Q waves > 2 mm, > 40 ms follow in those leads showing ST elevation, if the infarct evolves (Table 12.1). They may appear within the first hour or, more commonly, within 2–6 hours (Figure 12.2). Differentiate from nonpathological septal Q waves in LI, LII, aVF or V₅,V₆, which are small (< 2 mm) and narrow.

Table 12.1 Infarct localisation—the ECG pattern distribution (early ST elevation, later Q waves)—will help to localise the site of infarction, and the usual coronary artery occluded

ECG pattern distribution	Site	Infarct-related artery
I, aVL	Lateral	Circumflex
II, III, aVF	Inferior	Right coronary, circumflex
V_2–4	Anterior	Left anterior descending (LAD)
V_1,2 (large R, ↓ST)	Posterior	Right coronary

Figure 12.2 Anterior AMI, later changes: Q waves, prominent coved ST elevation V_2–5

A nonpathological Q wave can occur in LIII; it is narrow, < 2 mm and < one-third the height of the QRS complex, and may disappear during deep inspiration. A small Q wave in LIII is significant if associated with one in LII.

Sometimes Q waves do not develop, but AMI can still be suspected if there are small R waves with ‘lack of progression of R waves’ across the anterior leads (normally the R wave increases in amplitude from V₂ to V₄). These infarcts are often associated with inverted T waves.

Non-Q AMI refers to subendocardial infarcts. Up to 40% of infarcts are not transmural, but they predispose to reinfarction. Blood should be sent for cardiac enzymes on arrival of the patient with chest pain so that, where there is no ECG evidence of AMI, the diagnosis is not missed.

R wave

A prominent R wave in V₁, and often V₂, suggests a posterior infarct, as well as incomplete right bundle branch block (RBBB), right ventricular hypertrophy (RVH) or left accessory pathway.

T waves

Hyperacute peaked T waves in V leads may be the only sign of AMI; they may occur in hyperkalaemia or without a known cause.

Left bundle branch block (LBBB)

New LBBB, with chest pain, indicates AMI. The location may be diagnosed by inspecting the affected leads to see whether there is concordance of ST segments with QRS complexes (in non-AMI LBBB, the ST segments are discordant with the QRS, i.e. they point in opposite directions).

In LBBB, AMI is present if:

• the QRS is upright and the ST is elevated > 5 mm

• the QRS is depressed and the ST is also depressed

• there are Q waves in LI and aVL, which indicate a lateral AMI.

Right bundle branch block (RBBB)

RBBB does not mask AMI, as ST elevation does not occur in non-AMI RBBB.

Unstable angina, acute coronary syndrome, acute ischaemia

The ECG may be normal, but acute ischaemia is confirmed by 2 mm or more ST depression in anterior or standard leads. This may be induced by exercise. If angina is prolonged greater than 20 minutes, then this can be regarded as pre-infarctional.

Left ventricular hypertrophy

• Left axis deviation (LAD)

• S inV₂ + R inV₅ > 35 mm

• ST depression anterior chest leads (LV strain)

Pericarditis

• Extensive ST elevation, concave upwards

• P-R depression

Aortic dissection

The ECG is nonspecific, with associated hypertensive changes in the majority.

If the dissection involves the coronary ostia, resultant myocardial ischaemia or infarction may be seen. The cardiac surgeon should be notified urgently.

Pulmonary embolus (PE)

Over 40% show no significant change; therefore, a normal ECG does NOT rule out a pulmonary embolus. ECG findings include:

• sinus tachycardia

• RBBB, usually partial

• R axis deviation

• S₁Q₃T₃ (acute cor pulmonale)

• ST elevation in aVR

• anterior T wave inversion V_1–4 (Figure 12.3); differentiate from the normal T-wave inversion found in some youths, athletes and Black people in V_1–3.

Figure 12.3 Acute pulmonary embolism: partial RBBB, inverted T waves V_1–4

Anticoagulation is indicated (see Chapter 10, ‘Pulmonary emboli and venous thromboses’). Consult urgently for compromised patients following massive PE as they may need urgent thrombolysis or embolectomy.

2 Collapse, palpitations, syncope, dizziness, altered consciousness

The ECG can help to determine a cardiac cause.

AMI, acute ischaemia, unstable angina or acute coronary syndrome

These can cause syncope or coma as a result of vasovagal reaction, cardiogenic shock, tamponade or any of the following arrhythmias.

Ventricular asystole

Absence of any electrical activity with a ‘flat’ ECG is asystole requiring cardiac massage, full cardiopulmonary resuscitation (CPR) and the use of adrenaline as in advanced life support (ALS) guidelines.

Ensure that leads are attached and recording amplitude is correct, as low voltage VF may be misinterpreted as asystole. Direct current reversion should be tried, if there is any doubt.

Ventricular fibrillation (VF)

This grossly irregular and variable amplitude arrhythmia is easy to recognise (Figure 12.4), unless it is low in amplitude, when it can be mistaken for asystole (if in doubt, treat as VF).

Figure 12.4 Ventricular fibrillation

It requires immediate defibrillation beginning with 200 J biphasic or 360 J monophasic according to full CPR and ALS protocols, with adrenaline 1 mg IV, repeated every 3 minutes as required, and lignocaine 1–1.5 mg/kg or 100 mg bolus IV or amiodarone 5 mg/kg or 300 mg bolus IV as the mainstays of drug therapy. Magnesium 5 mmol should also be considered.

Lack of response to treatment will lead to deterioration, agonal rhythm with a sine-wave pattern, asystole and death.

Rarely, continued ALS may still rescue a patient with a preterminal rhythm.

Ventricular tachycardia (VT)

A wide-complex tachycardia represents VT (Figure 12.5) in over 90% of cases, approaching 100% in patients with prior AMI. If in doubt, treat as VT.

Figure 12.5 Ventricular tachycardia: onset from sinus rhythm

Most VT occurs in the setting of structural heart disease, usually ischaemic.

If the patient is not haemodynamically compromised, chemical cardioversion should be attempted, with lignocaine 1–1.5 mg/kg (or standard 100 mg bolus), procainamide 1 mg/kg (or 100 mg bolus) IV over 1 minute or amiodarone 150 mg over 1–2 minutes. If the patient is unstable (chest pain, hypotension or acute pulmonary oedema), prompt synchronised electrical cardioversion beginning with 50–100 J biphasic should be performed (once sedated, or consciousness lost).

Pulseless VT is treated as for VF with immediate (unsynchronised) defibrillation (200 J biphasic) with CPR and ALS.

VT can occur in the absence of structural heart disease, and this type of VT may last for seconds to weeks and generally has a benign prognosis. Cardiology consultation regarding medical management is advised.

Diagnostic difficulty occurs in cases of supraventricular tachycardia (SVT) with aberrancy/intraventricular conduction defect, which can mimic the ECG appearances of VT. There should be typical LBBB or RBBB changes; otherwise it is not SVT with aberrancy, and must be regarded as VT.

Prolonged QTc interval

A QTc (corrected for the rate) of over 0.44 s predisposes to VT and torsades, and should be corrected as soon as possible. Table 12.2 lists the causes of a prolonged QTc, which may progress to torsades de pointes.

Table 12.2 Causes of prolonged QT interval and torsades de pointes

Cause	Specific drugs, conditions
Antiarrhythmics	Quinidine, procainamide, disopyramide, amiodarone, sotalol
Antipsychotics	Thioridazine, haloperidol, chlorpromazine
Antidepressants	Tricyclics
Antiinfective	Macrolides: erythromycin, clarithromycin Quinolones: ciprofloxacin, moxifloxacin, norfloxacin Antifungals: fluconazole Antimalarials: chloroquine, mefloquine, quinine

Miscellaneous Cisapride, cocaine, methadone, lithium, sumatriptan, organophosphates Cardiac disease Ischaemia, complete heart block Electrolyte disturbances Hypomagnesaemia, hypocalcaemia, hypokalaemia Hypothyroidism Congenital long QT syndrome

Any serious tachycardia associated with prolonged QTc should be treated by correcting the underlying cause, magnesium or cardioversion. Class 1B antiarrhythmics such as phenytoin (but not Class 1A drugs), and Class II antiarrhythmics such as propranolol may also be effective, particularly for the congenital type. Pacing may be needed.

Torsades de pointes

This is a polymorphic broad-complex VT with ‘twisting of the axes’, often several complexes alternating above and below the isoelectric line. The danger is it may degenerate into VF, but it is more often self-limiting. Causes include drugs which prolong the QT interval, electrolyte disturbances and ischaemia.

Treatment involves drug withdrawal, IV magnesium sulfate 2 g bolus over 1 minute, followed by an infusion, and correction of electrolytes and ischaemia. An isoprenaline infusion or transcutaneous pacing may be used to accelerate the heart rate and terminate the arrhythmia. Unsynchronised cardioversion 50–100 J biphasic is recommended for haemodynamic instability; however, torsades may be resistant to electrical therapy.

Brugada syndrome

This is a disorder which causes VF and polymorphic VT, and which can be inherited in an autosomal dominant pattern. It is more common in South East Asians and males, and there may be a family history of sudden cardiac death. There is an abnormality in the cardiac sodium (Na⁺) channel. It should be considered in any young male presenting with syncope, seizures, chest pain, sudden cardiac arrest, a family history of unexplained death or the incidental finding of a Brugada pattern on routine ECG.

The ECG features of Brugada are ST elevation and T wave inversion in leads V1–3, mimicking a RBBB. Figure 12.6 shows a type 1. These changes may be transient. The rarer types 2 and 3 have ‘saddleback’ ST segments with upright T waves

Figure 12.6 Brugada syndrome type 1

Dr Jitu Vohra, Cardiologist, Epworth & Royal Melbourne Hospitals, Victoria.

Treatment is insertion of an implantable cardiac defibrillator (ICD). Drug therapy with sotalol may be tried if the patient is assessed by a cardiologist as low risk.

Heart block

High-degree heart block, particularly if associated with AMI, may deteriorate to complete heart block requiring urgent pacing. Incomplete occlusions can cause intermittent blocks.

First-degree AV block

The P-R interval is > 0.2 s.

Second-degree, Mobitz type I, Wenckebach

The P-R interval increases progressively until a ‘dropped beat’, with no QRS/ventricular response, occurs. The subsequent P-R interval is shorter than the P-R before the dropped beat.

Second-degree, Mobitz type II

The P-R interval is constant, in association with frequent dropped beats, often regular, e.g. 1 in 3. Deterioration results in a high rate of progression to complete heart block.

No treatment is indicated for first- and second-degree blocks unless there is ischaemia or poor cardiac output, when atropine 0.3–0.6 mg IV may be given with supplementary oxygen.

Third-degree, complete AV/heart block (CHB)

There is no P to QRS relationship; all of the atrial impulses are blocked at the AV node, so that regular P waves (rate > 50) are seen with an independent, idioventricular, QRS with a rate of around 30–40. If the QRS complex arises just below the AV node, the QRS may be narrow and normal in appearance (junctional AV block). More distal rhythms are relatively wide (> 0.12 s). In general, the broader escape rhythms are more unstable, and more likely to progress to ventricular standstill. Patients with complete heart block (CHB) may decompensate with poor cardiac output, hypotension or loss of consciousness (Stokes-Adams attack). Urgent treatment with atropine 0.3–0.6 mg IV, isoprenaline infusion and/or pacing are indicated. Atropine appears to be more effective for narrow complex CHB, and may worsen the block in broad complex CHB.

Bundle branch block (BBB)

BBB generally indicates disease in the main conducting system, and syncope can result from an associated AMI with decompensation, progression to CHB and asystole.

LBBB (Figure 12.7), due to functional or anatomical block of the LBB and delayed depolarisation of the left ventricle, is seen as an rS in V₁ and a broad RR¹ in V_5,6 with a wide QRS (> 0.12 s). It can be benign, but it is more commonly associated with ischaemic heart disease (IHD) and hypertension. It is important to note that evidence of AMI may still be seen on the ECG (see above, under ‘Myocardial infarction’).

Figure 12.7 Left bundle branch block

RBBB (Figure 12.8), due to functional or anatomical block of the RBB and delayed depolarisation of the right ventricle, is seen as an RSR¹ pattern in V_1,2 with a wide QRS (> 0.12 s) and is often benign, but can also be a sign of acute right heart strain, such as acute pulmonary embolism. AMI is not disguised by a RBBB.

Figure 12.8 Right bundle branch block

Left anterior fascicular block, anterior hemiblock (LAFB) is seen as left axis deviation (q₁R₁S₃) and a normal duration QRS. In patients with chest pain, it signifies partial occlusion of the left anterior descending artery and occurs in about half of anterior infarctions. If the LAD occlusion is more extensive, RBBB will also be present.

Left posterior fascicular block, posterior hemiblock (LPFB) is rare and seen as right axis deviation (S₁R₃) and a normal duration QRS. Since the posterior fascicle is broad, its occurrence indicates a widespread lesion such as an inferolateral infarct, cardiomyopathy or cor pulmonale. If associated with RBBB, this signifies extensive coronary artery disease with high risk of complete AV block.

Atrial fibrillation (AF)

In atrial fibrillation, there are no P waves, and the rhythm is irregular (Figure 12.9). It is the most common supraventricular tachycardia and its incidence increases with age.

Figure 12.9 Atrial fibrillation

In acute AF, precipitating factors such as fever, pneumonia, recent cardiac surgery, alcohol or caffeine use and thyrotoxicosis should be sought. When caused by AMI or PE, with rapid ventricular response (130–180), AF may result in poor cardiac output with palpitations and syncope. It usually coexists with hypertensive, dilated, valvular or rheumatic heart disease, though up to 25% of patients have ‘lone’ AF with no structural heart disease.

Acute management involves ventricular rate control or reversion to sinus rhythm and will often require consultation with the cardiology unit. Asymptomatic AF may not need any emergency management. Rate control is best achieved with drugs which prolong AV nodal conduction, such as IV beta-blockers (e.g. metoprolol), calcium channel blockers (e.g. verapamil), or digoxin.

• Digoxin has long been the mainstay of therapy, but while it slows the rate, it may prolong the arrhythmia. Ensure the arrhythmia is not a Wolff-Parkinson-White (WPW) syndrome, as digoxin may precipitate VF in WPW.

• Reversion to sinus rhythm (‘rhythm control’) may be achieved by synchronised electrical cardioversion or by pharmacological means.

• Patients with haemodynamic instability due to rapid AF require sedation and synchronised cardioversion starting at 50–100 J biphasic. Synchronised cardioversion is often used in new-onset AF, if a trial of an antiarrhythmic agent has not been successful.

• Pharmacological reversion may be achieved using flecainide, sotalol or amiodarone.

• Flecainide may be given at a dose of 2 mg/kg IV over 30 minutes. It is often used in ‘lone’ AF. It is contraindicated in IHD and structural heart disease.

• Sotalol, at a dose of 80 mg IV, has rate control in addition to reversion properties, although it has a low reversion rate. It is contraindicated in asthma and congestive cardiac failure.

• Amiodarone 4–5 mg/kg IV (typical dose 300 mg) over 15–20 minutes may be used. It is effective, but maintenance therapy is associated with long-term toxicity, including pulmonary fibrosis and thyroid dysfunction.

• If AF has been present for over 48–72 hours, anticoagulation must be considered prior to reversion (electrical or pharmacological). This is to prevent systemic embolus (cerebral, mesenteric, peripheral) from left atrial thrombus. In many instances, it will be difficult to ascertain the exact duration/time of onset of AF.

• Transoesophageal echocardiography (TOE) is used to detect left atrial or left atrial appendage thrombus prior to reversion in AF > 48–72 hours duration.

• If left atrial thrombus is detected on TOE (or if TOE is unavailable), a period of 3 weeks anticoagulation prior to reversion followed by 4–6 weeks anticoagulation after reversion is advised. Anticoagulation consists of enoxaparin followed by warfarin.

• In patients in permanent AF, long-term antithrombotic therapy is given to prevent thromboembolism. The selection of antithrombotic agent (aspirin or warfarin) is based on the risk of stroke versus the risk of bleeding in a particular patient.

Atrial flutter

Generally, atrial flutter has an atrial rate of 300 with variable block (commonly 2:1 or 3:1).

It has the same causes as AF, and may be treated similarly. Despite its regular rate, it may still result in atrial thrombus.

Flutter waves may be most obvious in the inferior leads, and are described as having a sawtooth appearance. Rate control is as for AF. The most effective treatment is synchronised cardioversion, beginning with 25–50 J biphasic. Pharmacological agents are less effective in reverting atrial flutter than atrial fibrillation. The same precautions regarding anticoagulation apply for atrial flutter.

Paroxysmal supraventricular tachycardia (PSVT)

PSVT has a regular rate, usually 150–200 (range 100–280, see Figure 12.10). It is a junctional tachycardia, where the AV node is an integral part of the arrhythmia circuit.

Figure 12.10 Paroxysmal supraventricular tachycardia

AV nodal re-entry tachycardia (AVNRT) is where the circuit is within the AV node itself, while AV re-entry tachycardia (AVRT) is where an additional (accessory) pathway is involved.

Vagal manoeuvres such as carotid sinus massage may terminate PSVT.

Adenosine is effective and relatively safe to use for chemical reversion, given as IV boluses through a wide-bore (e.g. 18-gauge in cubital fossa) IV cannula of 6 mg, 12 mg up to 18 mg if needed. In some patients, it causes a feeling of impending doom which may be prevented or treated with a small dose of midazolam, 0.01 mg/kg IV. Verapamil 5 mg IV slowly at 1 mg/minute may be used with care, but it can cause intractable hypotension, CHB and asystole, especially if the patient is also on a beta-blocker or digoxin.

SVT with intraventricular conduction defect (aberrant conduction), such as when there is a concurrent BBB or WPW syndrome causing a broad QRS complex, is difficult to differentiate from VT. Adenosine is safe for SVT with BBB, but in WPW, it may cause hypotension and unstable VT.

Radiofrequency ablation (RA) may be needed if adenosine is unsuccessful

Wolff-Parkinson-White syndrome (WPW)

WPW is due to pre-excitation of the ventricles by an accessory pathway, bypassing the AV node, resulting in a short P-R interval, and a slurred upstroke or ‘delta wave’ on the R wave, best seen in V_2–6 (see Figure 12.11).

Figure 12.11 Wolff-Parkinson-White type A with typical delta waves

If associated with a dominant R in V₁ and inverted T waves in V_1–4, this is due to a left accessory path (type A WPW); otherwise the accessory path is on the right (type B WPW).

The ECG of type A WPW can be mistaken for a posterior AMI.

Serious paroxysmal tachyarrhythmias can occur by retrograde re-entry mechanisms or by rapid conduction of superimposed AF/atrial flutter, such as when digoxin is used for treating AF when WPW is unrecognised. Impulses may be rapidly conducted down the accessory path and cause a bizarre ECG with variable width QRS tachycardia, hypotension and eventual VF arrest.

Treat WPW tachyarrhythmias with IV procainamide 100 mg over 2–5 minutes, up to a total dose of 1 g, if stable (watch for and suspend if hypotension or QRS widening) or cardioversion if decompensated. Other drugs (but not digoxin) may be used, but there is risk of exacerbating aberrant conduction. Radiofrequency ablation or surgery may be needed.

Holter monitoring

Despite a history suggestive of an abnormal rhythm, none may be detected during emergency department assessment. The patient should be considered for admission for cardiac monitoring or Holter monitoring as an outpatient.

Holter monitoring involves attaching a patient to a portable personal ECG monitor, which records usually two ECG channels on tape or computer for 24 hours. A technician then scans the recordings by computer and identifies periods of arrhythmia, which are then presented to the cardiologist for review to see if episodes of palpitations, syncope, angina etc can be explained.

Sinus bradycardia < 35 bpm, sinus pauses < 3 s, Wenckebach, brief runs of AF, multiple atrial ectopics and isolated ventricular ectopic beats may all be found in otherwise normal persons, and do not warrant treatment.

Sustained arrhythmias are more significant, particularly in symptomatic patients.

Holter monitoring is also useful in checking response to antiarrhythmics.

Hypokalaemia or hypomagnesaemia may result in a prolonged QT, flattened T waves and small U waves; note that U waves may occur in healthy people in V_2–4, but the T waves are normal. ST depression and first- or second-degree heart block may also be seen. Lower levels can cause atrial and ventricular arrhythmias, notably torsades de pointes.

With severe hypothermia, cardiac effects can be related to the temperature. The initial response is a sinus tachycardia for temperatures down to 32^°C, then bradycardia for temperatures down to about 30^°C. Osborn waves, which are deflections at the end of the QRS complex and in the same direction as the QRS, appear at around 30^°C and increase in height as the temperature falls. Various arrhythmias occur down to 27^°C, when VF may occur and cause death. In some patients, VF does not occur, and the temperature can fall as low as 22^°C, culminating in fatal asystole. Gradual rewarming and ALS should be instituted early to avoid this.

Electrocution

Cardiac effects can vary from nil to ST changes, transient arrhythmias, BBB, heart block, myocardial necrosis and cardiac asystole. If the route from entry to exit points traverses the torso, cardiac damage is more likely.

A low current of 10–100 microamps, resulting from stray currents or earthing faults in household equipment, can cause a microshock, which can result in VF arrest.

If the skin resistance is lowered by moisture, a 0.24 milliamp (mA) current from a 240 volt source can be increased to a current of 240 mA and cause a macroshock, with resultant VF.

Contact with high-tension power lines (> 1000 A) or a lightning strike (> 12,000 A) can cause cardiorespiratory arrest from asystole (more commonly) or VF. Early advanced life support may save these patients, but the severity of their burns will determine their fate.

See also Chapter 31, ‘Electrical injuries’.

Axis (electrical pathway mapping)

Axis generally refers to the QRS axis and the direction of depolarisation in the ventricles as reflected in the frontal plane (the anterior chest wall). It is best illustrated by a clock face with each numerical division representing 30^° (see Figure 12.12).

Figure 12.12 The QRS frontal plane cardiac axial reference system

Yuen Derek, after Fisch C, Mirvis D, Goldberg A. Electrocardiography. In: Libby P, Bonow R et al (eds). Braunwald’s heart disease. 8th edn. Philadelphia: WB Saunders; 2007

The horizontal direction can be determined by inspecting LI, to see whether the QRS deflection is mainly up (positive impulse moving from right to left), or down (negative impulse from left to right).

The vertical direction is reflected in aVF (the vertical axis). If the QRS deflection is mainly up, the impulse is travelling towards the foot, and if the QRS is down, the impulse is towards the head.

Combining this information, the quadrant in which the QRS vector lies can be determined.

• QRS in LI up, in aVF up—vector in left lower quadrant (normal axis)

• QRS in LI up, in aVF down—vector in left upper quadrant (left axis deviation (LAD))

• QRS in LI down, in aVF up—vector in right lower quadrant (right axis deviation (RAD))

• QRS in LI down, in aVF down—vector in right upper quadrant (indeterminate or extreme RAD).

To determine the axis more accurately (within 30^°), note which limb or standard lead has the most isoelectric QRS (equally up and down); the axis is at 90^° to this in the predetermined quadrant (use Figure 12.12). The range of normal axis can extend from -30^° to +90^°, as patients who are obese can have a more horizontal heart (vector in left upper quadrant), while those who are asthenic have a more vertical heart (90^° axis). Thus, if the QRS is isoelectric in lead aVR, and the above criteria point to the left upper quadrant (left axis deviation), then a perpendicular (90^°) to the aVR axis gives an axis of –60^° in the left upper quadrant. The QRS axis is then –60^° in the frontal plane.

While the above are more accurate, a simple summary is:

• QRS in LI negative = RAD

• QRS in LII negative = LAD.