Fig. 46.1 Urine test strip. Reproduced from https://en.wikipedia.org/wiki/Urine_test_strip.
Urine dipsticks, microscopy, and biochemistry have replaced taste to help screen for infection, renal disorders, pregnancy, and pregnancy-related disorders but inspection (haematuria) and smell (smell of burnt sugar in maple syrup urine disease, an autosomal recessive metabolic disorder) are still useful!
Dip the test strip in the sample for 1–2 sec, then wait for 30 sec before reading the different tabs against the dipstick container. (See Fig. 46.1.) Most wards have automatic readers which give a printout of the urinalysis.
Fig. 46.1 Urine test strip. Reproduced from https://en.wikipedia.org/wiki/Urine_test_strip.
Are a product of incomplete fat metabolism and a measure of starvation. Used to help diagnose and monitor treatment response to DKA but this has been replaced by measuring blood ketones (beta-hydroxybutyrate) which is a more accurate measurement of ketosis.
Normally absent in urine. Can be caused by drugs (some antibiotics, steroids). If positive, requires a blood glucose (see 
p. 847).
Measures the amount of solute in urine compared to water (1.0) and so the kidney’s ability to concentrate urine. If <1.005, excessive hydration or inability to concentrate urine (glomerulonephritis, pyelonephritis, diabetes insipidus, AKI). If >1.035, indicates dehydration (diarrhoea/vomiting), SIADH, heart failure, proteinuria, or glucose.
The kidneys help regulate acid–base balance, with normal range anywhere between 4.5 and 8.0 (but usually 5–7).
Must rule out malignancy! Otherwise indicative of trauma, infection (if tropical travel, think of schistosomiasis), stones, clotting disorder, or a tumour (Wilms’ tumour). Also, haemolysis (e.g. sickle cell crisis, toxins). Ask if a female patient is currently menstruating.
White cells indicate infection (but also trauma, stones, tumour) so is a non-specific marker of inflammation.
Normally <150 mg/day excreted. Fever, exercise, hypertension, CCF, infection, nephrotic syndrome, pregnancy (think of pre-eclampsia if hypertensive), and multiple myeloma (although urine dipstick detects albumin and not Bence Jones proteins. Urine is collected over a 24-hour period for more accurate assessment of proteins and solutes).
More sensitive marker for infection (vs leucocytes) as urinary nitrates converted to nitrites by Gram-negative bacteria such as Escherichia coli. However, not all bacteria do this (e.g. enterococci) and so test is not very sensitive in infants who pass urine more often than adults.
Some hospitals still count microscopy as a bedside test but most samples are likely sent to the microbiology lab before culturing:
• RBCs: >2/mm3, abnormal (haematuria).
• Organisms: >50,000 colony-forming units, likely infection (although lower thresholds to treat in patients symptomatic of UTI).
• Crystals: may be normal but precursor to calculi (stones).
• Epithelial cells: marker for possible contamination with skin flora.
• Casts: hyaline—clear, colourless, normal in concentrated urine; granular—breakdown of plasma proteins, indicate CKD; tubular—indicates AKI; waxy—longstanding renal disease.
• Yeast cells: most commonly Candida.
Important to consider how urine was collected to know likelihood of contamination. A ‘clean catch’ is where the patient, after wiping the area around the urethral meatus, voids half the contents of the bladder (to flush off contaminants) and then collects the urine sample—easier said than done, especially in children. You should be alert to the possibility of contamination or colonization of indwelling catheter specimens. Use of in-out catheters, especially in infants, or suprapubic aspiration, reduces likelihood of contamination (but with pain/discomfort and possible complications). Do not use urine bags to obtain urine samples for ?UTI—they will likely be contaminated.
Urine strips can be bought over the counter for self-testing at home, which detects beta-hCG after the egg implants. Essential test to rule out ectopic pregnancy in women of child-bearing age who present with PV bleeding/acute abdominal pain.
For drugs of abuse (but beware over-the-counter medications, e.g. codeine tests positive for opiates).
A measure of solute concentration in the urine (more accurate than specific gravity), normally 400–800 mOsm/kg of water but dependent on hydration status. Low (<100 mOsm/kg): excessive fluid intake and with AKI (where kidneys unable to concentrate urine). High (>1100 mOsm/kg): in dehydration.
(Normal = 280–300 mOsm/kg.) When paired with urine osmolality can be used to diagnose SIADH (serum osmolality <270 mOsm/kg and a urine osmolality > than serum level). But this is the other way round in diabetes insipidus, with serum osmolality >320 mOsm/kg and urine osmolality <100 mOsm/kg.
The most commonly ordered blood test in rich country settings, the FBC (or complete blood count, CBC, in North America), has a wealth of information that is often overlooked. Be systematic. Remember, a recent transfusion will affect the results.
Amount of oxygen-carrying protein in the blood. A low Hb is <11.5 g/dL for women and <13.5 g/dL for men at sea level. Hb normal ranges vary for children. Anaemia, a low concentration of Hb, has many causes, the main clue being MCV.
Normal MCV is 76–96 femtolitres (fL). The MCV is used to classify the three main types of anaemia (see Table 46.1).
Table 46.1 Narrowing your differential for anaemia
Normal value 150–400 × 109/L. Involved in primary haemostasis, triggered by injury to vessel wall, forming a platelet plug. Reduced in bleeding disorders, autoimmune diseases (e.g. idiopathic thrombocytopenic purpura), marrow infiltration (e.g. leukaemia) and marrow suppression (e.g. chemotherapy). 
After blood loss, surgery, inflammation, and infection.
The space taken up by RBCs in blood as a %.
An in variation in RBC size (anisocytosis) is suggestive of iron deficiency.
WCC is the total number of white blood cells (WBCs) in a given volume of blood (normal range for adults 4–11 × 109/L), with the differential breaking down the number of five different types of infection (see Table 46.2).
Table 46.2 The differential white cell count
| Type of WBC | WCC |
 WCC |
| Neutrophils (2–7.5 × 109/L) | ||
| Lymphocytes (1.5–4.5 × 109/L) | ||
| Eosinophils (0.04–0.4 × 109/L) | ||
| Monocytes (0.2–0.8 × 109/L) | ||
| Basophils (0–0.1 × 109/L) |
• Myeloproliferative disorders |
Mass of Hb in RBCs, read alongside mean cell haemoglobin concentration (MCHC): concentration of haemoglobin inside RBCs, low in hypochromic anaemias (e.g. iron deficiency), high in hyperchromic anaemias (e.g. hereditary spherocytosis).
Top tip
• Filling plain blood tubes after those with anticoagulant (EDTA, clotting), which can affect results.
• Ensure clotting bottles are full (or lab will reject sample).
• Taking blood from an arm with an IV line (false electrolyte results).
Not part of the FBC but iron, total iron binding capacity (TIBC), and ferritin are looked at to interpret a low Hb level. Ferritin is also an acute phase reactant so can be raised in infection. (See Table 46.3.)
Table 46.3 Interpreting plasma iron studies
| Iron | TIBC | Ferritin | |
| Iron deficiency | |
|
|
| Anaemia of chronic disease | |
|
|
| Chronic haemolysis | |
|
|
| Haemochromatosis | |
|
|
| Pregnancy | |
 |
|
| Sideroblastic anaemia | |
|
|
Reproduced with permission from Wilkinson, Ian, et al., Oxford Handbook of Clinical Medicine 10th ed, Oxford University Press 2017, p327.
This is a measure of new red cell production (new RBCs contain RNA while mature RBCs do not—normal range 0.8–2%) as a percentage of total RBCs and can further help determine the cause of anaemia: raised in haemolytic anaemias (along with bilirubin); in bone marrow failure from cancer, infection, iron deficiency anaemia, and aplastic anaemia.
A haematological diagnosis can be made with careful examination of a peripheral blood film, including malaria. Some common blood film terms:
• Anisocytosis: varying RBC size (iron deficiency anaemia).
• Basophilic stippling: denatured RNA seen in RBCs secondary to haemoglobinopathy, lead poisoning, and megaloblastic anaemia.
• Blast cells: abnormal, nucleated precursor cells, diagnosis of leukaemia.
• Heinz bodies: denatured haemoglobin seen in oxidative haemolysis (e.g. G6PD deficiency).
• Howell–Jolly bodies: remnants of DNA usually removed from RBCs by the spleen, so seen post splenectomy or in hyposplenism (e.g. sickle cell disease).
• Hypochromia: pale staining of RBCs secondary to Hb.
• Left shift: immature neutrophils, seen in infection.
• Right shift: hypermature white cells seen in megaloblastic anaemia (e.g. vitamin B12 deficiency), liver disease.
• Rouleaux formation: RBCs stack up together (like rolls of new coins), seen in chronic inflammation (see ‘Erythrocyte sedimentation rate’ p. 847).
• Toxic granulation: granulation in neutrophils, from infection.
Clotting studies look at secondary haemostasis, the fibrin clot formation that occurs after primary haemostasis (platelet plug formation and vasoconstriction). This is made to happen via the coagulation cascade, which follows either the intrinsic or extrinsic pathways, joining in a final common pathway and fibrin clot formation (see Fig. 46.2). Knowing which part of the clotting profile tests which part of the cascade will help you to a diagnosis.
Tests the extrinsic system but is more often expressed as an INR to aid the monitoring of warfarin therapy (normal = 0.9–1.2). The PT/INR is prolonged (abnormal) by warfarin, liver disease (e.g. paracetamol overdose), vitamin K deficiency, or DIC.
Normal: 35–45 sec. Tests the intrinsic pathway and is prolonged by heparin, DIC, liver disease, and haemophilia (Factor VIII or IX deficiencies).
Normal: 10–15 sec. Used to assess function of fibrinogen. Prolonged by heparin and DIC.
Normal: 1.5–4 g/L. Tests fibrinogen activity. Reduced by consumption of fibrinogen from bleeding/trauma, liver disease, and DIC.
Fig. 46.2 Coagulation cascade. Reproduced from Marco Tubaro et al. (eds.), ESC Textbook of Intensive and Acute Cardiac Care, Oxford University Press, Oxford, UK, Copyright © European Society of Cardiology 2011, by permission of Oxford University Press.
The quickest way to measure blood glucose is with a bedside blood glucose test strip (often called a ‘BM’ which actually stands for a company that made them) but their accuracy is limited with either very low (important in hypoglycaemic neonates) or very high readings. Get someone to show you how to use one. A venous blood glucose level should be sent for either abnormally high or low readings. Remember the fitting or unconscious patient, ABC and DEFG (‘don’t ever forget glucose’).
• Children: 3–5.3 mmol/L.
Fasting venous glucose >7 mmol/L on two separate occasions or random level >11.1 mmol/L. Oral glucose tolerance test (OGTT), 2-hour value >11.1 mmol/L.
CRP is a marker of inflammation but one which must be taken in clinical context. A protein produced by the liver, it was first identified in patients in the 1930s with pneumococcal infection, where the protein reacted with a ‘C’ antigen of the pneumococcal bacterium. It rises quickly in infection and other inflammatory disorders but also goes down quickly with either resolution or the right treatment. However, a low CRP does not rule out a serious bacterial infection (could this level be an early rise?) so is of less use if thinking about discharging a patient from the ED. Also, highly sensitive CRP (hs-CRP) has begun to have a role in predicting cardiovascular disease outcomes in adults. (see Table 46.4).
Table 46.4 CRP levels: a rough guide
| Condition (adults) | CRP level (mg/L) |
| Normal | <10 |
| Mild inflammation (viral illness, steroids, obesity, ulcerative colitis) | 10–40 |
| Bacterial infection, Crohn’s | 40–200 |
| Sepsis, severe trauma | >200 |
An alternative marker of inflammation is the ESR (‘sed’ rate) but this goes up and down more slowly and takes longer to process in the lab. However, it is still used to screen for joint infections and inflammation (e.g. IBD). Upper limit of normal: men = age/2; women = age + 10/2.
The kidneys are vital to homeostasis in several areas:
• Acid–base balance, electrolyte levels (Na+, K+, Ca2+, and PO43−).
• Removing waste products (including urea).
• RBC production (erythropoietin).
• Vitamin D (hydroxylating 25-hydroxyvitamin D 
1,25 hydroxyvitamin D).
Know the differentials for pre-renal (poor blood supply, e.g. blood loss, heart failure, renal artery stenosis), renal (toxins, sepsis, cancer, trauma), and post-renal failure (preventing urinary flow and so backing up to the kidneys, e.g. bladder/prostate cancer, urinary retention, posterior urethral valves in male newborns).
U&E is a commonly ordered panel, especially for patients on fluid therapy or where fluid balance is an issue. In the 2009 National Confidential Enquiry into Patient Outcome and Death (NCEPOD), it was found that 43% of patients with post-admission AKI (see p. 420) were diagnosed late, and it recommended U&E for all emergency admissions.1 U&E are used as a simplified marker for disease and, hopefully, disease resolution in this highly complex organ. Always take a drug history to look for drug-induced causes of impaired renal function.
Normal: 135–145 mmol/L. Risk of seizures, arrhythmias if sodium <120 mmol/L (severe hyponatraemia, e.g. Addison’s, diuretics, DKA, D&V, nephrotic syndrome, cardiac failure, SIADH, iatrogenic) or >155 mmol/L (hypernatraemia, e.g. fluid deficit from D&V, burns, osmotic diuresis secondary to DKA, diabetes insipidus, iatrogenic). Remember that serum sodium needs to be corrected in the presence of hyperglycaemia, i.e. in DKA. Corrected (i.e. actual) Na = measured Na + 0.3 (glucose − 5.5) mmol/L.
Normal: 3.5–5 mmol/L. A high potassium (severe hyperkalaemia, >6.5 mmol/L) is an emergency. Remember, presumed artefactual results should be repeated. Causes include metabolic acidosis (e.g. DKA), renal failure, Addison’s, massive blood transfusion, burns, and drugs.
A low potassium (severe hypokalaemia, <2.5 mmol/L) can present with cramping pain, palpitations, muscle weakness, and muscle tone and can cause arrhythmias (ECG: prolonged PR interval, ST depression, small/inverted T waves, U waves). Causes include severe gastroenteritis, pyloric stenosis in infants, diuretics, intestinal fistula, Cushing’s (glucocorticoid excess), and Conn’s (aldosterone producing adenoma) syndromes.
Normal: 2.5–6.7 mmol/L (blood urea nitrogen, or BUN in North America). A waste product from protein metabolism produced by the liver (converted from toxic ammonia) that is excreted by the kidneys in urine. A raised serum urea points to renal failure, acute or chronic. Remember that urea can also be raised by dehydration and blood loss (e.g. a marker for upper GI bleeding). It is used alongside creatinine (see next paragraph) to monitor kidney function.
Normal: 70–150 μmol/L. The most common measure of renal function, ‘creatinine’ is derived from the Greek ‘κρέας’, or ‘flesh’, as it is derived from creatine phosphate, a waste product from muscle that is excreted by the kidneys. However, a ‘normal’ creatinine level depends on an individual’s muscle mass (see Fig. 46.2).
Normal: >90 mL/min. A more accurate way to test renal function than serum creatinine is an estimate of the glomerular filtration rate, i.e. how much the kidney is filtering, normally around 100 mL/min. An example of its importance is prescribing nephrotoxic drugs—an elderly patient’s creatinine may be ‘normal’ but his low muscle mass might be masking poor renal function, which would more likely to be picked up by eGFR.
There are logistical difficulties in finding out accurate creatinine clearance from both 24-hour urine collection and inulin clearance (requires IV inulin infusion) so most labs use the MDRD equation (Modification of Diet in Renal Disease Study Group), which calculates eGFR based on serum creatinine, sex, age, and ethnicity (African-Caribbean/non-African-Caribbean).
However, the MDRD’s accuracy is debated alongside that of the CKD-EPI and Cockcroft–Gault equations.2 You should be aware of the Cockcroft–Gault equation, which takes into account the patient’s serum creatinine, age, sex, and weight:
1. National Confidential Enquiry into Patient Outcomes and Death. Acute Kidney Injury (2009). Adding Insult to Injury. 
www.ncepod.org.uk/2009report1/Downloads/AKI_summary.pdf
2. Willems JM, Vlasveld T, den Elzen WP, et al. (2013). Performance of Cockcroft-Gault, MDRD, and CKD-EPI in estimating prevalence of renal function and predicting survival in the oldest old. BMC Geriatr 13:113.
Remember, clotting studies are also an important marker of the liver’s synthetic function, e.g. production of proteins (and the liver team will groan if a clotting has not been taken alongside LFTs in assessing a patient with suspected liver disease). There are some common patterns to liver disease but there are important caveats (e.g. other systems can upset the results). As with the kidney, look at the drug chart for potential culprits in liver disease.
Normal: 35–50 g/L. Alongside clotting, another marker of the liver’s synthetic function. It decreases when abnormal and is a marker for more chronic liver disease. It is also reduced in malnutrition, sepsis (leaky capillaries), and malabsorption. Albumin can also be a marker for protein loss, e.g. peeing out proteins in nephrotic syndrome or loss from burns. Oedema is the clinical sign of a low albumin.
Normal: 30–150 IU/L. Raised ALP is a marker for liver disease, primarily cholestasis but also in cirrhosis and malignancy. A high ALP is seen in bone metastases, healing fractures, and other bone disease but is normal during the growth spurt in children and in pregnant women (produced by the placenta).
Normal: both 5–35 IU/L. Raised with damage to hepatocytes (viral or drug-induced hepatitis). ALT is specific to the liver while AST is also raised with damage to cardiac and skeletal muscle. Can be normal in end-stage liver cirrhosis. An AST:ALT ratio of >2:1 is suggestive of alcoholic liver disease.
Normal: 0–45 IU/L. Raised in alcoholic liver damage, cholestasis, and secondary to drugs.
Normal: 3–17 μmol/L. Jaundice, the yellowing of skin and sclerae, is visible when the bilirubin level is 35–40 μmol/L. Bilirubin is formed by the breakdown of haemoglobin; unconjugated bilirubin is (1) taken up by the liver; (2) conjugated by hepatocytes with glucuronic acid, making it water soluble; then (3) excreted in bile, some of which is changed either to urobilinogen by gut bacteria (and then excreted by the kidneys) or stercobilinogen which makes stool brown.
A split bilirubin can point to whether the problem is:
• pre-hepatic (unconjugated): haemolysis from haemoglobinopathies, physiological jaundice in neonates, drugs (e.g. antimalarials)
• intra-hepatic (mixed picture): viral hepatitis, cirrhosis, drugs
• post-hepatic (conjugated): obstructive, e.g. gallstone obstructing biliary duct or carcinoma of the pancreas obstructing the CBD (NB: pale chalky stools and dark urine are signs of a conjugated hyperbilirubinaemia as bilirubin is concentrated in the urine but not making it to the stools—a crucial bit of information not to miss in a neonate who might have biliary atresia). (See Table 46.5.)
Table 46.5 Some common patterns in liver disease
| Type of liver disease | LFTs |
| Acute hepatitis (e.g. viral, drug-induced) | ALT/AST (>1000 μmol/L), ALP and bilirubin slightly raised, clotting abnormalities |
| Alcoholic liver disease | AST:ALT ratio of >2:1, GGT, MCV (macrocytosis), albumin |
| Obstructive jaundice (e.g. cholestasis) | ALP, GGT, bilirubin (conjugated) |
| End-stage liver disease | Albumin, AST (ALT often normal) |
Remember to include viral hepatitis in your differential in travellers, health workers, those at risk of STI, IV drug users, and patients with tattoos/body piercing. Hepatitis B and C are spread through exposure to infected body fluids (hepatitis D infections occur only in those already infected with hepatitis B). Hepatitis A and E are spread through the faecal-oral route—usually a self-limiting illness, although hepatitis E has a high mortality in pregnant women. Hepatitis A and B are vaccine preventable (also hepatitis D via hepatitis B vaccine).
Amylase: normal <100 IU/L (up to 180 IU/L in Asians, West Indians, and Chinese). Not a LFT but a marker for pancreatitis (if result >1000 IU/L or three times the upper limit of normal). Often ordered as part of the workup for an acute abdomen. It can also be raised in DKA, parotitis (salivary glands produce amylase), and severe gastroenteritis. Not useful for chronic pancreatitis as amylase levels drop after 48–72 hours.
The interplay of parathyroid hormone (PTH), calcium, phosphate, and Vitamin D is complex. When interpreting the bone profile, remember that PTH regulates the level of ionized calcium in the bloodstream (important for cardiac and muscle function and blood clotting). High phosphate levels are seen in chronic renal failure and can calciphylaxis, the deposition of calcium and phosphate in tissues other than bone.
Normal: 2.12–2.65 mmol/L. A corrected calcium is usually reported to account for calcium bound by the protein albumin. It is unbound, ionized calcium that is active.
If calcium is low (hypocalcaemia), PTH is released to grab stores from bone ( osteoclast activity)—a problem in patients with kidney failure who can’t replace calcium stores as the kidney is unable to process vitamin D, or for those who’ve had their parathyroid glands removed. Signs and symptoms, ‘SPASMODIC’:
• Spasms (e.g. Trousseau’s sign—carpopedal spasm on inflating BP cuff)
• Prolonged corrected QT interval (QTc) on ECG
• Chvostek’s sign (twitching of face when facial nerve tapped over parotid gland).
For hypercalcaemia, remember ‘bones, stones, groans, and moans’—bone pain, renal stones, depression, abdominal pain, lethargy, confusion; bony metastases, primary and tertiary hyperparathyroidism, TB, sarcoidosis, vitamin D overdose, and lithium are some of the causes. Also, can cardiac arrest (shortened QT on ECG).
Blood gas analysis is straightforward—honest!—if you look at the result in a systematic way. But also look at all the results—remember some gas machines will give blood glucose (DEFG—‘don’t ever forget glucose’), Hb, bilirubin, lactate, and carbon monoxide levels, any of which might need treating. Remember, you can get most of the information you need from a venous sample (or capillary sample in infants), thus avoiding a painful arterial stab, but venous gases are not as accurate for CO2 and O2 measurement.1
• pH: normal = 7.35–7.45. Below 7.35 and your patient is acidotic, above 7.45 and she is alkalotic.
• CO2: normal 4.7–6.0 kPa. Acidic, so if raised, e.g. with a respiratory problem, and the pH is <7.35, you have a respiratory acidosis. If the CO2 is down and the pH is >7.45, you have a respiratory alkalosis (from hyperventilation). If the pH is <7.35 but the CO2 is also low (e.g. 3.0 kPa), your patient is compensating for acidosis.
• HCO3−(bicarbonate): normal = 22–28 mmol/L. Alkaline, low in acidosis and raised in alkalosis. A change to HCO3− metabolic problem.
• Anion gap: normal = 10–18 mmol/L. An indirect measure of anions in plasma, e.g. ketones. Anion gap = cations (Na+ and K+) – anions (Cl− and HCO3−). Helpful to pin down cause of a metabolic acidosis. Anion gap: DKA (ketones), shock (lactic acidosis), drugs/toxins (e.g. salicylates) (see metabolic acidosis later in this topic for more detail).
Some examples:
• pH, pCO2: respiratory acidosis, e.g. a problem with alveolar ventilation (e.g. asthma, COPD), a neuromuscular problem, foreign body in airway, or depressed respiratory drive (e.g. opiate overdose)—this hypercapnia (raised pCO2) is type 2 respiratory failure. Type 1 respiratory failure is hypoxaemia with a normal CO2, where the problem is either a low ambient oxygen level (e.g. altitude) or V/Q mismatch (e.g. PE, acute pulmonary oedema) where oxygen is not getting into the blood.
• pH, pCO2: respiratory alkalosis, from hyperventilation (e.g. stroke, and other central causes, anxiety, pregnancy).
• pH, HCO3−: metabolic acidosis. If you have this picture, work out the anion gap (see earlier in topic) to help determine the underlying cause—‘MUDPILES’:
• Ethylene glycol intoxication
• Salicylate intoxication.
A normal anion gap—renal tubular acidosis, diarrhoea, GI fistula.
• pH, HCO3−: metabolic alkalosis, e.g. vomiting, burns, ingestion of alkali/base.
Fig. 46.3 Blood gas analysis. Reproduced with permission from Wilkinson, Ian, et al., Oxford Handbook of Clinical Medicine 10th ed, Oxford University Press 2017, Fig 14.2.
Honours
The above, standard approach to blood gas analysis is what we tend to use in everyday clinical practice but be aware that this is based mainly on the carbonic acid reaction, using pH, PCO2, HCO3/base excess to work out the respiratory and/or metabolic causes underlying a patient’s presentation. There is now growing interest in Canadian physiologist Peter Stewart’s strong ion theory which, alongside the carbonic reaction, shows the following also affect pH:
• strong ion difference (SID)—difference between positively charged ions (cations, e.g. sodium) and negatively charged ions (anions, e.g. chloride)
• the action of non-volatile weak acids, e.g. plasma proteins, mainly albumin
Standard blood gas analysis is a simplification!2
References
1. Byrne AL, Bennett M, Chatterji R, et al. (2014). Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology 19(2):168–75.
2. Samuels M, Wieteska S (Eds) (2016). Advanced Paediatric Life Support: A Practical Approach to Emergencies. Oxford: Wiley.
The electrocardiogram, or electrocardiograph (ECG or EKG in the US), provides a snapshot of the heart’s electrical activity, the patterns of which change with various disease processes. This summary cannot possibly teach all the normal variants and caveats that come with looking at ECGs on the wards and reading elsewhere in greater depth on how to interpret them is recommended. The following basics apply to adults (there are several important age-dependent variants in children).
Top reference for ECG interpretation
Hampton JR (2013). The ECG Made Easy. 8th ed. Edinburgh: Churchill Livingstone.
Be systematic in your approach and you will not miss important pathology—it is worth checking:
• P-wave morphology, PR interval
• P wave: depolarization of atria (remember, repolarization is hidden behind the QRS complex) atrial contraction.
• QRS complex: depolarization of ventricles ventricular contraction.
• T wave: repolarization of the ventricles.
• Limb leads: I, II, aVL—left cardiac lateral surface; aVR—the right atrium; III and aVF—the inferior surface of the heart.
• Chest leads: V1, V2—right ventricle; V3, V4—ventricular septum; V5, V6—left ventricle.
Fig. 46.4 Placement of ECG leads. 1, right sternal edge, 4th intercostal space. 2, left sternal edge, 4th intercostal space. v3, between 2 and 4; 4, 5th intercostal space, mid-clavicular line. 5, anterior axillary line. 6, mid-axillary line. (7, posterior axillary line.) Reproduced with permission from Wilkinson, Ian, et al., Oxford Handbook of Clinical Medicine 10th ed, Oxford University Press 2017, Fig 3.6.
Normal heart rate in adults = 60–100 bpm (sinus tachycardia >100 bpm, sinus bradycardia <60 bpm). Normal sinus rhythm means that a P wave always precedes a QRS complex (i.e. the atria contract before the ventricles). Atrial fibrillation will have no easily identifiable P waves and the QRS complexes will be ‘irregularly irregular’—like the patient’s pulse (you can prove this to yourself by placing a piece of paper over the top of three successive R waves, marking them and then moving the paper along to the next set of R waves on the rhythm strip—they will not line up). Remember that in children and young people, the heartbeat can vary with respiration and so the irregularly spaced QRS complexes—which are all preceded by a P wave—are normal (sinus arrhythmia).
The sum of all the competing electrical forces during depolarization of the ventricles. If you imagine a clock over the front of the heart, the normal path of depolarization runs from 11 o’clock to 5 o’clock. As this spreads towards leads I, II, and III, the QRS complexes are predominantly positive (i.e. the R wave is greater than the S wave).
• If the right ventricle enlarges (hypertrophies)—e.g. due to conditions that put a strain on the right side of the heart—the depolarization wave spreads towards the right (or 7–8 o’clock), causing lead I to be negative (downward deflection) while III is positive. This is right axis deviation (RAD).
• If depolarization spreads towards the left (2 o’clock), there will be a negative deflection in lead III (and more pronounced if also in lead II). This is left axis deviation (LAD), a sign of left ventricular hypertrophy. RAD can be normal in tall, thin patients and LAD normal in short patients with a raised BMI but look for pathology with either, especially LAD.
Fig. 46.5 Planes represented by the limb ‘leads’. Reproduced with permission from Wilkinson, Ian, et al., Oxford Handbook of Clinical Medicine 10th ed, Oxford University Press, 2017, Fig 3.4.
Must be present before each QRS complex for sinus rhythm. Normal PR interval = 0.12–0.2 sec (3–5 small squares). If >0.2 sec, it signifies first-degree heart block (prolonged conduction time between atria and ventricles).
Right atrial hypertrophy (P pulmonale).
Left atrial hypertrophy (P mitrale). A shortened PR interval suggests faster atrioventricular conduction, e.g. Wolff–Parkinson–White syndrome (which also has a ‘slurred upstroke’ known as a delta wave at the start of the QRS complex).
Normal is <0.12 sec duration (3 small squares), i.e. narrow complexes. Broad complexes (i.e. >0.12 sec) associated with bundle branch block (conduction problem) and left ventricular hypertrophy. Q waves >0.04 sec wide (1 small square) or >2 mm deep indicate myocardial infarction, with the lead indicating where the ischaemic damage has occurred. Normal Q waves can be seen in leads V6, I, and aVL, mirroring septal depolarization.
Should be at the same level as the line of the PR interval, i.e. isoelectric. ST elevation (the ST segment moves to a level >1 mm higher than the line of the PR interval) indicates acute myocardial infarction (death of cardiac muscle) or, if across most leads, pericarditis. ST depression indicates myocardial ischaemia (lack of blood supply and therefore oxygen to the heart).
Normally upright except in aVR, V1, and up to V3 in children. An inverted or ‘flipped’ T wave can be a sign of bundle branch block, myocardial ischaemia, treatment with digoxin, or ventricular hypertrophy. Peaked T waves in hyperkalaemia, flattened T waves in hypokalaemia.
Calculated to look for a prolonged QT interval (measured from start of QRS to end of T wave). Calculated as follows: QTc = QT ⁄ √RR. Causes of prolongation include congenital, certain drugs (e.g. tricyclics, macrolides), electrolyte abnormalities (hypokalaemia/hypocalcaemia/hypomagnesaemia), and myocardial ischaemia.