19 Clinical data interpretation

The first step in making sense of an electrocardiogram (ECG) printout is to understand the electrical conduction process in the normal heart.

In their resting state, the surface of cardiac myocytes (muscle cells) is polarized with a potential difference of 90mV across the cell membrane (negatively charged intracellularly and positively charged extracellularly).

Depolarization (reversal of this charge) results in movement of calcium ions across the cell membranes and subsequent cardiac muscle contraction. It is this change in potential difference that can be detected by the ECG electrodes and represented as deflections on a tracing.

It is easiest to imagine an electrode ‘looking’ at the heart from where it is attached to the body.

Depolarization of the myocytes that spreads towards the electrode is seen as an upwards deflection, electrical activity moving away from the electrode is seen as a downwards deflection and activity moving to one side but neither towards nor away from the electrode is not seen at all (see Fig. 19.1).

In the normal heart, pacemaker cells in the sinoatrial (SA) node initiate depolarization. The depolarization first spreads through the atria and this is seen as a small upward deflection (the ‘P’ wave) on the ECG.

The atria and the ventricles are electrically isolated from each other. The only way in which the impulse can progress from the atria to the ventricles normally is through the atrioventricular (AV) node. Passage through the AV node slows its progress slightly. This can be seen on ECG as the isoelectric interval between the P wave and QRS complex, the ‘PR interval’.

Depolarization then continues down the rapidly conducting Purkinje fibres—bundle of His, then down left and right bundle branches to depolarize both ventricles (see Fig. 19.2). The left bundle has two divisions (fascicles). The narrow QRS complex on ECG shows this rapid ventricular depolarization.

Repolarization of the ventricles is seen as the T wave. Atrial repolarization causes only a very slight deflection which is hidden in the QRS complex and not seen.

The P wave and QRS complex show the electrical depolarization of atrial and ventricular myocardium respectively, but the resultant mechanical muscle contraction—which usually follows—cannot be inferred from the ECG trace (e.g. in pulseless electrical activity (PEA)).

Electrodes are placed on the limbs and chest for a ‘12-lead’ recording. The term ‘12-lead’ relates to the number of directions that the electrical activity is recorded from and is not the number of electrical wires attached to the patient.

The 6 chest leads (V_{1  –  6}) and 6 limb leads (I, II, III, aVR, aVL, aVF) comprise the 12-lead ECG. These ‘look at’ the electrical activity of the heart from various directions. The chest leads correspond directly to the 6 electrodes placed at various points on the anterior and lateral chest wall (see Fig. 19.3). However, the 6 limb leads represent the electrical activity as ‘viewed’ using a combination of the 4 electrodes placed on the patient’s limbs—e.g. lead I is generated from the right and left arm electrodes.

Remember there are 12 ECG leads—12 different views of the electrical activity of the heart—but only 10 actual electrodes placed on the patient’s body.

Additional leads can be used (e.g. V_{7  –  9} extending laterally around the chest wall) to look at the heart from further angles such as in suspected posterior myocardial infarction.

When a wave of myocardial depolarization flows towards a particular lead, the ECG tracing shows an upwards deflection. A downward deflection represents depolarization moving away from that lead. The key to interpreting the 12-lead ECG is therefore to remember the directions at which the different leads view the heart.

The 6 limb leads look at the heart in the coronal plane (see Fig. 19.4).

The 6 chest leads examine the heart in a transverse plane ...

Although each of the 12 leads gives a different view of the electrical activity of the heart, for the sake of simplicity when considering the standard ECG trace, we can describe the basic shape common to all leads (see Fig. 19.5).

The cardiac axis, or ‘QRS axis’, refers to the overall direction of depolarization through the ventricular myocardium in the coronal plane.

Zero degrees is taken as the horizontal line to the left of the heart (the right of your diagram).

The normal cardiac axis lies between –30 and +90 degrees (see Fig. 19.6). An axis outside of this range may suggest pathology, either congenital or acquired.

Note, however, that cardiac axis deviation may be seen in healthy individuals with distinctive body shapes. Right axis deviation if tall and thin; left axis deviation if short and stocky (Box 19.1).

Look at Fig. 19.7. Leads I, II, and III all lie in the coronal plane (along with aVR, aVL, and aVF). By calculating the relative depolarization in each of these directions, one can calculate the cardiac axis. To accurately determine the cardiac axis, you should use leads I, II, and III as described in Fig.19.7. There are less reliable short cuts, however.

There are many shorter ways of roughly calculating the cardiac axis. These are less accurate, however.

An easy method is to look at only leads I and aVF. These are perpendicular to each other and make a simpler diagram than the one described above.

An even easier method is to look at the print-out. Most computerized machines will now tell you the ECG axis (but you should still have an understanding of the theory behind it).

In the normal ECG each P wave is followed by a QRS complex. The isoelectric gap between is the PR interval and represents slowing of the impulse at the AV junction. Disturbance of the normal conduction here, leads to ‘heart block’ (Fig.19.8).

Causes of heart block include ischaemic heart disease, idiopathic fibrosis of the conduction system, cardiomyopathies, inferior and anterior MI, drugs (digoxin, ?-blockers, verapamil), and physiological (1st degree) in athletes.

PR interval fixed but prolonged at >0.20 seconds (5 small squares at standard rate). See rhythm strip 1 (Fig. 19.8).

Not every P wave is followed by a QRS complex.

Also called complete heart block. See rhythm strip 4 (Fig. 19.8). There is no conduction of the impulse through the AV junction. Atrial and ventricular depolarization occur independent of one another. Each has a separate pacemaker triggering electrical activity at different rates.

Depolarization of both ventricles usually occurs rapidly through left and right bundle branches of the His–Purkinje system (see Fig. 19.9). If this process is disrupted as a result of damage to the conducting system, depolarization will occur more slowly through non-specialized ventricular myocardium. The QRS complex—usually <0.12 seconds’ duration—will become prolonged and is described as a ‘broad’ (Fig.19.9).

Conduction through the AV node, bundle of His, and left bundle branch will be normal but depolarization of the right ventricle occurs by the slow spread of electrical current through myocardial cells. The result is delayed right ventricular depolarization giving a second R wave known as R' (‘R prime’).

RBBB suggests pathology in the right side of the heart but can be a normal variant (Fig.19.10).

(See Box 19.2 for bundle branch block mnemonic.)

Conduction through the AV node, bundle of His, and right bundle branch will be normal but depolarization of the left ventricle occurs by the slow spread of electrical current through myocardial cells. The result is delayed left ventricular depolarization (Fig.19.11).

LBBB should always be considered pathological.

LBBB on the ECG causes abnormalities of the ST segment and T wave. You should not comment any further on these parts of the trace.

Supraventricular rhythms arise in the atria. They may be physiological in the case of some causes of sinus brady- and tachycardia or may be caused by pathology within the SA node, the atria, or the first parts of the conducting system.

Normal conduction through the bundle of His into the ventricles will usually give narrow QRS complexes.

This is a bradycardia (rate <60 beats per minute) at the level of the SA node. The heart beats slowly but conduction of the impulse is normal. (Rhythm strip 1, Fig. 19.12.)

This is a tachycardia at the level of the SA node—the heart is beating too quickly but conduction of the impulse is normal. (Rhythm strip 2, Fig. 19.12.)

These are tachycardias (rate >100bpm) arising in the atria or the AV node. As conduction through the bundle of His and ventricles will be normal (unless there is other pathology in the heart), the QRS complexes appear normal (Fig.19.13).

There are four main causes of a supraventricular tachycardia that you should be aware of: atrial fibrillation, atrial flutter, junctional tachycardia, and re-entry tachycardia.

This is disorganized contraction of the atria in the form of rapid, irregular twitching. There will, therefore, be no P waves on the ECG.

Electrical impulses from the twitches of the atria arrive at the AV node randomly, they are then conducted via the normal pathways to cause ventricular contraction. The result is a characteristic ventricular rhythm that is irregularly irregular with no discernible pattern.

This is the abnormally rapid contraction of the atria. The contractions are not disorganized or random, unlike AF, but are fast and inadequate for the normal movement of blood. Instead of P waves, the baseline will have a typical ‘saw-tooth’ appearance (sometimes known as F waves).

The AV node is unable to conduct impulses faster than 200/min. Atrial contraction faster than that leads to impulses failing to be conducted. For example, an atrial rate of 300/min will lead to every other impulse being conducted giving a ventricular rate (and pulse) of 150/min. In this case, it is called ‘2:1 block’. Other ratios of atrial to ventricular contractions may occur.

A variable block at the AV node may lead to an irregularly irregular pulse indistinguishable from that of AF on clinical examination.

The area in or around the AV node depolarizes spontaneously, the impulse will be immediately conducted to the ventricles. The QRS complex will be of a normal shape but no P waves will be seen.

In Wolff–Parkinson–White (WPW) syndrome, there is an extra conducting pathway between the atria and the ventricles (the bundle of Kent)—a break in the normal electrical insulation. This ‘accessory’ pathway is not specialized for conducting electrical impulses so does not delay the impulse as the AV node does. However, it is not linked to the normal conduction pathways of the bundle of His.

Depolarization of the ventricles will occur partly via the AV node and partly by the bundle of Kent. During normal atrial contraction, electrical activity reaches the AV node and the accessory pathway at roughly the same time. Whilst it is held up temporarily at the AV node, the impulse passes through the accessory pathway and starts to depolarize the ventricles via non-specialized cells (‘pre-excitation’), distorting the first part of the R wave and giving a short PR interval. Normal conduction via the bundle of His then supervenes. The result is a slurred upstroke of the QRS complex called a ‘delta wave’.

This is an example of a ‘fusion beat’ in which normal and abnormal ventricular depolarization combine to give a distortion of the QRS complex (Fig. 19.14 and Box 19.3).

The accessory pathway may allow electrical activity to be conducted from the ventricles back up to the atria.

For example, in a re-entry tachycardia, electrical activity may be conducted down the bundle of His, across the ventricles and up the accessory pathway into the atria causing them to contract again, and the cycle is repeated. This is called a ‘re-entry circuit’ (Figs 19.15 and 19.16).

Most ventricular rhythms originate outside the usual conduction pathways meaning that excitation spreads by an abnormal path through the ventricular muscle to give broad or unusually shaped QRS complexes (Fig.19.17).

Here, there is a focus of ventricular tissue depolarizing rapidly within the ventricular myocardium. VT is defined as 3 or more successive ventricular extrasystoles at a rate of >120/min. ‘Sustained’ VTs last for >30 secs.

VT may be ‘stable’ showing a repetitive QRS shape (‘monomorphic’) or unstable with varying patterns of the QRS complex (‘polymorphic’).

It may be impossible to distinguish VT from an SVT with bundle branch block on a 12-lead ECG (see also Box 19.5).

This is disorganized, uncoordinated depolarization from multiple foci in the ventricular myocardium (Box 19.4).

These are ventricular contractions originating from a focus of depolarization within the ventricle. As conduction is via abnormal pathways, the QRS complex will be unusually shaped (Fig.19.19).

Ventricular extrasystoles are common and harmless if there is no structural heart disease. If they occur at the same time as a T wave, the ‘R-on-T’ phenomenon, they can lead to VF.

This occurs as a ‘back-up’ when conduction between the atria and the ventricles is interrupted (as in complete heart block).

The intrinsic pacemaker in ventricular myocardium depolarizes at a slow rate (30–40/min).

The ventricular beats will be abnormal and wide with abnormal T waves following them. This rhythm can be stable but may suddenly fail.

This is a complete absence of electrical activity and is not compatible with life.

There may be a slight wavering of the baseline which can be easily confused with fine VF in emergency situations.

This is a slow, irregular rhythm with wide ventricular complexes which vary in shape. This is often seen in the later stages of unsuccessful resuscitation attempts as the heart dies. The complexes become progressively broader before all recognizable activity is lost (asystole).

Represents depolarization of the small muscle mass of the atria. The P wave is thus much smaller in amplitude than the QRS complex.

Represents repolarization of the ventricles. The T wave is most commonly affected by ischaemic changes. The most common abnormality is ‘inversion’ which has a number of causes.

This is the portion of the ECG from the end of the QRS complex to the start of the T wave and is an isoelectric line in the normal ECG. Changes in the ST segment can represent myocardial ischaemia and, most importantly, acute MI (Fig.19.21).

The degree and extent of ST elevation is of crucial importance in ECG interpretation as it determines whether reperfusion therapy (thrombolysis or primary PCI) is considered in acute MI.

ST depression can be horizontal, upward sloping, or downward sloping.

In the first hour following a MI, the ECG can remain normal. However, when changes occur, they usually develop in the following order:

The leads in which these changes take place allow you to identify which part of the heart has been affected and, therefore, which coronary artery is likely to be occluded.

If the heart is faced with having to overcome pressure overload (e.g. left ventricular hypertrophy in hypertension or aortic stenosis) or higher systemic pressures (e.g. essential hypertension) then it will increase its muscle mass in response. This increased muscle mass can result in changes to the ECG.

This can lead to changes to the P wave.

This can lead to changes to the cardiac axis, QRS complex height/depth, and the T wave.

Temporary or permanent cardiac pacing may be indicated for a number of conditions such as complete heart block or symptomatic bradycardia. These devices deliver a tiny electrical pulse to an area of the heart, initiating contraction. This can be seen on the ECG as a sharp spike (Fig.19.22).

Many different types of pacemaker exist, and can be categorized according to:

On the ECG look for the pacing spikes which may appear before P waves if the atria are paced, before the QRS complexes if the ventricles are paced, or both.

Be careful not to mistake the vertical lines that separate the different leads on some ECG print-outs as pacing spikes!

Paced complexes do not show the expected changes described elsewhere in this section. You are, therefore, unable to diagnose ischaemia in the presence of pacing.

Peak expiratory flow rate (PEFR) is the maximum flow rate recorded during a forced expiration. Predicted readings vary depending on age, sex, height, and ethnicity (Fig.19.23).

See Chapter 18 for how to perform this test.

See Boxes 19.6 and 19.7 for other tests.

PEFR readings less than the patient’s predicted, or usual best, demonstrate airflow obstruction in the large airways.

PEFR readings are useful in determining the severity, and therefore the most appropriate treatment algorithm, for asthma exacerbations:

Improvement in PEFR or FEV₁ ?15% following bronchodilator therapy (e.g. salbutamol) shows reversibility of airflow obstruction and can help to distinguish asthma from poorly reversible conditions such as COPD.

Spirometry measures airflow and functional lung volumes; this can aid diagnosis of a number of conditions, but is primarily used to distinguish between restrictive and obstructive lung diseases.

Patients are asked to blow, as fast as possible, into a mouthpiece attached to a spirometer. This records the rate and volume of airflow.

Most spirometers are now hand-held computerized devices which will print a spirometry report for you and calculate normal values.

Two key values are:

Flow volume loops can also be generated from spirometry data and show the flow at different lung volumes. These are useful in distinguishing intra- and extra-thoracic causes of obstruction as well as to assess for small airways obstruction (Figs 19.24 and 19.25).

When airflow is obstructed, although FVC may be reduced, FEV₁ is much more reduced, hence the FEV₁/FVC ratio falls. It can also take much longer to fully exhale. Note that FVC can be normal in mild/moderate obstructive conditions.

Conditions causing an obstructive defect include COPD, asthma, and bronchiectasis as well as foreign bodies, tumours, and stenosis following tracheotomy (all localized airflow obstruction).

The airway patency is not affected in restrictive lung conditions, so the PEFR can be normal. But the FEV₁ and FVC are reduced due to the restrictive picture.

Conditions causing a restrictive defect include fibrosing alveolitis of any cause, skeletal abnormalities (e.g. kyphoscoliosis), neuromuscular diseases (e.g. motor neuron disease), connective tissue diseases, late-stage sarcoidosis, pleural effusion, and pleural thickening (Table 19.1 and Fig. 19.26).

The printout from the ABG machine can have a bewildering number of results. Initially, just focus on the pH, PaCO₂, and HCO₃^– in that order (Box 19.8):

Note what FiO₂ the patient was breathing when the sample was taken.

Hypoxia is PaO₂ of <8.0kPa and can result from a ventilation–perfusion mismatch (e.g. pulmonary embolism) or from alveolar hypoventilation (e.g. COPD, pneumonia).

If the PaO₂ is very low consider venous blood contamination.

Mechanisms controlling pH are activated when acid–base imbalances threaten. Thus, renal control of H⁺ and HCO₃^– ion excretion can result in compensatory metabolic changes. Similarly, ‘blowing off’ or retaining CO₂ via control of respiratory rate can lead to compensatory respiratory changes.

A compensated picture suggests chronic disease.

A relative excess of cations (e.g. H⁺), unless adequately compensated, will result in acidosis (more correctly acidaemia) (Table 19.2).

It is useful to calculate the anion gap to help distinguish causes of metabolic acidosis (Box 19.9).

An increased anion gap points to increased production of immeasurable anions.

A relative excess of anions (e.g. HCO₃^–), unless adequately compensated, will result in alkalosis (more correctly alkalaemia). (See Box 19.10.)

CSF is produced by the choroid plexus lining the cerebral ventricles and helps cushion and support the brain. Samples are usually obtained by lumbar puncture (see Table 19.3).

CSF glucose is abnormal if <50% of blood glucose level.

Premature babies, newborns, children, and adolescents have different normal ranges.

Bedside dipstick urinalysis offers speedy and non-invasive testing that can help with the diagnosis of common conditions such as UTIs and diabetes mellitus. Samples can be sent to the laboratory for further analysis, including MCS.

Dipstick testing gives semi-quantitative analysis of:

Microscopy allows identification of bacteria and other microorganisms, urinary casts (formed in the tubules or collecting ducts from proteins or cells), crystals, and cells (including renal tubular, transitional epithelial, leukocytes, and red blood cells). Organism growth and antibiotic sensitivities and can also be determined.

Asymptomatic bacteriuria is more common in pregnancy (up to 7%) and can lead to pyelonephritis and potential fetal complications.

Fluid in the pleural space can be classified as:

At borderline levels, if the pleural protein is >50% serum protein then the effusion is an exudate. Blood, pus, and chyle (lymph with fat) can also form an effusion. See Chapter 18.

See Box 19.11 for other tests.

Transudates are largely cause by increased venous or reduced oncotic pressure.

Exudates are largely caused by increased capillary permeability.

Fluid in the peritoneal cavity can result in abdominal distension and breathlessness. As with pleural fluid, analysis of an aspirated sample can aid diagnosis. See Chapter 18 for ascitic tap guidance. See Box 19.12 for other tests.