investigations and interpretations

Published on 24/06/2015 by admin

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ESSENTIALS OF ELECTROCARDIOGRAM READING

There are a few common electrocardiogram (ECG) abnormalities that can be encountered in the long case setting. It is very important to be able to identify such abnormalities and interpret them accurately. On many occasions the candidate will be presented with a normal ECG and asked for an opinion. Therefore, you should not always expect abnormal ECGs or be surprised to see a normal ECG at the examination. Candidates should have the audacity to decide that the ECG is normal and not to fabricate findings.

The major components to observe in the interpretation of an ECG are the rhythm, rate, axis and morphology, as shown by the P wave, P-R interval, QRS complex, ST segment, T wave and Q-T interval (see box).

Interpretation of ECG

1. Confirm the name and the date of birth/age of the patient and the date on which the ECG was recorded.

2. Ascertain the number of leads on display (usually 12 leads).

3. Check the calibration: standard paper speed is 25 mm/s (where each small 1 mm square denotes 0.04 s or 40 ms horizontally); vertically each 1 cm square denotes 1 mV.

4. Check the rate.

5. Check the rhythm (regular, irregular): this is best seen in lead II—the rhythm strip.

6. Check the axis (normal axis is between –30° and +120°; if between –90° and –30° it is left-axis deviation and if between +120° and +180° it is right-axis deviation).

7. Analyse the P wave (morphology, regularity and relationship to the QRS complex).

8. Assess the P-R interval (normal is 200 ms).

9. Analyse the QRS complex: morphology (e.g. presence of delta waves), width (normal is 120 ms), height of R wave and depth of S wave, presence of Q waves and R wave progression in the precordial leads.

10. Analyse the ST segment: depression and elevation in relation to the isoelectric line and its significance according to the context.

11. Check the Q-T interval (this is a rate-dependent phenomenon; < 430 ms is normal for the adult male, < 450 ms for the adult female).

12. Study the T wave: height and morphology.

13. Look for special features (e.g. bundle branch block) and possible diagnosis according to the clinical context.

It is not necessary to describe the ECG in the traditional and pedantic way, opening with the rate, rhythm and axis and then going on to describe the rest if they are normal. At the examination this may sound superfluous, and there is no time to waste! Candidates should identify the name of the patient and the date the ECG was done, and immediately start describing the abnormalities with references to the clinical findings. The following is a discussion of the various ECG findings commonly encountered in the long case examination.

Acute (transmural) myocardial infarction

ST elevation of more than 1 mm in two contiguous leads. In anterior infarcts this would be in the chest leads V₂–V₆. Left heart infarcts show this in leads I, II and aVL. In inferior infarcts it is seen in leads II, III and aVF. Posterior infarctions show up as reciprocal changes in the anterior leads, and the classic findings include R waves, ST segment depression or tall T waves in leads V₁ and V₂. Acute myocardial infarction can sometimes present as a new bundle branch block.

Q waves are pathological if they are broader than 1 mm or deeper than 2 mm (or > 25% of the height of the following R wave).

Subendocardial ischaemia

ECG changes consistent with subendocardial ischaemia (acute coronary syndrome) are ST segment depression of 1 mm or more, 0.08 seconds after the J point and corresponding T wave changes. The slope of the ST segment may provide some clues to the severity of the ischaemic phenomenon. Upward sloping indicates less severe disease, horizontal sloping indicates more severe disease, while downward sloping is usually considered the most significant and severe. The T wave changes include T wave flattening and T wave inversion.

Left ventricular hypertrophy

Left ventricular hypertrophy is described according to voltage criteria and strain/repolar-isation criteria.

Voltage criteria

1. Length of the deepest S wave in leads V₁ or V₂, or height of the tallest R wave of lead V₅ or V₆ > 25 mm

2. Sum of the lengths of the S wave of V₁ and the R wave of either V₅ or V₆ > 35 mm

3. Height of the R wave in aVL > 12 mm and height of the R wave in aVF > 20 mm

4. Sum of the lengths of the S wave in lead III and R wave of lead I > 25 mm

Repolarisation criteria

1. Non-specific ST segment depression and T wave inversion in the left precordial leads

2. Incomplete or complete left bundle branch block

Right ventricular hypertrophy

This may be associated with pulmonary stenosis or pulmonary hypertension.

1. Tall R wave in leads V₁ and aVR (the height of the R wave exceeds the length of the S wave)

2. Right axis deviation

3. Prominent S waves in leads V₅ and V₆

4. Poor R wave progression

Left atrial hypertrophy/strain

1. Biphasic P waves in lead V₁

2. Notched P waves in the limb leads

Right atrial hypertrophy/strain

This is associated with right atrial overload, as in pulmonary hypertension and right heart failure.

1. P waves taller than 2.5 mm, best seen in leads II and V₁

Right bundle branch block

This is seen in right heart strain associated with pulmonary hypertension, chronic lung disease, pulmonary emboli and mitral valve pathology. Some people may have non-pathological right bundle branch block, which is of no significance.

1. Broad QRS complex

2. Right axis deviation

3. rSR pattern in lead V₁ with a smaller r wave followed by a broad and deep S wave and a dominant R wave

4. qRS pattern in V₆ with a small q wave followed by a broad and tall R wave and deep S wave

Left bundle branch block

This is seen in ischaemic heart disease, hypertension, aortic stenosis and cardio-myopathy. Features to notice:

1. Broad QRS complex

2. Notched R waves in leads I, II, aVL, aVF, V₅ and V₆

3. R waves may be tall in the left precordial leads (V₅, V₆)

4. Deep S waves and Q waves in the right precordial leads (V₁)

5. The ST segment and T wave changes are non-specific in this setting.

Left anterior hemiblock

This is the most common cause of left-axis deviation. There is marginal prolongation of the QRS complex with left-axis deviation. Also notice terminal R waves in leads aVR and aVL, deep S wave in lead II, and RSR pattern in leads II, III and aVF. This feature is commonly seen in anterolateral or inferior myocardial infarcts.

Left posterior hemiblock

This abnormality is associated with right-axis deviation of about 120°, Q waves in leads II, III and aVF, R waves in leads I and aVL. When left posterior hemiblock is present it is almost always associated with right bundle branch block. This combination has a poor prognosis, and progression to complete heart block needing a pacemaker is the likely eventuality.

Bifascicular block

Right bundle branch block in combination with a left-sided hemiblock or left bundle branch block. There is a high likelihood of progression to complete heart block requiring a permanent pacemaker.

First-degree heart block

The rate is usually normal and the main abnormality is a prolonged P-R interval (> 200 msec or 5 mm).

Second-degree heart block

Type I (Wenckebach phenomenon)

The sinus rate is normal but the ventricular rate is slower than normal. The main abnormality is the gradual prolongation of the P-R interval until one P wave is not conducted to the ventricles. A new cardiac cycle begins following the non-conducted P wave. Rhythm is usually irregular. This pattern has an association with inferior myocardial infarctions.

Type II

The sinus rate is normal but the ventricular rate is a definite fraction of the sinus rate. There are more P waves than QRS complexes, as only one P wave is conducted for several subsequent P waves. Note the block, which is 2:1, 3:1 or more. This condition is usually associated with anterior myocardial infarctions.

Complete heart block

The sinus rate is normal but the ventricular rate is much slower. The ventricular rate is dependent on the site of the escape pacemaker (if it is in the AV junction, the rate would be around 40–60 bpm; if ventricular, the rate would be < 30 bpm). The P-R interval changes constantly and the P wave has no relationship to the QRS complex (AV dissociation).

Tachyarrhythmias

Ventricular tachycardia

A broad complex tachycardia with a rate exceeding 100 bpm. In practice, however, it is common to see the rate at 140–200. The rhythm is regular. It is called sustained ventricular tachycardia if it persists beyond 30 seconds. The QRS complex is longer than 140 milliseconds. There is evidence of AV dissociation, fusion beats and variable retrograde conduction. QRS pattern of all precordial leads should be in concordance. There may be features of left-axis deviation in the presence of right bundle branch block. A broad complex ventricular rhythm at a rate of less than 100 bpm is called accelerated idioventricular rhythm.

Atrial tachycardia

The rhythm is regular and the rate is 140–280 bpm. QRS complex follows each P wave, but the P wave may also be buried in the QRS complex or the T wave and not be visible.

Atrial flutter

The rhythm is most often regular but may vary if the degree of AV nodal block changes. Ventricular rate may vary between 60 and 150, again depending on the block. There are characteristic atrial oscillations described as ‘sawtooth’-shaped flutter waves. These flutter waves occur regularly at a rate of 250–300 per minute. Depending on the block, the rhythm should be described as atrial flutter with 2:1, 3:2 or 4:1 block.

Junctional tachycardia (AV nodal re-entry tachycardia)

The rhythm is regular and the rate is 100–200 bpm. The P wave appears inverted and is located immediately before or after the QRS complex due to retrograde conduction.

Wolff-Parkinson-White syndrome

This conduction defect occurs due to ventricular pre-excitation due to the presence of an accessory AV conduction pathway. The P-R interval is shorter than 110 milli-seconds and the QRS complex has a slurred upstroke (delta wave). The patient may be in atrial fibrillation. A negative delta wave in lead V₁ suggests a right-sided bypass tract.

Hypertrophic obstructive cardiomyopathy

Patients with hypertrophic obstructive cardiomyopathy may show non-specific ECG features. Evidence of left ventricular hypertrophy and diffuse, widespread, deep and broad Q waves are some commonly seen abnormalities.

HAEMATOLOGICAL STUDIES

Blood test results encountered in the examination include the full blood count, electrolyte profile, renal function indices, liver function studies, endocrine studies and serology. Serological tests can be either infective or autoimmune serology.

Full blood count

Here the focus should be on haemoglobin level, haematocrit, mean cell volume, mean cell haemoglobin concentration, and white cell count with differential and platelet count.

Candidates should know the normal values of all the above so that an abnormal value can be spotted immediately and interpreted accurately. When an abnormality in the blood count is present, ask for the report of the blood film for further clarification and, if appropriate, ask for other tests such as the results of the bone marrow biopsy, haemolytic screen, iron studies and vitamin B₁₂ and folate levels in anaemia, results of the blood culture in the setting of significant leucocytosis and febrile illness, and antiplatelet antibodies in idiopathic thrombocytopenia.

Figure 14.1 ECG showing atrial and ventricular paced rhythm with pacing spikes clearly visible before each atrial and ventricular complex. Also note the left bundle branch block (LBBB) pattern due to the early stimulation of the right ventricle by the pacing lead located there.

Figure 14.2 ECG showing ventricular tachycardia

Figure 14.3 ECG showing Wolff-Parkinson-White (WPW) syndrome. Notice the short P-R interval and the delta wave visible in most QRS complexes.

Figure 14.4 ECG showing atrial flutter with variable AV nodal block

Figure 14.5 ECG showing supraventricular bigeminy and left axis deviation

Figure 14.6 ECG showing left ventricular hypertrophy with non-specific ST–T changes

Figure 14.7 ECG showing left bundle branch block (LBBB)

Figure 14.8 ECG showing right bundle branch block (RBBB)

Figure 14.9 ECG showing atrial fibrillation

Figure 14.10 ECG showing supraventricular tachycardia with aberrancy

Neutrophilia

Neutrophilia is diagnosed when the neutrophil count is elevated above 7.5 × 10⁹/L. The possible causes are:

1. Bacterial sepsis

2. Inflammatory conditions (as guided by the clinical setting)

3. Tissue damage due to infarction or trauma

4. Glucocorticoid excess

5. Haematological malignancy—chronic myeloid leukaemia, polycythaemia rubra vera and myelofibrosis.

Lymphocytosis

Lymphocytosis is diagnosed when the lymphocyte count is elevated above 4 × 10⁹/L. The possible causes are:

1. Viral sepsis

2. Intracellular bacterial sepsis

3. Lymphoma

4. Chronic lymphocytic leukaemia.

Eosinophilia

Eosinophilia is diagnosed when the eosinophil count is elevated above 0.5 × 10⁹/L. The possible causes are:

Basophilia

Basophilia is diagnosed when the basophil count is elevated above 0.1 × 10⁹/L. The possible causes are:

1. Chronic myeloid leukaemia

2. Polycythaemia rubra vera

3. Myelofibrosis

4. Ulcerative colitis.

Leucopenia

Leucopenia is diagnosed when the white cell count is less than 4 × 10⁹/L. The possible causes are:

1. Viral sepsis

2. Drugs—chloramphenicol, carbimazole, propylthiouracil, chlorpromazine, ganciclovir, myelosuppressive agents

3. Felty’s syndrome

4. SLE

5. Bone marrow infiltration by sepsis and malignancy.

Microangiopathic haemolytic anaemia (MAHA) should be suspected in an anaemic and coagulopathic patient if the blood film report shows fragment cells, helmet cells, polychromasia and reticulocytosis. The possible causes include:

1. Disseminated intravascular coagulation due to severe sepsis, severe organ failure (liver, heart and kidney), massive trauma and disseminated malignancy

2. Haemolytic-uraemic syndrome (ask for renal function indices)

3. Thrombotic thrombocytopenic purpura

4. Malignant hypertension.

Blood film

Red cell morphology:

1. Pencil cells—in iron deficiency anaemia

2. Teardrop poikilocytosis—in myelofibrosis

3. Spherocytes—in hereditary spherocytosis, autoimmune haemolytic anaemia

4. Target cells—in liver disease, iron deficiency, thalassaemia

5. Polychromasia—reflects a high reticulocyte count.

Thrombophilic screen

This should be performed in cases of thromboembolic disease with a strong family history or recurrent spontaneous venous thrombosis in any patient, arterial throm-bosis in a patient aged under 30 years, and venous thrombosis in a patient aged under 40 years without a predisposing condition.

Thrombophilic screen involves testing for the following:

1. Lupus anticoagulant and antiphospholipid antibody

2. Factor V Leiden

3. Protein C and S levels, looking for deficiency

4. Antithrombin III levels, looking for deficiency

5. Dysfibrinogenaemia

6. Prothrombin gene mutation.

Electrolyte profile

Look at the sodium level, potassium level, chloride level, bicarbonate level and the renal function indices. If any abnormality is noticed, try interpreting it in the context of the clinical setting or a causative medication.

Sodium

The normal serum sodium level is 136–144 mmol/L.

Hypernatraemia

This can be caused by hypovolaemia and dehydration as well as primary hyperaldosteronism, Cushing’s syndrome and excess salt intake. Patients present with lethargy, irritability, fever, nausea, vomiting and confusion. Management is with controlled hydration using 4% dextrose with 1/5 normal saline or 5% dextrose solution together with judicious diuretic therapy.

Hyponatraemia

This can be caused by inappropriate secretion of antidiuretic hormone (SIADH), congestive cardiac failure, severe hepatic failure, Addison’s disease, aldosterone insufficiency, hypothyroidism, diuretic therapy, salt-losing nephropathy, renal tubular disorders and water retention.

SIADH can be due to small cell lung cancer, central nervous system disorders such as meningitis and subarachnoid haemorrhage, lung disease such as asthma, pneu-monia and tuberculosis, and drug therapy with tricyclic antidepressants, carbamazepine and monoamine oxidase inhibitors. The phenomenon of pseudohyponatraemia occurs in hyperglycaemia, alcohol excess and hyperuricaemia. Significant hyponatraemia (serum sodium of < 125 mmol/L) presents with lethargy, confusion, convulsions and coma. Management of severe symptomatic hyponatraemia uses controlled infusion (1–3 mL/kg/h) of hypertonic saline (3% NaCl) with judicious diuretic therapy. Chronic, asymptomatic hyponatraemia can be well managed with fluid restriction to 1 L/day. Resistant hyponatraemia due to SIADH can also be treated with regular oral demeclocycline.

Potassium

The normal serum potassium level is 3.5–5.0 mmol/L.

Hyperkalaemia

This can be caused by ACE inhibitor therapy, potassium-sparing diuretics, inadvertent potassium supplementation, acidosis, blood transfusion, haemolysis, severe renal failure, rhabdomyolysis and hypoaldosteronism.

Patients present with severe muscular weakness, paralytic ileus, symptomatic brady-cardia and heart block. Management of hyperkalaemia includes administration of 10 mL 10% calcium gluconate if there are electrocardiographic changes of hyperkalaemia (peaked T waves, small P waves and wide QRS complexes). Rapid reversal of potassium levels can be achieved by giving 50% glucose with insulin infusion, but the levels may rise again in a few hours. Concurrently administer oral or per rectum resonium 15–30 g and repeat administration as guided by subsequently measured serum potassium levels. Hyperkalaemia of severe renal failure needs haemodialysis.

Hypokalaemia

Causes of hypokalaemia include loop diuretic therapy, primary hyperaldosteronism, Cushing’s syndrome, renal tubular disease, alkalosis and hyperthyroidism. Therapy with drugs such as verapamil, beta-agonists and amiodarone should be excluded.

Hypokalaemia presents with muscle weakness or tetany. Significant hypokalaemia can lead to rhabdomyolysis. To manage hypokalaemia, usually oral supplementation alone will suffice. If the level is < 2.9 mmol/L, parenteral supplementation with KCl 10 mmol/L over an hour through a central venous line is indicated. The patient’s cardiac function should be monitored during this infusion. It should be repeated as guided by the subsequently performed serum potassium levels.

Calcium

The normal serum calcium level is 2.2–2.5 mmol/L. The serum calcium level varies with the serum albumin level, and the correction can be made using the following formula:

Hypercalcaemia

This can be caused by primary hyperparathyroidism, squamous cell carcinoma of the lung, cancer with bony metastases, multiple myeloma, sarcoidosis, vitamin D intoxi-cation, milk-alkali syndrome and thiazide diuretics.

Significant hypercalcaemia presents with anorexia, nausea, vomiting, constipation, polyuria, severe weakness, stupor and eventually coma.

Steps in the management of hypercalcaemia include, first, hydration with adequate amounts of normal saline, together with loop diuretic therapy. More severe hypercalcaemia needs treatment with a bisphosphonate such as etidronate or pamidronate. Calcitonin injected subcutaneously or intravenously (200 units, 6-hourly) has a short-lived effect. Hypercalcaemia due to multiple myeloma, sarcoidosis or vitamin D toxicity can be treated also with glucocorticoids. Oral phosphate is useful when there is hypercalcaemia together with hypophosphataemia.

Hypocalcaemia

Causes of hypocalcaemia include hypoparathyroidism, vitamin D deficiency, osteomalacia, acute pancreatitis, chronic renal failure, malignancy with osteoblastic metastases, and pseudohypoparathyroidism.

Patients present with circumoral and distal limb paraesthesias, painful muscle cramps, tetany and seizures. Patients may also have Chvostek’s sign and Trousseau’s sign.

Symptomatic hypocalcaemia and corrected serum levels of < 1.88 mmol/L should be treated with parenteral calcium in the form of 10% calcium gluconate.

Acid–base status

Metabolic acidosis

This diagnosis should be suspected when plasma bicarbonate (HCO₃) is less than 10 mmol/L and PaCO₂ is low with a low pH (a low HCO₃ value can be seen in respiratory alkalosis as well as in metabolic acidosis). The anion gap helps the interpretation of metabolic acidosis in more detail, and is calculated as follows: