Is the patient adequately oxygenated? PaO2 >7 kPa; therefore ade- quately oxygenated Has the patient got an A \200\223a gradient? 23 \200\223 [11 + (6.5/0.8)] = 4.2 kPa (remember, the PIO2 is 23 because he is on 24% O2) >2 kPa hence, yes; therefore may have de veloped an aspiration pneumonia. USE OF A \200\223A GRADIENT DIAGRAM: EXAMPLES 797 Fig. A1.3 Examples of using A \200\223a gradient. Three things blood gasses tell you about gas exchange \200 How much is the patient ventil ating their alveoli? \200\224PaCO2 \200 Is the PaO2 high enough to adequately oxygenate t issues and thus prevent anaerobic metabolism? Is there any evidence of a V/Q mismatch, assessed from the alveolar \200\223 arterial (A \200\223a) gradient for oxygen? APPENDIX 1 Blood gasses and acid \200\223base balance 798 Acid \200\223base balance Normal ranges pH 7.37 \200\2237.43 (H+ 37 \200\22343 nmol/L), PaCO2 4.7 \200\2235.9, base e xcess 3 mmol/L. Interpretation Acid \200\223base relationships are best plotted as a PaCO 2 vs. pH graph, because these are the two primary measurements made by a blood gas machine (everything else to do with acid \200\223base balance is calcu- lated). This is shown oppos ite. Normal acid \200\223base is the area labeled N, the pH between 7.37 and 7.43, the PaCO2 aro und 5 kPa. As ventilation is decreased or increased (PaCO2 going up or down, respectively), the pH will change, the amount depending on the buffering capacity of the blood (CO2 is an acid gas, com- bining with water to give [H+] and [HCO3 ] ions). Without buffering, the p H would fall disastrously following small rises in PaCO2. This buffering capacity depends m ainly on hemoglobin and other proteins, producing the normal buffer line running through N on the graph. Therefore, acute hypoventilation and hyperventilation will move the patient up and down thi s line, in the direction b or c, respectively. If the hypoventilation at point b comes chro nic (e.g. as it may in COPD), then the kidney retains bicarbonate (by excreting hydrogen io ns) to try and correct the pH towards normal, and the patient moves onto a new iso [HCO3 ] buffer line displaced to the right, e.g. the one labeled + 10 meq/L (35 meq/L). The degree of displacement represents the metabolic com- ponent to the acid \200\223base status, and in this case, because the [HCO3 ] has risen, will be higher than the normal \201 gure of about 25 meq/L. When the raised \201 gure is quoted relative to the normal 25 meq/L (by subtracting 25), this is called the base excess. Thus, buffer lines to the right of the nor mal buffer line represent a metabolic alkalosis or base excess. These \201 gures are calculated assuming a normal or \200\230standard \200\231 PaCO2, ca lled the \200\230standard bicarbonate \200\231 (SBC on the blood gas machine printout), or \200\230standard base excess \200\231 (usually BE). The other similar \201 gures on som e printouts (usually HCO \200\223 3 and TCO2) are calculated at the patient \200\231s actua l PaCO2 and are not much use. Chronic hyperventilation (e.g. at altitude due to the hypoxia) produces the opposite, a res orption of [H+] by the kidney, and the buffer line shifts to the left giving a negative val ue for the \200\230base excess \200\231, a base de \201 cit. Thus, a metabolic acidosis c ompensates for a respiratory alkalosis. Note that these corrections rarely bring the pH bac k to normal as there needs to be an error signal to keep the correction process going. A metabolic acidosis (such as in ketoacidosis) will also move the line to the left (a), pro ducing a base de \201 cit (or negative base excess), followed by hyperventilation to try a nd correct it (i.e. a respiratory alkalosis to correct a metabolic acidosis). This pure ven tilatory stimulation in the absence of abnormal lungs often produces deep breathing with li ttle increase in rate and is called Kussmaul \200\231s breathing. Thus, lines to the left o f the normal buffer line represent a metabolic acidosis or base de \201 cit. A metabolic a cidosis due to anaerobic metabolism (and hence lactic acid production) can reverse the comp ensatory metabolic alkalosis secondary to chronic hypercapnia during a severely hypoxic COP D exacerbation, removing the evidence for chronic CO2 retention. ACID \200\223BASE BALANCE 799 Finally, a metabolic alkalosis, e.g. during hypokalaemia (when the kidney is forced to use hydrogen ions instead of potassium ions to swap for the sodium that needs resorbing from th e tubular \202 uid) moves the buffer line to the right (d), but with only limited hypoven tilation available to compen- sate, due to the inevitable ventilatory stimulation the atten dant hypox- aemia produces. Thus, the mixture of respiratory and metabolic contributions to a patient \200\231s acid \200\223base disturbance can be established by plotting the PaCO2 and pH on the graph. Fig. A1.4 Acid \200\223base balance: PaCO2 \200\223pH. APPENDIX 1 Blood gasses and acid \200\223base balance 800 Anion gap The anion gap [(Na+ + K+) \200\223(Cl + HCO3 )] shows the amount of other anio ns, apart from Cl + HCO3 , that exist, and helps differentiate the cause of any metaboli c acidosis. Depending on methods of measurement, the normal value is between 8 and 16 mmol/ L (or meq/L) and mainly due to albumin. High anion gap indicates loss of HCO3 without a s ubsequent increase in Cl . Electroneutrality is maintained by increase in anions such as k etones, lactate, PO4 , and SO4 . Because these anions are not part of the anion-gap calcu lation, a high anion gap results. An acidosis with a normal anion gap will be a simple HCO3 /Cl exchange such as might occur, for example, in: \200 Renal tubular acidosis \200 Acetazo lamide therapy \200 HCO3 loss from profuse diarrhea. An anion gap is likely to be prese nt, for example, when the metabolic acidosis is due to: \200 Diabetic, starvation, or alc ohol induced ketoacidosis (ketones are acids) \200 Renal failure (although can be in the normal range too) \200 Lactic acidosis \200 Salicylate poisoning \200 Methanol poison ing \200 Ethylene glycol (anti-freeze) poisoning. Three things arterial samples tell you about acid \200\223base balance \200 Is there a ve ntilatory/respiratory contribution from an abnormally high or low PaCO2? Is there a metabolic component evidenced by a shift of the buffer line to the left or right, numerically the base excess (or de \201 cit)? If there is an acidosis, is there an increased anion gap? Further information Williams AJ. ABC of oxygen. http://www.bmj.com/cgi/content/full/317/716 7/1213 This page intentionally left blank APPENDIX 1 Blood gasses and acid \200\223base balance 802 Conversion between arterial oxygen saturation and oxygen tension (hemoglobin dissociation c urve) 100 pH=7.5, 7.4, 7.3 80 ) % ( 2 O a S / n o i t a r u t a s 60 Right shift caused by: fall in pH rise in temperature increase in 2,3-DPG 50% 40 n e g y x O 20 P 50 at pH 7.40 0 2 4 6 8 60 pO2 10 12 14 16kPa 120mmHg 80 100 0 20 40 Fig. A1.5 Hemoglobin dissociation curve. A fall in pH (more acidotic), or a rise in body temperature, will move the dissociation cur ve to the right. This has the effect of making the PaO2 higher for any given SaO2, e.g. at pH 7.20 a measured saturation (e.g. by oximetry) of 90% is equivalent to a higher PaO2 of 9 .7 kPa (73 mmHg) than the usual 7.7 kPa (58 mmHg): a rise in body temperature to 41 C will do the same, and the effects of pH and temperature are additive. Conversely, for a given PaO2, pyrexia and acidosis will lower the SaO2 and thus oxygen carr iage to the tissues. A PaO2 of 7.7 kPa (58 mmHg) will normally give a SaO2 of 90%, but if t he temperature rises to 41 C, and pH falls to 7.20, then the SaO2 falls to 70%. Increasing 2,3-DPG levels shift the curve to the right, but levels \202 uctuate unpredictably and a ny changes are small. Changes in body temperature are often the reason why measured pulse oximetry saturations ap parently \200\230do not agree \200\231 with the measured blood gasses (pH is taken into ac count in the theoretical calculation of SaO2 by blood gas analysers, but the patient \200 \231s correct body temperature is rarely entered and thus not taken into account). This is particularly important in hypothermia when the curve is left shifted leading to impaired ox ygen unloading anyway. Furthermore, an apparently adequate oximetry reading can mask a low PaO2, which will further lessen oxygen availability to the tissues (although somewhat mitig ated by the reduced metabolic rate of hypothermic tissues). ARTERIAL OXYGEN SATURATION AND OXYGEN TENSION 803 Table A1.1 Conversion chart* % Saturation kPa mmHg 98 15.0 112 97 12.2 92 96 10.8 81 95 9.9 74 94 9.3 70 93 8.8 66 92 8.4 63 91 8.1 60 90 7.7 58 88 7.3 55 86 6.8 51 84 6.5 49 82 6.2 47 80 5.9 45 75 5.4 40 70 4.9 37 65 4.5 34 60 4.2 31 55 3.8 29 50 3.5 27 Assumes a normal position of the hemoglobin dissociation curve. kPa and mmHg: conversion factor, 7.5 x kPa = mmHg. This page intentionally left blank 805 Appendix 2 BMI calculator; height and weight converter APPENDIX 2 BMI calculator, height, and weight 806 BMI = weight in kilograms, divided by height in meters squared e.g. 70 kg man, 1.8 m tall. BMI = 70/(1.8 \227 1.8) = 21.6 Weight (pounds) Stone 90 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 110 130 150 170 190 210 230 250 270 290 3 10 330 350 2 6 6 Underweight BMI<18.5 Normal range BMI18.5-25 Overweight BMI 25-30 Obese BMI>30 40 1.9 6 3 ) s e h c n ) s e r t e m 1.8 5 11 i d n a ( t e e f ( t h g e H 1.7 5 7 i t h g e H i 1.6 5 3 1.5 4 11 40 50 60 70 80 90 100 110 120 130 140 150 160 Weight (kilograms) Fig. A2.1 BMI calculator. 807 Appendix 3 CT anatomy of the thorax Level of C7 808 Level of T2 809 Level of T4 810 Level of T6 811 Level of T7 812 Level of T9 813 These are not standard images set for mediastinal or lung viewing, but have been adjusted t o aid anatomical labeling. Contrast was used to highlight the vessels. 8 0 8 A P P E N D X Trachea Left clavicle I 3 Subclavian artery C T Common carotid a n a t o m y Axillary vein Axillary artery Axillary artery Subclavian o f Common carotid artery t h e Scapula t h o r a x Vertebral artery Esophagus Fig. A3.1 CT anatomy of the thorax: level of C7. Brachiocephalic vein Right brachiocephalic artery Common carotid artery Brachiocephalic vein Subclavian artery Top of inominate artery C T A N A T O M Y O F Esophagus Upper lobe Upper lobe Spinal cord T H E Fig. A3.2 CT anatomy of the thorax: level of T2. T H O R A X 8 0 9 8 1 0 A P P E N D X I Anterior mediastinal fat and thymic remnants 3 Internal thoracic artery and vein C T a n a t o m y Aortic arch Superior vena cava Trachea o f t h e Upper lobe Esophagus t h o r a x Upper lobe Fig. A3.3 CT anatomy of the thorax: level of T4. Upper lobe Pulmonary trunk Ascending aorta Upper lobe Superior vena cava Superior pulmonary vein Upper lobe bronchus Left pulmonary artery Superior pulmonary vein Left main bronchus Right main bronchus C T A N A T O M Y O F Descending aorta Esophagus Azygos vein Oblique fissure Oblique fissure Lower lobe Lower lobe T H E Fig. A3.4 CT anatomy of the thorax: level of T6. T H O R A X 8 1 1 8 1 2 Middle lobe Right ventricle A P P E N D X Ascending aorta/ outflow tract Right atrium I 3 Upper lobe C T Superior vena cava a n a t o m y Left ventricular wall Oblique fissure Left atrium Inferior left pulmonary vein o f Lower lobe bronchus t h e Left pulmonary arteries t h o r a x Pulmonary artery Lymph node Azygos vein Descending aorta Fig. A3.5 CT anatomy of the thorax: level of T7. Pericardium Right ventricular wall Right ventricular cavity Left ventricular cavity Right atrium Left ventricular wall Liver C T A N A T O M Y O F Esophagus Dome of left diaphragm Azygos vein Descending aorta T H E Fig. A3.6 CT anatomy of the thorax: level of T9. T H O R A X 8 1 3 This page intentionally left blank 815 Appendix 4 CT patterns of lung disease APPENDIX 4 CT patterns of lung disease 816 Term Process Causes Air space consolidation Fluid/secretion accumulation in alveoli Pneumonia, pulmonary oedema or hemorrhage, ARDS, COP, lymphoma, drugs, bronchoalveolar cell carcinoma, eosinophilic pneumonia Fig. A4.1 Chronic organizing pneumonia (COP). Air bronchograms clearly present. Fig. A4.2 Extensive airspace consolidation due to eosinophilic pneumonia. CT PATTERNS OF LUNG DISEASE 817 Term Process Causes Air trapping Partial small airway obstruction Asthma, obliterative bronchiolitis, COPD Inspiration Expiration Fig. A4.3 Subject prone. On expiration the denser area becomes more dense indi- cating the lung has de \202 ated: other parts of the lung remain lucent, indicating that air is trapp ed behind narrowed airways. Lobular pulmonary artery Pulmonary veins and lymphatics Lobular bronchiole Central bronchovascular core 1 cm Acinus Visceral pleural surface Interlobular septum Fig. A4.4 Structure of two secondary pulmonary lobules abutting the pleural surface. The se condary pulmonary lobule is the smallest anatomical area visible on CT. Tree in bud appeara nce will be in the acinus around the central bronchovascular core. Reticular patterns will be centered on the interlobular septae and/or draining lymphatics. Mosaic patterns and air trapping will tend to follow outlines of the lobule or sets of lobules. APPENDIX 4 CT patterns of lung disease 818 Term Process Causes Cystic air spaces Clearly de \201 ned air-containing space with de \201 nable wall LAM, LCH, end-stage UIP, PCP, LIP, septic emboli Fig. A4.5 Langerhans \200\231 cell histiocytosis (LCH). Walls are thin, but more pro- nounc ed, irregular, and widely spread than emphysematous holes. Fig. A4.6 Peripheral cysts (honeycombing) of usual interstitial pneumonitis (UIP), characte ristic subpleural distribution. Fig. A5.7 Holes in the lungs due to emphysema. No real \200\230walls \200\231. CT PATTERNS OF LUNG DISEASE 819 Term Process Causes Sarcoidosis. Also described in Kaposi \200\231s sarcoma Fissural, bronchovascular, and sub-pleural nodularity Nodules seen along the pulmonary \201 ssures, along the bronchovascular bundles, and sub- pleurally Fig. A4.8 Sarcoidosis, perihilar, and bronchovascular distribution of nodularity. Fig. A4.9 Sarcoidosis, subpleural nodules. Fig. A4.10 Irregular/nodular thickening of \201 ssures and bronchovascular bundles. APPENDIX 4 CT patterns of lung disease 820 Term Process Causes Parenchymal in \202 ammatory conditions, such as sarcoidosis, alveolitis, early UIP and ot her IIPs, hyper- sensitivity pneumonitis, pulmonary oedema or hemorrhage, PCP, alveolar pro teinosis, drug/radiation injury Ground-glass shadowing Gray appearance to lung interstitium; air in bronchus looks blacker Fig. A4.11 Subtle ground-glass shadowing in early usual interstitial pneumonitis. Airways a ppear blacker, but lung is diffusely more dense. Early reticular pattern at right base also . Fig. A4.12 More marked ground-glass shadowing in UIP. Very early honeycombing and traction bronchial dilatation (bronchiectasis) as well. CT PATTERNS OF LUNG DISEASE 821 Term Process Causes Honeycomb lung End-stage \201 brotic lung UIP, asbestosis Fig. A4.13 Honeycombing in usual interstitial pneumonitis (UIP). Usually mainly peripheral. Fig. A4.14 More subtle honeycombing at the lung periphery with other features of UIP. Tract ion bronchial dilatation due to surrounding lung \201 brosis and a reticular pattern begi nning to outline the secondary pulmonary lobule. APPENDIX 4 CT patterns of lung disease 822 Term Process Causes Indicates small airways disease such as asthma, vascular disease such as PE, or in \201 lt rative disease such as obliterative bronchiolitis, hypersensitivity pneumonitis Well-de \201 ned areas of normal lung abutting abnormal lung, giving a mosaic pattern. See n particularly in expiration Mosaic attenuation pattern Fig. A4.15 Bronchiectasis with small airways disease that is causing the mosaic pattern. In addition, there are markedly bronchiectatic airways in the left lower lobe with considerab le airway crowding due to distal lung collapse. Fig. A4.16 Non-speci \201 c interstitial pneumonitis (NSIP) showing patchy and mosaic- lik e pattern of increased attenuation. CT PATTERNS OF LUNG DISEASE 823 Term Process Causes Metastases, sarcoidosis, pneumoconiosis, hypersensitivity pneumonitis, miliary TB, fungal i nfection, idiopathic pulmonary hemorrhage, alveolar microlithiasis, varicella pneumonitis Nodularity Small discrete dots 1 \200\22310 mm, may be in air spaces or interstitium Fig. A4.17 Multiple dense nodules of varying size due to metastases. Fig. A4.18 Sarcoid. Multiple small nodules throughout lung, but usually associated with oth er features of sarcoid, such as \201 ssural nodularity and bilateral hilar node enlargeme nt. APPENDIX 4 CT patterns of lung disease 824 Term Process Causes Hypersensitivity pneumonitis, RB-ILD Poorly de \201 ned centrilobular nodules Peribronchiolar in \202 ammation in the absence of intraluminal secretion Fig. A4.19 Soft centrilobular nodularity due to hypersensitivity pneumonitis (also called e xtrinsic allergic alveolitis, EAA). Fig. A4.20 Another example of hypersensitivity pneumonitis enlarged to show position of sof t nodules in the center of the secondary pulmonary lobules. CT PATTERNS OF LUNG DISEASE 825 Term Process Causes ILD (e.g. UIP, asbestosis), pulmonary oedema, drug-induced \201 brosis, pulmonary hemorrh age, lymphangitis Reticular (or linear) pattern Linear \201 ne lines, indicating thickened interlobular septa. Sub-pleural reticulation Fig. A4.21 Lymphangitis carcinomatosis. In \201 ltrated lymphatics widen and thicken the i nterlobular septa. Fig. A4.22 Pulmonary oedema due to left heart failure. Fluid-distended lymphatics outlining the secondary pulmonary lobules. Worse in dependent areas. Fluid in the \201 ssures, bil ateral pleural effusions, and some air-space \201 lling with pulmonary oedema. APPENDIX 4 CT patterns of lung disease 826 Term Process Causes Small airways disease, particularly infection including mycobacteria, Haemophilus in \202 uenzae, diffuse panbronchiolitis, CF, yellow nail syndrome, primary pulmonary lymphoma Tree in bud Mucus/pus/secretions \201 lling bronchioles and causing dilatation Fig. A4.23 Extensive tree in bud appearance in the left lower lobe from opportu- nistic myc obacterial disease. Fig. A4.24 Tree in bud appearance enhanced by a post-processing technique called \200\230m aximum intensity projection \200\231. Effectively this squashes denser structures from seve ral thin cuts into one allowing branching structures to be viewed in their entirety. 827 Appendix 5 Lung function testing Flow \200\223volume loop1 828 Flow \200\223volume loop2 830 Spirometry, peak \202 ow meas urements, and CO transfer 831 Respiratory muscle function, body plethysmography, and lung volumes 834 Peak \202 ow reference ranges 836 APPENDIX 5 Lung function testing 828 Flow \200\223volume loop 1 A good starting point to the understanding of lung function test s is the \202 ow \200\223volume loop. This plots inspiratory and expiratory \202 ow aga inst lung volume during a maximal expiratory and maximal inspiratory maneuver. B C Expiratory flow RV TLC D A Inspiratory flow Fig. A5.1 Flow \200\223volume loop. At the beginning of expiration from a full breath in, the expiratory muscles are at their s trongest, the lungs at their largest, and hence the airways are at their most open (A). Bec ause the lungs are at their largest, the radial attachments to the airways, effectively the alveolar/capillary membranes and their connective tissue, are pulling the hardest and supp orting the airways against dynamic compression during the exhalation maneuver. This means that the highest \202 ow rates are possible at the beginning of the blow; henc e, the sudden rise to a peak expiratory \202 ow rate in the \201 rst 100 ms or so of th e forced breath out (B). This is the peak \202 ow and is essentially what a peak \202 o w meter measures. As the lung empties and the lung volume drops, the dilatory pull on the airways from the ra dial attachments of the surrounding lung tissue reduces (C). Hence the airways narrow and b ecome less supported, and are less able to resist dynamic compression. This means that the maximal air \202 ow obtainable, regardless of effort, falls too. Eventually, the expiratory muscles come to the end of their \200\230travel \200\231 and ca nnot squeeze the chest anymore. Also, increasingly with age, the small airways may actually close off, preventing anymore emptying (D). The volume at which this begins to happen is c alled the closing volume. As maximal inspiration starts, although the inspiratory muscles are at their strongest, the airways are at their smallest. Thus, \202 ow rates start low and increase as the airways open up. However, as the lung expands the inspiratory muscles are approaching the end of t heir \200\230travel \200\231 and are weakening; this means the \202 ow rates fall again, hence the different, rounded appearance of the inspiratory limb of the \202 ow \200\223v olume curve. Thus, normally the inspiratory and expiratory \202 ow rates depend on lung volume and are termed \200\230volume-dependent \200\231. If there is a \201 xed upper airway narrowing , such as from a solid hard tumor partially blocking the trachea, then the size of the airw ay at this point may become so narrow that it now limits maximal \202 ows. However, its d iameter will vary very little with lung volumes and hence \202 ow will become \200\230vo lume-independent \200\231. Figure A5.2 shows this. FLOW \200\223VOLUME LOOP 1 829 Expiration B C D A E Inspiration Fig. A5.2 Volume-independent \202 ow. At A, the rise in \202 ow will initially be normal, but at some point the maximum \202 ow imposed by the upper airway narrowing will cut in (B). From that point onwards the \202 ow rate will be \201 xed at this maximum (C) until at much lower lung volumes the lo wer recoil and narrowing small airways again determine the maximum \202 ow (D). The \202 ow \200\223volume curve has been severely \200\230clipped \200\231 with a squarish ap pearance. The same clipped appearance will be present on the inspiratory limb (E), giving r ise to the so-called \200\230square box \200\231 appearance. Sometimes, such upper airways restriction may be variable, rather than \201 xed, and only obstruct during inspiration (e.g. paralyzed and collapsing vocal cords) due to the obstruc ting elements being sucked in, and then blown open again on expiration. \200 Thus, a square inspiratory limb, but normal expiratory limb, provides evidence of a mobile extrathoracic upper airways obstruction. Conversely, a mobile intrathoracic upper airway obstruction (e.g. soft \202 eshy tumor at the carina, or retrosternal thyroid) may obstruct more during expiration (when the expirat ory effort is compressing the lung), compared with inspiration when the chest is being expa nded. \200 Thus, a square expiratory limb, but normal inspiratory limb, is evidence of a variable intr athoracic upper airways obstruction. Sometimes ratios of maximal inspiratory to maximal expiratory \202 ows are used to charac terize intra- or extrathoracic airway obstruction. APPENDIX 5 Lung function testing 830 Flow \200\223volume loop 2 The other, more common, causes of airway obstruction are due to nar- rowing of the lower airways (asthma, COPD). In these conditions the airway caliber (an d thus \202 ow rates) still remains dependent on lung volume. Hence, the \202 ow rates decrease as the lung volume decreases, but particularly so at low lung volumes. This is bec ause resistance to \202 ow is proportional to the airway radius raised to the power of 4 (r4) and therefore most signi \201 cant when airways are already small. Hence, increasing air \202 ow obstruction produces expiratory \202 ow \200\223volume curves like those in Figure A5.3. This greater effect of small airways narrowing at low lung volumes has led som e units to report \202 ow rates at, for example, 25% expired lung volume, or averaged bet ween 25% and 75% of the total expired lung volume. Expiration RV A Fig. A5.3 Expiratory \202 ow volume curves \200\223lower airways obstruction. Airways can be so small so that during expiration they begin closing off earlier than norma l (the closing volume); hence a full breath out is not possible, producing air trapping and a raised residual volume (RV) (A). Sensitive tests of small airways narrowing have to conc entrate on \202 ows at low lung volumes, and peak \202 ow measurements are relatively i nsensitive. \200 Note, however, that peak \202 ow measurements are the most sensitive to upper airway narr owing and a good way to follow changes in upper airway narrowing during, for example, radio therapy for a central airway obstructing lung cancer. SPIROMETRY, PEAK FLOW MEASUREMENTS, AND CO TRANSFER 831 Spirometry, peak \202 ow measurements, and CO transfer \200 The ordinary spirometer (mechanical or electronic) records volumes against time, rather tha n \202 ows against volume The two essential measures are FEV1 and VC. The vital capacity (VC) is the maximum amount of air that can be blown out completely. This will be reduced if the lungs are stiff (preventing a full breath in), the inspiratory musc les are weak (preventing a full breath in), or the airways are narrowed such that the small airways collapse during expiration (preventing a full breath out). The FEV1 is the amount (forced expiratory volume) that can be blown out in 1 s. Because the value is taken over a second, much more \202 ow is being captured during the breath out than the PEFR, but it is still occurring when the airways are larger. It is less dependent on effort and generally more robust. The ratio of the two \201 gures (FEV1/VC) tells us a bout the degree of air \202 ow obstruction. \200 A ratio of FEV1/VC of less than about 70 \200\22375% indicates air \202 ow obstruction. This ratio is very useful because it is hardly affected by age, sex, height, ethnic origin, etc. \200\224it is self-normalizing. The individual measures of FEV1 and VC do need correc tions for the above factors and are usually quoted as % predicted. The range of normality i s considerable, and it may not be clear if results are simply at the bottom end of normal, or considerably reduced from the patient \200\231s normally much higher \201 gures. Seria l measure- ments indicating continuing deterioration may be the \201 rst clue. If the FEV 1/VC ratio is normal, then the VC can be interpreted as to whether there is a reduced total lung volume, such as from interstitial lung disease. This is called a restrictive pattern, and a low FEV1/VC ratio is called an obstructive pattern. The FEV1/VC ratio may actually b e raised in interstitial lung disease as the airways are better supported by the \201 bro sed radial attach- ments, which reduces dynamic compression, improving expiratory \202 ow . The slope of the volume \200\223time plot from a spirometer is effectively the \202 ow ra te at any particular point: because \202 ow is dropping during expiration the slope progr essively \202 attens off. However, if there is any \201 xed upper airways obstruction ( as discussed above) the expiratory \202 ow rate will be constant for a while, and hence t he spirometer line will be straighter than usual. An interesting index to detect possible u pper airway obstruction, the Empey index, has been described: Empey Index = [FEV1 (mL)/PEFR (L/min)] Because PEFR is clipped \201 rst by the presence of upper air \202 ow obstruc- tion, rel ative to the FEV1, the above index gets larger with such a problem. A \201 gure over 10 i s suggestive of upper air \202 ow obstruction, but it is only a pointer, and there will be false positives and negatives. Although one-off measures of lung function can be made, more inter- esting information come s from serial measurements, e.g. in asthma, PEFR will \202 uctuate with characteristic mo rning \200\230dips \200\231. APPENDIX 5 Lung function testing 832 Spirometry \200\223 how to do it Everyone has their own way to do spirometry, but this is a way that works for the authors. Say to the patient:- \200\230This is a test of how big y our lungs are, and how fast you can empty them. What I would like you to do is take an enor mous breath in, the biggest you can manage, then seal your lips around the tube, and blow a s hard and as fast and as long as you pos- sibly can \200\231. Then demonstrate the maneuve r yourself with a spare tube (not connected to the spirometer) so that they can then mimic it. Whilst they are blowing, say \200\230Excellent, well done, keep blowing, come on, come on, come on, keep blowing \200\231. There are various recommendations as to numbers of blo w etc. These are the arguments. Standing or sitting? High intrathoracic pressure generated may cause the patient to pass out. Therefore, sitting down is safer, but better and more consistent \201 gures are obtained standing. Have a c hair behind patient to sit on if dizzy. Nose clip? Prevents escape through the nose which would give falsely low \201 gures, but is uncomfor table. Vast majority of patients do not need it, but if the line appears to fall off toward s the end of the blow, or inconsistent volumes, try a nose clip. Best of 3 blows? Need to demonstrate that maximal blow has been achieved, usually by seeing two identical tr acings. A device showing the actual spirometer tracing is extremely helpful. If two tracing s are identical, this is probably enough, but may need more if blowing is erratic, until sa tis \201 ed it is maximal. Keep going to end of page (6 s) or not? Need to establish correct VC. Therefore if line still rising, then VC not reached, but have to stop somewhere. In restrictive disease, or normals, usually maximal by 3 s; in obstruct ive disease may need to do slow VC to establish real value. Repeat with a sub-maximal effort? Sometimes useful to ask patient to repeat with slightly less effort, when emphysema suspect ed. Will often give better expiratory volume in 1 s, and VC, suggesting major dynamic airwa ys compression. SPIROMETRY, PEAK FLOW MEASUREMENTS, AND CO TRANSFER 833 Carbon monoxide (CO) transfer Usually done in the lung function laboratory and essentially measures the amount of gas exchanging surface area available. A gas mixture containing CO i s inhaled, the breath held for 10 s, then exhaled. The amount of CO that has disappeared (b y crossing the alveolar capillary membrane and being taken up by red cells) is calculated. A correction for the hemoglobin concentration is required, as the amount of CO transferred will fall as the available hemoglobin is reduced. The total amount of CO transferred is the TLCO (total lung, TL). When divided by the total lung volume during the breath hold, it is called the kCO, gas transfer per unit lung volume. The total lung volume \200\230reached \200\231 by the CO is the amount breathed in plus the amount of air already in the lung at the start of the breath in. This is measured by including helium in the inhaled gas mixture that is diluted by the air already in the lung; by comparing inspired helium concentration with expired, this total lung volume can be calculated. \200 The kCO is reduced most in emphysema when alveoli have been destroyed The kCO is also reduc ed in interstitial lung diseases where the alveolar capillary membrane may be thick enough to reduce CO passage The kCO may also be raised when lungs are poorly expanded by, say, wea k respiratory muscles, because the lung is \200\230more concentrated \200\231 and transfer s CO better when quoted per unit volume The kCO may also be raised for a few days when ther e has been profuse lung hemorrhage, as can occur in, SLE, Wegener \200\231s, and Goodpastur e \200\231s. This is because the free red cells lining the alveoli take up CO directly and \200\230falsely \200\231 elevate the \201 gure. As the hemoglobin is broken down, the kC O returns to normal, unless there is another bleed. This helps to distinguish re-bleeding f rom other causes of lung in \201 ltrates such as infection This test requires more cooperation than simple spirometry, as well as a minimum inspired v olume, and therefore cannot always be obtained. APPENDIX 5 Lung function testing 834 Respiratory muscle function, body plethysmography, and lung volumes Respiratory muscle func tion Respiratory failure and small VCs may be due to weak respiratory muscles. It is theref ore useful to be able to assess inspiratory and expira- tory muscle power. There may be glo bal weakness, or speci \201 c inspiratory weakness, usually due to diaphragm paralysis. In the clinic the simplest test is a lying and standing VC. If the diaphragm is paralyzed the n on lying down the abdominal contents will push up the diaphragm and limit inspiration. On standing the abdominal contents drop and aid inspiration. \200 \200 \200 A fall in VC of less than 10% on lying down is probably normal A fall of 10 \200\22320% is suspicious of diaphragm paralysis A fall of more than 20% is abnormal and suggests signi \201 cant, usually bilateral, diaphragm paralysis. In the laboratory there are various ways to test respiratory muscle function. The patient c an blow against a pressure meter after a maximum inspiration, and inspires against the mete r after a full expiration. This is, of course, highly effort dependent. A maneuver such as a sniff is very stereotypic and patients can reproduce this. Measuring the inspiratory pres sure pro- duced at the nose during this maneuver is a reasonably reliable way of screening for inspiratory muscle weakness. More accurate assessments of inspiratory muscle function, particularly the diaphragm, can be obtained using two oesophageal balloons placed above and below the diaphragm and connected to pressure transducers. The transdiaphragmatic pressure s during maximal inspiratory efforts, snif \201 ng, and breathing to TLC all provide repro ducible measures of diaphragm function, but depend on good co- operation and effort by the patient. Activating the phrenic nerve directly with a super \201 cial electrical stimulato r, or by using high-intensity magnetic stimulation over the nerve roots of C3 \200\223C5, p rovides non-effort-dependent ways to test diaphragm function. Body plethysmography requires the patient to climb into an airtight cabinet and breathe through a shuttered mouthpiece c onnected to the outside world. It has two particular advantages over simpler lung function tests. It is able to measure the total lung volume or capacity (TLC) in the thorax, and it provides a measure of airways obstruction involving little or no effort by the patient. The other main method of measuring TLC involves helium dilution as described during the TLC O measurement above. However, in the presence of lower airways obstruction, the helium may not \200\230reach \200\231 all parts of the lung during the 10 s breath hold, and the volu me of dilution will therefore be lower than the real TLC. The body plethysmograph relies on the pressure changes that occur when all the air in the chest is alternately compressed an d expanded by the patient making breathing efforts against an airway closed by a shutter at the mouth. The pressure changes produced in the oral cavity versus in the box are then pro portional to the volume of air being compressed and rare \201 ed, thus allowing calculatio n of the volume in the chest at the time. Note that this volume will include any bullae and the difference between the plethysmographic lung volume and the RESPIRATORY MUSCLE FUNCTION 835 helium dilution volume will re \202 ect the bullae volume, as well as areas not reached by the helium due to increased airways resistance. Measurement of airways resistance with the body box relies on a similar principle. If there were no airways resistance, then breathing in and out would not compress or rarefy the air in the chest. With increasing resist- ance, the air in the chest will be compressed during expiration and rare \201 ed on inspiration. It is this phenomenon that allows calculation of the airways resistance during quiet breathing or panting (the latter ensures the vocal chords are fully open and not contributing to the measured resistance). VC TLC VC TLC FRC RV VC RV FRC FRC TLC RV Normal Obstructive Restrictive Fig. A5.4 Lung volumes in normal, obstructive, and restrictive lung conditions. TLC = total lung capacity; VC = vital capacity; RV = residual volume; FRC = func- tional residual capa city; FEV1 = forced expiratory volume in 1 s. Derivative Obstructive Restrictive dd d FEV1 (% predicted) d or l d d VC (% predicted) l or i (increased recoil) d FEV1/VC ratio i or l i TLC (% predicted) d RV (% predicted) i d FRC (% predicted) i (gas trapping) l or d RV/TLC ratio Further reading Gibson GJ. Clinical Tests of Respiratory Function, 2nd edn. Hodder Arnold, 1995. APPENDIX 5 Lung function testing 836 Peak \202 ow reference ranges 680 660 640 620 600 580 560 540 520 500 480 460 440 420 400 380 360 340 320 Men 190/75 183/72 175/69 167/66 160/63 ) n m i / l ( w o l f k a e P Height (cm/in) Women 175/69 167/66 160/63 152/60 145/57 40 45 50 55 60 65 70 15 20 25 30 35 Age (years) Fig. A5.5 Normal values for peak \202 ow based on original Gregg and Nunn values (BMJ 197 3), but corrected for new EU scale peak \202 ow meters. Normal range is about 15% or ro ughly 100 l/min in men and 50 l/min in women. Old Wright peak \202 ow meters over-read in the middle of the scale (e.g. reading about 400 when actual value was 350 l/min), and were replaced from October 2004 by a corrected scale. Conversion calculator available at: http://www.mortonmedical.co.uk/ clement_clarke_mini_wri ght_EU.htm 837 Appendix 6 Plain radiograph and lobar collapses Posterior to anterior view 838 Left lateral view 839 Lobar collapses 840 8 3 8 Sterno-clavicular joint Posterior part of 5th rib Aortic knuckle Anterior part of 3rd rib L eft pulmonary artery Left atrial appendage Trachea Clavicle Right para-tracheal stripe (air both sides) A P P E N D X I 6 Carina Position of azygos vein P l a i n r a d o g r a p h Horizontal fissure i Right pulmonary artery Left border of descending aorta Left ventricle Right atrial edge Right pulmonary veins (entering mediastinum lower than arteries) Right ve ntricle a n d Left diaphragm visible across to aorta l o b a r Gastric bubble c o l l a p s e s Fig. A6.1 Normal PA chest radiograph. Trachea Scapula Approximate position of oblique fissure Brachiocephalic vessels Anterior mediastinal window Aortic arch Pulmonary trunk (right PA ant, left PA post) and hilum Approximate position of horizontal (right) fissure P L A N R A D O G R A P H A N D I Pulmonary arteries I Left atrium Right ventricle Vertebral bodies: each one should be darker than one above Right atrium L O B A R Right and left diaphragms C O L L A P S E S Fig. A6.2 Normal left lateral chest radiograph. 8 3 9 840 APPENDIX 6 Plain radiograph and lobar collapses Left upper lobe collapse