Open thorax: Pressure gradient distending the lung (transmural = alveolar – intrapleural) Pressure gradient driving air along airways (mouth – alveolar) Intrapleural Alveolar pressure Mouth –0.5 0.5 –0.1 0 0 0.1 –0.75 –0.5 0 0.5 Volume above FRC (L) Intrapleural pressure relative to atmospheric (kPa) Alveolar pressure (kPa) Airflow (L/sec) Inspiration Expiration Inspiration Expiration (b) (a) Functional residual capacity (c) (d) (e) Air Air Outward recoil of chest wall Inward recoil of lungs ‘Negative’ intrapleural pressure Chest wall expands ‘Zero’ pressure Lungs collapse Intrapleural pressure, –0.5 kPa Alveolar pressure, 0 kPa Heart Oesophageal pressure, –0.5 kPa Table 1 Tidal volume (VT) (at rest) Vital capacity (VC) Inspiratory reserve volume (IRV) Expiratory reserve volume (ERV) 500 mL 5500 mL 3300 mL 1700 mL Inspiratory capacity (IC) 3800 VT VC IRV IC ERV TLC FRC 0 RV (i) (ii) (i) (ii) 14 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 14. Functional residual capacity functional residual capacity (FRC) intrapleural space outward recoil inward recoil barrel chest Intrapleural pressure visceral pleura parietal pleura intrapleural pressure oesophageal pressure − − − − Pressures, flow and volume during a normal breathing cycle alveolar pressure + + Lung volumes simple water-filled spirome- ter tidal volume rest- ing tidal volumes inspiratory reserve volume (IRV) expiratory reserve volume (ERV) vital capacity (VC = VT + IRV + ERV) residual volume total lung capacity helium dilution body plethysmography nomograms Pressures and volumes during normal breathing Structure and function 15
  • 15. r4 Gas laws (a) Altitude, barometric pressure, O2 fraction and PO2 Mt Everest summit 8850 m (29035 ft) Sea level 0m (0ft) 5486 m (18 000 ft) PB = 250 mmHg (33.3 kPa) 1⁄3 sea level value FO2 dry air = 0.209 (20.9% O2) ∴ PO2 dry air = 0.209 x 250 = 52 mmHg (7 kPa) PB = 380 mmHg (50.6 kPa) 1⁄2 sea level value FO2 dry air = 0.209 (20.9% O2) PO2 dry air = 0.209 x 380 = 79 mmHg (10.6 kPa) PB = 760 mmHg (101.3 kPa) FO2 dry air = 0.209 (20.9% O2) PO2 dry air = 0.209 x 760 = 159 mmHg (21 kPa) Barometric pressure with increasing altitude 800 700 600 500 400 300 200 100 0 0 10000 10 000 12000 13000 14 000 16000 18000 20000 30000 40000 50 000 60 000 20000 4000 6000 8000 Altitude (metres) Altitude (feet) Barometricpressure(PB ,mmHG) Sea level (0m, 0ft) Mexico City (2240 m, 7349 ft) Lhasa, Tibet (3600 m, 11810 ft) La Rinconda, Peru* (5100 m, 16 732 ft) Mt Everest summit (8850 m, 29 035 ft) Cruising altitude typical passenger jet (11 278 m, 37 000 ft) *Highest permanently inhabited town PB = barometric pressure; FO2 = O2 fraction (b) Correction factors for gas volumes Volume (BTPS) = volume (ATPS) Volume (STPD) = volume (ATPS) 273 + 37 273 + tO C PB – PH2O PB – 6.3* *47 if PB and PH2O are in mmHg *760 if PB and PH2O are in mmHg (c) Partial pressure of a gas in a liquid Gas phase (Pg) Liquid phase liquid X (PXg) Gas phase (Pg) Liquid phase liquid Y (PYg) P1 Liquid X containing dissolved gas, g, is exposed to a gas phase containing g at three different partial pressures, P1, P2, P3. Only when the Pg = P2 does the number of gas molecules leaving the liquid per minute ( ) equal the number entering the liquid ( ) – i.e. the liquid and gas phases are in equilibrium. ∴ Partial pressure of gas, g, in liquid X (PXg) =P2 Liquid Y also contains gas, g, and is also in equilibrium with the gas phase when Pg = P2 ∴ Partial pressure of gas, g, in liquid Y (PYg) =P2 However, the solubility of gas, g, in liquid Y is less than in liquid X, so at the same partial pressure, liquid Y contains a lower concentration of g. 273 273 + tO C PB – PH2O 101* 2 P3 P1 2 P3 Note: In the bottom left flask, gas moves against its concentration gradient. P P PB=760mmHg 101.3kPa PB=380mmHg 50.6kPa PB=250mmHg 33.3kPa 16 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 16. Fractional concentration and partial pressure of gases in a gas mixture Dalton’s law ∼= = F ≈ P = F × P = . × = . altitude Water vapour pressure saturated water vapour pressure ◦ ◦ relative humidity × ◦ Fo Fn ◦ Pb − Pb − partial pressure of moist inspired oxygen PIO2 = . × P − ◦ Pio = × Po Pio ◦ Pio Pio The effect of pressure and temperature on gas volumes Boyle’s law ∝ = + ◦ Charles’ law ∝ ambient temperature and pressure satu- rated with water (ATPS) body temperature and pressure saturated with water (BTPS) standard temperature and pressure dry (STPD) ◦ Ph o = ≈ Gases dissolved in liquids Henry’s law = × partial pressure of a gas in a liquid gas tension Note on time derivative symbols Gas laws Structure and function 17
  • 17. r5 Diffusion (a) The alveolar–capillary membrane (c) Diffusion through a sheet of tissue (d) The diffusion path through the alveolar–capillary membrane Alveolar epithelium O2 Alveolus Red blood cells Capillary (e) The oxygen cascade: oxygen tension from ambient air to mitochondria mmHg PO2 200 150 100 50 0 25 20 15 10 5 0 kPa Ambient,sea level Trachea (moistureadded) Alveolar(O 2takenup,CO 2added) Pulmonarycapillary(equilibrateswithalveolar) Arterial(R toLshunt,e.g.bronchialcirculation) M eantissuecapillary(veryvariable) M itochondria tissuecells(veryvariable) Restingmixed venousblood (venousvarieswithtissue) (b) Transfer of gases across alveolar–capillary membrane Alveolar Capillarypartial pressure 0 0 0 .25 0.5 0.75 Time along pulmonary capillary (second) CO O2 N2O Mixed venous blood T = thickness P1 A = area P2 Interstitial fluid Endothelium O2 O2 O2 O2 Red blood cells Pore of Kohn (gap between alveoli) Endothelium Alveolar epithelium Collagen and elastin fibres Alveolus AlveolusAlveolus Plasma pressure of N20, 02 or CO 18 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 18. bulk flow diffusion The alveolar–capillary membrane alveolar epithelium pulmonary capillaries elastin collagen fibres alveolar epithelium capillary endothelium alveolar–capillary membrane < μ Type I pneumocytes type II pneumocytes Diffusion and perfusion limitation Pn o Pn o perfusion-limited Pco diffusion-limited Factors affecting diffusion across a membrane (Fick and Graham’s laws) ∝ P − P = √ P P diffusing capacity D , = D P − PC , D o = o P o − P o D o Po P o D o D co Pco D co = co P co D co Pco D co Kco D o D co T o T co Factors affecting DLco (TLco) D co D co Kco D co D co D co D co P co The oxygen cascade Po Po Po Po Po Diffusion Structure and function 19
  • 19. r6 Lung mechanics: elastic forces (a) Static pressure–volume loop Volume%TLC 100 50 0 FRC RV ΔP ΔV CL = slope ΔV/ΔP 0 1 2 10 20 cmH2O kPa Transmural pressure (= – intrapleural pressure since measurements taken at zero airflow) RV TLC = Residual volume = Total lung capacity FRC CL = Functional residual capacity = Lung compliance (c) Surface tension Laplace’s equation T= Surface tension Pressure above ambient = P 1 P2 P1 > P2 ∴ When tap is opened the small bubble empties into the large (d) Effect of surface area R1 Water molecule Surfactant molecule R2 R2 < R1 but T2 < T1 because surface concentration of surfactant is higher when the alveolus is small The fall in R is more than offset by the fall in T, ∴ since P = 2T , P does not rise, but falls as the alveolus shrinks P= 2T R (b) Dynamic pressure–volume loop If intrapleural pressure and volume are recorded continuously (lower panel), a pressure–volume loop (upper panel) can be constructed from pairs of simultaneous measurements of volume, e.g. (b) with pressure (b'). Alternatively the pressure and volume signals can be fed into an X-Y plotter. Volume above FRC (litre) Intrapleural pressure relative to atmospheric 0.5 0 –0.5 –1.0 Inspiration Expiration Inspiration Expiration VolumeaboveFRC(litres) 0.5 0.4 0.3 0.2 0.1 0 –0.5 –0.6 –0.7 –0.8 –0.9 –1.0 Intrapleural pressure relative to atmospheric (kPa) a,a' b,b' c,c' d,d' e,e' f,f' g,g' h,h' i,i' j,j' a b c d e f g h i j a’ b’ c’ d’ e’ f’ g’ h’ i’ j’ R R P 20 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 20. airway resistance elastic resistance Assessing the stiffness of the lungs: lung compliance = static pressure–volume (P–V) curve hysteresis Static lung compliance restrictive disease elastic recoil emphysema TLC FRC FEV FVC Dynamic pressure–volume loops and dynamic compliance dynamic pressure–volume loop dynamic compliance static compliance The air–fluid interface lining the alveoli surface tension = law of Laplace = 1 2 atelectasis surfactant Surfactant phospholipids type II pneumocytes alveolar lining fluid hydrophilic hydrophobic alveolar interdependence neonatal respiratory distress syndrome (NRDS) Lung mechanics: elastic forces Structure and function 21
  • 21. r7 Lung mechanics: airway resistance (a) Laminar and turbulent flow Laminar flow Turbulent flow (b) Main factors influencing bronchomotor tone (d) Dynamic compression of airways = Flow–volume curve for maximum effort from partly filled lungs A = Peak expiratory flow rate with lungs filled to total lung capacity B = Peak expiratory flow rate for partly filled lungs filled (RV + 3 L) TLC = Total lung capacity, RV = Residual volume Normal curve Obstructive airway disease of smaller airways. Note: • concave appearance of forced expiratory curve • forced inspiratory flow affected less than forced expiratory flow Upper airway obstruction (e.g. tracheal stenosis). Note: • flat topped flow–volume curve • forced inspiratory flow affected as much as expiratory flow Restrictive lung disease. Low peak flow rates are related to low volume. (Note: this figure is drawn to show the relationship between these traces by using absolute lung volume which cannot actually be obtained from a flow–volume loop alone). (c) The effect of effort on inspiratory and expiratory airflow Effort dependent 600 300 0 300 600 Airflow(L/min) ExpirationInspiration TLC RV Volume (L) Effort independent A B (e) Maximum flow–volume loops 6 4 2 0 Lung volume (L) 6 5 4 3 2 1 1 2 3 4 5 6 600 300 0 300 600 Airflow(L/min) ExpirationInspiration Beginning of inspiration Alveolus Intrathoracic airway Intrapleural space –0.5 0 8.7 8 6 4 0 +8.0 Numbers are pressures in kPa (1 kPa = 7.5 mmHg) 0 0 During forced expiration Airway smooth muscle Synapse Vagal efferents Pulmonary stretch receptors (inhibit) Vagal afferents Brainstem (Chapter 12) Airway irritant receptors (activate) NANC nerves (excitatory) Mast cells, eosinophil (Chapter 23) Histamine, Prostagladins Leukotrienes etc β2-Receptor β-Adrenergic agonists (e.g. adrenaline and saltbutamol) NANC nerves (inhibitory) NO and VIP CO2 ACh via M3 receptors BronchodilationBronchoconstriction SP and neurokinins = Receptor = Nerve ending Nitric oxide Vasoactive intestinal peptide Substance P NO = VIP = SP = ACh = M3 = Acetylcholine Muscarinic type 3 receptor 22 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 22. = = − = laminar flow η l Poiseuille’s equation = = π η ∴ = η π silent zone turbulent ∝ √ Factors affecting airway resistance Bronchial smooth muscle and epithelium parasympathetic bron- choconstrictor β epinephrine Transmural (airway–intrapleural) pressure gradient = = effort-dependent effort-independent Peak expiratory flow rate dynamic compression of airways RAW in disease forced expiratory volume in 1 second forced vital capacity forced expiratory ratio = obstructive pulmonary disease air trap- ping Expiratory wheezes (rhonchi) Lung mechanics: airway resistance Structure and function 23
  • 23. r8 Carriage of oxygen (a) Haemoglobin structure Haemoglobin is composed of four subunits, each containing a protein chain (globin) and a haem group. Normal adult haemoglobin, HbA, contains two identical α-chains composed of 141 amino acids and two β-chains composed of 146 amino acids. The haem group ( ) is attached to each chain at a histidine residue, and each has an iron atom in the ferrous form, which binds to an oxygen molecule. The haem groups lie in crevices in the crumpled ball of globin chains. The exact 3D (or quaternary) structure of haemoglobin can change and alter the accessibility of the oxygen-binding site. Each molecule of haemoglobin can bind up to four molecules of oxygen in a series of reactions which can be summarized as: Hb4 + 4O2 Hb4(O2)4 (b) The oxygen–haemoglobin dissociation curve, haemoglobin concentration (150g/L) 100 75 50 25 0 200 150 100 50 0 10 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 kPa PO2 50 100 150mmHg a v pH, PCO2, temperature 2,3-DPG pH, PCO2, temperature 2,3-DPG Dissolved oxygen O2 αβ O2 O2 O2 0 Oxygencontent(mL/L) Oxygensaturation(%) a PO2 = Normal arterial blood = 13.3 kPa (100mmHg) v PO2 = Resting mixed venous = 5.3 kPa (40mmHg) = 150 mL/L = 75% (c) Anaemia and carbon monoxide poisoning 200 150 100 50 0 0 2 4 6 8 10 12 14 16 kPa PO2 0 20 40 60 80 100 mmHg120 Oxygencontent(mL/L) Tissues remove 50mL/L C B A Hb = 150g/L Hb = 75g/L Hb = 150g/L COHb = 50%Tissues remove 50mL/L = 200 mL/L = 97% O2 content O2 saturation Note: For simplicity the Bohr shift is ignored O2 content O2 saturation 24 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 24. Po Po solubility Po haemoglobin oxygen capacity Po oxygen saturation / / × cooperative binding oxygen–haemoglobin dissocia- tion curve Po Po Po < Po Po Pco Bohr effect Pco Po P = Pco = = ◦ P = P 2,3-di(or bi)phosphoglycerate P Anaemia and carbon monoxide poisoning anaemia Po = Po Po = = Po Po carboxyhaemoglobin ∼ cyanosis Other respiratory pigments Fetal haemoglobin, HbF adult haemoglobin, HbA γ β double Bohr shift Pco Po Myoglobin Po Carriage of oxygen Structure and function 25
  • 25. r9 Carriage of carbon dioxide (a) CO2 dissociation curve 550 500 450 CO2content(mL/L) 5.5 6.0 6.6 7.0 40 45 50 55 (mmHg) The red line (A-X) shows what the relationship between blood PCO2 and CO2 content would be if Hb remained 98% saturated. However, as mixed venous blood HB is only 75% saturated, more CO2 can be carried for any given PCO2, as shown by the dashed line A-V (the Haldane effect, see box and text). (kPa) (c) How CO2 is carried in arterial and venous blood 480mLCO2/L 520mLCO2/L The basis of the Haldane effect When haemoglobin is fully oxygenated, each of the four Hb subunits is bound to one O2: Hb4(O2)4 As O2 is released, i.e. the ability of each reduced (deoxygenated) Hb subunit (H•Hb) to buffer H+ and form Hb•COOH (carbaminohaemoglobin) is greatly increased This enhances carriage of CO2 by blood by: (a) buffering red cell acidity and therefore facilitating formation of HCO3 – (b) formation of Hb•COOH When blood is reoxygenated in the lungs, the reverse occurs, facilitating removal of CO2 in the breath (b) CO2 uptake and O2 delivery in the tissues – role of red cells CA = carbonic anhydrase Hb = haemoglobin subunit H•Hb = reduced haemoglobin O2 Red cell CA H2O H2O Chloride shift Carbamino formation Hb4(O2)4 Hb4(O2)3 Hb4(O2)2 Hb4(O2) Normal mixed venous Normal arterial 75% O2 saturation 98% O2 saturation Haldane effect Arterial Mixed venous 5% 87% 8% Dissolved 10% HCO3 – Carbamino 30% 60%A V X CO2 + H2O H2CO3 HCO3 – + H+ CO2 + H•Hb Hb4(O2)4 Hb4(O2)3 Hb•COOH Cl– Cl– HCO3 – CO2 26 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 26. CO dissociation curve Bicarbonate − + ⇔ ⇔ + + − carbonic anhydrase + + chloride shift + + haemoglobin acts as a buffer + + Haldane effect Pco + + · ⇔ · + Carbamino compounds + · ⇔ · · CO2 in solution ∼ Hypoventilation and hyperventilation P co Vco V P co ∝ Vco V P co P co Pco P co P co Po difference Hypoventilation hyperventilation P co hypoventilating P co hyperventilating P co − Po Hypoventilation hypercapnia P co hypoxia P o P co hypocapnia Respiratory gas exchange ratio ≈ Carriage of carbon dioxide Structure and function 27
  • 27. r10 Control of acid–base balance CO2 + H2O H2CO3 HCO3 + H+ [HCO3] x [H+] [H2CO3] K = [HCO3] [H2CO3] log K = log [H+] + log [HCO3] [H2CO3] –log [H+] = –log K + log [HCO3] [H2CO3] pH = pK + log [HCO3] PCO2 x s pH = 6.1 + log But: [H2CO3] [CO2] (pKA = 6.1) and: [CO2] = PCO2 x s (solubility) K = dissociation constant; KA = corrected for [CO2] instead of [H2CO3] Solubility (s) = 0.23 mmol / L / kPa 0.03 mmol / L / mmHg Relationship between PCO2, HCO3 and pH, and the Henderson–Hasselbalch equation (from law of mass action) (a) Plasma[HCO3](mmol/L) 40 30 20 10 7.1 7.2 7.3 7.4 7.5 7.6 7.7 pH PCO2 60 mmHg (7.8 kPa) PCO2 40 mmHg (5.3 kPa) PCO2 20 mmHg (2.6 kPa) (b) Davenport diagram [H+ ] (nmol/L) pH 120 100 80 60 40 20 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 0 0 2 4 6 8 10 10 20 30 40 50 60 70 80 PaCO2 (mmHg) PaCO2 (kPa) (d) Flenley acid–base nomogram Metabolic acidosis Normal range Polycythaemia ( red cells) Plasma buffer line C B A Plasma[HCO3](mmol/L) 40 30 20 10 7.1 7.2 7.3 7.5 7.6 7.7 pH PCO2 60 mmHg (7.8 kPa) PCO2 20 mmHg (2.6 kPa) (c) Compensation and base excess C B A Base excess D F E G Renal compensation Metabolic alkalosis Respiratory compensation Respiratoryalkalosis Renal compensationMetabolic acidosi s Respiratoryacidosis Acute respiratory acidosis Chronic respiratory acidosisMetabolic alkalosis Respiratory alkalosis Whole blood buffer line PCO2 40 mmHg (5.3 kPa) 7.4 24 28 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 28. + = acid–base status Buffers + buffer curve bicarbonate − haemoglobin − + Pco − Henderson–Hasselbalch equation Pco × − Pco − ∝ − P Pco − Haemoglobin blood proteins Acidosis, alkalosis and compensation − Pco Davenport diagram − Pco buffer line Pco − − Pco Pco acute respiratory failure − Pco respiratory acido- sis respiratory alkalosis chronic respiratory failure compensated + − − Pco renal compensation − metabolic acidosis alkalosis − + metabolic acidosis Pco respiratory compensation metabolic alkalosis Base excess Pco − Pco Po Base excess base deficit calculated Pco Pco − − Pco Pco in vitro Flenley nomogram Pco Common causes of acid–base disorders Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis − + Control of acid–base balance Structure and function 29
  • 29. r11 Control of breathing I: chemical mechanisms (d) Central chemoreceptors Pons Medulla oblongata V VII VIII IX X XI Cranial nerves Central chemoreceptors (f) Peripheral chemoreceptors Vagus nerve Aorta Carotid sinus nerve Bifurcation Carotid sinus Common carotid artery Glosso- pharyngeal nerve Heart Groups of cells surrounded by fenestrated sinusoidal capillaries Sheath (type II) cells Glomus (type I) cells Dense granules containing neurotransmitters Carotid sinus nerve fibres Glial cells Capillary Neurone Blood–brain barrier Chemoreceptor Blood HCO3 H+ CO2 O2 H+ , HCO3 CO2 + H2O H2CO3 H+ + HCO3 – [H+ ] at chemoreceptor PCO2 / [HCO3 – ] PCO2 from blood, and [HCO3 – ] from CSF CSF CSF Carbonic anhydrase (a) (b) (c) (e) (g) Ventilation(L/min) 60 50 40 30 20 10 0 4 5 6 7 8 9 Alveolar PCO2 (kPa) Effect of CO2, pH and O2 on ventilation: Metabolic acidosis Metabolic alkalosis Normal pH Low PO2 ~5 kPa High PO2 ~60 kPa Normal PCO2 5 kPa High PCO2 6 kPa PO2 (kPa) Ventilation(L/min) 60 50 40 30 20 10 0 4 5 6 7 8 9 Alveolar PCO2 (kPa) Ventilation(L/min) 60 50 40 30 20 10 0 4 8 12 16 Normal PO2 ~13 kPa Carotid body (not part of sinus) Aortic bodies 30 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 30. Chemical control of ventilation central periph- eral chemoreceptors Pco Po brainstem Pco Pco Po Ventilatory response to changes in PAco2 and PAo2 Pco P co P co P co ∼ P co P co metabolic acidosis + − metabolic alkalosis + Pco respira- tory acidosis P o ∼ P o P co P co P co P o ∼ P o P co synergistic P o P co The central chemoreceptor central chemoreceptor not Po blood–brain barrier + − Pco − Pco Pco ∼ The peripheral chemoreceptors peripheral chemoreceptors carotid aortic bodies ∼ glomus sheath Pco + Po not Pco Po Pco Po + + Adaptation: chronic respiratory disease and altitude Pco − Pco P co Po hypoxic drive Po P o Po hypocapnia − Pco acclimatization to altitude Control of breathing I: chemical mechanisms Structure and function 31
  • 31. r12 Control of breathing II: neural mechanisms (a) Pneumotaxic centre (b) Dorsal respiratory group Hypothalamus Emotion Temperature Cortex (g) Voluntary control of breathing via pyramidal tracts Spinal cord Respiratory muscles Lungvolumeandmuscleload Damage,inhaledirritants (c) Ventral respiratory group Medulla Pons (f) Input from central and peripheral chemoreeceptors (e) Lung receptors Stretch Proprioceptors Irritant Juxtapulmonary (d) Descending respiratory motor neurones to diaphragm, intercostals and ancilliary respiratory muscles Cut here Gasping Cut here No effect on breathing but loss of higher control Cut here Abolition of breathing – apnoea Nucleus parabrachialis Kölliker-Fuse nucleus Bötzinger complex Nucleus ambiguus and retro ambiguus Nucleus tractus solitarius 32 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 32. central pattern generator sensors chemoreceptors mechanoreceptors Brainstem and central pattern generator central pattern generator pons medulla inspira- tory expiratory Reciprocal inhibition The medulla dor- sal respiratory group nucleus tractus solitarii nucleus ambiguus caudal rostral ventral respiratory groups pre-B¨otzinger B¨otzinger gasping pneumotaxic centre nucleus parabrachialis K¨olliker–Fuse nucleus pons apneusis apneustic centre pyramidal tracts Ondine’s curse origin of the respiratory rhythm switching concept Lung receptors and reflexes Stretch receptors slowly adapting Hering–Breuer inspiratory reflex deflation reflex > Juxtapulmonary or ‘J’ receptors apnoea Irritant receptors Proprioceptors (position/length sensors) Other receptors that may modulate respiration: Pain receptors trigeminal region larynx Arterial baroreceptors Control of breathing II: neural mechanisms Structure and function 33
  • 33. r13 Pulmonary circulation and anatomical right-to-left shunts (a) Pulmonary and systemic circulation and normal anatomical right-to-left shunts Pulmonary capillary pressure: Arterial end 14 mmHg Venous end 8 mmHg Bronchial artery Pulmonary artery pressure: 24/9, mean 15 mmHg VCM Aortic pressure: 120/70, mean 90 mmHg VCM = venae cordis minimae (thebesian veins) Alveoli Venous end 10 mmHg Arterial end 30 mmHg Systemic capillary pressure: Aorta Tissue LARA RV LV The PO2 and PCO2 that result from these O2 and CO2 contents can be found from the O2 and CO2 dissociation curves: 700 600 500 400 300 200 100 0 –1 31 75 119 13 15 PO2/PCO2 (kPa) O2 and CO2 dissociation curves O2 CO2 Normal O2 and CO2 pressures and contents (b) The initial effects of a 20% right-to-left shunt on arterial O2 and C02 contents and partial pressures Arterial O2 content = Arterial CO2 content = + x + x O2andCO2content(mL/L) 80 100 20 100 x 200 15 = 190mL/L 80 100 20 100 x 480 520 = 488mL/L O2 content CO2 content = 200mL/L = 480mL/L O2 and CO2 pressures and contents following mixing 20% mixed venous blood with 80% blood undergoing normal gas exchange *Note: The mixed venous contents used are normal values. In fact, the abnormal arterial contents would lead to abnormal mixed venous contents so this simple analysis underestimates the effects on arterial contents. *O2 content *CO2 content = 150 mL/L = 520 mL/L 80% 34 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 34. Pulmonary circulation compared with the systemic circulation pulmonary circulation systemic circulation Pulmonary vascular resistance pul- monary artery pressure hypoxic pulmonary vasocon- striction Pco autoregulation Starling forces The Cardiovascular System at a Glance Capillary oncotic pressure ∼ interstitial oncotic pressure interstitial hydrostatic pressure − Pulmonary oedema mitral stenosis left ventricular failure Inspira- tory crepitations Anatomical or true right-to-left shunts bronchial circulation venae cordis minimae (Thebe- sian veins) right-to-left shunts Po Po At- electasis consolidation pneumonia cyanotic congenital heart disease tetralogy of Fallot left-to-right shunts Effect of right-to-left shunts on arterial blood gases Po Pco P o P co P co Po P co P o P co Pulmonary circulation and anatomical right-to-left shunts Structure and function 35
  • 35. r14 Ventilation–perfusion mismatching VA/Q (a) Different types of VA/Q regions PO2 and O2 contents of blood from these regions breathing air and oxygen Normal Dead space Dead-space effect Shunt effect True/anatomical shunt VA Q VA/Q = Normal = Normal = Normal (close to 1) VA Q VA/Q = Normal = 0 = ∞ VA Q VA/Q = Normal = Low = High VA Q VA/Q = Low = Normal = Low VA Q VA/Q = 0 = Normal = 0 PO2 kPa (c) The effect of a mixture of high and low VA/Q regions on arterial blood gases VA/Q = 4 Q = 1 VA/Q = 0.3 Q = 15 Small flow with: High PO2 Normal O2 content Low PCO2 Low CO2 content Large flow with: Low PO2 Low O2 content High PCO2 High CO2 content Combined to give: Low O2 content High CO2 content Low PO2 Slightly high PCO2 Peripheral and central chemoreceptors Ventilation Final picture: Low O2 content Normal or low CO2 content Low PO2 Normal or low PCO2 3 2 1 0 Alveoli at start and end of breath Blood vessels at different heights (d) Alveolar air equation This predicts the PO2 in the functioning or ‘ideal’ alveoli PAO2 ~ PΙO2 – PaCO2 R = 0 10 20 02 content (mL/L) 200 0 0 10 20 02 content (mL/L) 200 0 0 10 20 02 content (mL/L) 200 0 0 10 20 02 content (mL/L) 200 0 PO2 kPa PO2 kPa PO2 kPa O2 content of blood draining the region breathing air ( ) and breathing O2-enriched air ( ): Normal Unchanged No blood draining this region Low Increased Low Unchanged Normal Unchanged (b) Variation of ventilation, VA, perfusion, Q and ventilation–perfusion ratio, VA/Q withvertical height in the upright lung VA Q R = The respiratory gas exchange ratio = (R is usually about 0.8) PΙO2 = Inspired O2 partial pressure PaCO2 = Arterial CO2 partial pressure (≈ alveolar) CO2 production O2 consumption VA = 4 VA = 5 Ventilation,VA,perfusion,Q(arbitraryunitsper unitlungvolume)andventilation–perfusionratio,VA/Q Base Apex 36 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 36. = = ∞ dead-space effect Po Pco shunt effect venous admixture Po Pco Po Effect of the upright posture on perfusion, ventilation and VA/Q P o Ventilation–perfusion matching in disease Hypoxic vasoconstriction Effect of ventilation–perfusion mismatching on arterial blood gases Po Po < P o P o P co P co P o P o P co oxygen-enriched air Po Assessment of ventilation–perfusion mismatching Po Po alveolar air equation A–a Po gradient = Po = Po < Ventilation–perfusion mismatching Structure and function 37
  • 37. r15 Exercise, altitude and diving PvCO2 Table 1 Typical values in a healthy but sedentary 20-year-old man at rest and in max. exercise Rest Maximal exercise Heart rate (bpm) 70 200 Stroke volume (mL) 75 90 Cardiac output (mL/min) 5 250 18 000 Arterial–mixed venous O2 content* (mL/mL) 0.048 0.167 O2 consumption (mL/min) 250 3 000 Ventilation (mL/min) 7 500 140 000 Respiratory frequency (breaths/min) 15 56 Tidal volume (mL) 500 2 500 (*= O2 extraction) mmHg Rest Oxygen consumption Anaerobic threshold kPa pHa PO2/PCO2 20 7.2 7.4 0 0 1 2 3 4 L/min 0 25 50 75 100 VO2 20 40 60 80 100 120 140 0 20 40 60 80 100 120 140 160 Ventilation (L/min) V . 15 10 5 0 kPa 6 5 0 (a) Typical changes in ventilation V, arterial PO2 (PaO2), arterial PCO2 (PaCO2), arterial pH (pHa), mixed venous PO2 (PvO2) and mixed venous PCO2 (PvCO2) in a fit young man as oxygen consumption is increased from its resting value of 0.25 L/min to his maximum oxygen consumption of 4 L/min. 14 Alveolar ventilation 12 10 Alveolarventilation(L/min) 8 6 4 2 0 0 1000 2000 3000 Altitude (m) 4000 5000 6000 120 A Alveolar PO2 100 80 60 40 20 0 0 1000 2000 3000 Altitude (m) 4000 5000 6000 45 Alveolar PCO2 40 35 AlveolarPCO2 30 25 20 15 10 5 0 0 1000 2000 3000 Altitude (m) 4000 5000 6000 B A B A B (b) Typical alveolar ventilation, PCO2 and PO2, at altitudes between sea level (0 m) and 6000 m for subjects exposed acutely (red solid line) and chronically (blue solid line) following acclimatiza- tion. The dashed line shows the values that would have occurred if alveolar ventilation remained at its sea level value. PaO2 pHa PaCO2 PvO2 4 3 2 1 mmHg kPa 16 12 0 AlveolarPCO2 8 4 mmHg . 38 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 38. Exercise Oxygen delivery × Oxygen extraction oxygen consumption = × Po Pco + maximum oxygen consumption (VO2 max) V Po Pco P o P co anaerobic threshold P co Altitude Po × P − P Po P o P co ∝ P co P co Acute mountain sickness high-altitude pulmonary oedema high-altitude cerebral oedema acclimatization P o P co Erythropoietin 2,3-diphosphoglycerate P co P co chronic mountain sickness (Monge’s disease) Diving diving response SCUBA diving Pn Pn nitrogen narcosis Decompression sick- ness the bends Exercise, altitude and diving Structure and function 39
  • 39. r16 Development of the respiratory system and birth 2 (a) Branching morphogenesis Epithelium Mesoderm Signalling factors Factors released by mesoderm cells cause the epithelium to grow inwards towards them as a bud; inhibitory factors prevent budding either side (b) Week 4 Week 5 Week 6 Week 8 4th pharyngeal pouch Trachea Embryonic oesophagus Bronchial buds Laryngo- tracheal tube Secondary bronchi Mesoderm Endoderm/ epithelium Segmental bronchi + + + + – – RA RV LV LA 1 7 3 4 6 5 (c) Fetal circulation Foramen ovale Fetal liver Pulmonary artery Ascending aorta Portal vein Aorta Inferior vena cava Umbilical vein Umbilical arteries Superior vena cava Ductus arteriosus Ductus venosus Placenta 8 Before birth: Pulmonary vascular resistance > Systemic vascular resistance Ductus arteriosus OPEN Foramen ovale OPEN Ductus venosus OPEN O2 saturation in aorta ~67% PO2 in aorta ~4 kPa, 30 mmHg After birth: Systemic vascular resistance > Pulmonary vascular resistance Ductus arteriosus CLOSED Foramen ovale CLOSED Ductus venosus CLOSED O2 saturation in aorta ~97% PO2 in aorta ~13 kPa, 100 mmHg 40 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 40. embryological origins endoderm splanchnic mesoderm branch- ing morphogenesis 1. Embryonic period laryngotracheal tube bronchial buds 2. Pseudoglandular period segmental bronchopulmonary segment 3. Canalicular period ter- minal sacs type I alveolar pneumocytes alveolocapillary membrane type II alveolar pneumocytes neonatal respiratory distress syndrome 4. Saccular (terminal sac) period 5. Alveolar period Fetal breathing oligohydram- nios Fetal circulation and birth placenta ductus venosus foramen ovale ductus arteriosus P o ∼ At birth surfac- tant Po Development of the respiratory system and birth Structure and function 41
  • 41. r17 Complications of development and congenital disease (a) Relationship between prematurity and development of NRDS %Neonatesdeveloping NRDS 80 60 40 20 0 Birth weight: Gestational age: <1250 <30 <1500 30–34 <1700g 34–37 weeks Other factors such as socioeconomic status, maternal health, race and sex also affect incidence of NRDS (d) Some genetic diseases in which the lung is a primary site of injury Disease Inheritance Lung pathology Alpha1-antitrypsin deficiency Ciliary dyskinesia Cystic fibrosis Familial idiopathic fibrosis Lipoid proteinosis (Urbach–Wiethe syndrome) Tracheobroncho-megaly (Mounier–Kuhn syndrome) Congenital cartilage deficiency (Williams–Campbell syndrome) AD AR AR AR AR AR ? Protease–antiprotease imbalance Impaired mucociliary clearance Abnormal chloride transport Unknown Lipoglycoprotein deposition in upper respiratory tract causing mucosal thickening and airway obstruction Saccular bulges between cartilage rings resulting from atrophy of elastic and smooth muscle tissue and causing impaired mucociliary clearance Deficiency of subsegmental bronchial cartilage with airway collapse Emphysema Airway infection, bronchiectasis Airway infection, bronchiectasis Diffuse fibrosis Hyalinized or granular deposits in the tracheo-bronchial submucosa Recurrent airway infections Recurrent airway infections, bronchiectasis AD = Autosomal dominant, AR = Autosomal recessive (c) Trachea Atresia Fistula Bronchi Oesophagus Oesophageal atresia and tracheo-oesophageal fistula (85%) Tracheo-oesophageal fistula (5%) Trachea Fistula Bronchi Oesophagus Pathogenesis Heart Diaphragm Intestine in thoraxLiver Stomach (b) Congenital diaphragmatic hernia Hypoplastic compressed lung 42 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 42. Problems associated with premature birth Neonatal respiratory distress syndrome corticosteroids exogenous surfactant pulmonary surfac- tant protein B Bronchopulmonary dysplasia ECMO Partial fluid ventilation Congenital diseases Congenital diaphragmatic hernia ∼ eventration of the diaphragm Tracheo-oesophageal fistula oesophageal atresia polyhy- dramnios tracheal atresia/stenosis inherited disorders of haemoglobin synthesis thalassaemia sickle cell disease Congenital influences on respiratory disease Complications of development and congenital disease Structure and function 43
  • 43. r18 Lung defence mechanisms and immunology • Traps particles >5μm in mucus • Mucociliary clearance to mouth • Irritant receptors initiate coughing Larynx, trachea and bronchi Alveolar ducts and alveoli • Squamous epithelium (no cilia) • Alveolar macrophages • Surfactant protein A from type II pneumocytes • Warms/humidifies air • Traps particles >10μm • Irritant receptors initiate sneezing Nasopharynx (a) Physical and physiological defences (b) Ciliated columnar epithelium IgA Invading bacteria Macrophage Cilia Gel phase Mucus Sol phase Epithelial cell Basement membrane LumenEpitheliumLaminapropria Submucosal gland Secretory component Goblet cell (c) Immune response IgA IgG Complement Phagocyte Plasma cells Differentiation proliferation IL-4, IL-3, IFN-γ IL-2 TH lymphocyte TC lymphocyte Infected cell Dentritic cell Antigen B-lymphocyte IgM 44 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 44. Physical and physiological defences μ Mucociliary transport μ humidifying warming Mucus and airway secretions μ gel phase sol phase goblet cells submucosal glands cilia mucociliary transport cilia dyskinesia cystic fibrosis bronchiectasis ntiproteases α -antitrypsin α -antitrypsin deficiency Surfactant protein A opsonizing Lysozyme Secretory immunoglobulin A plasma cells secretory component Lung macrophages mononuclear phagocytes phagocytosis anti-inflammatory cytokines β β Basics of immunity T B lymphocytes BALT CD4+ T lymphocytes antigen- presenting cells dendritic cells cytokines γ γ CD8+ T lym- phocytes γ plasma cells complement Immunology at a Glance Lung defence mechanisms and immunology Structure and function 45
  • 45. r19 History and examination O2 Table 1. Causes of Clubbing Common: Bronchial carcinoma Suppurative lung infection - bronchiectasis - lung abscess - empyema Interstitial fibrosis Uncommon Bacterialendocarditis Cyanotic heart disease Inflammatory bowel disease Malabsorption Atrial myxoma Cirrhosis Familial Idiopathic Pleural mesothelioma Pulse Clubbing Increased curvature Loss of angle Normal Peripheral cyanosis Nicotine staining Coarse flap of CO2 retention Hands Neck JVP Cervical lymph nodes Tracheal position Face Conjunctiva for anaemia Lips + tongue for central cyanosis Features of systemic disease Chest inspection Measure respiratory rate (normal 8–14/min) Look for: • use of accessory muscles - intercostal recession - paradoxical abdominal movement • chest wall shape + hyperinflation • scars (radiotherapy, surgery) • engorged veins (e.g. SVC obstruction) • chest wall movement - symmetrical, reduced Chest palpation Examine • position of trachea + apex beat • symmetry of movement of two sides • amount of chest wall movement • axillary lymph nodes • vocal fremitus Chest percussion Compare the percussion note over comparable areas on both sides of the chest (including apices). Note dullness or hyper-resonance Chest auscultation Examine for: • nature and intensity of breath sounds - i.e. diminished or absent - i.e. vesicular or bronchial • added sounds (crackles, wheeze, rubs) • character + intensity of vocal resonance Sputum pot Look inside bedside sputum pot Disorder Percussion Note Breath AddedChest Wall Movement Sounds Sounds Consolidation Bronchial Coarse crackles Collapse Absent or None bronchial Pleural effusion Diminished* None (±rub) Interstitial Vesicular or Fine inspiratory cracklesfibrosis diminished Pneumothorax Diminished** NoneNormal or hyper-resonant Asthma/COPD Normal Vesicular with Expiratory prolonged expiration wheeze Table 2. Typical physical signs associated with specific respiratory disorders * Bronchial breathing may occur above the effusion; ** an audible click (in time with cardiac systole) may occur on the left side. Check charts for: - Temperature - Peak expiratory flow rate - Saturation (SaO2 ) CHECK SaO 2 GIVE OXYGEN to prevent hypoxaemia On affected side On affected side On both sides On affected side On both sides Normal or ± On affected side Dull Dull Stony dull 46 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 46. History 1 General features: 2 Presenting complaint: 3 History of the presenting complaint: r Chest pain: r Breathlessness: r Cough: r Sputum: r Haemoptysis: Aspergillus 4 Past medical history: 5 Medications: β allergies 6 Family, occupational and social history: Smoking history = Alcohol abuse Occupation Environmental Travel Examination General examination S o r Hands: r Face and neck: Chest examination r Inspection: r Palpation: > r Percussion: r Auscultation: ‘Vesicular’ breath sounds Bronchial breath sounds Crepitations Vocal resonance tactile vocal fremitus History and examination History, examination and investigation 47
  • 47. r20 Pulmonary function tests (a) Volume–time spirograms during forced expiration from total lung capacity Middle 50% FVC FEF25–75 = v/t Normal forced expiratory trace (c) The body plethysmograph for measuring lung volumes Pmouth Shutter Pbox Calibrating syringe The subject inhales against a closed shutter Lung volume expands from V1 to V1 + ΔV ΔV can be deduced from the rise in box pressure, Pbox (calibrated with known volumes) Mouth (= alveolar) pressure falls from P1 to P2 From Boyle’s law: V1 x P1 = P2(V1 + ΔV) Hence the original volume in the lungs, V1, can be found (b) Helium dilution for measuring functional residual capacity* Spirometer filled with volume, V ,1 and helium concentration, [He], C1 Starting at the end of a normal expiration (lung volume = FRC), the subject breathes in and out from the spirometer until equilibrium is reached. Since helium is poorly soluble in blood: V1 x C1 = (V1+ FRC) x C2 *Note: To measure TLC or RV, the subject is asked to breathe in fully or breathe out fully before breathing the helium gas mixture. Volume [He] = FRC = 0% Volume [He] = V1+ FRC = C2 ∴ FRC = V1 x C1 – C2 C2 FEV1 7 6 5 4 3 2 1 0 0 1 2 3 4 65 Time (second) VolumeBTPS(L) 7 6 5 4 3 2 1 0 0 1 32 64 5 Time (second) VolumeBTPS(L) Traces from three subjects of same age, sex and height v t FVC A B C = Normal respiratory system = Obstructive airway disease = Restrictive lung disease = Forced expiratory volume in 1 second = Forced vital capacity = Mean forced expiratory flow from 25–75% of FVC FEV1 FVC FEF25–75 V1, P1, V1 + ΔV, P2 A B C 48 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 48. nomograms Airway resistance body plethysmograph Lung compliance oesophageal pressure Forced expiratory tests Peak expiratory flow rate (PEFR) volume against time (spirogram) airflow against volume Forced vital capacity (FVC) forced expiratory volume in ‘t’ seconds (FEV ) FEV = FEV /FVC Forced mid-expiratory flow (FEF ) Maximal voluntary ventilation (MVV) Lung volumes Restrictive ventila- tory defects (RVDs) helium dilution body plethysmog- raphy transdiaphrag- matic pressure P P P P = P − P P P Diffusing capacity D = T D co D o D co KCO = D co/ D co D co D co D co < Arterial blood gases P o P co arterial oxygen saturation Pulmonary function tests History, examination and investigation 49
  • 49. r21 Chest imaging and bronchoscopy 6 Chest radiograph interpretation(a) (b) (c) Normal chest X-ray Normal lateral X-ray Date: Name: AP/PA: Is it AP (anteroposterior) or PA (posteroanterior)? (Heart size cannot be measured if AP) Is it well positioned? The trachea should be midway between clavicles Penetration: The disc spaces should be just visible through the cardiac shadows (underpenetrated = plethoric lungs overpenetrated = dark lungs) Soft tissues and breast shadows (mastectomy in a female) Right diaphragm 2 cm higher than left (raised when paralysed, flat in asthma/COPD) Check ribs for fractures, metastases Right heart border = right atrium Hilium = bronchi, arteries and veins Superior vena cava Aortic arch Heart size less than 50% of chest width Thoracic vertebral bodies Scapula Pulmonary trunk and hilium Descending aorta Head of clavicle Trachea Arch of aorta Ascending aorta Anterior space (thymus) Heart Sternum Diaphragm Left heart border = left ventricle Pulmonary vessels 3 4 5 6 7 8 9 10 11 12 1 2 13 14 4 7 8 9 10 11 12 13 14 15 16 7 16 3 4 5 6 7 8 9 10 11 12 1 2 Oesophagus Right lung Rightmainbronchus Right pulmonary artery and branches Superior vena cava Ascendingaorta Pulmonary trunk Mediastinum and heart Left pulmonary artery and branches Left main bronchus Left lung Descending aorta 3 4 5 6 7 8 9 10 11 12 1 2 3 4 7 8 9 10 11 12 1 2 Chest radiograph interpretation 10 14 5 Evaluation of the CXR includes all the following: Trachea and main bronchi Lung fields 15 16 5 1 3 4 6 9 10 12 8 11 7 2 6 5 50 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 50. Standard (two-dimensional) chest X-rays Computed tomography: r Bronchial carcinoma: r Lung parenchymal disease: r Mediastinal masses: r Pleural disease: r Pulmonary emboli (PE): Ventilation–perfusion (V/Q) scans Pulmonary angiography Positron emission tomography (PET) Bronchoscopy Pneumocystis carinii Chest imaging and bronchoscopy History, examination and investigation 51
  • 51. r22 Public health and smoking (b) Progressive decline in lung function in smokers and non-smokers and the effect of stopping smoking at 45 and 65 years old 100 50 0 25 50 75 Stopped at 65 Stopped at 45 Disability Death Smoked regularly and susceptible Never smoked not susceptibile %FEV1at25yearsold Age (years) Adapted from: Fletcher and Peto (1977) BMJ 1:1645 (a) All UK deaths in 2004 All UK deaths in 2004 Ischaemic heart disease Non-respiratory cancer All deaths from respiratory disease Respiratory disease • Pneumonia and TB • Lung cancer • Progressive non-malignant causes COPD + asthma Pulmonary circulatory disease Pneumoconiosis Cystic fibrosis Sarcoidosis • Others (congenital etc.) 587808 106081 122 512 117 456 Cases % 35814 34721 35979 28859 3926 3024 139 31 10527 30.5 29.6 30.6 24.6 3.3 2.6 0.1 0.03 9 (c) Total UK emergency medical admissions by diagnosis (2004) COPD Angina CCF Pneumonia Gastroenteritis Diabetes + complications 111000 79000 62000 57000 54000 18000 Factors associated with respiratory disease 1 Smoking-related disease (SRD) r COPD 52 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 52. r Lung cancer < > < 2 Environmental and social factors ± r Asthma 3 Working conditions Smoking cessation > β Management a Behavioural Strategies r A r A r A r A r A b Pharmacotherapy r Nicotine replacement therapy (NRT) ∼ r Antidepressants Bupropion (Zyban) Nortryptiline r Varenicline Public health and smoking Diseases and treatment 53
  • 53. r23 Respiratory failure (a) Causes of respiratory failure Central drive CNS-depressant drugs (e.g. barbiturates) Head injury Cerebrovascular accident Primary alveolar hypoventilation Airway obstruction Foreign body or tumour Asthma COPD Spinal cord Transection (apnoea if above C3) Poliomyelitis Chest wall Crush injury — flail chest Kyphoscoliosis Lung parenchyma Fibrosis Emphysema Pneumonia Lung resection Pneumothorax Atelectasis NRDS/ARDS Respiratory muscles Muscular dystrophies Peripheral nerves Guillain–Barré Neuromuscular junction Myasthenia gravis Muscle relaxants (b) Mechanisms of arterial hypoxia (low PaO2) Normal Normal alveolar- capillary membrane >98% cardiac output passing through gas- exchanging alveoli Normal PaO2 Normal alveolar ventilation Normal PΙO2 Matching of ventilation and perfusion throughout the lungs (c) Effects of hypoxia and hypercapnia Low PaO2 (hypoxaemia/ hypoxia) High PaCO2 (hypercapnia) Acute Impaired CNS function: irritability, confusion, drowsiness, convulsions, coma, death Central cyanosis (not very sensitive; may be absent in anaemia) Cardiac arrhythmias Hypoxic vasoconstriction* of pulmonary vessels Low arterial pH (respiratory acidosis) Peripheral vasodilatation warm flushed skin, bounding pulse Cerebral vasodilatation intracranial pressure headache, worse on waking if nocturnal ventilation Impaired CNS/muscle function: irritability, confusion, somnolence, coma, tremor, myolonic jerks, hand flap Cardiac arrhythmias Chronic—compensation and complications Erythropoietin from hypoxic kidney polycythaemia oxygen carriage despite low PaO2 but if excessive (haematocrit >55%) the viscosity impairs tissue blood flow Polycythaemia florid complexion; increased cyanosis Pulmonary hypertension* right ventricular hypertrophy Fluid retention/right heart failure (cor pulmonale*) peripheral oedema/ascites/ jugular venous pressure/enlarged liver Renal compensation (compensatory metabolic alkalosis) arterial [HCO3 – ] arterial pH returned to near normal Cerebrospinal fluid (CSF) compensation CSF [HCO3 – ] CSF pH returned to near normal respiratory drive less at any given PaCO2 than in acute hypercapnia *Hypercapnia accentuates the effects of hypoxia on pulmonary blood vessels and therefore contributes to the development of cor pulmonale (see above) Other Cyanotic congenital heart disease Pulmonary emboli Pulmonary oedema 2. Hypoventilation – Inadequate alveolar ventilation low alveolar PO2 4. Ventilation–perfusion mismatching – Blood from areas with high VA/Q mixes with blood from low VA/Q areas low pulmonary venous PO2 5. Right-to-left shunt – Shunted blood fails to undergo gas exchanges, mixes with pulmonary capillary blood low pulmonary Air or alveolar gas with normal PO2 Air or alveolar gas with reduced PO2 Deoxygenated blood (‘mixed venous’ or right-sided) Normal, fully oxygenated Incompletely oxygenated blood venous/left ventricular PO2 3. Diffusion impairment – Pulmonary capillary blood fails to reach equilibrium with alveolar gas low pulmonary end-capillary PO2 1. Low inspired PO2 – e.g. altitude (low PB) or low inspired O2 concentration low alveolar PO2 54 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 54. Po type 1 respira- tory failure Pco type 2 or ventilatory failure Pco acute chronic acute on chronic dyspnoea Po tachypnoea Mechanisms leading to hypoxia and hypercapnia hypoventilation P co P ∝ A–a Po gradient right-to-left shunts ventilation–perfusion mismatching diffusion impairment Effects of hypoxia and hypercapnia Cyanosis peripheral cyanosis central cyanosis Respiratory failure in asthma P co P co Respiratory failure in chronic obstructive pulmonary disease pink puffer blue bloater P o P co P co P co P co F o P o Management Respiratory failure Diseases and treatment 55
  • 55. r24 Asthma: pathophysiology (a) Cartoon of airway wall EpitheliumMucusSmooth muscle (b) Hyperrresponsiveness (c) Main causes of asthma Bronchoconstriction hyperresponsiveness, remodelling Epithelial damage Mucus hypersecretion Mucosal oedema Inflammatory cell infiltration Airwayresistancetoairflow Severe asthma Mild asthma Healthy Dose of stimulus (e.g. inhaled histamine) Housedustmite Pollen Dander Spores 5 15 Minutes 4 86 10 2 4 Inflammation, mucosal oedema, mucus, epithelial damage Hyperresponsiveness, bronchoconstriction and airway remodelling Bronchoconstriction DaysHours (e) Cellular mechanisms Goblet cell Sub-mucosal gland Mucus Smooth muscle growth Vascular leak Mucosal oedema TH2 lymphocyte Antigen presenting cell Cytokines Cytokines Eosinophil Histamine, PgD2 LTC4, LTD4 Epithelium Antigen 65% 80% 40% 20% Patients often allergic to more than one allergen FEV1 Allergen challenge (d) Typical response of an atopic asthmatic to inhaled antigen Mucus Smooth muscle IgE Mast cell Cyto kines PAF,LTC4 , LTD 4 MBP,ECP Immediate response Late-phase response Recurrent attacks 56 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 56. 1 Narrowing of the airways 2 hyperresponsiveness 3 inflammatory cells hypersecretion of mucus mucus plugs oedema epithelial shedding re- modelling of the airway wall Prevalence antigens tobacco smoke exhaust fumes emo- tional stress exercised-induced asthma viral infections occupational asthma Classification extrinsic intrinsic IgE antibodies allergic atopic asthma IgE-independent Atopic asthma house dust mite Dermatophagoids pteronyssinus DerP pollen domestic pets fungal spores imme- diate response β late-phase response iso- cyanates isolated late phase recurrent asthma attacks type I hypersensitivity mast cell degranulation histamine prostaglandin D leukotriene C D type IV cell-based hypersensitivity TH2 lymphocytes cytokines eosinophils neutrophils antigen presenting cells leukotrienes PAF ma- jor basic protein eosinophil cationic protein Drug-associated asthma β β β Asthma: pathophysiology Diseases and treatment 57
  • 57. r25 Asthma: treatment (a) Step-wise approach to asthma therapy (adult) Based on British Thoracic Society guidelines, 2009, update Move down to the lowest step for adequate control Move up to improve control (but review compliance) Inhaled short-acting β2- agonist as required Step 1 ADD: Inhaled low-dose steroid Step 2 ADD: Inhaled long- acting β2-agonist If improvement but still poor control, increase inhaled steroid (to 800 μg/day) If no improvement, increase steroid and trial leukotriene receptor antagonist or SR theophyline Consider trials of: Increased inhaled steroid to high dose 2000 mg/day Addition of 4th drug: leukotriene receptor antagonist SR theophyline oral β2-agonist ADD: Oral steroid, lowest dose possible Consider other treatments to minimize use of oral steroids Step 3 Step 4 Step 5 Control of asthma is defined as: • No daytime symptoms • No need for rescue medication • No limitations on activity • No night-time awakening due to asthma • No exacerbations • Normal lung function • Remove the cap and shake the inhaler • Tilt the head back slightly and exhale • Position the inhaler in the mouth (or preferably just in front of the open mouth) • During a slow inspiration, press down the inhaler to release the medication • Continue inhalation to full inspiration • Hold breath for 10 seconds • Actuate only one puff per inhalation (c) Pressurized metered dose inhaler Maintain high-dose inhaled steroid Refer to specialist (b) Most common drug classes used in asthma Type Route and example Effect Adverse effects β2–agonist (adrenoreceptor agonists) Inhaled, oral, intravenous (IV) Short-acting: salbutamol (albuterol) Long-acting: salmeterol, formoterol Muscle tremor (most common) Tachycardia, palpitations (high dose) Corticosteroids Xanthines Muscarinic receptor antagonists Antileukotrienes Receptor antagonist Lipoxygenase inhibitor Inhaled: Oral: IV: Beclometasone proprionate Prednisolene Hydrocortisone Oral, IV: Theophylline, aminophylline Slow release (SR) formulations Inhaled: Ipratropium bromide Oral: Montelukast, zafirlukast Zileuton (not licensed in UK) Anti-inflammatory (Suppress activation of inflammatory genes) Bronchodilators Some anti-inflammatory action (increase cAMP) Bronchodilators May stabilize mast cells (increase cAMP) Bronchodilators Reduce mucus secretion (block cholinergic effects) Bronchodilators May reduce mucosal oedema (block action of LTC4, LTD4) Inhaled: oral candidiasis, cough, hoarseness Oral/high dose: Retarded growth, water retention, osteoporosis, hypertension, weight gain, eye problems, diabetes, psychosis Headache, nausea, diuresis, cardiac arrhythmias, vomiting, epilepsy; many drug interactions affect xanthine plasma levels Rare, bitter taste None-significant described Mild and intermittent asthma Regular preventer therapy Initial add-on therapy Persistent poor control Frequent oral steroid 58 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 58. Management of asthma Assessment Lung function: morning dipping Bronchial provocation tests hyperresponsiveness Skin prick tests Therapy step-wise treatment regimens inhaled MDI relievers preventers Short acting β -adrenoceptor agonists Long-acting β -agonists β tolerance Corticosteroids Inhaled steroids Oral corticosteroids Combination therapies β Muscarinic receptor antagonists β Xanthines β Antileukotriene therapy Cromones Allergen-specific immunotherapy: Bronchial thermoplasty Poorly controlled Severe uncontrolled asthma Indications: life-threatening Treatment: β + − β Asthma: treatment Diseases and treatment 59
  • 59. r26 Chronic obstructive pulmonary disease (d) Typical signs and symptoms of COPD Chronic bronchitis Emphysema Chronic cough, producing sputum Hypoventilation, little respiratory effort Cyanosis, hypoxaemia with secondary polycythaemia CO2 retention/chronic hypercapnia – leading to peripheral vasodilatation and bounding pulse Oedema Cor pulmonale Normal lung volumes, DLCO, lung compliance Note: Most patients may present with both chronic bronchitis and emphysema Chronic breathlessness (dyspnoea) Cyanosis unusual; normoxic at rest, hypoxic on exercise Barrel chest (hyperinflation), underweight Rarely exhibit oedema or cor pulmonale Increased TLC, RV, lung compliance Reduced DLCO Risk factors for COPD Spirometry. FEV1/FVC ratio decreases in COPD Smoking Age >50 years old; prevalence ~5–10% Male gender Childhood chest infections Airways hyperreactivity • asthma/atopy Low socioeconomic status α1-Antitrypsin deficiency Heavy metal exposure • cadmium Atmospheric pollution Pathophysiology of chronic bronchitis and emphysema Volume 1 second 4 seconds Normal FEV1/FVC = >0.8 COPD Irreversible with bronchodilators <15% increase in FEV1 COPD FEV1/FVC = <0.8 FVC FEV1 FVC FEV1 Normal lung parenchyma provides lung's elastic recoil Loss of alveolar septa and capillaries reduces the lung's elastic recoil. Large air spaces (bullae) develop Pressure collapsing airway in expiration is greater than lung's elastic recoil causing distal airways collapse Chronic bronchitis Emphysema Mucosal inflammation and mucous secretion cause narrowing (± obstruction) of some airways Increased upper airway pressure (purse-lip breathing, CPAP) will tend to hold airways open and allows increased alveolar emptying Poor ventilation and collapse of some alveoli (e.g. mucous plugs) cause V/Q mismatch + hypoxaemia Collapse of distal airways in expiration causes gas trapping and alveolar hyper- inflation Pressure collapsing airway in expiration balanced by lung's elastic recoil and airway held open Pressure collapsing Elastic recoil (a) (c) (b) 60 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 60. Chronic obstructive pulmonary disease (COPD) irreversible chronic bronchitis emphysema acute exacerbations respiratory failure pulmonary hypertension reversible Diagnosis and pathophysiology reduced FEV /FVC ratio < dyspnoea Chronic bronchitis chronic mucosal inflammation mucous gland hypertrophy mucus hypersecretion bronchospasm D co CO retention Hypoxaemia polycythaemia increased pulmonary artery pressure hypoxic pulmonary vasoconstriction peripheral oedema cor pulmonale Emphysema enlarged airways and airspaces hyperinflation α1-antitrypsin deficiency D co barrel chest purse-lipped breath- ing Management β2-agonists anticholinergics Xanthines mucolytics Inhaled cor- ticosteroids < oral corticosteroids Pulmonary rehabilitation O therapy α -antitrypsin deficiency lung volume reduction transplantation Prevention of acute COPD exacerbations Haemophilus in- fluenzae Overall prognosis Chronic obstructive pulmonary disease Diseases and treatment 61
  • 61. r27 Pulmonary hypertension 1. Pulmonary arterial hypertension (PAH): Idiopathic (IPAH) Familial (FPAH) (e.g. mutation in bone morphogentic protein receptor (BMPR) Associated with (APAH) connective tissue diseases, congenital systemic- pulmonary shunts, portal hypertension (cirrhosis), HIV infection, drugs and toxins + disorders (e.g. thyroid) Associated venous or capillary involvement: pulmonary veno-occlusive disease and pulmonary capillary haemangiomatosis Persistent PH in the newborn (PPHN) 2. PH associated with left heart disease including left-sided valvular heart disease 3. PH associated with lung diseases and/or hypoxia including COPD, interstitial lung disease, sleep-disordered breathing, hypoventilation, high altitude exposure + developmental abnormalities 4. PH due to chronic thrombotic and/or embolic disease including thromboembolic obstruction of pulmonary artery and non-thrombotic pulmonary embolism (e.g. tumour, parasites) Dyspnoea, Loud P2 Chronic thromboembolic disease (b) Evaluation of suspected pulmonary hypertension Echocardiogram Congenital heart disease LV dysfunction Valvular disease Parenchymal lung disease Other studies: • Autoantibodies • HIV • Liver function • Sleep study Right heart catheterization Ventilation/ perfusion scan Chest X-ray/ CT scan RV LV Secondary to thrombotic disease: Chronic thromboembolic disease Embolic obliterative disease Disorders directly affecting the vasculature: Interstitial lung disease (Chapter 30) Vasculitis (Chapter 29) Emphysema (Chapter 26) Schistosomiasis Secondary to respiratory disease: Alveolar hypoxia - COPD (Chapter 26) Interstitial lung disease (Chapter 30) ARDS (Chapter 41) Sleep-disordered breathing (Chapter 44) (a) Causes of pulmonary hypertension (Venice/WHO 2003) 1.1 1.2 1.3 1.4 1.5 Pulmonary venous hypertension: Left ventricular heart failure Mitral stenosis/insufficiency Fibrosing mediastinitis Left atrial myxoma Veno-occlusive disease 62 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 62. Pulmonary hypertension 25 mmHg 30 mmHg ∼ pulmonary vascular resistance back-pressure secondary PH pulmonary arterial hypertension Types of pulmonary hypertension Secondary to respiratory disease: hypoxic pulmonary vasoconstriction Pulmonary venous hypertension: con- gestive heart failure Mitral insufficiency stenosis Secondary to thrombotic disease: thromboembolism Disorders directly affecting the vasculature: capillary resistance Interstitial lung diseases fibrosis scleroderma sarcoidosis emphy- sema Pulmonary arterial hypertension familial sporadic Clinical features progressive right-sided heart failure remodelling right ventricular dys- function Diagnosis echocardiography Right heart catheterization Treatment thromboembolic disease anticoagulation prostacyclin Pulmonary hypertension Diseases and treatment 63
  • 63. r28 Venous thromboembolism and pulmonary embolism (a) Pulmonary angiograms (A, D) and V/Q scans (B, E = ventilation scans, C, F = perfusion scans) in a healthy patient and a patient with a massive right- sided pulmonary embolism. The angiogram (D) shows complete occlusion of the right pulmonary artery. On the V/Q scan there is loss of right lung perfusion (F) but normal ventilation (E) (c) Risk factors for DVT and PE (d) DVT prophylaxis (b) Contrast CT scan showing contrast in the heart and pulmonary arteries (PA). Both the right and left PA show irregular defects, consistent with pulmonary emboli Normal Pulmonary embolism Ventilation scan Perfusion scan Normal right lung ventilation No right lung perfusion Normal PA LMWH = low-molecular-weight heparin UFH = unfractionated heparin CVA = cerebrovascular accident Hip, knee, gynaecological procedures Spinal trauma Age, obesity, smoking, oral contraceptive pill (OCP) Malignancy, sepsis, stroke, autoimmune disease Low flow states (e.g. cardiac failure and immobility) Vascular injury (e.g. atherosclerosis and catheters) Deficiencies (e.g. antithrombin III, protein C and protein S) Clotting disorders (e.g. factor V leiden, antiphospholipid syndrome and dysfibrinogenaemias) Surgery Trauma General factors Underlying disease Cardiovascular disease Inherited disorders (less common) Occluded right PA Right pulmonary artery Left pulmonary artery Heart and pulmonary trunk Pulmonary embolus Aorta Pulmonary embolus A D B C E F Regime Early ambulation Compression stockings Low-dose heparin (UFH or LMWH) Full-dose LMWH or warfarin Patient <40 years old, minor surgery (<1 h) Minimal immobility >40 years old, surgery (>1 h), cardiac, medical problems, CVA, hypercoagulability Complicated surgery, hip or knee surgery, hip fracture, trauma Risk of DVT Low (<1%) Moderate (5–10%) High (>15%) 64 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 64. Venous thromboembolism pul- monary embolism (PE) deep venous thrombo- sis (DVT) Deep venous thrombosis ∼ Pulmonary embolism increase in minute ventilation P co atelectasis Hypoxaemia V /Q mismatch Pulmonary infarction Clinical features dyspnoea pleuritic chest pain haemoptysis apprehension tachypnoea RV failure Arterial blood gas abnormalities widened A–a gradient hypoxaemia hypocapnia Diagnosis Deep venography pulmonary angiography V/Q scanning Non-invasive imaging pulmonary angiography Spi- ral/helical computed tomography Echocardiography pericardial tamponade Transoesophageal echocardiography Treatment anticoagulation unfraction- ated heparin (UFH) low-molecular-weight heparin (LMWH) warfarin inferior vena cava (IVC) filter fibrinolysis thrombolytics Venous thromboembolism and pulmonary embolism Diseases and treatment 65
  • 65. r29 Pulmonary vasculitis Vasculitides (a) CT scan of patient with Wegener’s granulomatosis, showing large cavitating masses (b) Histological section showing necrobiotic regions with multinucleate giant cells (arrows) Disease Table 1 Feature Diagnostic antibodies Comment Collagen vascular disease Rheumatoid arthritis Scleroderma SLE Arteries Fibrosis in arterioles Capillaritis Uncommon CREST syndrome Alveolar haemorrhage Wegener’s granulomatosis Churg–Strauss syndrome Microscopic polyangiitis Goodpasture’s syndrome Lymphomatoid granulomatosis Granulomatous inflammation Arteriolar/venular vasculitis Capillaritis, fibrinoid necrosis Necrotizing vasculitis in small arteries, arterioles and venules Granulomas, eosinophils Fibrinoid necrosis Arteriole/venule vasculitis Capillaritis, fibrinoid necrosis Intra-alveolar haemorrhage Linear IgG in basement membrane Minimal inflammation Angiodestructive lymphocytes Plasma cells, atypical lymphocytes PR3-ANCA >> MPO-ANCA MPO-ANCA >> PR3-ANCA MPO-ANCA > PRS-ANCA Anti-GBM antibodies Occassionally PR3-ANCA Alveolar haemorrhage Asthma, eosinophilia Related to Wegener’s Hepatitis B, C Alveolar haemorrhage Smoking, recent infection Epstein–Barr virus Lymphoproliferative 66 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 66. vasculitides collagen vascular disease rheumatoid arthritis scleroderma systemic lupus erythematosus (SLE) primary vasculitides Wegener’s granulomatosis, Churg–Strausssyndrome,microscopicpolyangiitis,lymphomatoid granulomatosis angiitis Goodpasture’s syndrome anti-neutrophil cytoplasmic antibodies ANCA Collagen vascular diseases Rheumatoid arthritis pulmonary hyper- tension Caplan’s syndrome Limited cutaneous scleroderma pulmonary capillaritis SLE pulmonary arterial hypertension Vasculitides Wegener’s granulomatosis granulomas Churg–Strauss syndrome allergic granulomatosis angiitis Treatment: Microscopic polyangiitis Treatment Goodpasture’s syndrome anti-glomerular basement membrane D co Treatment: Lymphomatoid granulomatosis Epstein–Barr virus Treatment: Pulmonary vasculitis Diseases and treatment 67
  • 67. r30 Diffuse parenchymal (interstitial) lung diseases (a) Classification and diagnostic process in DPLD 1. Idiopathic interstitial pneumonitis (IIP) 2. DPLD due to specific causes 3. Granulomatous DPLD 4. Rare causes of DPLD Usual insterstitial pneumonitis (UIP/IPF) Non-usual interstitial pneumonitis (non-UIP, e.g. NSIP, DIP) • Drug-induced • Hypersensitivity pneumonitis • Connective tissue disease • Occupational lung disease Sarcoidosis and other granulomatous diseases • Infiltrative (e.g. amyloidosis) • Malignant (e.g. lymphangitis carcinomatosis) • Post-inflammatory (ARDS) • Post-infective (e.g. HIV) • Bone marrow transplants • Langehams cell histiocytosis History, examination, CXR and lung function tests TBBx, BAL diagnostic in sarcoidosis in 60–90%Possible IIP HRCT scan Not IIP (e.g. drug-related, occupational, CTD, sarcoidosis and ARDS) Characteristic clinical and CT features of UIP Surgical biopsy not required Features diagnostic of another DPLD e.g. sarcoidosis, LCH Atypical clinical or CT features for UIP or suspected other DPLD or non-UIP IIP (e.g. NSIP and DIP) TBBx, BAL or other relevant test If non- diagnostic Surgical lung biopsy UIP Non-UIP IIP NSIP DIP RB-ILD COP LIP AIP Not IIP (b) Drug induced DPLD Antibiotics (e.g. nitrofurantoin) Antiarrythmias (e.g. Amiodarone and tocainide) Anti-inflammatory (e.g. gold and penacillamine) Anticonvulsants (e.g. dilantin) Antihypertensives (e.g. hydralazine) Chemotherapeutic agents (e.g. bleomycin, mitomycin C, methotrexate and busulphan) Oxygen toxicity Paraquat Narcotics (inhaled or intravenous) Therapeutic radiation (c) Collagen vascular disease involvement in DPLD Rheumatoid arthritis (5% but commonest cause in view of disease frequency) Scleroderma (>70%) Polymyositis/dermatomyostis (20–50%) Systemic lupus erythematosus (5%) Sjogrens syndrome (25%) Ankylosing spondylitis (2%) (g) Clinical features, age at onset, histologic pattern and radiographic features of idiopathic interstitial pneumonias Clinical name Age, sex Clinical features, relation to smoking and response to treatment Typical CT findings CT distribution UIP/IPF 50–80 yrs M>>F Gradual onset. Acute exacerbations. Worse in smokers. BAL shows neutrophils (±eosinophils). Poor response to steroids and immunosuppressive agents. Median survival 2–3 years from diagnosis Reticular abnormality + volume loss, honeycombing, traction bronchiectasis, focal GGO Peripheral, basal + subpleural (Fig. d) NSIP 40–50 yrs M=F Gradual onset 6–30 months or subacute. Not related to smoking. BAL lymphocytosis. Prognosis better than UIP, especially in cellular (inflammatory) disease. Most patients improve or recover with steroid (±immunosuppressive) therapy GGO, consolidation, reticular opacities Peripheral, subpleural, basal (Fig. e) COP ~55 yrs M=F Subacute, related to CTD or lower respiratory tract infections and more common in smokers. Most patients recover with steroids but may be slow (>6 months) Patchy consolidation and/or nodules Subpleural, peribronchial RB-ILD 40–50 yrs M:F 2:1 Usually occurs in heavy smokers (>30 packs a year). Characterized by pigmented intraluminal macrophages in bronchioles. Many patients improve with smoking cessation but steroid therapy may be required Bronchial wall thickening, patchy GGO, centrilobular nodules Diffuse DIP 40–50 yrs M>>F A form of severe RB-ILD. Characterized by BAL pigment-laden alveolar macrophages which fill alveolar spaces. Nearly always due to smoking. Prognosis >10 years following smoking cessation and/or steroid therapy in 70%. Progression to fibrosis in <20%. GGO++, reticular lines Lower zone, mainly peripheral (Fig. f) AIP Any age M=F Rapidly progressive disease, indistinguishable from ARDS. Often presents after a viral URTI. No effective therapy and mortality is >50% and occurs within 4–8 weeks of onset. Recurrence or progressive fibrosis may occur in survivors. Consolidation, GGO (lobular sparing), late traction bronchiectasis Diffuse LIP Any age F>M Often due to an underlying systemic condition (e.g. rheumatoid arthritis, systemic lupus erythematosus and myasthenia gravis). BAL lymphocytosis. Most respond to steroids but ~30% progress to diffuse fibrosis. Centilobular nodules, GGO bronchovascular +septal thickening Diffuse IPF = idiopathic pulmonary fibrosis; UIP = usual interstitial pneumonia; NSIP = non-specific interstitial pneumonia; DIP = desquamative interstitial pneumonia; RB = respiratory bronchiolitis; RB-ILD = respiratory bronchiolitis-interstitial lung disease; AIP = acute interstitial pneumonia; DAD = diffuse alveolar damage; COP = cryptogenic organizing pneumonia; LIP = lymphocytic interstitial pneumonia; GGO = ground glass opacification; BAL = bronchoalveolar lavage; CTD = connective tissue disease, SLE = systemic lupus erythematosus IPF = idiopathic pulmonary fibrosis; TBBx = transbronchial biopsy; BAL = bronchoalveolar lavage; UIP = usual interstitial pneumonia; NSIP = non-specific interstitial pneumonia; DIP = desquamative interstitial pneumonia; RB = respiratory bronchiolitis; AIP = acute interstitial pneumonia; COP = organising pneumonia; LIP = lymphoctic interstitial pneumonia; DPLD = diffuse parenchymal lung disease; CTD = connective tissue disease (d) HRCT scan showing subpleural honeycomb fibrosis in UIP (e) HRCT scan showing subpleural sparing, coarse reticular shadowing and traction bronchiectasis in NSIP (f) HRCT scan showing ground glass opacification (GGO) and mosaic pattern typical of alveolitis in DIP Subpleural honeycomb fibrosis Coarse reticular opacities Traction bronchodilation Subpleural sparing GGO and mosaic patterning Normal lung 68 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 68. Clinical features: ± Pulmonary function tests D co Chest X-ray > Bron- choalveolar lavage HRCT scans (±histology) Classification: 1 Idiopathic interstitial pneumonitis r Usual interstitial pneumonia Pathogenesis Incidence Clinical features HRCT scans Histology Treat- ment: Median survival < r Non-usual interstitial pneumonitis ± > ≤ 2 DPLD due to specific causes r Drug-induced DPLD r Hypersensitivity pneumonitis r Connective tissue disease (CTD) DPLD r Occupational lung disease 3 Granulomatous DPLD: 4 Rare causes of DPLD Diagnosis (Fig. 30a): HRCT scans Surgi- cal biopsy Management: Supportive ther- apy Pharmacological therapy N Diffuse parenchymal (interstitial) lung diseases Diseases and treatment 69
  • 69. r31 Sarcoidosis (a) Causes of lung granuloma Idiopathic: Sarcoidosis Infective: Tuberculosis, leprosy, brucellosis, fungal, schistosomiasis, cat-scratch fever, syphilis Malignancy: Lymphoma Gastrointestinal: Crohn’s disease, primary biliary cirrhosis Allergic: Extrinsic allergic alveolitis Occupational: Berylliosis, silicosis Vasculitic: Wegener's granulomatosis, giant cell arteritis, polyarteritis nodosa, Takyasu’s arteritis Others: Thyroiditis, Langerhans’ cell histiocytosis, hypogammaglobulinaemia, orchitis (b) Causes of bihilar lymphadenopathy on CXR Sarcoidosis Tuberculosis Lymphoma, leukaemia Fungal infections (e.g. histoplasmosis) Berylliosis Hypogammaglobulinaenia (+recurrent infection) (e) Radiographic staging in sarcoidosis and likelihood of spontaneous resolution Stage Finding Likehood of spontaneous resolution 0 I II III IV Normal chest radiograph Bilateral hilar lymphadenopathy (BHL) BHL plus pulmonary infiltrates Pulmonary infiltrates (without BHL) Pulmonary fibrosis (± bullae) >90% 60–90% 40–60% 10–20% <20% (d) Initial evaluation of sarcoidosis History (+occupational/environmental exposure) Examination including fundoscopy Full blood count including lymphocyte count Biochemistry, calcium, liver function, LDH, SACE, ECG, CXR, urine analysis (±calcium excretion) Spirometry and gas transfer (DLCO) Mantoux test (to exclude tuberculosis) (g) Criteria for steroid therapy in sarcoidosis Progressive symptomatic pulmonary disease Asymptomatic pulmonary disease with ongoing loss of lung function Cardiac disease Neurological disease Eye disease not responding to topical therapy Symptomatic hypercalcaemia Other symptomatic/progressive extrapulmonary disease LDH = lacate dehydrogenase; SACE = serum angiotensin-converting enzyme; ECG = electrocardiogram; CXR = chest X-ray BHL RPTA (c) Characteristic CXR features in pulmonary sarcoidosis (i) Bihilar lymphadenopathy (BHL) and right paratracheal adenopathy (RPTA) (ii) Upper lobe fibrosis (ULF) (iii) Perihilar infiltrates ULF Perihilar infiltrates Peri- bronchovascular nodularity Parenchymal nodules Fissural ‘beading’ on HRCT Hilar adenopathy (f) CT scan of pulmonary sarcoidosis showing hilar adenopathy and peri- bronchovascular nodules. Inset shows fissural nodules/‘beading’ on HRCT 70 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 70. Sarcoidosis > Incidence Aetiology: Histopathology γ Clinical features: > 1 Pulmonary sarcoidosis ∼ ∼ ∼ ∼ (a) Acute sarcoidosis (b) Progressive, interstitial lung disease ± Diagnosis: ± Disease progression ±D co r SACE r CXR < r High-resolution CT scans r Histological confirmation ∼ r Pulmonary function tests D co Management: r Steroid therapy > r Immunosuppressive therapy α r Lung transplant 2 Extrathoracic disease r Skin ∼ r Eye > ± r Cardiac disease ∼ r Neurosarcoid Prognosis: D co Sarcoidosis Diseases and treatment 71
  • 71. r32 Pleural diseases (a) Causes of pleural effusions (b) CXR showing large pleural effusion in left lung (contrast with pneumothorax CXR in Chapter 35) (c) CT scan demonstrating irregular (lumpy) pleural thickening of mesothelioma over lateral right chest wall (see arrows) Exudative (protein ratio pleural/serum >0.5 or LDH ratio pleural/serum >0.6 or pleural LDH >0.66 of top normal serum value) Infectious Para-pneumonic • aerobic bacterial pneumonia • anaerobic bacterial pneumonia Empyema Tuberculosis Parasitic • amoeba • echinococcus • paragonimus Viral Autoimmune/collagen vascular Systemic lupus erythematosus Rheumatoid arthritis Neoplastic Lung cancer Metastatic disease Mesothelioma Abdominal Pancreatitis/pseudocyst Oesophageal rupture Liver abscess Splenic abscess Miscellaneous Pulmonary embolism Drug reactions Asbestos exposure Haemothorax Chylothorax Post-cardiac surgery Post-myocardial infarction Meig’s syndrome Transudative (meets none of the criteria for exudative) Congestive heart failure Cirrhosis Hepatic hydrothorax Myxoedema Nephrotic disease Peritoneal dialysis 72 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 72. The pleurae parietal visceral pleurae transudative Pneumothorax Chylothorax Empyema Pleurisy Pathophysiology pleural effusion inflam- matory pulmonary mechanics pleuritic chest pain dull aching pain fullness of the chest dyspnoea Compressive atelectasis transudative exuda- tive Transudative effusions congestive heart failure Exudative effusions ∼ Treatment Specific conditions Pneumonia Streptococcus pneumoniae Staphylococcus aureus Tuberculosis pleurisy Primary lung malignancies metastases pleurodesis Mesothelioma Pleural diseases Diseases and treatment 73
  • 73. r33 Occupational and environmental-related lung disease (a) Common examples of irritant gases and other agents causing lung-specific responses Agent Source Response Ammonia Chlorine gas Hydrogen sulphide Nitrogen dioxide Nitrogen oxides Ozone Sulphur dioxide Acrolein, aldehydes Diesel particulates (<10μm) Heavy metals (cadmium, mercury) Paraquat Polycyclic hydrocarbons Hydrocarbons Industrial refrigeration leaks, fertilizers Industrial leakage, water purification including swimming pools, household bleach (liquid/powder) interactions Sewers and manure pits, fossil fuel extraction Vehicle exhausts, welding, power stations, oil refineries, gas and oil burning equipment, organic decomposition, structural or polymer fires Vehicle exhausts, welding, copiers, ozone generators, bleaching, water treatment, plasma welding Combustion of fossil fuels, power stations, oil refineries, smelters, oil burning heaters, mining, ore refining, cement manufacturing, refrigeration plants Structural or wildland fires, other combustion Diesel engines Welding, brazing, metal cutting, metal reclamation Ingestion of herbicides Diesel exhaust, tobacco smoke Ingestion of hydrocarbons (children) Low exposure Exacerbations of asthma and COPD Enhanced response to allergen Moderate exposure Mild mucosal irritation Airway inflammation and bronchiolitis Severe exposure Epithelial damage leading to diffuse alveolar damage Pulmonary oedema and ARDS In some cases – late response (2–8 weeks) Bronchiolitis obliterans after initial recovery Airway/alveolar inflammation Increased deaths in elderly Acute pneumonitis 12–24 hours after exposure Accelerated, chemically induced pulmonary fibrosis Cancer Aspiration hydrocarbon pneumonitis (b) Typical causes of allergic alveolitis Disease/occupation Material Causative agent Farmer’s lung Bagassosis Mushroom workers Humidifier fever Pigeon fancier’s (breeder’s) lung Farmers, sawmill, tobacco, esparto grass and brewery workers Cheese, laboratory, cork workers Household – other bacterial causes Mouldy hay or other vegetable matter Sugarcane Compost Contaminated water Feathers and excreta Fungal contamination of materials Fungal contamination of materials Fungal infestations of damp walls and woodwork Contamination of water , wood shavings, etc. Thermophilic actinomycetes bacteria (Saccharopolyspora rectivirgula, Thermoactinomyces species) – Also Klebsiella oxytoca, amoebae Avian proteins Primarily Aspergillus species Primarily Penicillium species Multiple fungal species Bacillus subtilis, Klebsiella, Epicoccum nigrum, non-tubercular mycobacteria Also: direct bronchoconstriction, especially in asthmatics Also: strongly pro-inflammatory (esp. acrolein) 74 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 74. asthma Response to acute lung irritants pulmonary oedema acute respiratory distress syndrome bronchiolitis obliterans Inhalation of mineral dusts (pneumoconiosis) Coal worker’s pneumoconiosis simple CWP < progressive massive fibrosis D co Caplan’s syndrome Asbestos μ μ blue as- bestos white asbestos Asbestos bodies Asbestosis D co honeycomb lung Mesothelioma Silicosis silicotic nodules Inhalation of organic material Extrinsic allergic alveolitis hypersensitivity pneumonitis farmer’s lung thermophilic actinomycetes interstitial fibrosis granulomas D co Management Dif- ferential diagnosis Byssinosis Occupational and environmental-related lung disease Diseases and treatment 75
  • 75. r34 Cystic fibrosis and bronchiectasis (a) Mean survival of CF patients 100 50 0 %Survival Age (years) 250 50 (b) Development of respiratory problems in CF Impaired lung function Progressive respiratory failure Cell damage, DNA Treatment Gene therapy (potential) Bronchodilators (c) Other conditions associated with CF Condition % of CF patents Delayed development, puberty 100% Male infertility (absent/obstructed vas deferens and epididymis) 98% Female infertility 20% Nasal polyps Symptomatic sinusitis 15–20%, most in 2nd decade Rectal prolapse 20% children Rare in adults Bone demineralization (vitamin D deficiency) Common Hypertrophic osteoarthropathy 15% adults Dysfunctional gallbladder or gallstones 10–30% Biliary cirrhosis 5% adults (d) Some conditions associated with bronchiectasis Allergic bronchopulmonary aspergillosis (Chapter 33) α1-Antitrypsin deficiency (Chapters 18, 26) Bronchial obstruction (foreign bodies, mucus, tumour) Congenital cartilage deficiency (Williams–Campbell syndrome) Cystic fibrosis Fibrotic disease and alveolitis (Chapters 30 and 33) HIV and immunodeficiency (Chapter 39) Infection (e.g. measles and pertussis), pneumonia (Chapters 36 and 37) Lung transplant Primary ciliary dyskinesia (Kartagener’s syndrome, Chapter 18) Rheumatoid arthritis Tuberculosis (Chapter 38) Tracheobronchomegaly (Mounier–Kuhn syndrome) 10% children 25% adults CFTR gene mutation (e.g. ΔF508) Defective CFTR Defective epithelial ion transport Mucus viscosity and stasis Chronic infections Inflammation and bronchiectasis Amiloride, nucleotide triphosphates Postural drainage, inhaled DNase, aerosolized saline Antibiotics, immunization Steroids Pancreatic insufficiency 85% 76 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 76. Cystic fibrosis chronic bronchopulmonary infection exocrine pancre- atic insufficiency increased viscosity subsequent stasis of epithelial mucus increased salt content of sweat autosomal recessive trait cystic fibrosis transmembrane conductance regulator reduced mucus hydration increased viscosity F508 Clinical features fin- ger clubbing bronchiectasis pneu- mothorax haemoptysis meconium ileus equivalent Diagnosis family history sweat chloride sodium Management control infection, promote mucus clearance improve nutrition Clearance: Other therapies: β Nutrition: Bronchiectasis Bronchiectasis > mucociliary clearance persistent respiratory infections Man- agement Cystic fibrosis and bronchiectasis Diseases and treatment 77
  • 77. r35 Pneumothorax (c) Aspiration Small pneumothorax <30% Moderate pneumothorax Complete pneumothorax Tension pneumothorax 'Blunt dissection' technique for chest drain insertion (d) Type of pneumothorax Primary Secondary Traumatic/ latrogenic Arrows depict edge of collapsed lung Aspirate/ chest drain Chest drain Chest drain Aspirate Chest drain Chest drain Observe Chest drain Observe/ chest drain Complete Moderate Degree of collapse Small Local anaesthetic above rib edge (avoid neurovascular bundle) Blunt dissect tract into pleural space with forceps Safe triangle for chest drain insertion Ultrasound guidance is always preferred Deviated trachea Mediastinal shift Edge of pectoralis muscle Nipple line Lung Pneumothorax Position in apex of chest cavity Finger into pleural space to enlarge tract Intercostal drain gently inserted with forceps NOT TROCAR Tie drain in place Connect to underwater seal Compressed lung >30% (a) Pneumothorax (b) Pneumothorax management Local anaesthetic Aspirate using three-way tap Plastic cannula 50mL Lung Pntrxm Dischar aspirated air through underwater seal euoo ge ha 78 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 78. Pneumothorax classification Primary spontaneous pneumothorax (PSP) > > Secondary pneumothorax Traumatic (iatrogenic) pneumothorax Tension pneumothorax tension pneumothorax Clinical assessment < Monitoring Blood gases CXR Computed tomography (CT) scan Management < > always bronchopleural fistula Air leaks Pneumomediastinum subcutaneous em- physema (SE) pneumopericardium Pneumothorax Diseases and treatment 79
  • 79. r36 Community-acquired pneumonia Age: >65, <5 years old Chronic disease (e.g. renal and lung) Diabetes mellitus Immunosuppression (e.g. drugs and HIV) Alcohol dependency Aspiration (e.g. epilepsy) Recent viral illness (e.g. influenza) Malnutrition Mechanical ventilation Postoperative (e.g. obesity and smoking) Environmental (e.g. psittacosis) Occupational (e.g. Q fever) Travel abroad (e.g. paragonimiasis) Air conditioning (e.g. Legionella) (e) Complications and infection specific features of pneumonia Table 2. Risk factors for pneumonia(a) Pneumonia affecting the right lower lobe Consolidation right lower lobe Consolidation lingula lobe (b) Pneumonia affecting lingula lobe * = Rare ** = Very rare Cold agglutinins, e.g. Mycoplasma ** often present with cerebral symptoms Meningitis ** e.g. Streptococcus pneumoniae Pneumatocoeles**, e.g. Staph. aureus Pleural effusions or empyema (often occur with S. pneumoniae + S. aureus) Cholestatic jaundice** e.g. Legionella Bacteraemia Septicaemia arthritis Haemolysis** (e.g. Mycoplasma) Respiratory failure Haemoptysis*, e.g. Klebsiella Sinus infection* Myocarditis** Hypotension Pericardial infection** Lung abscess (often with S. aureus or aspergillus) Streptococcus pneumoniae Haemophilus influenzae Klebsiella pneumoniae Pseudomonas aeruginosa Gram-negative (E. coli) Mycoplasma pneumoniae Legionella pneumophila Coxiella burnetii Chlamydia psittaci Aspergillus Histoplasmosis Candida Nocardia Bacterial infections Atypical infections Fungal infection Influenza Coxsackie Adenovirus Respiratory syncytial Cytomegalovirus Pneumocystis carinii Toxoplasmosis Amoebiasis Paragonimiasis Aspiration Lipoid pneumonia Bronchiectasis Cystic fibrosis Radiation Viral infections Protozoal infections Other causes Score 1 point for each of: • Confusion (mental test score <8 or new disorientation) • Respiratory rate >30/min • Blood pressure (SBP<90mmHg or DBP <60mmHg) • Age >65 years 3 or 4 (33–48%) Urgent hospital admission 1 or 2 (5–12%) Consider hospital referral 0 (1.2%) CRB-65 score (Associated mortality) Likely suitable for home treatment Score 1 point for each of: • Confusion (mental test score <8 or new disorientation) • Urea >7 mmol/L (i.e. includes use of laboratory tests) • Respiratory rate >30/min • Blood pressure (SBP<90mmHg or DBP <60mmHg) • Age >65 years 3 or more (17–57%) Manage in hospital as severe pneumonia Assess for ICU admission especially if CURB-65 is >4 2 (13%) Consider hospital- supervized treatment Options include: a) Short stay in- patient b) Hospital-supervized outpatient 0 or 1 (1–3%) CURB-65 score (Associated mortality) Likely suitable for home treatment Table 1. Microorganisms and pathological insults that cause pneumonia (c) Non-hospital (i.e. community) management of CAP using the recently validated CRB-65 score (d) Management of CAP in patients admitted to hospital using the recently validated CURB-65 score acute lower respiratory tract (LRT) illness infection fever focal chest symptoms (±signs) new shadowing on chest X-ray (CXR) Classification microbiological classification anatomical 80 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 80. r Community-acquired pneumonia (CAP): Streptococcus pneumoniae Mycoplasma pneumoniae Chlamydia pneumoniae Legionalla Haemophilus influenzae Moraxella catarrhalis r Hospital-acquired (nosocomial) pneumonia ∼ ∼ r Aspiration/anaerobic pneumonia: r Opportunistic pneumonia r Recurrent pneumonia: Epidemiology Annual incidence: Mortality: Seasonal variation: Mycoplasma Staphylococcus Mycoplasma Risk factors Specific risk factors age Mycoplasma occupation environment geographical Coxiella burnetti Legionella pneu- mophila Diagnosis diagnosis complications severity classification Clinical features Symptoms Signs Mycoplasma non-respiratory features Complications Investigations Routine blood tests: Mycoplasma Legionella Mycoplasma Blood gases: Microbiology: Serology: Mycoplasma Legionella Radiology: Severity assessment Clinical: Laboratory: Po < × > × Severity scoring: c u r < < b 65 Management Supportive measures: P o S o < ± Ventilatory support: Physiotherapy and bronchoscopy: Initial antibiotic therapy: r Non-hospitalized patients: S. pneumoniae β r Hospitalized patients: S. pneumoniae β H. influenzae Community-acquired pneumonia Diseases and treatment 81
  • 81. r37 Hospital-acquired (nosocomial) pneumonia (a) (i) CXR; (ii) CT scan from a patient with hospital-acquired pneumonia (HAP) showing consolidation, cavitation and abscess formation (i) Table 1. Risk factors and modifiable risk factors for HAP and VAP • Antimicrobial therapy in the previous 90 days • Current hospitalization of >5 days • High frequency of local antibiotic resistance • Presence of risk factors for HCAP Hospitalization for >2 days in the previous 90 days Residence in a nursing home Home wound care or intravenous therapy Chronic dialysis within 30 days Family member with MDR pathogen • Immunosuppressive disease and/or therapy Table 2. Risk factors for multidrug-resistant pathogens causing hospital-acquired pneumonia (b) Pathogenesis of hospital aquired pneumonia (c) Likely pathogens and empirical antibiotic treatment of hospital-acquiredt pneumonias ONSET + MDR PATHOGEN RISK Early-onset (<4 days in hospital) + no risk factors for MDR pathogens Late-onset (>4 days in hospital) + risk factors for MDR pathogens LIKELY PATHOGENS Hospitalization + antibiotic therapy Gastro-oesophageal aspiration Cough reflex (e.g. drugs and pain) Colonization of the nasopharynx by Gram-negative bacilli Aspiration of nasopharyngeal secretions Infected ventilators/circuits Direct access to LRT (ET/tracheostomy tubes) Blood spread from distant focus (iv lines, infected emboli, abdominal sepsis) Streptococcus pneumoniae Haemophilus influenza S. aureus (methicillin-sensitive) Antibiotic-sensitive Gram-negative bacilli, e.g. E. coli, Proteus spp. Klebsiella pneumoniae, Serratia All the early-onset HAP pathogens + MDR pathogens e.g. Pseudomonas aeruginosa, Klebsiella pneumoniae, Acinetobacter spp., MRSA, Legionella pneumophilia TREATMENT Narrow-spectrum (single-agent) antibiotic therapy e.g. ceftriaxone or fluoroquinolones (e.g. ciprofloxacin) or co-amoxiclav or ertapenem Broad-spectrum (multiagent) antibiotic therapy Antipseudomonal cephalosporin (e.g. ceftazidine) or Antipseudomonal carbapenem (e.g. imipenem) or β-lactam/ β-lactamase inhibitor (e.g. piperacillin-tazobactam) + Antipseudomonal fluoroquinolones (e.g. levofloxacin) or Aminoglycoside (e.g. amikacin, gentamicin) + Vancomycin or linezolid (if risk factors for MRSA) HAP or VAP or HCAP Supine positioning Impaired consciousness (e.g. drugs) Swallowing difficulty + vomiting Immobility + debility Instrumentation (e.g. NG tube) (ii) Consolidation Fluid-filled abscess Cavitation Unmodifiable risk factors Modifiable risk factors 1. Host related • Malnutrition • Age: >65, <5 years old • Chronic disease (e.g. renal) • Diabetes • Immunosuppression (e.g. SLE) • Alcohol dependency • Aspiration (e.g. epilepsy) • Recent viral illness • Obesity • Smoking 2. Therapy related • Mechanical ventilation • Postoperative 3. Epidemiological factors • Environmental (e.g. psittacosis) • Occupational (e.g. Q fever) • Travel abroad (e.g. paragonomiasis) • Air conditioning (e.g. Legionella) 1. Host related • Nutrition (e.g. enteral feeding) • Pain control, physiotherapy • Limit immunosuppressive therapy • Posture, kinetic beds • Preoperative smoking cessation 2. Therapy related • Semi-recumbent position (30˚ head up) • Early removal of iv lines, ET and NG tubes • minimize sedative use • Avoid gastric overdistention • Avoid intubation + re-intubation • Maintain ET cuff pressure >20cmH2O* • Subglottic aspiration during intubation • Change + drain ventilator circuits • Sucrulfate for stress ulcer prophylaxis 3. Infection control • Hand washing, sterile technique • Patient isolation • Microbiological surveillance Mucociliary clearance Immunity Local lung defences 82 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 82. Hospital-acquired (nosocomial) pneumonia (HAP) ventilator-associated pneumonia (VAP) healthcare-associated pneumonia (HCAP) Definitions HAP: VAP: HCAP: Epidemiology Incidence: Risk factors: prevented Mortality: Early-onset HAP/VAP < late-onset HAP/VAP > Pathogenesis ± Aetiology Klebsiella pneumoniae Pseudomonas aeruginosa Escherichia coli Staphylococcus aureus Streptococ- cus pneumoniae Haemophilus influenza S. aureus S. aureus Diagnosis clinical microbiological Clinical: > ◦ Diagnostic tests: ± complications Management Supportive therapy oxygen P o S o < intravenous fluids (±vasopressors/inotropes) ventilatory support Phys- iotherapy analgesia Semi-recumbent ◦ Antibiotic therapy r early-onset HAP/VAP monotherapy β β r late-onset HAP/VAP combination therapy P. aeruginosa S. aureus > Other pneumonias Aspiration/anaerobic pneumonia: Bacteroides Pneumonia during immunosuppression Aspergillus Pneumocystis carinii Hospital-acquired (nosocomial) pneumonia Diseases and treatment 83
  • 83. r38 Pulmonary tuberculosis Giant cells (multinucleate) Central caseation (‘cheesy pus’) Lymphocytes Acid-fast bacilli Ghon focus and hilar lymphadenopathy = ‘Primary complex’ (a) (c) Pulmonary complications Apical cavitiesMycetoma Pneumothorax Collapsed lung Pleural fluid Miliary TB • Malaise • Weight loss • Low-grade fever Tuberculosis (b) CXR of patients with TB General • Malaise • Fever and weight loss • Night sweats Large joint TB Neurological TB • Meningitis • Cerebral abscess • Nerve lesions Cardiac TB • Pericardial TB • Calcification and tamponade Spinal TB • Vertebral collapse • Paralysis Skin TB • Lupus vulgaris Lymph node TB • Painless lymph node enlargement Respiratory TB • Dyspnoea • Cough/sputum • Haemoptysis • Crackles Renal TB • Haematuria • Sterile pyuria • Chronic renal failure Abscess Upper lobe shadowing and cavitation 84 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 84. Pathogenesis Primary pulmonary TB Mycobac- terium tuberculosis granuloma Ghon focus primary complex tuberculin Mantoux Heaf Post-primary pulmonary TB tuberculous pneumonia pleural effusions miliary TB Clinical features Primary pulmonary TB erythema nodosum bronchiecta- sis Post-primary TB Miliary TB Investigation Blood tests Mantoux test: > Heaf test Microbiology: Histopathology: Chest radiography Drug therapy compliance with drug ther- apy Complications Prevention and contact tracing BCG must be notified Pulmonary tuberculosis Diseases and treatment 85
  • 85. r39 The immunocompromised host (b) Infectious causes of respiratory disease in immunocompromised patients Immunological defect Clinical conditions Types of infection Neutropaenia Chemotherapy, leukaemia, aplastic anaemia Bacterial (e.g. E. coli, staph aureus) Fungal (e.g. aspergillus) Infectious • Bacterial pneumonia • Fungal pneumonia (e.g. aspergillosis) • Opportunistic pneumonia (e.g. PCP) • Viral pneumonoia Non-infectious • Pulmonary oedema, ARDS • Radiation pneumonitis • Drug-induced, e.g. amiodarone, busulphan • Malignant infiltration • Pulmonary haemorrhage • Non-specific interstitial pneumonitis (a) Causes of new pulmonary infiltrates (c) Clinical features of AIDS Causes of respiratory disease and CXR infiltrates in HIV-infected patients Cerebral HIV encephalopathy, dementia Cerebral toxoplasmosis Cryptococcus neoformans Primary brain lymphoma General Weight loss, fatigue Lymphadenopathy CMV retinitis Respiratory Pneumocystis pneumonia Mycobacterium avium complex Mycobacterium tuberculosis Pneumonia (e.g. S. pneumoniae) Infection* • Bacterial (e.g. S. Pneumoniae) • Pneumocystis pneumonia • Fungal (e.g. cryptococcus) • Mycobacterial infection (e.g. MTB, MAC) • Viral (e.g CMV) Drug toxicity e.g. amiodarone, busulphan Gastrointestinal Diarrhoea Cytomegalovirus colitis Oral + oesophageal candida Small bowel lymphoma Skin Herpes simplex Kaposi’s sarcoma Dermatitis Interstitial pneumonitis e.g. Non-specific interstitial pneumonitis Lymphocytic interstital pneumonitis Blood Lymphopaenia Bacteraemia Malignancy Non-Hodgkin lymphoma Kaposi’s sarcoma Burkitt’s lymphoma Lung cancer Malignancy Non-Hodgkins lymphoma Burkitts lymphoma Clinical features and diseases that are indicators of AIDS Causes of chest disease + CXR infiltrates in HIV- infected patients (*commonest) General causes Heart failure, pulmonary oedema Sepsis-induced acute respiratory distress syndrome (ARDS) Radiation pneumonitis Pulmonary haemorrhage (e) Cerebral toxoplasmosis with ring enhancement on a post-contrast CT brain scan (d) Pneumocystis Jirovecii pneumonia (PCP) showing bilateral diffuse infiltrates Mass lesion with ring enhancement Impaired T-cell function Impaired B-cell function Impaired compliment Mannose lectin deficiency, complement deficiency Lymphoma, leukaemia, myeloma, hypogammaglobulinaemia Transplantation, steroids, lymphoma, HIV infection, chemotherapy Streptococcus pneumonia Streptococcus pneumoniae, Haemophilus influenza Bacteria (e.g. mycobacteria), fungi (e.g. PCP), viruses (e.g. CMV) 86 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 86. Clinical presentation Investigations Aspergillus Pneumocystis jiroveci Cryptococcus Diagnosis r Infection r Non-infectious causes Treatment r Antibiotic ± r Steroid therapy r Supportive therapy Respiratory manifestations in the HIV-positive patient 1 Infectious causes r Bacterial pneumonia Streptococcus pneumoniae Staphy- lococcus aureus Nocardia Legionella r Pneumocystis jirovecii pneumonia < × ∼ > ∼ r Mycobacteria Mycobacterium tuberculosis My- cobacterium avium r Viral Cytomegalovirus r Fungal . Aspergillus Cryptococcus neoformans ± histoplasmosis coccidioidomycosis 2 Non-infectious causes r Malignancie Kaposi’s sarcoma Non-Hodgkin’s lymphoma Lung cancer r Interstitial pneumonitis r Drug-induced heart failure The immunocompromised host Diseases and treatment 87
  • 87. r40 Lung cancer (a) Mass on CT: a >3cm spiculated mass is seen in upper lobe of the right lung (c) CXR showing squamous cell tumour in hilar region (b) Fibreoptic bronchoscopy showing tumour invading bronchus (e) Survival for non-small cell cancer Stage T (tumour) N (node) M (metastasis) Key IA IB IIA IIB IIIA IIIB IV T1 T2 T1 T2 T3 T1, 2, 3 T3 T1, 2, 3, 4 T4 T1–4 N0 NO N1 N1 N0 N2 N1 N3 N1, 2 N0–3 M0 M0 M0 M0 M0 M0 M0 M0 M0 M1 (d) Staging system for non-small cell lung cancers T1: T2: T3: T4: ≤3cm without division >3cm, or invasion of main bronchus >2cm from main carina, or invades visceral pleura, or bronchus causing obstruction Invades chest wall or pleura, or main bronchus <2cm from main carina Invades adjacent structure, malignant effusion, satellite nodules N0: N1: N2: N3: No lymph node metastasis Ipsilateral hilar lymph nodes Ipsilateral mediastinal or subcarinal lymph nodes Contralateral, scalene or supraclavicular lymph nodes M0: M1: No distant metastasis Any distant metastasis %Survival 100 50 0 0 5 Years Stage IA Postresection pathological diagnosis Inoperable clinical diagnosis IB IIA IIIA IIIA IIIB IV IIB 88 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 88. lung cancer worse prog- nosis 5-year survival 13% Risks Cigarette smoking > < Passive smoking Asbestos exposure Radon gas Classification small cell SC non-small cell NSC NSC squamous cells large cells adenocarci- noma Adenocarcinomas < > Squamous cell carcinomas Large cell carcinoma SC Presentation extrathoracic metastasis Paraneoplastic syndromes autoantibodies parenchymal nodules Evaluation malignancy staging suitability for therapy Computed to- mography CT) scans Positron emission tomography (PET) scanning Staging SC cancer limited extensive Limited disease Extensive disease NSC cancer tumour node metastasis T3 T4 TNM categories stage I II > surgical resection stage IIIA stage IIIB IV chemotherapy radiation therapy Stage IV Platinum taxol-based Lung cancer Diseases and treatment 89
  • 89. r41 Acute respiratory distress syndrome 3. Normal alveoli As normal alveoli are easiest to inflate, they are damaged by overinflation = 'volutrauma'. This causes increased membrane permeability and flooding Use low tidal volumes (6 mL/kg) IL-1, IL-8 Increased permeability and consolidation Pathophysiology Widespread alveolar and dependent consolidation Loss of surfactant and increased permeability Alveolar flooding NO increases blood flow past ventilated alveoli Consolidated alveoli NO NO Back Front Reduces shunt Consolidated lung (a) Acute respiratory distress syndrome (b) Ventilator-induced lung damage (c) Common causes of ARDS (d) V/Q matching CXR of aspiration-induced ARDS 1. Loss of surfactant Repeated alveolar collapse and re-expansion cause damage. Aim to prevent alveolar collapse and encourage alveolar recruitment This is achieved with PEEP and increased mean airways pressure (i.e. reverse I:E ratio) to hold open alveoli Direct pulmonary Infective (pneumonia, tuberculosis) Pulmonary trauma Near-drowning Toxic gas inhalation Smoke NO2, NH3, Cl2 Phosgene Oxygen toxicity (FiO2 >0.8) Inhalation of gastric contents (pH <2) Indirect Sepsis Non-thoracic trauma Burns Haemorrhage, multiple transfusion Post arrest Bowel infarction Anaphylactic Pancreatitis Uraemia, toxins, eclampsia Drugs (salicylates, barbiturates) 2.Damaged/fibrosed/ consolidated alveoli: difficult to inflate (reduced compliance) High peak inspiratory pressures (PIP) cause alveolar damage, 'barotrauma' and pneumothorax in normal lung tissue Use low PIP (<30 cmH2O) Direct alveolar damage (aspiration/pneumonia) Systemic inflammatory response (sepsis/trauma) Endothelial and alveolar cell damage Normal lung Blood flow greatest in dependent lung V/Q matching improved 1. PEEP: recruits collapsed alveoli 2. Nitric oxide 3. Prone position Endotoxin IL-1, IL-6, TNFα White cellactivation Whitecell adhesionandmigration Decreased surfactant with alveolar collapse H2O Dependent consolidation with air bronchograms CT scan of ARDS 90 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 90. Acute respiratory distress syndrome (ARDS) internationally agreed criteria 1 Severe hypoxaemia P o F o < ± P o F o = = 2 Bilateral diffuse pulmonary infiltrates on chest X-ray 3 Normal or only slightly elevated left atrial pressure < Acute lung injury (ALI) P o F o < Epidemiology and prognosis incidence high (>40%) ∼ ∼ ∼ > multiorgan failure MOF Pathogenesis (Fig. 41a and b) and causes (Fig. 41c) acute inflammatory phase healing fibroproliferative phase Clinical features acute inflammatory phase healing fibroprolifer- ative phase Investigations Monitoring: to assess fluid balance and ensure adequate tissue oxygen delivery Radiological: diffuse bilateral pulmonary infiltrates diffuse patchy infiltrates dependent consolidation pneumothoraxes pneu- matoceles fibrosis Management establish and treat the underlying cause F o > limit pressure- induced damage, optimize oxygenation avoid circulatory com- promise < Alveolar recruitment > Excessive fluid loading must be avoided Essential general measures No drug therapy has been consistently beneficial Inhaled ni- tric oxide prone position Extracorporeal mem- brane oxygenation (ECMO) Acute respiratory distress syndrome Diseases and treatment 91
  • 91. r42 Mechanical ventilation (a) Indications for mechanical ventilation or support in adults Surgery General anaesthesia with neuromuscular blockade Postoperative management following major surgery Respiratory centre depression Usually when PaCO2 >7–8kPa (50–60mmHg) Head injury Drug overdose, e.g. opiates, barbiturates Raised intracranial pressure: cerebral haemorrhage/ tumours/meningitis/encephalitis Status epilepticus Lung disease Pneumonia Acute respiratory distress syndrome (ARDS) Severe asthma attack Acute exacerbation of chronic obstructive pulmonary disease (COPD), cystic fibrosis Trauma–lung contusion Pulmonary oedema Cervical cord damage above C4 Neck fractures Neuromuscular disorders– when VC <20–30mL/kg Guillain–Barré Myasthenia gravis Poliomyelitis Polyneuritis Other Cardiac arrest Severe circulatory shock Resistant hypoxia in type 1 respiratory failure (reduces oxygen consumption) (c) Airway pressure profiles in different types of ventilation cmH2O 20 0 SV INPV CPAP BiPAP IPPV (CMV) IPPV + PEEP (5cmH2O) SIMV Timing SV = spontaneous ventilation, INPV = intermittent negative pressure ventilation, CPAP = continuous positive airway pressure, BiPAP = biphasic continuous airway pressure (trace shown is fixed time period BiPAP), IPPV = intermittent positive pressure ventilation (= CMV), CMV = controlled mechanical ventilation, PEEP = positive end-expiratory pressure, SIMV = synchronized intermittent mandatory ventilation. If a spontaneous breath occurs in the timing window it triggers a synchronized ventilator breath and if not a mandatory breath is given soon after the timing window. (d) Complications of mechanical ventilation Risks during endotracheal intubation or tracheostomy Myocardial depression from anaesthetic Aspiration of gastric contents Fall in PaO2 during apnoea Reflex bronchoconstriction and laryngospasm Risks associated with sedation and paralysis Cardiac depression Depression of respiratory drive (delays weaning) Increases danger of disconnection/ventilator failure Risks associated with high inspired oxygen (see Chapter 43) Chest wall disorders Kyphoscoliosis Trauma: especially flail segment (multiple rib fractures section of chest wall unattached) Synchronized breath Spontaneous breath (b) Nasal mask and NIPPV Unsynchronized mandatory breath Risks of endotracheal intubation and tracheostomy Intubation of the oesophagus Intubation of a bronchus Blockage/accidental extubation Laryngeal/tracheal damage or stenosis Infection Risks associated with mechanical ventilation High airway pressure barotrauma Alveolar overdistension volutrauma: • Pneumothorax, pneumomediastinum • Subcutaneous emphysema (= air in skin) • Structural damage to lung, airways and capillaries • Bronchopulmonary dysplasia (see Chapter 17) 92 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 92. Types of mechanical ventilation intermittent negative pressure ventila- tion (INPV) tank ventilator iron lung Jacket cuirass ventilators intermittent positive pressure ventilation IPPV controlled mechanical ventilation, CMV , = / , = / , = × ≈ / / = P co P co P co permis- sive hypercapnia P o Fo Po synchronized intermittent mandatory ventilation, SIMV mandatory minute ventilation, MMV positive end-expiratory pressure, PEEP P o P o Po > Non-invasive respiratory support continuous positive airway pressure (CPAP) obstructive sleep apnoea ARDS non-invasive intermittent positive pressure ventilation (NIPPV) CPAP NIPPV Weaning Complications of mechanical ventilation Mechanical ventilation Diseases and treatment 93
  • 93. r43 Oxygenation and oxygen therapy (a) Indications for acute oxygen therapy (d) Oxygen delivery devices (c) Risks associated with high-dose oxygen therapy 1. Cardiac and respiratory arrest 2. Hypoxaemia (PaO2 <8kPa, SaO2 <90%) 3. Hypotension (systolic BP <100 mmHg) 4. Low cardiac output 5. Metabolic acidosis (bicarbonate <18 mmol/L) 6. Respiratory distress (respiratory rate >24/min) 1. Carbon dioxide retention: ~10% of breathless patients, mainly COPD, have type 2 respiratory failure (RF). ~40–50% of COPD patients are at risk of type 2 RF 2. Rebound hypoxaemia: occurs if oxygen is suddenly withdrawn in type 2 RF 3. Absorption collapse O2 in poorly ventilated alveoli is rapidly absorbed whereas N2 absorption is slow, so high FO2 can cause collapse 4. Pulmonary oxygen toxicity FiO2>60% may damage alveolar membranes causing ARDS if inhaled for >24–48 hrs (Chapter 41). Hyperoxia can cause coronary and cerebral vasospasm 5. Fire Deaths and burns occur in smokers during O2 therapy 6. Paul–Bert effect Hyperbaric O2 can cause cerebral vasoconstriction and epileptic fits Are independent of the patient’s pattern of breathing and inspiratory volume Used in patients with COPD and respiratory failure to avoid CO2 retention This system delivers more gas than is inspired (i.e. >30 L/min). Consequently, FiO2 is less affected by the breathing pattern. The resulting masks are high flow, low concentration and fixed performance Figure (iv) illustrates that a fixed O2 flow through a Venturi valve entrains the correct proportion of air to achieve the required O2 concentration 2. Fixed performance devices Air is entrained during breathing whilst oxygen is delivered from a reservoir (i.e. mask, reservoir bag, nasopharynx) e.g. Figure (i) ‘Low-flow face masks’, O2 flows at ~2–10 L/min into the mask and is supplemented by air drawn into the mask. The FiO2 achieved depends on ventilation Examples of variable performance devices are ‘low-flow’ facemasks (see i), nasal cannulae (see ii) and non- rebreathing face masks with reservoir bags (see iii) These devices cannot be used if accurate control of FiO2 is desirable, e.g. COPD with hypercapnia Ventilation = 25 L/min O2 flow = 2 L/min; air (21% O2) flow = 23 L/min FiO2 = (2+0.21 x 23)/25 x 100 = 27% Ventilation = 5 L/min O2 flow = 2 L/min; air (21% O2) flow = 3 L/min FiO2 = (2+0.21 x 3)/5 x 100 = 53% The FiO2 delivered to the lungs depends on the oxygen flow rate, the patient’s inspiratory flow, respiratory rate and the amount of air entrained 1. Variable performance devices Continuous positive airways pressure (CPAP) masks Use a tight fitting mask and a flow generator to deliver a fixed FiO2 with a positive pressure (5–10 cm/H2O) throughout the respiratory cycle Venturi valves are colour coded and deliver 24, 28, 31, 35, 40 or 60% FiO2 for a fixed flow rate 28 L/min entrained air 5 L/min inspired 5L/min inspired Venturi Valve (iv) ‘High-flow’ (Venturi), low concentration face mask (iii) Non-rebreathing and anaesthetic masks (i) ‘Low-flow’ facemask (ii) Nasal cannulae High (10–15 L/min) flow rates of O2 provide high FiO2 > 60% and up to 100% Non-rebreathing masks have a reservoir bag which should be filled before use. They increase FiO2 by preventing O2 loss during expiration FiO2 is 60–100% at O2 flow rates of 10–15 L/min FiO2 can be 60% at 15 L/min O2 FiO2 is between 24 and 35% One-way valve stops exhaled air entering reservoir bag Reservoir bag O2 flow 10–15 L/min O2 flows at ~2–15 L/min into the mask and is supplemented by air drawn into the mask. Flow rate must be > 5 L/min to prevent CO2 rebreathing 3 L/min air drawn into mask The O2 flow is constant so FiO2 varies with ventilatory volume. More comfortable and not removed during eating or coughing. O2 inhaled even when mouth breathing O2 flow rates up to 4 L/min. Higher rates dry mucosa 30 L/min into mask at FiO2 24% 25 L/min escapes from mask 2 L/min jet of oxygen 30 L/min total gas flow at fixed O2 concentration 2L/min oxygen into mask 2 L/min oxygen 94 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 94. Tissue hypoxia low arterial Po blood O2 content tissue blood flow haemoglobin concentration oxygen dissocia- tion curve poisoning of intracellular oxygen usage Measuring tissue hypoxia S o pulse oximeter P o blood gas analysis S P o S o mixed venous oxygen partial pressure P −o Po P o S o P o Oxygen therapy type 2 (hyper- capnic, CO2 retaining) respiratory failure r In normal patients S > P r In patients at risk of type 2 respiratory failure S S r High-dose supplemental oxygen (>60%) S r Moderate-dose supplemental oxygen (40–60%) S r Low-dose (controlled) supplemental oxygen (24–28%) CO2 retaining, type 2 respira- tory failure S P co S P co S P co > < CO poisoning P Stop oxygen therapy S S Other techniques to improve oxygenation 1 Anaemia: 2 Block of airways by mucus and retention of secretions 3 Fluid restriction 4 Alveolar recruitment 5 Ventilatory support Oxygenation and oxygen therapy Diseases and treatment 95
  • 95. r44 Sleep apnoea EOG (eye movement) EEG SaO2 (blood O2 saturation) Thoracic movement Airflow (a) Normal (b) Obstructive sleep apnoea (c) Central sleep apnoea Desaturation Arousal No airflow Continued effort Desaturation No effort Arousal No airflow Polysomnogram (simplified) (e) Cheyne-Stokes respiration Time VentilationO2saturation Cheyne-Stokes respiration occurs in heart failure and at altitude, and is characterized by slowly increasing and decreasing depth of each breath Pharynx Blocked airway Tongue Uvula (d) Obstructive sleep apnoea Normal airflow Obstructed airflow 96 The Respiratory System at a Glance, 3e. By J.P.T. Ward, J. Ward, R.M. Leach. Published 2010 Blackwell Publishing Ltd.
  • 96. Sleep apnoea obstructive sleep apnoea central sleep apnoea (CSA) polysomnogra- phy REM ∼ NREM P o P co Obstructive sleep apnoea loud snoring daytime hypersomnolence gain weight nocturnal hypoxia apnoea plus hypopnoea index AHI obesity hy- poventilation syndrome pulmonary hypertension Therapy ≥ nasal con- tinuous positive airway pressure CPAP Central sleep apnoea loss or inhibition of central respiratory drive Cheyne-Stokes respiration Therapy NIPPV Sleep apnoea Diseases and treatment 97
  • 97. Case studies: questions Case 1 Questions 1 You are worried whether either or both could have a pulmonary embolus (PE). From the history and findings so far, is this likely in either or both of these patients? If these patients had not had surgery recently but had presented with the same symptoms and signs in Accident and Emergency, would your answer be different? 2 Which of these oxygen saturations is ‘typical’ of a pulmonary embolus? 3 Pulmonary emboli produce an area of lung that is ventilated but not perfused; that is, they produce alveolar dead space and therefore increase physiological dead space. Does increased physiological dead space inevitably lead to a reduced arterial o2? 4 What other aspects of the history might be relevant? 5 d-dimer tests are a useful addition to the diagnostic armoury but false-positives are common. False-negatives also occur. Which sort of PE is most likely to be associated with a false-negative PE? How long do D-dimers remain elevated? 6 What is the role of chest X-ray (CXR) and electrocardiogram (ECG)? How will they be affected in the presence of a pulmonary embolus? 7 What other investigations are appropriate? 8 What are the treatment options for Elizabeth and Alice? Case 2 μ μ Questions 1 Is this peak flow normal? Apart from the nomogram values, can you think of any other peak flow reading with which it would be useful to compare today’s clinic reading? 2 If you measured the following: r FEV1/FVC r Airway resistance r Functional residual capacity (FRC) r Lung compliance r Arterial o2 and arterial co2 – how would they compare with the normal for a boy of his age and size? On a school trip to a countryside park, Tom becomes breathless running across a field. His teacher is alarmed by his noisy breathing and asks you, a passing medical student, to assess whether they need to get him to hospital. 3 What simple observations can you make that will help you decide how severe this attack is? In his backpack he has a salbutamol inhaler, a salmeterol inhaler, a sodium cromoglycate inhaler and a beclometasone inhaler. Which should he use? 4 If you had been able to measure the following during his episode of breathlessness: r FEV1/FVC r Peak flow rate r Airway resistance r Functional residual capacity r Lung compliance r Arterial o2 and arterial co2 – how do you think they would compare with the normal for a boy of his age and size? 5 If you had had your stethoscope with you, what would you have heard on examining his chest? At 18 years of age, Tom goes to college in London. He stops taking regular medication, as he feels he has ‘grown out’ of his asthma. He keeps a salbutamol inhaler in his room ‘just in case’. During the first term he is well, apart from a couple of wheezy episodes while playing football. In the second term, he develops a heavy cold, and over 24 hours he becomes progressively more breathless despite frequent puffs of salbutamol. His friends call out his GP, who finds the following: Tom is fully alert, but talking in broken sentences because he is very breathless. He is not cyanosed. He is using his accessory muscles of respiration. On auscultation, there are widespread expiratory rhonchi (wheezes). BP is 115/80 mmHg, HR 110 beats/min, respiratory rate 30 breaths/min, peak flow 200 L/min. 6 Which observations suggest that this is a fairly severe attack? 7 If the GP had measured airway resistance, FRC, lung compliance, arterial o2 and co2, how would they compare to the predicted values? His GP decides that this attack warrants hospital admission, and he calls an ambulance. Unfortunately, owing to heavy traffic it is 40 minutes before he arrives at the local Accident and Emergency department. By this time, Tom is confused, too breathless to talk and unable to produce a peak flow reading. The Accident and Emergency 98 Cases and self assessment Case studies: questions
  • 98. officer notices he is now cyanosed, although the widespread rhonchi noted in the GP’s letter have now disappeared. Arterial blood gases show arterial o2 = 7 kPa and arterial co2 = 5.5 kPa while breath- ing 60% oxygen. 8 Discuss the features that suggest this asthma attack is life- threatening. Do the reduced rhonchi on auscultation contradict the other findings? 9 What is the cause of the low arterial o2? Was the inhaled oxygen helpful, and if so was the correct concentration used? Is this co2 normal, and how does it affect your assessment of the severity of this attack? Case 3 Physical examination Chest radiograph D co Questions 1 What would you expect the patient’s FRC and residual volume (RV) to be? 2 Why is the cardiac point of maximal impulse (PMI) shifted to the midline? 3 Why is the FVC low? 4 Why is the Lco low? 5 What will happen to the patient’s oxygenation with exercise? Why? 6 Why is the patient’s jugular venous pressure elevated? 7 What are the most likely diagnosis and pathophysiology of his dis- ease? Case 4 D co Questions 1 What patterns of abnormalities do these patients exhibit? 2 Based on the lung function results, what is the most likely patho- physiology explaining each patient’s symptoms? 3 What is the likely explanation for the differences in FRC and RV between the two patients? 4 What is the differential diagnosis for Patient A? 5 What is the differential diagnosis for Patient B? 6 Both patients have hypoxaemia. Which patient is more likely to have hypercapnia? Case 5 Figure 45 Case studies: questions Cases and self assessment 99
  • 99. < Questions 1 What are the most common causes of haemoptysis, and from which circulation does bleeding occur? 2 Is haemoptysis life-threatening, and how is the severity of bleeding classified? 3 What are the clinical features that may help establish the diagnosis? What is the most likely cause in this case? 4 What investigations would you perform to establish the diagnosis in this case? 5 What is bronchiectasis, and what causes it? 6 How should a large haemoptysis be managed? Case 6 P Questions 1 Why is each patient hypoxaemic and what will happen when the FiO2 is raised to 1.0 (i.e. 100% oxygen therapy)? Precise answers cannot be calculated but assume reasonable values for unknown data. 2 How will you ensure improved oxygenation in each patient? Case 7 Questions 1 What are the risks associated with cigarette smoking? 2 Why is smoking addictive? 3 How would you advise the wife regarding smoking cessation? 4 Following smoking cessation what is the risk of developing cancer? 5 What are the effects of passive smoking on children? Case 8 Questions: 1 What brings you to suspect PSP? 2 How do you confirm your diagnosis? 3 What causes PSP, and is it likely to happen to James again? 4 What treatment would you prescribe? 5 You advise him neither to play another game for at least some months nor to climb Mount Kilimanjaro, which he had intended to do for charity. Why? 100 Cases and self assessment Case studies: questions
  • 100. Case studies: answers Case 1: Pulmonary emboli 1 2 P o 3 Po P co 4 5 d d d 6 7 8 Case 2: Asthma 1 2 Case studies: answers Cases and self assessment 101
  • 101. 3 r r > r r > r β 4 Pco 5 6 7 Pco Po Pco 8 9 P o Pco Pco Pco Case 3: Severe breathlessness 1 2 ◦ 3 4 D co 5 D co < 6 7 α 102 Cases and self assessment Case studies: answers
  • 102. Case 4: Restrictive ventilatory defect 1 D co 2 D co D co 3 4 5 r r r r 6 Case 5: Haemoptysis 1 ∼ ∼ 2 < > 3 bronchiectasis ∼ ∼ Aspergillus 4 d Case studies: answers Cases and self assessment 103
  • 103. Figure 46(a) Aspergillus Aspergillus > 5 6 Immediate Bronchial angiography embolization ∼ ∼ Aspergillus < Final diagnosis: Case 6: Oxygenation and oxygen therapy Patient 1 1 P co P o = P o − P co R P o ≈ P o = P o = F o × − = × − = R ∼ P co = co F o P o = F o × − = × − . = P o ≈ P o = − . . = 2 P co P o P co Patient 2 1 P o P o P co P o F o = P o P o = − . = P o 104 Cases and self assessment Case studies: answers
  • 104. 70.0 14.0 7.0 PaO2(kPa) 0.2 0.6 1.0 FiO2 Hypoxaemia caused by true right to left shunt is refractory to supplemental O2 when ‘shunt fraction’ exceeds 30% Shunt fraction = QS/QT (%) Effect of true shunt (QS/QT) on the arterial oxygen tension (PaO2) response to inspired oxygen fraction (FiO2) 50% shunt 30% shunt 10% shunt Figure 47 2 F o ∼ type 1 respiratory failure P co ∝ Patient 3 1 P o F o P o × P o F o P o ∼ 2 P o F o Case 7: Smoking cessation 1 2 3 A A A A A Nico- tine replacement therapy Bupropion (Zyban) Varenicline (Champix) 4 5 Case studies: answers Cases and self assessment 105
  • 105. Case 8: Primary spontaneous pneumothorax 1 2 3 > 4 5 106 Cases and self assessment Case studies: answers
  • 106. Self-assessment questions best Chapter 1: Structure of the respiratory system: lungs, airways and dead space 1.1 The pulmonary nerve plexus 1.2 The pleural space 1.3 Type II pneumocytes 1.4 Alveolar dead space Chapter 2: The thoracic cage and respiratory muscles 2.1 Intercostal spaces 2.2 The diaphragm 2.3 Accessory inspiratory muscles include all of the following EX- CEPT 2.4 Paradoxical breathing Chapter 3: Pressures and volumes during normal breathing 3.1 Functional residual capacity 3.2 Intrapleural pressure 3.3 From the trace produced when a subject breathes in and out of a simple water-filled spirometer, it is possible to measure 3.4 The predicted lung volumes for a subject Chapter 4: Gas laws 4.1 Fractional concentration of oxygen in the air = 4.2 Saturated water vapour pressure Self-assessment questions Cases and self assessment 107
  • 107. 4.3 A man has eaten a lunch of baked beans on toast and drunk a bottle of cola after which he goes on a hot air balloon ride. As he ascends he experiences abdominal pain. The gas law that best explains his problem is ∝ ∝ ∝ = × 4.4 When the lid was removed from the bottle of cola, bubbles formed in the liquid and rose to the surface. ∝ ∝ ∝ = × Chapter 5: Diffusion 5.1 Diffusion through the alveolar–capillary membrane 5.2 Diffusion-limited uptake of a gas through the alveolar– capillary membrane 5.3 Carbon monoxide (CO) diffusing capacity (transfer factor) P P 5.4 One condition that does NOT reduce the carbon monoxide diffusing capacity (transfer factor) is Chapter 6: Lung mechanics: elastic forces 6.1 When producing a pressure–volume loop for the measurement of static lung compliance 6.2 Surfactant 6.3 Low static lung compliance 6.4 Dynamic pressure–volume (P–V) loops differ from static pressure–volume loops in that Chapter 7: Lung mechanics: airway resistance 7.1 Airway resistance in the human lung is 7.2 Airway smooth muscle constriction is 7.3 During a forced expiration 108 Cases and self assessment Self-assessment questions
  • 108. 7.4 Airway resistance Chapter 8: Carriage of oxygen 8.1 Haemoglobin Pco 8.2 In an anaemic patient P P 8.3 A low P50 8.4 Replacing inspired air with a gas mixture contains 60% oxygen P Chapter 9: Carriage of carbon dioxide 9.1 CO2 is transported in mixed venous blood as approximately < 9.2 Decreased pH within the red blood cell 9.3 The Haldane effect states that Pco Pco Pco Pco 9.4 Hyperventilation P co < Chapter 10: Control of acid–base balance 10.1 The Henderson–Hasselbalch equation Pco 10.2 Which of the following statements about buffers is true? = 10.3 Why do CO2 and bicarbonate provide a good buffer system for the blood? 10.4 An arterial blood sample from a patient has a pH of 7.25, Pco2 of 6.6 kPa, and a base excess of −3. What is the mostly likely acid–base status of the patient? (hint: look at Chapter 10, panel c) Chapter 11: Control of breathing I: chemical mechanisms 11.1 Ventilation is NOT increased by P co P 11.2 The peripheral chemoreceptors Pco 11.3 The central chemoreceptor − 11.4 The ventilatory response to increased Pco2 P P Self-assessment questions Cases and self assessment 109
  • 109. Chapter 12: Control of breathing II: neural mechanisms 12.1 The receptors located on the bronchial walls close to the cap- illaries are 12.2 Ascending input from the lung receptors 12.3 Stretch receptors in the lung 12.4 Which of the following has NOT been implicated in the gen- eration of basic respiratory rhythm? Chapter 13: Pulmonary circulation and anatomical right-to-left shunts 13.1 Compared to the systemic circulation, the pulmonary circu- lation 13.2 The forces affecting fluid movement across the pulmonary capillaries 13.3 All of the following are examples of conditions that usually give a pure right-to-left shunt EXCEPT: 13.4 Some right-to-left shunting occurs in healthy people P P Chapter 14: Ventilation–perfusion mismatching 14.1 In a person with ventilation–perfusion mismatching Pco Po Po Pco 14.2 Oxygen-enriched inspired air 14.3 In a young asthmatic patient with arterial hypoxia during a severe attack Pco Pco Pco 14.4 The A–a PO2 gradient P Chapter 15: Exercise, altitude and diving 15.1 In exercise, as the work load increases progressively Pco 15.2 On acute ascent to high altitude 110 Cases and self assessment Self-assessment questions
  • 110. 15.3 A person travels from sea level to an altitude of 4000 m (13 000 ft). A week after arriving Pco P 15.4 During diving Chapter 16: Development of the respiratory system and birth 16.1 Airway smooth muscle 16.2 The lung increases in size over the first 3 years after birth 16.3 The PaO2 of fetal blood P 16.4 At birth P Chapter 17: Complications of development and congenital disease 17.1 Neonatal respiratory distress syndrome (NRDS) ∼ < 17.2 Which of the following congenital diseases affecting the lung is most common? 17.3 Which option is NOT correct concerning oesophageal atresia? 17.4 Bronchopulmonary dysplasia Chapter 18: Lung defence mechanisms and immunology 18.1 Physical defences in the upper airways μ 18.2 Mucus 18.3 Removal of invading materials/organisms from the alveoli 18.4 Which form of immunoglobulin is secreted across the epithe- lium? Chapter 19: History and examination 19.1 What is the most common cause of haemoptysis? 19.2 On examination of the hands of a patient with type 2 respira- tory failure, which of the following would be most common? 19.3 On auscultation of the patient’s chest you hear fine inspiratory crackles; with which condition is this most often associated? 19.4 The sound on percussion of a patient’s chest is hyperresonant; which condition might this reflect? Self-assessment questions Cases and self assessment 111
  • 111. Chapter 20: Pulmonary function tests 20.1 When trying to determine whether a breathless patient has obstructive or restrictive pulmonary disease 20.2 Forced expiratory volume in 1 second (FEV1) > 20.3 The best single measurement indicating a respiratory prob- lem and which is reproducible and best correlates with func- tion and prognosis is 20.4 In patients with restrictive ventilatory defects Kco = D co D co Chapter 21: Chest imaging and bronchoscopy 21.1 A routine screening chest X-ray (CXR) 21.2 Which of the following is NOT normally an indication for computed tomography? 21.3 What is the gold standard for diagnosing pulmonary emboli? 21.4 Bronchoscopy Chapter 22: Public health and smoking 22.1 Respiratory disease ∼ 22.2 Smoking-related disease ∼ 22.3 Progressive decline in lung function (FEV1) 22.4 Smoking cessation Chapter 23: Respiratory failure 23.1 Hypercapnia is in inevitable when the cause of hypoxia is P 23.2 Respiratory failure P Pco P P co P 23.3 Typical symptoms and signs caused by a high Paco2 include 23.4 Chronic arterial hypoxia combined with chronic arterial hy- percapnia Pco 112 Cases and self assessment Self-assessment questions
  • 112. Chapter 24: Asthma: pathophysiology 24.1 Which of the following is NOT a characteristic of asthma? 24.2 The most common allergens associated with asthma in the UK are (in order of importance) 24.3 The immediate response of asthma involves 24.4 Chronic asthma is associated with: Chapter 25: Asthma: treatment 25.1 Which test is NOT used during diagnosis or monitoring of asthma? 25.2 Which drug is the most commonly prescribed preventer ther- apy in asthma? β 25.3 Long-acting β2-adrenoreptor agonists 25.4 Which of the following is NOT a common adverse effect of low-dose inhaled steroids? Chapter 26: Chronic obstructive pulmonary disease 26.1 Which of the following is NOT normally associated with chronic bronchitis? 26.2 Which of the following is NOT normally associated with em- physema? D co 26.3 Why do patients with emphysema often exhibit purse-lipped breathing? 26.4 Which of the following statements about COPD is NOT true? α β Chapter 27: Pulmonary hypertension 27.1 Pulmonary hypertension is defined as > ∼ > > > > > 27.2 The most common cause of pulmonary hypertension is 27.3 Idiopathic pulmonary arterial hypertension 27.4 Which of the following drugs is NOT used for treatment of pulmonary hypertension? Chapter 28: Venous thromboembolism and pulmonary embolism 28.1 Deep vein thrombosis Self-assessment questions Cases and self assessment 113
  • 113. 28.2 Pulmonary embolism 28.3 The diagnostic standard for pulmonary embolism is 28.4 Standard treatment for pulmonary embolism is Chapter 29: Pulmonary vasculitis 29.1 Pulmonary vasculitis 29.2 Which of the following is NOT a primary vasculitides? 29.3 Which of the following is NOT normally associated with vas- culitides? 29.4 What is the most common therapy for pulmonary vasculitis? Chapters 30 and 31: Diffuse parenchymal (interstitial) lung diseases/Sarcoidosis 30.1 The most common form of DPLD is 30.2 DPLD is commonly associated with D co 30.3 The most frequent form of non-usual interstitial pneumonitis is 30.4 Which of the following is least likely to respond to treatment with steroids? Chapter 32: Pleural diseases 32.1 Pleurisy 32.2 The fluid between the parietal and visceral pleurae > 32.3 Exudative pleural effusions 32.4 Mesothelioma > Chapter 33: Occupational and environmental-related lung disease 33.1 The most common form of occupational and environmental lung disease 33.2 Which of the following statements about inhaled irritants is UNTRUE? 33.3 Pneumoconiosis 33.4 Which of the following statements about Farmer’s lung is UNTRUE? 114 Cases and self assessment Self-assessment questions
  • 114. Chapter 34: Cystic fibrosis and bronchiectasis 34.1 Cystic fibrosis is < 34.2 The cystic fibrosis transmembrane conductance regulator (CFTR) 34.3 The most important treatment for cystic fibrosis is 34.4 Which statement is NOT true concerning bronchiectasis? Chapter 35: Pneumothorax 35.1 A pneumothorax that causes mediastinal shift and compres- sion of the functioning lung is called 35.2 Primary pneumothorax 35.3 A pneumothorax of <30% 35.4 Secondary pneumothorax is a particular risk for Chapters 36 and 37: Community-acquired pneumonia/Hospital-acquired (nosocomial) pneumonia 36.1 Concerning community acquired pneumonia < > 36.2 Concerning hospital acquired pneumonia Streptococcus pneumonia 36.3 Which of the following statements in NOT true concerning the management of pneumonia? S o > 36.4 Which of the following does NOT suggest increased risk of mortality in patients admitted to hospital for pneumonia? > > > > Chapter 38: Pulmonary tuberculosis 38.1 Which statement is INCORRECT concerning TB? 38.2 Investigations of TB Mycobacterium tuberculosis 38.3 Which of the following is NOT a common feature of TB? 38.4 Treatment of TB Chapter 39: The immunocompromised host 39.1 Which of the following is NOT normally associated with im- munosuppression? Self-assessment questions Cases and self assessment 115
  • 115. 39.2 Which of the following is NOT a consequence of chemother- apy? 39.3 The HIV-positive patient Pneumocystis jirovecii pneumonia Cytomegalovirus 39.4 Which statement is NOT true concerning identification of respiratory infections in the Immunocompromised host? ∼ Chapter 40: Lung cancer 40.1 Lung cancer < 40.2 The least common type of lung cancer is: 40.3 In the context of lung cancer, which of the following is NOT a paraneoplastic syndrome? 40.4 Staging for small cell cancer limited disease extensive disease Chapter 41: Acute respiratory distress syndrome 41.1 Which of the following is NOT part of the criteria for diagnosis of ARDS? 41.2 Which of the following statements about ARDS is true? 41.3 Clinical features of ARDS 41.4 Which of the following is NOT generally beneficial in early ARDS? Chapter 42: Mechanical ventilation 42.1 Mechanical ventilation 42.2 In a paralysed patient on intermittent positive pressure ven- tilation (IPPV) P co ∼ 42.3 Which statement is INCORRECT concerning continuous positive airway pressure (CPAP)? 42.4 Non-invasive intermittent positive pressure ventilation, NIPPV, Chapter 43: Oxygenation and oxygen therapy 43.1 Tissue hypoxia S o 43.2 In O2 therapy the initial target Sao2 116 Cases and self assessment Self-assessment questions
  • 116. Pco 43.3 Preferred method for O2 delivery in patients at the risk of type 2 respiratory failure 43.4 Which is NOT a recognized risk for high-dose O2 therapy? Chapter 44: Sleep apnoea 44.1 Which of the following is NOT commonly associated with sleep apnoea? 44.2 Which statement is NOT true concerning obstructive sleep apnoea (OSA)? 44.3 Which is generally the most long-term therapy for OSA? 44.4 Central sleep apnoea Self-assessment questions Cases and self assessment 117
  • 117. Answers 118 Cases and self assessment Answers
  • 118. Index Note f f f Acinetobacter f f f f f f f V Q f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f α f f f f f f f f f f f f f f Aspergillus f f f f f f f f f f f f f β f f f f Bacteroides f f f f f f f f f f f f f f Index 119
  • 119. Cont. f f f f f f f f f f f f Candida f f f f f f f f f f f f f f f f co f f f f f f f + f f f f f f f f f Chlamydia psittaci f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f Coxiella burnetti f Coxsackie f f f f Cryptococcus neoformans f f f f f f f f f f f f f f f f f f f f f f 120 Index
  • 120. f f f f f f f f f f f f β f f f Epicoccum nigrum f f f f f f Escherichia coli f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f Haemophilus influenza f f f f f f f f f f f f Histoplasmosis f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f Index 121
  • 121. f f f f f f f Klebsiella pneumoniae f f f β f β f f f f f f f Legionella pneumophila f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f Staphylococcus aureus f f f Moraxella catarrhalis f f f f f f f f f f Mycobacterium tuberculosis Mycoplasma pneumoniae f f f f f f f f f f f f Nocardia f f f f f f f f f f f f f f f f f f 122 Index
  • 122. f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f Pneumocystis carinii f Pneumocystis jiroveci f f f f f f f f Pneumocystis jiroveci f f f f f f f f f f f f f f f f f f f f Proteus f f Pseudomonas aeruginosa f f f f f f f f f f f f f f f f f f f f f f f Index 123
  • 123. Cont. f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f f Saccharopolyspora rectivirgula f f f f f f f f f f f f f Serratia f f f f f f f f f f f f f f f f Staphylococcus aureus f f f f f Streptococcus pneumoniae f f f f f f f f f f f f f f f f H f f f f f f f f f f f f f 124 Index
  • 124. β β f f f f f f f f f f f f f f f f f f f f f f f f VA Q f f f f f f f f f f f f f f f f f f Index 125