tenderness Avoid heavy lifting for at least 6wk (except for scalp or face wounds) \200 Drive when yo u can perform an emergency stop and check the view over your shoulder (see b p605). _OHFP.indb 561 _OHFP.indb 561 30/05/2014 16:18 30/05/2014 16:18 562 CHAPTER 16 Procedures Reduction of fractures and dislocations Consent verbal Level F1 Diffi culty 3/5 Indication traumatic injury resulting in a fracture or dislocation. Contraindications relat ive neurological or vascular defi cit (get senior help immediately), open fracture. Closed Colles \200\231 fracture reduction Equipment three personnel (two to manipulate the fracture, one to apply backslab plaster), plaster, crepe bandage, tube stocking, water, sling and equipment for Bier \200\231s block or haematoma block (b p558). Checks X-rays of fracture from two views showing displacement; no neuro vascular defi cit; adequate analgesia. Patient position: sitting up with upper limb held at side at roughly 90 . Procedure: Your assistant applies traction backwards distal to the elbow whilst you apply f orward traction gently to unlock the two bone fragments. You may also apply downwards press ure to the bone fragments in order to help them come into alignment. When aligned, fl ex an d deviate the wrist towards the ulna. In this position, the plaster is applied. Only once t he cast has set can traction on the limb be released. Neurovascular status should be re-che cked and a check X-ray performed. If position is not satisfactory on X-ray, a further attem pt at closed reduction can be made. If this fails surgery may be required. Slings, crutches and analgesia should be provided as appropriate for patients being dischar ged home. All fractures require orthopedic follow-up to ensure adequate union of bone, eith er as an in-patient or via out-patient fracture clinics. Shoulder dislocations Around 96% of shoulder dislocations are anterior dislocations and the re are many methods that can be used to reduce them. The technique employed should reduce t he dislocation without causing additional trauma. The method used depends on patient condit ion, deepness of sedation, and your competence at the technique. Two of the most commonly u sed methods are outlined here. Posterior and inferior dislocations frequently require reduc tion under general anesthetic, so techniques to reduce these are not covered here. OHFP.indb 562 OHFP.indb 562 30/05/2014 16:18 30/05/2014 16:18 563 REDUCTION OF FRACTURES AND DISLOCATIONS Never attempt a technique you are not fully familiar with. Dislocations of the shoulder are diagnosed clinically and on X-ray. Anterior dislocations are normally obvious on AP should er views, and confi rmed on scapular \200\230Y \200\231-view (the humeral head sits anteri or to the glenoid). Posterior dislocations can look normal or show the \200\230lightbulb s ign \200\231 (due to internal rotation of the humerus) on AP view. They are confi rmed on \200\230Y \200\231-view (the humeral head sits posterior to the glenoid). Equipment 2 \200\2233 personnel, one to perform and monitor sedation if used (eg midazolam) and 1 or 2 to perform the reduction, sling. Checks X-rays (2 views minimum) to diagnose dislocation and check for associated fractures, except in patients with a history of recurrent atraumatic dislocation, no neurovascular de fi cit, and specifi cally axillary nerve function (see \200\230Complications \200\231), ad equate analgesia/sedation. Patient position lying fl at on their back. External rotation technique (single-person technique). The arm is slightly abducted and ben t at the elbow to 90 . Support the elbow with one hand and the patient \200\231s wrist wit h the other. Slowly ask the patient to allow their forearm to rotate away from their body ( externally rotate), stopping whenever pain or muscle spasm is felt. Support their arm in th at position until pain/spasm resolves and then ask them to allow their hand to fall to the side again. Repeat as many times as required, with the hand moving further each time. When externally rotated to between 70 and 110 , the shoulder should click back into position. Traction-countertraction technique (two-person technique). With the patient relaxed, abduc t the arm and apply traction at the distal forearm through the length of the arm whilst you r assistant applies counter-traction using a sheet wrapped around the patient \200\231s axi lla. Apply traction steadily until rotator cuff muscles relax enough to allow the shoulder to click back into position. For any reduction method, neurovascular status should be docu- mented before and after the procedure and a shoulder X-ray must be performed after reducti on. The patient should have a broad arm sling applied, be given adequate analgesia and have orthopedic follow-up. Complications axillary nerve and blood vessel injury (ensure the \200\230badge-patch \200 \231 area on the lateral side of the upper arm over the deltoid muscle, is checked for sens ation and this is documented pre- and post- procedure); Bankart lesions and Hill \200\223Sa chs deformities in recurrent dislocations, requiring elective surgery; failure of reduction leading to emergency reduction in theater. Alternatives other techniques exist for anterior dislocation reduction. These include the S paso, modifi ed-Milch, chairback and scapular manipula- tion techniques (single operator te chniques that are relatively atraumatic). Older techniques include Kocher \200\231s method and the Hippocratic method; however these techniques have higher levels of associated injur y and are not generally used in the UK. _OHFP.indb 563 _OHFP.indb 563 30/05/2014 16:18 30/05/2014 16:18 This page intentionally left blank Chapter 17 Interpreting results 565 Blood tests Full blood count (FBC) 566 Clotting 567 Cardiac markers 567 Infl ammatory respo nse 567 Urea and electrolytes (U+E) 568 Liver function tests (LFT) and amylase 569 Calcium and phosphate 570 Endocrine tests 571 Cardiology Electrocardiogram (ECG) 572 Respiratory Chest X-ray (CXR) 582 Arterial blood gasses (ABGs) 584 Respiratory function tes ts 586 Gastrointestinal Abdomen X-ray (AXR) 588 Urine tests 590 Neurological CSF 592 Musculoskeletal Autoantibodies and associated diseases 593 Cervical spine radiographs 594 S keletal radiographs 596 _OHFP.indb 565 _OHFP.indb 565 30/05/2014 16:18 30/05/2014 16:18 566 CHAPTER 17 Interpreting results Full blood count (FBC) There are three main components: red cells (measured by hemoglobin o r Hb), white cells (leucocytes or WCC), and platelets (plts). Remember these components rep resent the three cell lines from bone marrow. Main FBC abnormalities b p392 d Hb b p478 FBC often initially normal b p482 i WCC, i plts ii WCC b p396 Persistent change in \211 1 cell line b p396 Anemia Acute blood loss Infection/infl ammation Hematological malignancies Bone marrow diso rders Hb \200\223 red bloods cells (male: 130 \200\223180g/L: female: 115 \200\223160g/L) \200 dHb Anemia, classifi ed according to MCV, see b p392 for causes, investigations, and management iHb Dehydration (b p378), secondary polycythaemia, eg heart/ lung disease, polycythaemia ve ra (b p396). Consider prophylactic LMWH (b p406) due to the increased thrombosis risk. Reticulocytes (50 \200\223100 \227 109/l or 0.5 \200\2232.5%) these are immature red cells released from bone marrow in response to haemolysis or blood loss (response detectable aft er a few hours, not hyperacutely). They are also raised secondary to infl ammation and infe ction. WCC \200\223 white blood cells (4 \200\22311 \227 109/l; Table 17.1) Table 17.1 Causes of abnormal white cell diff erentials Cell Neutrophils (2.0 \200\2237.5 \227 109/l) Causes i Bacterial infection, infl ammation, acute illness, myeloid leukemia, steroid therapy d Viral infection, sepsis, drugs (chemotherapy, steroids, carbimazole), splenomegaly, bone marrow failure, d B12 or folate, autoimmune disease i Viral infection, infl ammation, lymphocytic leukemia d Steroids, chemotherapy, HIV, autoi mmune disease, Lymphocytes (1.3 \200\2233.5 \227 109/l) bone marrow failure i Parasitic/fungal infection, asthma, atopy, lymphoma d Rarely pathological Eosinophils (0.04 \200\2230.44 \227 109/l) Plts \200\223 platelets (150 \200\223400 \227 109/l; Table 17.2) Table 17.2 Causes of abnormal platelet counts i Infl ammation, infection, acute illness, re covery from splenectomy, essential thrombocytosis, polycythaemia [rubra] vera (see b p396) d HIT (b p406), idiopathic thrombopenic purpura (ITP) (b p405), chronic alcoholism, bone marrow failure, DIC (b p405), viral infections, splenomegaly, HELL P (b p505) OHFP.indb 566 OHFP.indb 566 30/05/2014 16:18 30/05/2014 16:18 567 INFLAMMATORY RESPONSE Clotting Clotting is often measured before procedures and surgery if there is suspi- cion o f an abnormality (eg liver failure). It is also measured to allow correct dosing of warfari n and IV heparin. Prothrombin time (PT) is a measure of the extrinsic pathway and should be quoted unless the patient is on war- farin therapy when the international normalized ratio (INR) is used; activated partial thromboplastin time (APTT) is a measure of the intrinsic pathway and should be quoted unless the patient is on IV heparin therapy when the APTT rati o (APTTr) is used (Table 17.3). See b p405 for clotting defects. Table 17.3 Causes of abnormal clotting Test Causes i Warfarin, liver disease, DIC, sepsis, defi ciency of factors PT (11 \200\22316s) [INR 0.8 \200\2231.2] II, V, VII or X, heparin d Rarely pathological i Heparin, hemophilia A+B, von Willebrand disease, APTT (35 \200\22345s) [APTTr 0.8 \200\2231.2] DIC, sepsis, defi ciency of factors II, V, VII, IX, X, XI, or XII, liver disease, warfarin d Rarely pathological i DIC, sepsis, liver disease, warfarin, heparin PT and APTT Cardiac markers These tests are used to diagnose MI, and to distinguish MI from stable and unstable angina (b p241). Assays for cardiac troponins (either I or T) diff er between hosp itals. Due to diff erent kinetics of release and excretion, meas- urement of creatine kinas e (CK or CK-MB) can also be useful in patients with ongoing chest pain after a recent MI (s ee b p243). See Table 17.4. Table 17.4 Causes of abnormal cardiac markers Test Causes i MI (raised after 6 \200\22312h), small rise may Troponin (upper limit of normal depends on assay used \200\223 check local advice) CK (25 \200\223195units/l) be seen with CRF, PE, septicaemia, blunt chest trauma i MI, rhabdomyolysis (muscle breakdown \200\223 check renal function), exercise, recent su rgery, hypothyroidism, blunt chest trauma In \202 ammatory response Acute or chronic infl ammation can aff ect a wide range of blood results, including: \200 i ESR \200 i CRP \200 i Ferritin i Plts \200 i WCC \200 d Albumin. A very high ESR (>100mm/h) should raise suspicions of giant-cell arteritis (b p429), polymy algia rheumatica (b p454), or myeloma (b p389). _OHFP.indb 567 _OHFP.indb 567 30/05/2014 16:18 30/05/2014 16:18 568 CHAPTER 17 Interpreting results Urea and electrolytes (U+E) These are measured to assess renal function and the concentrati on of the two main electrolytes in the blood. Main urea and electrolyte abnormalities iurea, iCr iK+, iiurea, iCr iurea, iiCr, dHb iiurea, others normal dNa+, iK+, iurea, iCr b p378 b p372 b p373 b p299 b p332 Dehydration Acute renal failure Chronic renal failure Upper GI bleed Addison \200\231s dise ase Urea and creatinine (Table 17.5) Urea and creatinine (Cr) are metabolic waste products whic h are excreted by the kidney. An increase in either test suggests a degree of renal dysfunc - tion. If both urea and creatinine are raised the patient has renal failure. Check previou s U+E results to distinguish between chronic and acute renal failure. Acute renal failure i s an emergency, see b p372. Table 17.5 Causes of abnormal urea and creatinine Test Causes i Dehydration, upper GI bleed, acute illness, pre-renal Urea (2.5 \200\2237.8mmol/l) failure d Rarely pathological, can be caused by pregnancy or a lack of protein, eg alcoholism, anor exia, liver failure, malnutrition i Renal failure, may be acute, chronic or acute on Creatinine (Cr) (70 \200\223150micromol/l) chronic; muscle injury d Rarely pathological, can be seen in pregnancy or dBMI i Renal failure, check K+ and ECG Urea and creatinine Sodium and potassium (Table 17.6) Numerous diseases can aff ect electrolyte levels, these a re discussed in the section on electrolyte imbalance (b p385). Small changes in K+ can indu ce fatal arrhythmias in the heart so abnormal K+ levels should be treated as an emergency ( b p384). Table 17.6 Causes of abnormal sodium and potassium Electrolyte Na+ \200\223 sodium (133 \200\223146mmol/l) Causes i See b p387 d See b p386 i Urgent ECG, inform senior, see b p385 d Urgent ECG, info rm senior, see b p385 K+ \200\223 potassium (3.5 \200\2235.3mmol/l) OHFP.indb 568 OHFP.indb 568 30/05/2014 16:18 30/05/2014 16:18 569 LIVER FUNCTION TESTS (LFT) AND AMYLASE Liver function tests (LFT) and amylase These are measured to detect jaundice, liver disease , biliary disease and pancreatitis. Liver dysfunction may aff ect clotting, particularly PT . Main liver function abnormalities ibilirubin (unconjugated), dHb, ireticulocytes, d haptoglobin ibilirubin (mixed), iiALT/AST , iGGT b p318 ibilirubin (conjugated), iiALP, iGGT b p318 b p313 ii AST/ALT, i GGT, iALP b p313 ibilirubin, iPT, dalbumin iGGT, iMCV, dplts b p395 iiamylase/lipase, dCa2+, iglucose, iiCRP b p296 b p505 iAST/ALT, iGGT, dHb, dplts b p318 Pre-hepatic jaundice Hepatic jaundice Cholestatic jaundice Hepatocellular damage Liver failure Alcoholism Pancre atitis HELLP (pregnant) Liver function tests (Table 17.7) See b p312 \200\223319 for the investigation and manageme nt of liver disease. Table 17.7 Causes of abnormal liver function tests Test Causes i Hepatocellular damage, biliary disease, alcohol, ALT or AST (3 \200\22335units/l) muscle damage, MI, pancreatitis d Rarely pathological, consider dvitamin B6 ALP (30 \200\223130units/l) i Biliary disease/damage, liver disease, alcohol, bone disease (especially Paget \200\231s), pregnancy, bony metastases d Rarely pathological i Biliary or liver disease, alcohol d Rarely pathological i Jaundice (b p318 \200\223 haemolysis, liver disease, G GT(10 \200\22355units/l) Bilirubin (3 \200\22321micromol/l) obstruction of biliary system), Gilbert \200\231s syndrome d Rarely pathological i Dehydration d Infl ammation, cirrhosis, pregnancy, chronic disease Albumin (35 \200\22350g/l) Amylase and lipase (Table 17.8) Table 17.8 Causes of abnormal amylase and lipase Test Cause i Acute or chronic pancreatitis, abdominal disease (eg perforation), burns, anorexia, salivar y adenitis, renal disease Amylase (0 \200\223120units/l) Lipase (5.0-65units/l) iii Acute pancreatitis (eg 3 \227 upper limit of normal) Depending on the laboratory and the patient population, lipase tends to be slightly more sp ecifi c for pancreatic pathology than amylase. There is no indication for requesting both. _OHFP.indb 569 _OHFP.indb 569 30/05/2014 16:18 30/05/2014 16:18 570 CHAPTER 17 Interpreting results Calcium and phosphate Calcium and phosphate are electrolytes predominantly stored in bones. Blood levels are aff ected by many diseases including parathyroid and bone abnormalities. See Tables 17.9 and 17.10. Main calcium and phosphate abnormalities b p389 iCa2+, iALP 4 \200\223, dPTH b p388 dCa2+, iPO3 4 \200\223, iALP, iPTH iCa2+, dPO3 b p389 iCa2+, iurea, iCr, dHb, iESR b p389 4 \200\223 b p389 iiALP, nCa2+, nPO3 Bone metastases Hypoparathyroidism Primary hyperparathyroidism Myeloma Paget \200\231s Table 17.9 Causes of abnormal calcium and phosphate Test Ca2+ \200\223 calcium (2.2 \200\2232.6mmol/l) Causes i Primary/tertiary hyperparathyroidism, malignancy (myeloma, bone metastases, PTH-related p eptide secreting tumors), excess vitamin D supplements, sarcoidosis d Vitamin D defi ciency (Asians, Africans, chronic renal failure), hypoparathyroid, acute p ancreatitis, alkalosis, magnesium defi ciency i Chronic renal failure, dPTH, myeloma, excess vitamin D, rhabdomyolysis, cell lysis (eg po st-chemo), acidosis 3 \200\223 \200\223 phosphate PO4 (0.8 \200\2231.5mmol/l) d Malabsorption/malnutrition, alcohol, iPTH, burns, alkalosis, post-DKA treatment Table 17.10 Eff ects of parathyroid hormone disease on blood tests 3 \200\223 PO4 d d i i Ca2+ i d i d Disease PTH i i i d Primary hyperparathyroidism Secondary hyperparathyroidism Tertiary hyperparathyroidism1 Hyp oparathyroidism 1 The hyperphosphataemia in tertiary hyperparathyroidism results from the inability of the diseased kidneys to excrete it rather than as a function of the high levels of PTH, per se. OHFP.indb 570 OHFP.indb 570 30/05/2014 16:18 30/05/2014 16:18 571 ENDOCRINE TESTS Endocrine tests Cortisol (b p332) Short Synacthen test \200 Take blood for cortisol ide ally at 9am. Occasionally ACTH is also tested; it needs to be transported on ice. Call biochemistry to check which bottle to use Give 250micrograms Synacthen IM/IV \200 Take blood for cortisol 30min later \200 A ba seline or 30min cortisol level above 550nmol/l is normal and excludes primary adrenal insuffi ciency If 30min cortisol <550nmol/l and dACTH l ACTH defi ciency \200 If 30min cortisol <550nmol /l and iACTH lAddison \200\231s disease (b p332). Glucose This test is performed when the p atient is not acutely unwell and on a normal diet. The patient is fasted overnight. 75g glu cose in 300ml water is given after the baseline fasting glucose blood sample has been taken . A 2h plasma glucose sample is also taken. See Table 17.11. Table 17.11 Interpretation of oral glucose tolerance test Fasting glucose Glucose after 2h Diagnosis Any value \211 7mmol/l <7mmol/l 6.1 \200\2236.9mmol/l <6.1mmol/l \211 11.1mmol/l Any value 7.8 \200\22311.0mmol/l \211 7.7mmol/l \211 7.7mmol/l Diabetes mellitus Diabetes mellitus Impaired glucose tolerance (IGT) Impaired fasting gluco se (IFG) Normal Thyroid function (Table 17.12; b p334) Table 17.12 Thyroid function T4 i T3 i i TSH dd dd d ii Hyperthyoidism T3 hyperthyroidism Subclinical hyperthyroidism 1 hypothyroidism (thyroid d isease) 2 hypothyroidism (pituitary disease) Subclinical hypothyroidism normal normal d d normal d d d or normal i normal normal _OHFP.indb 571 _OHFP.indb 571 30/05/2014 16:18 30/05/2014 16:18 572 CHAPTER 17 Interpreting results Electrocardiogram (ECG) Examine all ECGs in a systematic manner to avoid missing the basics . Never be tempted to trust the automated interpretation: these are rarely accurate. Check patient details, date and time of ECG, speed of paper (25mm/s). Rate at 25mm/s each large s quare represents 0.2s and each small square 0.04s. To calculate rate divide 300 by the numb er of large squares between one R wave and the next R wave (see Table 17.13). Table 17.13 Calculating heart rate from the ECG Large squares Heart rate (bpm) Large square s Heart rate (bpm) 1 1 3/5 2 2 1/5 2 2/5 300 188 150 136 125 2 3/5 2 4/5 3 4 5 115 107 100 75 60 Rhythm Sinus rhythm each QRS has a P wave before it. Atrial \201 brillation no P wave and the QRS complexes are irregularly irregular. Atrial \202 utter the baseline is described as saw-tooth and the QRS are often regularly spaced. Ventricular rhythm QRS is wide (>0.12 s or >3 small squares) and has no association with P waves. Nodal rhythm P wave may be abse nt or part of the QRS complex, but rhythm is regular. Regularly irregular rhythms suggest a degree of heart block (b p258). Axis Look at lead I and count the number of small squares that make up the height of the R wave (positive defl ection). Next count the number of smal l squares that make up the Q and/or S wave (negative defl ections). Work out the diff erenc e between the R and Q/S wave (ie R wave squares \200\223 Q/S wave squares). Do the same fo r lead aVF. Draw a large cross (Fig. 17.1a) and plot the numbers for lead I and aVF. The li ne between where they meet and the middle is the cardiac axis. An example is shown where le ad I has a 10 square R wave and 7 square S wave (10 \210\222 7 = 3) and lead aVF has an 8 square R wave and 1 square S wave (8 \210\222 1 = 7). The normal axis is from \210\22230 to +90 (Fig. 17.1b). aVR aVL ( \210\22230 ) I ( \210\2220 ) Lead I Axis 67 II III Lead aVF aVF (+90 ) (a) (b) Fig. 17.1 (a) Calculating the cardiac axis; (b) the normal cardiac axis. Table 17.14 shows a quick way of working out the rough position of the axis by comparing the size of the R wa ve to the size of the Q wave. Table 17.14 Calculating the cardiac axis from the ECG Lead I R > Q/S 0 to 90 0 to \210\22290 R < Q/S 90 to 180 \210\22290 to 180 Lead aVF R > Q/S R < Q/S OHFP.indb 572 OHFP.indb 572 30/05/2014 16:18 30/05/2014 16:18 573 ELECTROCARDIOGRAM (ECG) P wave absent in AF (b p252) and atrial fl utter (b p253). Bifi d P wave suggests left atri al hypertrophy. Peaked P waves are seen in right atrial hypertrophy (eg pulmonary hypertens ion) and transiently in dK+. PR interval normally 0.12 \200\2230.2s (3 \200\2235 small squa res). Longer in heart block (b p258) and shorter in WPW (b p253). See Fig. 17.2. QRS comple x normally <0.12s (<3 small squares). Wider QRS implies ventricular rhythm (eg 3rd-degree h eart block) or bundle branch block (causes in Table 17.15). Paced rhythms may also have wid e QRS complexes. Hypertrophy left (LVH): sum of S wave in V3 and R wave in aVL >28mm (men) or >20mm (women)1 is suggestive of LVH (not diag- nostic); right (RVH): R>Q or S wave in V1 , deep S wave in V6, T wave inversion in V2, V3, V4, right axis deviation. ST segment usually level with baseline; elevation >1mm (for causes see Table 17.15, infarction b p244 ); depression >0.5mm suggests ischaemia (b p245 \200\223246). T wave inversion (pointing do wn) in leads I, II or V4 \200\223V6 suggests ischaemia. Often peaked in iK+ and acute MI, f l attened in dK+. Other components of the ECG \200 QT interval is dependent on heart rate . The QTc (QT interval corrected for heart rate) is calculated by most ECG machines. An abnormal QTc is >450ms (4) and >470m s (5) (b p254). QTc prolongation is associated with increased risk of ventricular arrhythmi as U wave (positive in most leads) follows the T wave and precedes the P wave; if present it i mplies d K+ though can be a normal fi nding \200 Z wave a slurred upstroke to the QRS com plex found in conduction defects eg WPW b p253 J wave an upwards wave seen immediately after the QRS complex and before the T wave in hypothermia. Hints and tips being able to read an ECG systematically is much more important than a spot ECG diagnosis. The common ECG abnormalities which should not be missed are: AF, MI or ischa emia, LBBB/RBBB, 3rd- degree heart block and ventricular tachycardia. Electrocardiograph Normal ECG PR interval QRS interval QT interval PR and QT intervals vary with heart rate R 0.12 \200\2230.20s <0.12s 0.33 \200\2230.43s ST segment P U T PR interval Q S QT interval QRS interval Fig. 17.2 The normal QRS complex and normal ECG intervals. 1 Cornell voltage criteria for L VH, from Casale et al. Improved sex specifi c criteria of left ven- tricular hypertrophy for clinical and computer interpretation of electrocardiograms: valida tion with autopsy fi ndings. Circulation. 2010 75(3):565 \210\22272. _OHFP.indb 573 _OHFP.indb 573 30/05/2014 16:18 30/05/2014 16:18 574 CHAPTER 17 Interpreting results Table 17.15 Causes of \200 ST elevation STEMI, pericarditis, ventricular aneurysm, LBBB, hypothermia, coronary artery spasm (Prinzm etal \200\231s angina), early repolarisation (high takeoff ) Acute MI, ischaemic heart dise ase, hypertensive heart disease, cardiomyopathy, aortic valve disease LBBB RBBB Left axis deviation Right axis deviation Normal, heart failure, PE, pulmonary hypertension Left ventricular hypertrophy, inferior MI , left anterior hemiblock, hyperkalaemia Right ventricular hypertrophy, chronic lung diseas e, normal in children, left posterior hemiblock Coronary artery territories and the ECG (Fig. 17.3 and Table 17.16) Aorta Pulmonary artery (trunk) Superior vena cava Right atrium Circumflex branch of left coronary artery Left atrium Left marginal artery Left main corona ry artery Left anterior descending coronary artery Right coronary artery Right ventricle Inferior vena cava Left ventricle Fig. 17.3 Simplifi ed structure of the heart and its coronary blood supply. Left anterior d escending artery (LAD) and its many branches supply the anterior and anteriolateral walls o f the left ventricle, and the anterior two-thirds of the septum. Left circum \202 ex artery (LCX) and its branches supply the posterolateral wall of the le ft ventricle. Right coronary artery (RCA) supplies the right ventricle, the inferior and posterior walls of the left ventricle and the posterior third of the septum; the RCA also gives off the AV nodal coronary artery in 785% of individuals, with the LCX supplying this in the remaining 15% of people. Table 17.16 Territories of the heart on the ECG I Lateral II Inferior III Inferior aVR Multiple aVL Lateral aVF Inferior V1 Septal V2 Septal V3 Anterior V4 Anterior V5 Lateral V6 Lateral OHFP.indb 574 OHFP.indb 574 30/05/2014 16:19 30/05/2014 16:19 _ _ O O H H F F P P i i n n d d b b 5 5 7 7 5 5 E L E C T R O C A R D O G R A M I ( E C G Fig. 17.4 Left bundle branch block: Note W pattern in V1 and M pattern in V5/V6, also no Q wave in V5/V6 and inverted T wave in I and aVL. Remember \200\230WiLLiaM and MaRRoW \200 \231. ) 5 7 5 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 1 1 9 9 : : O O H H F F P P i i n n d d b b 5 5 7 7 6 6 5 7 6 C H A P T E R 1 7 I n t e r p r e t i n g r e s u l t s Fig. 17.5 Right bundle branch block: Note M pattern (RSR) in V1, W pattern in V5/V6 and inv erted T wave in V1. Remember \200\231 WiLLiaM and MaRRoW \200\231. 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 : : 1 1 9 9 _ _ O O H H F F P P i i n n d d b b 5 5 7 7 7 7 E L E C T R O C A R D O G R A M I ( E C G ) Fig. 17.6 Acute inferolateral ischaemia: Note ST depression in leads I, II, III, aVF and V3 to V6, also T wave inversion in aVR (normal variant) and aVL. 5 7 7 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 1 1 9 9 : : O O H H F F P P i i n n d d b b 5 5 7 7 8 8 5 7 8 C H A P T E R 1 7 I n t e r p r e t i n g r e s u l t s Fig. 17.7 Acute inferolateral myocardial infarction: Note ST elevation in leads II, III and aVF (inferior leads) and also in V5 and V6 (lateral leads). The ST depression in I, aVL an d V2 are reciprocal changes and often seen with large infarcts. 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 : : 1 1 9 9 _ _ O O H H F F P P i i n n d d b b 5 5 7 7 9 9 E L E C T R O C A R D O G R A M I ( E C G ) Fig. 17.8 Acute anterior myocardial infarction: Note the ST segment elevation in leads V1 t o V4 and slightly in V5 and the evolving Q wave. 5 7 9 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 1 1 9 9 : : O O H H F F P P i i n n d d b b 5 5 8 8 0 0 5 8 0 C H A P T E R 1 7 I n t e r p r e t i n g r e s u l t s Fig. 17.9 Acute posterior myocardial infarction: Note dominant R wave and ST depression in V1-V3 (often seen with ST elevation in V5/V6 refl ecting posterolateral infarction). 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 : : 1 1 9 9 _ _ O O H H F F P P i i n n d d b b 5 5 8 8 1 1 E L E C T R O C A R D O G R A M I ( E C G Fig. 17.10 Ventricular tachycardia: Note the broad nature of the QRS and regular repeating rhythm. ) 5 8 1 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 1 1 9 9 : : 582 CHAPTER 17 Interpreting results Chest X-ray (CXR) The main patterns of acute disease are: \200 Pneumonia (b p276) asymmet rical shadowing (consolidation), blunting of angles, blurring of heart and diaphragm border s, air bronchograms Pulmonary oedema (b p282) enlarged heart, symmetrical hazy/ reticular shadowing, blunted costophrenic angles or pleural eff usions, indistinct hilar ve ssels, enlarged upper lobe vessels, Kerley B lines, distinct septa Pleural eff usion (b p279) featureless white area at the base with loss of costophrenic and /or costocardiac angles on the aff ected side meniscus (upper surface sloping up to the chest wall) Asthma/COPD (b p273 \200\223274) hyperinfl ated, fl attened diaphragm, barrel chested Pneumothorax (b p279) line of separated pleura with peripheries lacking lung markings \200 \223 may be large and deviating mediastinum (eg tension). tension). Adequacy of a CXR \200 \223 interpret cautiously unless the following are normal \200 Rotation heads of the clav icles should be the same distance from the vertebral bodies on each side; the spinous proce sses should be in the middle of the vertebral bodies Penetration intervertebral disks should be visible behind the heart and the lung fi elds should have markings Inspiration \211 7 posterior ribs should be visible. Develop a routine so you spot all the abnormalities: \200 Lung outline: blunting/loss of costophrenic and cardiophrenic angles \200 indistinct heart border, lung border or diaphragm edges \200 pneumothorax best seen by inverting the image or rotating by 90 \200 Kerley B lines 1 \200\2232cm horizontal lines at the edges, extending to the plerural margin pleural plaques/thickening does the edge look whiter in some areas? Lung \201 elds: color too dark suggests pneumothorax, emphysema or high penetration, while white shadowing suggests pulmonary oedema, pneumonia, eff usion or under -penetration. Describe shadowing as nodular (lumpy), reticular (fi ne lines eg pulmonary oe dema) or alveolar (fl uff y eg consolidation). Air bronchograms may be seen (air fi lled br onchus seen against surrounding opacifi ed alveoli) suggesting an airspace process (eg oede ma, consolidation) vascular markings the upper lobe vessels should be thinner than lower lobe ones cavities ie dark circles, consider bronchiectasis, bullae or abscesses (may have an air/fl uid level) localized white lesions eg carcinoma or abscess Lung size there should be \211 7 posterior ribs (see Figs 17.11 and 17.12), \211 10 hyper infl ated, \211 6 poor inspiratory eff ort; for anterior ribs the numbers are two lower OHFP.indb 582 OHFP.indb 582 30/05/2014 16:19 30/05/2014 16:19 583 CHEST X-RAY (CXR) Diaphragm: Is there a pneumoperitoneum (eg perforated bowel), thin black line under the diaphragm? Is the right side slightly higher than the left? If not consider pressure from within abdomen or diaphragmatic paralysis as causes Are the domes convex? Flat suggests hyperexpansion Mediastinum: This should be <8cm wide at the aortic arch, wider suggests abnormal tissue eg aortic disse ction or lymphadenopathy The heart should be <50% the width of the chest on a PA fi lm, larger suggests cardiomegaly (diffi cult to interpret on AP fi lms) Is there collapse or consolidation behind the heart? Trachea should be central and uncompressed \200 Hila these should have a concave shape wi th distinct vessels \200 Bones look at the spine, clavicles, scapulae, shoulder and ribs. Look for fractures, osteolytic and osteosclerotic lesions. Is the spine straight? \200 S oft tissues surgical emphysema (pneumothorax), breast lesions. Aortic arch Trachea Right middle lobe Carina (T6) Spine Right ventricle Left atrium Lower lobe Right hemi diaphragm Left ventricle Left hemi diaphragm Gastric bubble Fig. 17.11 Major features of a lateral CXR. Trachea Clavicle Aortic arch 2nd rib 1st rib Right upper lobe Scapula Left upper lobe Posterior rib Carina Right middle lobe Anterior rib Left ventricle Cardiophrenic angle Left lower lobe Gastric bubble Right lower lobe Right atrium Spine Costophrenic angle Fig. 17.12 Major features on an anteroposterior CXR. Central lines (b p534) check for pneum othorax and haemothorax; note the position of the end of the line, it should be at the leve l of the carina. Feeding NG tubes (b p549) the end of the tube should be seen below the dia phragm; if not advance the tube 5cm and repeat CXR. If tube in bronchus, remove completely and resite. Chest drains (b p540) the end should be within the ribcage, ideally angled down wards for eff usions and up for pneumothoraces; note the size of pneumothorax or eff usion and any surgical emphysema. _OHFP.indb 583 _OHFP.indb 583 30/05/2014 16:19 30/05/2014 16:19 584 CHAPTER 17 Interpreting results Arterial blood gasses (ABGs) \200\223 in a ABG analysis measures PaO2 and PaCO2, and calcu lates HCO3 heparinised specimen (can also be undertaken on venous or capillary blood or on fl uid aspirated from the chest or abdomen). Base excess and anion gap are also calculated. In addition, pH, O2 saturation, and concentrations of Na+, K+, Ca2+, Cl \200\223 and lacta te are measured. For advice on how to perform an ABG see b p522. See Table 17.17. Table 17.17 Normal ranges (patient breathing room air) Parameter Value Parameter HCO \200\223 Base excess (BE) O2 saturation Value pH PaO2 PaCO2 7.35 \200\2237.45 10.6 \200\22313.3kPa 4.7 \200\2236.0kPa 22 \200\22328mmol/l \210\2222 to +2 95 \200\223100% 3 NB Note that a low or normal PaO2 in a patient on a high concentration of inspired O2 is ve ry worrying and suggests signifi cantly impaired gas exchange. First look at the pH: \200 pH <7.35 = acidaemia \200 pH 7.35 to 7.45 = normal pH \200 pH >7.45 = alkalaemia. Next look at the PaCO2 and bicarbonate (HCO3 17.19): \200\223) (Tables 17.18 and Table 17.18 Types of acidaemia dHCO \200\223 3 Metabolic acidosis Mixed acidosis Mixed acidosis nHCO \200\223 3 iHCO \200\223 3 dPaCO2 X X nPaCO2 iPaCO2 X Acute respiratory acidosis X Chronic respiratory acidosis X \200\223 incompatible Table 17.19 Types of alkalaemia dHCO \200\223 3 nHCO \200\223 3 iHCO \200\223 3 dPaCO2 Chronic respiratory alkalosis X X Acute respiratory alkalosis X X Mixed alkalosis nPaCO2 iPaCO2 Mixed alkalosis Metabolic alkalosis X \200\223 incompatible OHFP.indb 584 OHFP.indb 584 30/05/2014 16:19 30/05/2014 16:19 585 ARTERIAL BLOOD gasses (ABGS) Base excess This is the amount of \200\230base \200\231 needed to restore pH to the normal range (Table 17.20): \200 Base excess >+2, patient has excess base present (ie alkalosis ) \200 Base excess < \210\2222, patient has insuffi cient base present (ie acidosis). Table 17.20 Causes of acid \200\223base disturbance Acidosis Alkalosis Shock DKA Renal/liver failure Drug overdose (eg TCA) Renal tubular acidosis Lactate (b p477 ) Refer to \200\230anion gap \200\231 box Vomiting Diarrhea Hypokalaemia Metabolic Respiratory Severe asthma/COPD Cranial lesions (eg stroke) Anxiety/hyperventilation Severe pneumonia Severe pulmonary oedema Myasthenia gravis Drugs (eg sedatives, opioids) Ch est trauma/scoliosis Obesity If all else fails calculate the anion gap or speak to a biochemist If the diff erentials fo r a metabolic acidosis are still unclear then calculate the anion gap which should answer a ny remaining problems (see box); alternatively ask a senior or speak directly to the clinic al biochemist in the laboratory. The anion gap This is calculated by ([Na+] + [K+]) \200\223 ([Cl \200\223 ] + [HCO3 Normal value is 6 \200\22316mmol/l. It helps to distinguish the diff erent causes of a metabolic acidosis: \200 Raised anion gap (>16mmol/l): \200\223 ]). lactic acidosis (b p477 shock, sepsis/infection) \200 urate (renal failure) \200 ketone s (DKA, alcohol, starvation) \200 drugs/toxins (salicylates, biguanides, ethylene glycol, methanol) Normal anion gap (6-16mmol/l): Addison \200\231s disease \200 pancreatic fi stula \200 ammonium chloride ingestion. renal tubular acidosis \200 diarrhea \200 drugs (acetazolamide) _OHFP.indb 585 _OHFP.indb 585 30/05/2014 16:19 30/05/2014 16:19 586 CHAPTER 17 Interpreting results Respiratory function tests Peak expiratory \202 ow rate (PEFR) Indications used for the diagnosis, monitoring (eg da ily diary/obs) and severity assessment of asthma (Table 17.21). Method reset the tab and fi t a clean mouthpiece. Ask the patient to stand up and hold it i n their hands (not covering the scale), breathe in deeply and blow as hard and fast as they can (with encouragement). Use the best reading of three attempts. Table 17.21 PEFR in asthma (exacerbation severity) PEFR1 Asthma severity >80% Normal Mild \200\223moderate 80 \200\22350% 55 \200\22333% Severe <33% Life-threatening 1 Compared with best or predicted (see Fig. 17.14). Spirometry Indication diagnosis and monitoring of respiratory disease. Before testing omit morning inhalers or nebulisers (unless severely ill) to allow reversibility assessment. Method can be performed by technicians in a respiratory function laboratory or by you at th e patient \200\231s bedside. The patient must inhale as deeply as they can then exhale as f ast and as long as they can manage. The following measurements are made (Table 17.22): \200 Forced expiratory volume in 1s (FEV1), the volume exhaled in the fi rst second after deep inspiration and forced expiration, similar to PEFR \200 Forced vital capacity (FVC), the total volume exhaled from maximal inspiration to maximal exhalation. Beyond spirometry respiratory function laboratories can also measure: Residual volume (RV), the volume of gas remaining in the lungs after a maximum expiration Total lung capacity (TLC) is the combination of FVC and RV. Table 17.22 Spirometry \201 ndings in lung disease Obstructive dd d Normal n n Restrictive d dd FEV1 FVC FEV1/FVC RV TLC <75% i i 75 \200\22380% n n >80% d d Obstructive asthma, COPD, emphysema. Restrictive interstitial lung disease, sarcoid, connec tive tissue disorders, neuromuscular disease (including myasthenia gravis and Guillain \200 \223Barr ). OHFP.indb 586 OHFP.indb 586 30/05/2014 16:19 30/05/2014 16:19 587 RESPIRATORY FUNCTION TESTS Other spirometry measurements Reversibility asthma (a reversible obstruction) is diagnosed if there is \211 250ml and \211 15% improvement in PEFR or FEV1 with bronchodilators. Ast hma can coexist with COPD (non-reversible obstruction). Gas transfer also called transfer factor; is measured using carbon monoxide. It is reduced in emphysema, acute asthma, anemia and interstitial lung disease and increased with chronic asthma, left heart failure, polycythaemia and exercise. Flow volume loops graphical representations of the results with volume on the x-axis and fl ow rate on the y-axis. Exhalation is above the line and inhalation below the line. There a re four main patterns (Fig. 17.13). Upper airway obstruction lesion occluding the bronchi, trachea or larynx associated with st ridor, see b p284. Normal Obstructive Restrictive Upper airway obstruction Fig. 17.13 Flow volume loops (fl ow on y-axis, volume on x-axis). 700 Age (yrs): 20 \200\22325 30 40 50 60 20 \200\22325 30 40 50 60 Men Women 11 650 ) n m / ( 10 600 ) s / ( i l l w o fl 550 9 w o fl y r o t a r i p x e k a e P 500 y r o t a r i p x e k a e P 8 450 7 400 6 350 4 11 \235 5 3 \235 5 7 \235 5 11 \235 300 5 1.6 m 1.7 m 1.8 m 1.9 m 1.4 m 1.5 m Height (m) = meters, = feet, \235 = inches Fig. 17.14 Normal peak expiratory fl ow values. _OHFP.indb 587 _OHFP.indb 587 30/05/2014 16:19 30/05/2014 16:19 588 CHAPTER 17 Interpreting results Abdomen X-ray (AXR)