 \200 \200 RAST or radio-allergosorbent blood tests are more speci \201 c, but less sensitive and mor e expensive than skin prick tests, but give similar infor- mation. There is no risk of anap hylaxis and the patient does not need to stop steroids or antihistamines for the test to be performed. Unconventional tests Electrodermal allergy testing (using a Vegatest machine) w as developed as an aid to homeopathic prescribing, and is widely used in complementary medi cine to assess allergic status to food and envi- ronmental allergens. It is based on small changes in skin electrical imped- ance at acupuncture points, in response to allergens plac ed in an electrical circuit. There are no RCT data to show that this method can identify at opic from non-atopic individuals, as identi \201 ed from skin prick tests. METHACHOLINE CHALLENGE TESTING 769 Technique of induced sputum \200 \200 Used to investigate for infection (e.g. TB, PCP) or airway in \202 ammation Patients rinse their mouth and clean their teeth to minimize oral con- tamination. Give inhaled salbutamo l, to minimize bronchoconstriction Nebulized hypertonic (2.7 \200\2235%) saline is administ ered via a face mask. Afterwards the patient expectorates sputum into a sterile pot If tran smission of infection (e.g. TB) is likely, perform the test in a nega- tive pressure room, with appropriate protection of staff and other patients. Do not perform on the open ward or out-patient department Send sputum promptly to microbiology for staining and culture, and direct immuno \202 uorescent testing for PCP (if indicated). Sputum for cell counts is mix ed with 0.1% dithiothreitol, diluted with saline, and then \201 ltered and centrifuged. Methacholine challenge testing \200 Methacholine induces bronchospasm in people with hyperreactive airways. Helpful if there is diagnostic doubt regarding the diagnosis of asthma Should be performed by experienced pers onnel, with facilities to deal with acute bronchospasm Increasing nebulized doses of methac holine are given systematically, with the FEV1 measured after each dose If there is a 20% f all in FEV1, or if the highest dose of methacholine has been given, the test is stopped The concentration of drug causing the 20% fall is known as the PC20 Asthma is indicated by a P C20 < 8 mg/mL. Normal subjects have a PC20 >16 mg/mL. \200 This page intentionally left blank 771 Chapter 68 Pleural biopsy 772 CHAPTER 68 Pleural biopsy Indications for Abrams \200\231 pleural biopsy \200 Diagnosis of tuberculous pleural effu sion \200 Abrams \200\231 biopsy is used for the diagnosis of malignant pleural disease i n many centers, although a recent randomized controlled trial has shown that CT-guided cutt ing-needle biopsy has a greater sensitivity (sensi- tivity 87% in CT-guided biopsy group vs . 47% in Abrams \200\231 group). Technique An assistant is required. 1. Discuss procedure with patient and obtain written co nsent 2. Insert IV cannula 3. Consider sedation (e.g. midazolam 2 \200\2235 mg IV, with oxy gen saturations monitoring) 4. Position patient sitting forward, leaning on a pillow over a table with their arms folded in front of them 5. Double-check correct side from chest examination and CXR 6. Choose biopsy site: 1 \200 \2232 intercostal spaces below upper level of effu- sion on percussion. Use posterior or lateral approach (although avoid very posterior approa ches close to spine, as intercostal artery drops medially to lie in mid-intercostal space) 7. Sterile skin preparation. Wear sterile gloves and gown 8. In \201 ltrate skin, intercos tal muscle, and parietal pleura with 10 mL of 1% lidocaine. Aim just above the upper border of the appropriate rib, avoiding the neurovas cular bundle that runs below each rib. Anesthetize area behind rib below the insertion poin t 9. Whilst waiting for anesthetic to work, assemble Abrams \200\231 reverse bevel biopsy nee dle. The needle consists of an outer sheath with a triangular opening (biopsy port) that ca n be opened or closed by rotating an inner sheath 10. Verify that the insertion site is correct by aspirating pleural \202 uid with a green (21G) needle. If unable to aspirate \202 uid, do not proceed 11. Make small (5 mm) skin incision; dissect intercostal muscles with blunt forceps (e.g. Spencer \200\223Wells) 12. Insert biopsy needle gently with biopsy port closed. Do not apply force; the needle should slip into the pleural space without resistance. When in the pleura l cavity, \202 uid can be withdrawn by attaching a syringe to the needle and opening the biopsy port 13. To take a biopsy, attach a syringe to the needle. Open the biopsy port and angle it dow nwards, and then pull the biopsy port \201 rmly against the parietal pleura on the rib be neath the entry point (6 o \200\231clock posi- tion relative to entry point). Close the bio psy port, thereby pulling a sample of parietal pleura into the needle 14. Remove the biopsy needle, open the biopsy port, and remove biopsy sample 15. Repeat procedure 4 \200\2236 times in positions 4 \200\2238 o \200\231clock, always sam pling below the insertion point (to avoid the neurovascular bundle beneath the rib above) 16. Send biopsy samples in saline for analysis for tuberculosis and in for- malin if malignancy is suspected PLEURAL BIOPSY 773 17. Apply dressing to biopsy site. May require a single stitch 18. CXR to exclude pneumotho rax. Complications include pain, pneumothorax, haemothorax, and empyema. Hemorrhage from tr auma to an intercostal artery may neces- sitate emergency thoracotomy. Fatalities are well documented, but rare. Further information Maskell NA et al. Standard pleural biopsy versus CT-guided cutting-need le biopsy for diagnosis of malignant disease in pleural effusions: a randomized controlled trial. Lancet 2003; 361: 1326 \200\22331. This page intentionally left blank 775 Chapter 69 Pleurodesis Chemical pleurodesis 776 776 CHAPTER 69 Pleurodesis The aim of pleurodesis is to seal the visceral pleura to the parietal pleura with adhesions to prevent pleural \202 uid or air accumulating. Successful pleurodesis is dependent upo n two factors. \200 Lung re-expansion following removal of pleural \202 uid or air, which allows the appositi on of visceral and parietal pleura. This may be encouraged by applying suction to an interc ostal drain In \202 ammation of the pleural surfaces, which is required to produce pleural \201 brosis and adhesions. This may be induced by a chemical scle- rosing agent or by pl eural abrasion at thoracoscopy. Indications \200 Recurrent and symptomatic pleural effusion (most commonly as a result of malignancy, althou gh pleurodesis is also rarely used in benign recurrent effusions) Recurrent pneumothorax (d ue to concerns regarding the long-term safety of intrapleural talc, surgical abrasion pleur odesis is usually the procedure of choice in younger patients; chemical pleurodesis may be used as a last resort in older patients who are un \201 t for surgery). Chemical pleurodesis Types of sclerosant Choice of sclerosing agents varies. The most com- monly used agents are sterile talc, tetracycline, and bleomycin. \200 Talc is the most effective (success rate about 90%), and can be adminis- tered either as a slurry via a chest drain or as a poudrage at thoracos- copy, but it carries a risk of induc ing ARDS (see later) Tetracycline is successful in about 65% cases Bleomycin has success ra tes of only 60%, and is expensive. \200 Other rarely used agents include doxycycline, minocycline, interferon, interleukins, cispla tin, or the patient \200\231s own blood. Corticosteroids may increase the failure rate of p leurodesis by inhibiting the pleural in \202 ammatory response and development of adhesion s, and should be discontinued beforehand. The effect of NSAIDs on the success of pleurodesi s is unclear. Technique Most centers will have a written pleurodesis protocol, usually invo lving premedication and intrapleural local anesthesia. A typical protocol is set out below. 1. Discuss procedure with patient and obtain written consent 2. Insert chest drain (p 760) : small bore (10 \200\22314F) chest tubes are suf- \201 cient for \202 uid drainage and pleurodesis, and are more comfortable than larger drains. Flush drain with 20 mL normal saline 6-hourly 3. Commence heparin 5000 IU bd as prophylaxis against thromboembo- lism (increased risk fol lowing pleurodesis, especially in patients with malignancy) 4. Drain \202 uid in a controlled manner. There is a small risk of re-expansion pulmonary oedema if large effusions are drained too quickly; control output by clamping drain; aim t o drain a maximum of 1 L/h CHEMICAL PLEURODESIS 777 5. CXR when drain output slows (<150 mL/day): Consider pleurodesis if \202 uid removed and lung fully or partially expanded on CXR (alt hough success rates are much lower in the setting of an incompletely expanded lung) Conside r trial of suction if lung only partially re-expanded. Aim to gradually increase pressure t o \200\22320 cmH2O. Use of suction may be limited by pain. For pleurodesis 6. Insert IV cannula and attach pulse oximeter 7. Pleurodesis is often extr emely painful. Consider premedication with opioid (diamorphine 2.5 mg IV), anti-emetic (metoclopramide 10 mg), and benzodiazepine (mid azolam 1 \200\2232 mg IV, titrate to conscious level; care in elderly and in patients with respiratory failure). The patient should be comfortable, but cooperative 8. Administer intrapleural local anesthetic (e.g. lidocaine 3 mg/kg, maximum 250 mg) via the chest drain, as intrapleural administration of sclerosants is frequ ently painful. Clamp drain and wait several minutes 9. Administer sterile talc slurry (4 g talc in 30 mL normal saline) 10. Flush drain with 20 mL saline 11. Further analgesia if required 12. Clamp drain for 1 h after administration o f sclerosant. Then unclamp drain and consider applying suction, \200\22320 cmH2O. Restart drain \202 ushes 13. Monitor pulse, blood pressure, temperature, respiratory rate, and oxygen saturations half-hourly for 2 h and then 6-hourly 14. Analgesia and antipyretics as required 15. Optimal duration of drainage following pleur odesis is unknown; con- sider drain removal within 12 \200\22372 h if there is adequate drainage of \202 uid and lung expansion on CXR. Can usually remove tube at 48 h 16. In cases of mesothelioma arrange prophylactic radiotherapy for the drain site (total of 21 Gy in 3 fractions over 1 week). Malignant seeding at drain site s in non-mesothelioma malignant effusions is uncommon and prophylactic radiotherapy is not required. Complications All sclerosants may cause chest pain and fever as side- effects. Use of steri le talc may rarely (<1%) result in respiratory failure due to adult respiratory distress sy ndrome, manifest as hypoxia and diffuse pulmonary in \201 ltrates within 48 h of pleurodes is. The risk appears to be reduced with lower talc doses (<5 g). \200\230Mixed \200\231 ta lc (containing small par- ticles) appears to be associated with greater systemic in \202 a mmation and greater deterioration in gas exchange than \200\230graded \200\231 talc (which has small particles removed), so routine use of graded talc is now recommended. Future dev elopments are likely to focus on more effective and safer sclerosing agents for pleurodesis , for example, transforming growth factor-B, which has been demonstrated to produce an effe ctive pleurodesis in rabbits. This page intentionally left blank 779 Chapter 70 Pneumothorax aspiration 780 CHAPTER 70 Pneumothorax aspiration Indications \200 Primary pneumothorax Consider aspiration if patient breathless and/or pneumothorax large (r im of air >2 cm on CXR) Secondary pneumothorax Consider aspiration if patient aged <50 year s, with small pneumothorax (rim of air <2 cm on CXR) and minimal breathlessness. Technique Refer to pp 380 \200\2231 for treatment algorithms. 1. Discuss procedure with pat ient and obtain written consent (unless emergency situation) 2. Insert IV cannula 3. Position patient sitting upright, supported on pillows 4. Double-ch eck correct side from chest examination and CXR 5. Choose aspiration site: second intercost al space in mid-clavicular line on side of pneumothorax 6. In \201 ltrate skin, intercostal muscle, and parietal pleura with 10 mL of 1% lidocaine. Aim just above the upper border of the appropriate rib, avoiding the neurovas cular bundle that runs below each rib. Parietal pleura is extremely sensitive; use the full 10 mL of lidocaine 7. Sterile skin preparation. Wear sterile gloves and gown 8. Whilst waiting for anesthetic to work, connect 50 mL syringe to 3- way tap, with tap turned \200\230off \200\231 to patient 9. Con \201 rm presence of pneumothorax by aspirating air with green (21G) needle 10. Insert large bore (e.g. 16G) cannula over upper border of rib. Remove inner needle, quickly connect cannula to three-way tap and 50 mL syringe 11. Aspirate 50 mL air with syringe, turn tap and expel air into atmo- sphere. Repeat until resistance felt, or 2.5 L of air aspirated (aspiration of >2.5 L sugge sts a large air leak, and aspiration is likely to fail). Halt procedure if painful or patie nt coughing excessively. 12. Remove cannula; cover insertion site with dressing 13. Repeat CXR. Ideal timing of CXR following aspiration is unknown; it may be advisable to wait several hours before performing the CXR in order to detect slow ai r leaks 14. Aspiration is successful if lung is fully re-expanded on CXR 15. If initial aspiration of a primary pneumothorax fails, repeat aspiration should be considered (unless \211 2.5 L has already been aspirated). At least one-third of patients will respond to a second aspir ation. 781 Chapter 71 Thoracentesis Diagnostic thoracentesis 782 Therapeutic thoracentesis 783 782 CHAPTER 71 Thoracentesis Thoracentesis ( \200\230pleural tap \200\231, or pleural \202 uid aspiration) may be diag nostic or therapeutic. Diagnostic thoracentesis Indication Undiagnosed pleural effusion. There are no absolute con traindications to pleural aspiration, although care should be taken if the patient is antic oagulated. Technique 1. Explain procedure to patient 2. Position patient sitting forward, leaning on a pillow over a table with their arms folded in front of them 3. Double-check correct side from chest examination and CXR 4. Choose aspiration site 1 \200\2232 intercostal spaces below upper level of effusion on percussion. Use posterior or lateral approach (although avoid very posterior approaches close to spine, as intercostal a rtery drops medially to lie in the mid-intercostal space) 5. Sterile skin preparation and aseptic technique 6. In \201 ltrate skin, intercostal musc le, and parietal pleura with 10 mL of 1% lidocaine. Aim just above the upper border of the appropriate rib, avoiding the neurovas cular bundle that runs below each rib. The pari- etal pleura is extremely sensitive; use th e full 10 mL of lidocaine 7. Aspirate pleural \202 uid with a green (21G) needle and 50 m L syringe 8. Following diagnostic tap: Note pleural \202 uid appearance \200 Send sample in sterile pot to biochemistry for me asurement of protein and LDH Send a fresh 20 mL sample in sterile pot to cytology for examination for malignant cells an d differential cell count. Use of a 3.8% sodium citrate tube may help preserve cells in cyt ology samples Send samples in sterile pot and blood culture bottles to microbiology for Gram stain and mi croscopy, culture, and AFB stain and culture Process non-purulent heparinized samples in arterial blood gas analyzer for pH (consult biochemistry laboratory for local policy of pH analysis beforehand ; never put purulent samples in the arterial blood analyzer) Consider measurement of cholesterol and triglycerides, haemato- crit, glucose (with paired blood sample), and amylase, depending on the clinical circumstan ces 9. There is no need for a routine CXR following aspiration If unable to aspirate \202 uid, further attempts should be made with ultra- sound guidanc e. Ultrasound guidance may also be required for small or loculated effusions, or to disting uish \202 uid from pleural thickening. THERAPEUTIC THORACENTESIS 783 If mesothelioma is likely, \200\230tattoo \200\231 the aspiration site with India ink (to guide prophylactic radiotherapy; pierce skin through ink) and perform aspiration in mid-axi llary line 6th \200\2237th intercostal space (corresponding to the site of thoracoscopy por t, to minimize area of radiotherapy required). Complications of thoracentesis include pneum othorax, cough, bleeding, empyema, spleen or liver puncture, and malignant seeding down asp iration site (particularly in mesothelioma). Therapeutic thoracentesis Indication Symptomatic relief of breathlessness due to a pleural effusion, most commonly due to malignancy. Technique In many cases, can be performed as a d ay-case procedure. 1. The initial procedure is identical to that of diagnostic thoracentesi s (steps 1 \200\2237 opposite). It is important to verify that the insertion site is correct by \201 rst aspirating pleural \202 uid with a green (21G) needle. If unable to aspirat e \202 uid, abort the procedure and ultrasound the chest to check the presence and locati on of \202 uid 2. Carefully advance a large bore intravenous cannula along the anaesthe- tized track 3. Remove the inner needle and attach the cannula to a 3-way tap 4. Aspirate \202 uid fro m the chest with a 50 mL syringe via the 3-way tap, and \202 ush the \202 uid into a pot through extension tubing. Drain a maximum of 1.5 L of \202 uid in one sitting (risk of re-expansion pulmo- nary oedema following sudde n removal of very large volumes). Stop the procedure if resistance is felt, or the patient experiences discom- fort or severe coughing 5. Apply dressing to aspiration site 6. Repeat CXR to document extent of improvement in eff usion size and to exclude pneumothorax or trapped lung This page intentionally left blank 785 Chapter 72 Thoracoscopy (medical) 786 CHAPTER 72 Thoracoscopy (medical) Thoracoscopy is the procedure of examining the chest wall, parietal pleura, visceral pleura , and diaphragm with a thoracoscope and taking biopsies. Chemical pleurodesis can also be p erformed. Performed by chest physicians using sedation and local anesthetic. There needs to be an adequate space into which the thoracoscope is inserted without damagin g the underlying lung. Patients suitable for thora- coscopy are therefore those who have an underlying pleural effusion or a pneumothorax, where the lung is away from the instrument insertion site. Indications for thoracoscopy \200 Undiagnosed pleural effusion \200\224usually an exudate (diagnostic sensitivity of medical thoracoscopy is 95%) Suspected mesothelioma Staging of pleural effusion in lung cancer Trea tment of recurrent pleural effusions with pleurodesis Pneumothorax requiring chemical pleur odesis, as an alternative to surgery, e.g. the patient un \201 t for surgical thoracoscopy . \200 \200 \200 Contraindications/proceed with caution \200 \200 \200 \200 \200 \200 Obliterated pleural space Pleural adhesions, as these may tear when pneumothorax is induced Bleeding disorder Hypoxia <92% on air Unstable cardiovascular disease Persistent uncontrol lable cough. Risks associated with thoracoscopy Mortality rates are low (<0.01% of cases) \200 \200 \200 \200 \200 \200 Hemorrhage \200\224may need diathermy in the pleural space. Rare Pulmonary perforations. Ra re Air or gas embolism during pneumothorax induction. Rare <0.1% Local wound infection Empy ema Fever, ARDS with talc poudrage (see p 777). Preparation of patient and consent \200 Patient should have written information >24 h before the procedure. Written consent taken b y doctor performing procedure Check recent CXR and any CT scans available Check FBC, coagul ation, U&E Send blood for group and save Nil by mouth for 4 h pre-procedure IV cannula in a rm on the same side as the thoracoscopy to make repeated sedative administration during the procedure easy Premedication with analgesia, such as a single dose of oral ibuprofen 800 m g, 1 \200\2232 h before. Also antibiotics, such as cefuroxime 1.5 g IV, for infection proph ylaxis Baseline oxygen saturations, pulse, BP, temperature. Measure oximetry throughout. \200 \200 \200 \200 THORACOSCOPY (MEDICAL) 787 Procedure The patient is placed in the lateral decubitus position, with the side of the ple ural effusion uppermost. Sedation is administered and allowed time to work. Oxygen (2 \200 \2234 L/min) is administered via nasal can- nulae. The skin is cleaned and local anesthetic inserted, in the same way as for a chest drain. The aspiration of \202 uid or air from t he pleural space con \201 rms it is safe to proceed to thoracoscopy. An incision is made a nd blunt dissection performed through the parietal pleura. The thoracoscope port is then in serted. The pleural effusion is drained via a suction tube through the thoracoscope port. A ir is allowed to enter the pleural space through this port so the lung does not re-in \202 ate, and effectively a pneu- mothorax is created. The thoracoscope, with its light source, can then be inserted through the port and the chest cavity inspected. A second smaller inc ision allows forceps or other instruments to be inserted and biopsies taken. Thoracoscopic biopsies are usually large and yield good diagnostic results. If the pleural surfaces have appearances consistent with malig- nancy, pleurodesis can be performed at the end of the procedure, using talc inserted via an insuf \202 ator. There is no evidence th at pleurodesis per- formed at thoracoscopy is more ef \201 cacious than pleurodesis perfor med via chest tube, but it may save the patient having a further procedure. Post thoracoscopy care \200 \200 Monitor oxygen saturations, pulse, blood pressure, and temperature The patient will have a chest drain in situ. This should be on free drainage initially, but continuous suction is r equired when the drain stops bubbling Analgesia as required, such as IV diamorphine 2.5 mg, dihydrocodeine 30 \200\22360 mg PO, paracetamol 1 g DVT prophylaxis with subcutaneous hepa rin (increased coagulopathy with talc pleurodesis) Mobile CXR on the morning after thoracos copy Remove chest drain when the lung is re-in \202 ated on CXR with minimal \202 uid or air drainage. Trapped lung occurs if the visceral pleura is too thick to allow lung re-in \202 ation (see p 350) If mesothelioma is diagnosed, refer for radiotherapy to thoracoscop y and chest drain tract sites. \200 Further information Daniel T. Diagnostic thoracoscopy for pleural disease. Ann Thorac Surg 1993; 56: 639 \200\22340 Loddenkemper R, Boutin C. Thoracoscopy: present diagnostic and therapeutic indications. Eur Respir J 1993; 6: 1544 \200\22355 This page intentionally left blank Part 00 Appendices Appendices 1 Blood gasses and acid \200\223base balance 2 BMI calculator, height and weight converter 3 CT anatomy of the thorax 4 CT patterns of lung disease 5 Lung function testing 6 Plain radiograph and lobar collapses 7 Radiological investigations and radiation doses 8 Useful websites 791 805 807 815 827 837 841 845 This page intentionally left blank 791 Appendix 1 Blood gasses and acid \200\223base balance Interpretation of arterial blood gasses: 1 792 Interpretation of arterial blood gasses: 2 7 94 Use of A \200\223a gradient diagram: examples 796 Acid \200\223base balance 798 Conversi on between arterial oxygen saturation and oxygen tension (hemoglobin dissociation curve) 80 2 APPENDIX 1 Blood gasses and acid \200\223base balance 792 Interpretation of arterial blood gasses: 1 Normal ranges Breathing air: PaO2 > 12 kPa (>10 in normal elderly), PaCO2 4.6 \200\2235.9. How to take \200 Arterial blood gasses Best taken from radial, rather than brachial, arte ry due to dual radial/ulnar supply to hand. Use a heparinized syringe, analyze immediately, or within 30 min if kept on ice. Always record date, time and the % inspired O2 \200 Arterialized capillary sample An unde r-used technique. Uses small glass pre-heparinized tube to draw up blood from a puncture on the end of the ear lobe. Blood gas machine must take microsamples (most do). PaCO2 levels are accurate enough for clinical practice, but good arteri- alization, with rubefacients (A lgipan/Deep Heat) or heat and vigorous rubbing, required for accurate PaO2: the latter is l ess important as oxygenation can be assessed by oximetry. Can easily be performed by nursin g staff, to monitor response to NIV and O2 therapy. The three main things blood gasses tell you about gas exchange \200 How much is the patient ventilating their alveoli? This is d erived from the PaCO2. PaCO2 \211 6 kPa = underventilating, PaCO2 \211 4.5 kPa = over-v entilating Is the PaO2 high enough to adequately oxygenate tissues and prevent anaerobic metabolism? PaO2 > 6 kPa (SaO2 \211\210 80%) is probably adequate; PaO2 > 7 kPa (SaO2 > 87%) is de \201 nitely adequate \200 Is there evidence of V/Q mismatch? Evidence of low V/Q units is derived from the calculated alveolar to arterial (A \200\223a) O2 grad ient The two main things blood gasses tell you about acid/base balance (see later section o n acid \200\223base balance) \200 What is the respiratory component to an abnormal pH? Th is is derived from the PaCO2 What is the metabolic component to an abnormal pH? This is derived from the standard base excess/de \201 cit. The A \200\223a gradient calculator graph sets out the graphical representation of gas exch ange \200 Point \236\212 = pO2 and pCO2 (virtually zero) of inspired air (atmospheric pr essure \211\210 100 kPa, air is 21% O2, and air is slightly \200\230diluted \200\231 by w ater vapor pressure (7 kPa) following humidi \201 cation by upper airways). 21% of 100 \200\2237 = 20 kPa. (Point \236\213 = pO2 and pCO2 when breathing 24% O2 via a Ventimask a nd point \236\214 = pO2 and pCO2 when breathing 28% O2 via a Ventimask) Point \236\215 = theoretical pO2/pCO2 of inspired gas when breathing air, if all the O2 rem oved and replaced by CO2 (equivalent to extreme hypov- entilation and impossible!), when th e respiratory quotient (RQ = CO2 produced/O2 consumed) is 0.8 (usual value) The line between \236\212 and \236\215with a gradient of 0.8 describes all possible combi nations of alveolar gas, moving towards \236\212 if breathing more, and towards \236\215i f breathing less, called the alveolar air line. INTERPRETATION OF ARTERIAL BLOOD gasses: 1 793 Point \236\216 = area in which PaO2 and PaCO2 of arterial blood sit normally. If lungs are perfect gas exchangers, then blood leaving the lungs and entering systemic art erial circulation ( \236\216) should be perfectly equili- brated with the alveolar gas (A). 4 16 28%O2 24%O2 14 Air 12 ) a P k ( 10 2 8 O C p 6 6 7 A5 4 2 3 1 2 0 0 2 4 6 8 10 12 pO2 (kPa) 14 16 18 20 22 24 Fig. A1.1 pCO2 vs pO2: alveolar air lines and A \200\223a gradient calculator. Point \236\217 = However, the mixed venous point (or the pulmonary arterial blood) is well to the left of the alveolar air line. This is because capil- lary PO2 falls more kPa than the PCO2 rises during gas exchange in the tissues (CO2 solubility curve is steeper than PaO 2 \200\223SaO2 dissociation curve). Thus, if the lungs fail to oxygenate mixed venous blood properly (e.g. area of consolidation, or low V/Q due to asthma/COPD) then it is as if mixed venous blood h as bypassed the lung and leaked into the arterial blood, which therefore moves the eventual arterial PaO2/PaCO2 point to the left of the alveolar air line, point \236\220 APPENDIX 1 Blood gasses and acid \200\223base balance 794 Interpretation of arterial blood gasses: 2 \200 The horizontal distance between the actua l arterial point and the \200\230ideal \200\231 alveolar air line is called the alveolar t o arterial (A \200\223a) gradient and is a measure of how ef \201 ciently mixed venous blo od is equilibrated with alveolar gas, i.e. it is a measure of V/Q mismatch, right-to-left s hunts, and very severe lung \201 brosis through reduced diffusion across the alveolar-cap illary membrane. As well as being read off the graph it can be mathematically calculated as shown in Fig. A1.2. Arterial PO2 Arterial PCO2 A \200\223a gradient=PIO2 \200\223(PaO2+PaCO2) 0.8 Inspired PO2 Respiratory quotient Fig. A1.2 Calculation of inspired PO2 breathing air or 24/28% O2: Air, 21% of (100 \200\223 7) \211\210 20 kPa (where 100 kPa is atmospheric pressure and 7 kPa is water vapor pressur e due to the inspired air being humidi \201 ed); 24%, 24% of (100 \200\2237) \211\21023 k Pa; 28%, 28% of (100 \200\2237) \211\21026 kPa In Fig. A1.1 the alveolar air line depends on the % inspired O2, and the two extra lines, f or 24% and 28% O2, are shown. In the calculation the PIO2 has to be adjusted accordingly, ( see Figure A1.2). In normal lungs matching of V/Q is not totally perfect due to relative under-perfusion of t he apices and over-perfusion of the bases (gravity effects on pulmonary arterial blood \202 ow, not fully compensated for by hypoxic vasoconstriction of pulmonary arterioles). Th ese imperfections in V/Q, and direct drainage of some of the cardiac muscle venous blood in to the left ventricular cavity and thus systemic arterial circulation, lead to a small A \200\223a gradient, 1 \200\2232 kPa in the young and middle aged, and 2 \200\2233 kPa in th e elderly. Figures in excess of these values are abnormal and indicate areas of low V/Q or increased shunt. This page intentionally left blank APPENDIX 1 Blood gasses and acid \200\223base balance 796 Use of A \200\223a gradient diagram: examples Case 1 Consider point W in the pO2 \200\223pC O2 graph (Fig. A1.3), the blood gasses on air of a young non-smoker complaining of chest pa in 7 days post- operatively. The PaO2 of 13 is normal. Does this reassure you or does it pr ovide supporting evidence for a pulmonary embolus? Ask the following questions \200 How m uch is the patient ventilating? PaCO2 = 2; therefore \211 4.5 kPa and indicates hyperventilation Is the patient adequately oxygenated? PaO2 >7 kPa; therefore, OK \200 Is there an abnorma l A \200\223a gradient? Read off graph, horizontal line between W and alveolar line, or calculate: 20 \200\223 [13 + (2/0.8)] = 4.5 kPa >2 kPa, hence yes; therefore the V/Q matching is not normal. This provides supporting evidence for a pulmonary embolus, but could just as well be due to consolidation from pneumonia, for example \200 Remember, PaO2 cannot be used to assess V /Q matching in the lung without an associated PaCO2 to tell you \200\230what the PaO2 ough t to be \200\231. Case 2 Consider point X on the pO2 \200\223pCO2 graph. These are the gass es on air from a young man following an overdose of methadone tablets. \200 How much is t he patient ventilating? PaCO2 = 11; therefore \211 6 kPa and indicates hypoventilation Is the patient adequately oxygenated? PaO2 only 6 kPa; therefore not enough and needs extra O2 Has the patient got an A \200\223a gradient? 20 \200\223 [6 + (11/0.8)] = 0.8 kPa <2 kPa, hence no; therefore there is nothing wrong with the lungs, despite the abnormal gas ses, this represents pure hypoventilation. After a messy stomach wash-out he is sent to the ward and 24 h later is febrile. Gasses on 24% O2 are point Y on the graph; thus both PaCO2 and PaO2 are better. \200 How much is th e patient ventilating? PaCO2 just \211 6 kPa; therefore is still hypoventilating a bit 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.