Myocardial Ischaemia

This page covers the ECG signs of myocardial ischaemia seen with non-ST-elevation acute coronary syndromes. ST-elevation / Q-wave myocardial infarction patterns are covered elsewhere (see links at bottom of page). Background Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two main entities:

Non-ST-elevation myocardial infarction (NSTEMI). Unstable angina (UA).

The differentiation between these two conditions is usually retrospective, based on the presence/absence of raised cardiac enzymes at 8-12 hours after the onset of chest pain. Both produce the same spectrum of ECG changes and symptoms and are managed identically in the Emergency Department. Patterns of Myocardial Ischaemia There are two main ECG abnormalities seen with NSTEACS:

ST segment depression T wave flattening or inversion

While there are numerous conditions that may simulate myocardial ischaemia (e.g. left ventricular hypertrophy, digoxin effect), dynamic ST segment and T wave changes (i.e. different from baseline ECG or changing over time) are strongly suggestive of myocardial ischaemia. Click on the links above to read more about the different causes of ST segment and T wave abnormalities. Other ECG patterns of ischaemia

Hyperacute (peaked) T waves or pseudonormalisation of previously inverted T waves (i.e. becoming upright) suggest hyperacute STEMI. Another, less well-known ECG feature of myocardial ischaemia is U-wave inversion.

Morphology Of ST Depression

ST depression can be either upsloping, downsloping, or horizontal (see diagram below).

Horizontal or downsloping ST depression 0.5 mm at the J-point in 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria). ST depression 1 mm is more specific and conveys a worse prognosis. ST depression 2 mm in 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (35% mortality at 30 days). Upsloping ST depression is non-specific for myocardial ischaemia.

ST depression: upsloping (A), downsloping (B), horizontal (C)

ST segment morphology in myocardial ischaemia

Distribution of ST segment depression ST depression due to myocardial ischaemia may be present in a variable number of leads and with variable morphology:

ST depression due to subendocardial ischaemia is usually widespread typically present in leads I, II, V4-6 and a variable number of additional leads. A pattern of widespread ST depression plus ST elevation in aVR > 1 mm is suggestive of left main coronary artery occlusion. ST depression localised to a particular territory (esp. inferior or high lateral leads only) is more likely to represent reciprocal change due to STEMI. The corresponding ST elevation may be subtle and difficult to see, but should be sought. This concept is discussed further here.

Widespread subendocardial ischaemia due to LMCA occlusion T wave inversion T wave inversion may be considered to be evidence of myocardial ischaemia if:

At least 1 mm deep Present in 2 continuous leads that have dominant R waves (R/S ratio > 1) Dynamic not present on old ECG or changing over time

NB. T wave inversion is only significant if seen in leads with upright QRS complexes (dominant R waves). T wave inversion is a normal variant in leads III, aVR and V1.

Widespread T wave inversion due to myocardial ischaemia (most prominent in the lateral leads) Wellens Syndrome

Wellens syndrome is a pattern of inverted or biphasic T waves in V2-4 (in patients presenting with ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery. Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next 2-3 weeks.

There are two patterns of T-wave abnormality in Wellens syndrome:

Type 1 Wellens T-waves are deeply and symmetrically inverted Type 2 Wellens T-waves are biphasic, with the initial deflection positive and the terminal deflection negative

Wellens Type 1

Wellens Type 2

Read more about Wellens syndrome here. Non-specific ST segment and T wave changes The following changes may occur with myocardial ischaemia but are relatively non-specific:

ST depression < 0.5 mm T wave inversion < 1 mm

T wave flattening Upsloping ST depression

More ECG Examples Example 1

Subendocardial ischaemia:

The most striking abnormality is the widespread ST depression, seen in leads I, II and V5-6. This is consistent with widespread subendocardial ischaemia. There is also some subtle ST elevation in V1-2 and aVR with small Q waves in V1-2, suggesting that the cause of the widespread ischaemia is a proximal LAD occlusion.

Example 2

Reciprocal change:

The most obvious abnormality is the horizontal ST depression in III and aVF. This could be misinterpreted as inferior ischaemia however, subendocardial ischaemia does not localise. Regional ST depression should prompt you to scrutinise the ECG for signs of reciprocal ST elevation In this case there is subtle ST elevation in aVL. This is a high lateral STEMI!

Dr Stephen Smith covers two similar cases on his excellent ECG blog.

Example 3

Wellens Syndrome:

There are abnormal T waves in V1-4 biphasic in V1-3 and inverted in V4. This pattern is known as Type 2 Wellens Syndrome and is highly specific for a critical stenosis of the proximal LAD artery.

Example 4a

Dynamic ST depression in a patient with chest pain:

Widespread ST depression (leads I, II, V5-6) indicates subendocardial ischaemia. Q wave in lead III with slightly elevated ST segment suggests the possibility of early inferior STEMI.

Example 4b

ECG of the same patient after treatment with oxygen, nitrates, heparin and antiplatelets:

The ST changes have now resolved. Inferior ST segments and Q waves are stable this patient had a history of prior inferior MI. Troponin was raised, confirming that the initial ST depression was due to NSTEMI.

Example 5

NSTEMI presenting with isolated U wave inversion:

There are inverted U waves, most prominent in leads V5-6. This is an infrequently recognised but very specific sign of myocardial ischaemia this patient had a 12-hour troponin of 4.0 ng/mL.

Premature Atrial Complex (PAC)

AKA atrial ectopics, atrial extrasystoles, atrial premature beats, atrial premature depolarisations.

Definition

A premature beat arising from an ectopic focus within the atria.

Origin Of Ectopic Beats

Groups of pacemaker cells throughout the conducting system are capable of spontaneous depolarisation. The rate of depolarisation decreases from top to bottom: fastest at the sinoatrial node; slowest within the ventricles. Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above.

However, if an ectopic focus depolarises early enough before the arrival of the next sinus impulse it may capture the ventricles, producing a premature contraction. Premature contractions (ectopics) are classified by their origin atrial (PACs), junctional (PJCs) or ventricular (PVCs).

Atrial Ectopics

These arise from ectopic pacemaking tissue within the atria. There is an abnormal P wave, usually followed by a normal QRS complex.

Electrocardiographic Features PACs have the following features:

An abnormal (non-sinus) P wave is followed by a QRS complex. The P wave typically has a different morphology and axis to the sinus P waves. The abnormal P wave may be hidden in the preceding T wave, producing a peaked or camel hump appearance if this is not appreciated the PAC may be mistaken for a PJC. PACS arising close to the AV node (low atrial ectopics) activate the atria retrogradely, producing an inverted P wave with a relatively short PR interval 120 ms (PR interval < 120 ms is classified as a PJC). PACs that reach the SA node may depolarise it, causing the SA node to reset this results in a longer-than-normal interval before the next sinus beat arrives (post-extrasystolic pause). Unlike with PVCs, this pause is not equal to double the preceding RR interval (i.e. not a full compensatory pause). PACs arriving early in the cycle may be conducted aberrantly, usually with a RBBB morphology (as the right bundle branch has a longer refractory period than the left). They can be differentiated from PVCs by the presence of a preceding P wave. Similarly, PACs arriving very early in the cycle may not be conducted to the ventricles at all. In this case, you will see an abnormal P wave that is not followed

by a QRS complex (blocked PAC). It is usually followed by a compensatory pause as the sinus node resets. Classification PACs may be either:

Unifocal Arising from a single ectopic focus; each PAC is identical. Multifocal Arising from two or more ectopic foci; multiple P-wave morphologies.

Patterns PACs often occur in repeating patterns:

Bigeminy every other beat is a PAC. Trigeminy every third beat is a PAC. Quadrigeminy every fourth beat is a PAC. Couplet two consecutive PACs. Triplet three consecutive PACs.

Clinical Significance

PACs are a normal electrophysiological phenomenon not usually requiring investigation or treatment. Frequent PACs may cause palpitations and a sense of the heart skipping a beat. In patients with underlying predispositions (e.g. left atrial enlargement, ischaemic heart disease, WPW), a PAC may be the trigger for the onset of a re-entrant tachydysrhythmia e.g. AF, flutter, AVNRT, AVRT.

Causes Frequent or symptomatic PACs may occur due to:

Anxiety. Sympathomimetics. Beta-agonists. Excess caffeine. Hypokalaemia. Hypomagnesaemia. Digoxin toxicity. Myocardial ischaemia

ECG Examples Example 1

This rhythm strip displays the typical pattern of frequent PACs (arrows) separated by post-extrasystolic pauses.

Example 2

Blocked PAC:

This hidden PAC gives a peaked appearance to the T wave (circled). The PAC is not not followed by a QRS complex, indicating that it has not been conducted to the ventricles (blocked PAC). It is followed by a compensatory pause.

Example 3

Normally and aberrantly-conducted PACs:

There is an aberrantly conducted PAC, best seen in aVL and aVF (circled). This could be mistaken for a ventricular ectopic however, it is clearly preceded by an abnormal P wave. A normally-conducted PAC is also present on the rhythm strip (circled).

First Degree Heart Block

Definition

PR interval > 200ms (five small squares) Marked first degree block if PR interval > 300ms

Examples First degree heart block (PR interval > 200 ms)

Marked first degree heart block (PR interval > 300 ms, P waves are buried in the preceding T wave)

Causes

Increased vagal tone Athletic training Inferior MI Mitral valve surgery Myocarditis (e.g. Lyme disease) Hypokalaemia AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone) May be a normal variant

Clinical significance

Does not cause haemodynamic disturbance No specific treatment is required

AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon)

Definition

Progressive prolongation of the PR interval culminating in a non-conducted P wave The PR interval is longest immediately before the dropped beat The PR interval is shortest immediately after the dropped beat

Other Features

The greatest increase in PR interval duration is typically between the first and second beats of the cycle. The RR interval progressively shortens with each beat of the cycle. The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

Example of a typical Wenckebach sequence

Arrows mark the first beat in each Wenckebach cycle Non-conducted P waves are hidden in the T wave before each pause

Mechanism

Mobitz I is usually due to reversible conduction block at the level of the AV node. Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).

Causes

Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone Increased vagal tone (e.g. athletes) Inferior MI Myocarditis Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

Clinical significance

Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block. Asymptomatic patients do not require treatment. Symptomatic patients usually respond to atropine. Permanent pacing is rarely required.

An Interesting Case of Wenckebach Mobitz I in an atrially-paced patient following mitral valve surgery

Small atrial pacing spikes precede the QRS complexes. The interval between the pacing spikes increases progressively until there is a nonconducted pacing spike.

AV Block: 2nd degree, Mobitz II

Definition

Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I). The PR interval in the conducted beats remains constant. The P waves march through at a constant rate. The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc).

Example of Mobitz II

Arrows indicate dropped QRS complexes (i.e. non-conducted P waves)

Mechanism

Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node). While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis). Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (bilateral bundle-branch block). In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes. In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes. Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal cells, Mobitz II is an all or nothing phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse. There may be no pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

Causes of Mobitz II

Anterior MI (due to septal infarction with necrosis of the bundle branches). Idiopathic fibrosis of the conducting system (Lenegres or Levs disease). Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair) Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease). Autoimmune (SLE, systemic sclerosis). Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis). Hyperkalaemia. Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

Clinical Significance

Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block. Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death. The risk of asystole is around 35% per year. Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker.

AV block: 2nd degree, fixed ratio blocks

Definition

Second degree heart block with a fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1). Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.

Examples 2:1 block

The atrial rate is approximately 75 bpm. The ventricular rate is approximately 38 bpm. Non-conducted P waves are superimposed on the end of each T wave.

3:1 block

The atrial rate (purple arrows) is approximately 90 bpm. The ventricular rate rate is approximately 30 bpm. Note how every third P wave is almost entirely concealed within the T wave.

Mobitz I or II?

It is not always possible to determine the type of conduction disturbance producing a fixed ratio block, although clues may be present. Mobitz I conduction is more likely to produce narrow QRS complexes, as the block is located at the level of the AV node. This type of fixed ratio block tends to improve with atropine and has an overall more benign prognosis. Mobitz II conduction typically produces broad QRS complexes, as it usually occurs in the context of pre-existing LBBB or bifascicular block. This type of fixed ratio block tends to worsen with atropine and is more likely to progress to 3rd degree heart block or asystole. However, this distinction is not infallible. In approximately 25% of cases of Mobitz II, the block is located in the Bundle of His, producing a narrow QRS complex. Furthermore, Mobitz I may occur in the presence of a pre-existing bundle branch block or interventricular conduction delay, producing a broad QRS complex. The only way to be certain is to observe the patient for a period of time (e.g. watch the cardiac monitor, print a long rhythm strip, take serial ECGs) and observe what happens to the PR intervals. Often, periods of 2:1 or 3:1 block will be interspersed with more characteristic Wenckebach sequences or runs of Mobitz II.

AV block: 2nd degree, high-grade AV block

Definition

Second degree heart block with a P:QRS ratio of 3:1 or higher, producing an extremely slow ventricular rate.

Unlike 3rd degree heart block there is still some relationship between the P waves and the QRS complexes. High-grade AV block may result from either Mobitz I or Mobitz II AV block.

Example

High-grade AV block (4:1 conduction ratio). Atrial rate is approximately 140 bpm. Ventricular rate is approximately 35 bpm.

AV block: 3rd degree (complete heart block)

Definition

In complete heart block, there is complete absence of AV conduction none of the supraventricular impulses are conducted to the ventricles. Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

Typically the patient will have severe bradycardia with independent atrial and ventricular rates, i.e. AV dissociation.

Example of complete heart block

The atrial rate is approximately 100 bpm. The ventricular rate is approximately 40 bpm. The two rates are independent; there is no evidence that any of the atrial impulses are conducted to the ventricles.

Mechanism

Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block. It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to increased vagal tone in the acute phase of an inferior MI). Alternatively, it may be due to sudden onset of complete conduction failure throughout the His-Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute anterior MI). The former is more likely to respond to atropine and has a better overall prognosis.

Causes of complete heart block The causes are the same as for Mobitz I and Mobitz II second degree heart block. The most important aetiologies are:

Inferior myocardial infarction AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin) Idiopathic degeneration of the conducting system (Lenegres or Levs disease)

Clinical significance

Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death. They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker.

Differential diagnosis Complete heart block should not be confused with:

High grade AV block: A type of severe second degree heart block with a very slow ventricular rate but still some evidence of occasional AV conduction. AV dissociation: This term indicates only the occurrence of independent atrial and ventricular contractions and may be caused by entities other than complete heart block (e.g. interference-dissociation due to the presence of a ventricular rhythm such as AIVR or VT).

ECG Examples Example 1

Complete Heart Block:

Atrial rate is ~ 85 bpm. Ventricular rate is ~ 38 bpm. None of the atrial impulses appear to be conducted to the ventricles. Rhythm is maintained by a junctional escape rhythm. Marked inferior ST elevation indicates that the cause is an inferior STEMI.

Example 2

Complete Heart Block:

Atrial rate is ~ 60 bpm. Ventricular rate is ~ 27 bpm. None of the atrial impulses appear to be conducted to the ventricles. There is a slow ventricular escape rhythm.

Example 3

Complete Heart Block:

Atrial rate 100 bpm Ventricular rate only 15 bpm! This patient needs urgent treatment with atropine / isoprenaline and pacing!

Example 4

Complete Heart Block with Isorhythmic AV Dissociation (long rhythm strip):

Atrial rate ~ 85 bpm Ventricular rate ~ 42bpm There is a junctional escape rhythm. As the ventricular rate is approximately half the atrial rate, this rhythm at first glance appears to be second-degree AV block with 2:1 conduction. However on closer inspection the PR interval varies, with some of the P waves superimposed on the QRS complexes. The ventricular rate remains regular. This confirms that the atrial impulses are not being conducted to the ventricles. The apparent relationship between the P waves and QRS complexes occurs merely by chance (= isorhythmic AV dissociation).

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LITFL | ECG Library | Interventricular Conduction Delay (QRS widening)

Interventricular Conduction Delay (QRS widening)

Definition

QRS duration > 100 ms in the presence of a supraventricular rhythm. Most commonly due to bundle branch block or left ventricular hypertrophy. The most important life-threatening causes of QRS widening are hyperkalaemia and tricyclic antidepressant poisoning.

Causes Follow the links to read more about each condition. Fascicular and bundle-branch blocks

Left anterior fascicular block Left posterior fascicular block Left bundle branch block Right bundle branch block Bifascicular block Trifascicular block

Ventricular hypertrophy and dilatation

Left ventricular hypertrophy Right ventricular hypertrophy Biventricular enlargement Dilated cardiomyopathy

Electrolyte abnormalities

Hyperkalaemia

Toxins

Sodium-channel blocker toxicity (e.g. TCA overdose) - wide QRS plus positive R wave in aVR.

Pre-excitation

Wolff-Parkinson-White syndrome wide QRS plus delta waves.

Arrhythmogenic cardiac conditions

Brugada syndrome - localised QRS widening in V1-2 with RBBB morphology. Arrhythmogenic right ventricular dysplasia (AVRD) - localised QRS widening in V1-2 plus epsilon waves and variable signs of right ventricular hypertrophy.

Non-specific IVCD

Not due to any of the causes above Before making this diagnosis, be sure to check the serum potassium level and scrutinise the ECG for any signs of TCA toxicity.

Differential Diagnosis Ventricular Rhythms

Ventricular tachycardia Accelerated idioventricular rhythm Ventricular escape rhythm Ventricular-paced rhythm

Pre-excitation Syndromes
Wolff-Parkinson-White Syndrome

First described in 1930 by Louis Wolff, John Parkinson and Paul Dudley White. Wolff-Parkinson-White (WPW) Syndrome is a combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia. Incidence 0.1 3.0 per 1000. Associated with a small risk of sudden cardiac death.

Pre-Excitation & Accessory Pathways

Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway. Accessory pathways, also known as bypass tracts, are abnormal conduction pathways formed during cardiac development and can exist in a variety of anatomical locations and in some patients there may be multiple pathways In WPW the accessory pathway is often referred to as the Bundle of Kent, or atrioventricular bypass tract. An accessory pathway can conduct impulses either anterograde, towards the ventricle, retrograde, away from the ventricle, or in both directions. The majority of pathways allow conduction in both directions, with retrograde only conduction occurring in 15% of cases, and antegrade only conduction rarely seen. The direction of conduction affects the appearance of the ECG in sinus rhythm and during tachyarrhythmias. Tachyarrythmia can be facilitated by the formation of a reentry circuit involving the accessory pathway, termed atrioventricular reentry tachycardias (AVRT). Tachyarrythmia may also be facilitated by direct conduction from the atria to the ventricles via the accessory pathway, bypassing the AV node, seen with atrial fibrillation or atrial flutter in conjunction with WPW

Re-entry circuit during AVRT (retrograde conduction via Bundle of Kent) ECG in Sinus Rhythm

The presence of a pre-excitation pathway results in a number of changes to the ECG in sinus rhythm. ECG features of WPW in sinus rhythm are:

PR interval <120ms Delta wave slurring slow rise of initial portion of the QRS QRS prolongation >110ms ST Segment and T wave discordant changes i.e. in the opposite direction to the major component of the QRS complex Pseudo-infarction pattern can be seen in up to 70% of patients due to negatively deflected delta waves in the inferior / anterior leads (pseudo-Q waves), or as a prominent R wave in V1-3 (mimicking posterior infarction).

The features of pre-excitation may be subtle, or present only intermittently. Pre-excitation may be more pronounced with increased vagal tone e.g. during Valsalva manoeuvres, or with AV blockade e.g. drug therapy WPW may be described as type A or B. o Type A has a positive delta wave in all precordial leads with R/S > 1 in V1 o Type B has a negative delta wave in leads V1 and V2 In patients with retrograde-only accessory conduction all antegrade conduction occurs via the AV node, thus no features of WPW are seen on the ECG in sinus rhythm (as no pre-excitation occurs). This is termed a concealed pathway. Patients with a concealed pathway can experience tachyarrythmias as the pathway can still form part of a re-entry circuit

Atrioventricular Reentry Tachycardias (AVRT)

AVRT is a form of paroxysmal supraventricular tachycardia. A reentry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement. During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit. AVRT often triggered by premature atrial or premature ventricular beats. AVRT are further divided in to orthodromic or antidromic conduction based on direction of reentry conduction and ECG morphology.

AVRT with orthodromic (left ) and antidromic (right) AV nodal conduction AVRT with Orthodromic Conduction In orthodromic AVRT antegrade conduction occurs via the AV node with retrograde conduction occurring via the accessory pathway. This can occur in patients with a concealed pathway. ECG features of AVRT with orthodromic conduction are:

Rate usually 200 300 bpm P waves may be buried in QRS complex or retrograde QRS Complex usually <120 ms unless pre-existing bundle branch block, or raterelated aberrant conduction QRS Alternans phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished from electrical alternans by a normal QRS amplitude T wave inversion common

ST segment depression

Treatment of orthodromic AVRT

Treatment of AVRT is based on the presence of haemodynamic instability e.g. hypotension, altered mental state, or pulmonary oedema. In patients who are haemodynamically stable vagal manoeuvres may be successful, followed by adenosine or calcium-channel blockers, and DC cardioversion may be considered if non-repsonsive to medical therapy. In a haemodynamically unstable patient urgent synchronised DC cardioversion is required.

AVRT with Antidromic Conduction In antidromic AVRT antegrade conduction occurs via the accessory pathway with retrograde conduction via the AV node. Much less common than orthodromic AVRT occuring in ~5% of patients with WPW. ECG features of AVRT with antidromic conduction are:

Rate usually 200 300 bpm. Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway.

Treatment of antidromic AVRT

AVRT with Orthodromic Conduction results in a wide complex tachycardia which may be mistaken for Ventricular Tachycardia. For discussion on differentiating wide complex tachycardias see here, here, and here. Stable patients may respond to drug therapy including amiodarone, procainamide or ibutilide, but may require DC cardioversion In a haemodynamically unstable patient urgent synchronised DC cardioversion is required. If in doubt treat as VT

Atrial Fibrillation & Atrial Flutter in WPW

Atrial fibrillation can occur in up to 20% of patients with WPW. Atrial flutter can occur in up to 7% of patients with WPW. The accessory pathway allows for rapid conduction directly to the ventricles bypassing the AV node. Rapid ventricular rates may result in degeneration to VT or VF.

ECG features of Atrial Fibrillation in WPW are:

Rate > 200 bpm Irregular rhythm Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway QRS Complexes change in shape and morphology Axis remains stable unlike Polymorphic VT

Atrial Flutter results in the same features as AF in WPW expect the rhythm is regular may be mistaken for VT. Treatment of AF with WPW

Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel blockers, beta-blockers may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into VT or VF In a haemodynamically unstable patient urgent synchronised DC cardioversion is required. Medical treatment options in a stable patient include procainamide or ibutilide, although DC cardioversion may be preferred.

Other Pre-Excitation Syndromes / Accessory Pathways Lown-Ganong-Levine (LGL) Syndrome

Proposed pre-excitation syndrome Accessory pathway composed of James fibres ECG features: o PR interval <120ms o Normal QRS morphology The term should not be used in the absence of paroxysmal tachycardia Existence is disputed and may not exist

Mahaim-Type Pre-excitation

Right sided accessory pathways connecting either AV node to ventricles, fascicles to ventricles, or atria to fascicles ECG features: o Sinus rhythm ECG may be normal o May result in variation in ventricular morphology o Reentry tachycardia typically has LBBB morphology

ECG Examples Sinus Rhythm Type A Pattern Example 1

Sinus rhythm with a very short PR interval (< 120 ms). Broad QRS complexes with a slurred upstroke to the QRS complex the delta wave. Dominant R wave in V1 this pattern is known as Type A WPW and is associated with a left-sided accessory pathway. Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy these changes are due to WPW and do not indicate underlying RVH. Negative delta wave in aVL simulating the Q waves of lateral infarction this is referred to as the pseudo-infarction pattern.

Example 2

Another example of the Type A WPW pattern with dominant R wave in V1 and right precordial T-wave inversions simulating RVH.

Sinus rhythm Type B Pattern Example 3

Sinus rhythm with very short PR interval (< 120 ms) Broad QRS complexes with a slurred upstroke to the QRS complexes the delta wave. Dominant S wave in V1 this pattern is known as Type B WPW and indicates a right-sided accessory pathway. Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular hypertrophy again, this is due to WPW and does not indicate underlying LVH.

Example 4

Another example of WPW Type B:

Negative delta waves in leads III and aVF simulate the Q waves of prior inferior MI (= pseudo-infarction pattern)

Sinus Rhythm Paediatric ECGs Example 5

An example of WPW in a 5-year old boy the ECG changes are more subtle than in adults:

The PR interval is short even allowing for the patients age. The QRS complexes do not appear particularly broad however, there is definite slurring of the upstroke of each R wave, most obvious in leads II, III, aVF and V4 (= delta waves). The RSR pattern with T wave inversion in V1-2 is a normal variant in children of this age; this is still a Type B pattern due to absence of a dominant R wave in V1. There are pseudo-infarction Q waves in lead aVL simulating lateral infarction.

For more information on interpretation of the paediatric ECG, check out our Guide to Paediatric ECG Interpretation.

Example 6

Another example of paediatric WPW, this time in a 7-year old child:

Slight QRS widening and delta waves are more evident in the older child. Again, there are pseudo-infarction Q waves in aVL. It is difficult to categorise this ECG as type A or B given that a dominant R wave in V1 is normal for the childs age.

Dysrhythmias Orthodromic atrioventricular re-entry tachycardia (AVRT) Example 7

Regular, narrow complex tachycardia at 225 bpm. No discernible P-waves. The QRS complexes are narrow because impulses are being transmitted in an orthodromic direction (A -> V) via the AV node. This rhythm is indistinguishable from AV-nodal re-entry tachycardia (AVNRT).

NB. Widespread ST depression (rate-related change) is present; this in common in SVT and does not necessarily indicate myocardial ischaemia. See what happened when this patient was given adenosine Example 8

Narrow complex tachycardia at 180 bpm with no discernible P waves this is another example of orthodromic AVRT.

See what happened when this patient was given adenosine Antidromic atrioventricular re-entry tachycardia (AVRT) Example 9

Antidromic AVRT in a 5-year old boy with WPW:

There is a regular, broad complex tachycardia at ~280 bpm; this would be very difficult to distinguish from VT. However, given the childs age, VT is very unlikely: > 95% of broad complex tachycardias in children are actually some form of SVT with aberrancy. This was the presenting ECG of the 5-year old boy from Example 5 (see above for his baseline ECG); the antidromic AVRT resolved with vagal manoeuvres.

Read more about differentiating VT from SVT with aberrancy.

Example 10

Another example of broad complex tachycardia due to antidromic AVRT in a 15year old boy with WPW. The AVRT resolved with vagal manoeuvres.

Atrial Fibrillation with WPW Example 11

Atrial fibrillation in a patient with WPW:

Rapid, irregular, broad complex tachycardia (overall rate ~ 200 bpm) with a LBBB morphology (dominant S wave in V1). This could easily be mistaken for AF with LBBB. However, the morphology is not typical of LBBB, the rate is too rapid (up to 300 bpm in places, i.e. too rapid to be conducted via the AV node) and there is a subtle beat-to-beat variation in the QRS width which is more typical of WPW (LBBB usually has fixed width QRS complexes).

Example 12

Another example of AF with WPW resulting in a very rapid (up to 300 bpm in places), irregular broad-complex tachycardia with varying QRS width. There are two narrow complexes (in V1-3), where the atrial impulses are presumably conducted via the AV node instead of via the AP. This rhythm is extremely difficult to differentiate from polymorphic VT; however it does not demonstrate the twisting morphology characteristic of torsades de pointes.

NB. Regardless of the aetiology, the most appropriate treatment for this rhythm (if sustained) would be immediate electrical cardioversion. Intermittent WPW Example 13

AF with WPW showing intermittent pre-excitation:

Some of the impulses are transmitted via the AP (= pre-excited beats), producing characteristic delta waves. Other impulses are transmitted via the AV node, producing narrow QRS complexes.

Example 14

Another example of AF with WPW with intermittent pre-excitation characteristic delta waves are best seen in V2.

Lown-Ganong-Levine Syndrome Example 15

This is a possible example of LGL syndrome:

Very short PR interval. Narrow QRS complexes. No evidence of delta waves.

Right Bundle Branch Block

RBBB Background

In RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle. The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged. The delayed right ventricular activation produces a secondary R wave (R) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads. Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads. In isolated RBBB the cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch.

Tall R' wave in V1 ("M" pattern) with wide, slurred S wave in V6 ("W" pattern) ECG changes in RBBB

Diagnostic Criteria

Broad QRS > 120 ms RSR pattern in V1-3 (M-shaped QRS complex) Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

Associated Features

ST depression and T wave inversion in the right precordial leads (V1-3)

Variations

Sometimes rather than an RSR pattern in V1, there may be a broad monophasic R wave or a qR complex.

Typical RSR' pattern ('M'-shaped QRS) in V1

Wide slurred S wave in lead I

Typical pattern of T-wave inversion in V1-3 with RBBB Causes of RBBB

Right ventricular hypertrophy / cor pulmonale Pulmonary embolus Ischaemic heart disease Rheumatic heart disease Myocarditis or cardiomyopathy Degenerative disease of the conduction system Congenital heart disease (e.g. atrial septal defect)

More ECG Examples of RBBB Example 1

Example 2

Example 3

Incomplete RBBB

Incomplete RBBB is defined as an RSR pattern in V1-3 with QRS duration < 120ms. It is a normal variant, commonly seen in children (of no clinical significance).

Incomplete RBBB (RSR' pattern in V1) in a 2-year old child

Differential Diagnosis of RBBB

An RSR pattern in V1-3 may also be caused by Brugada syndrome an ECG pattern associated with malignant ventricular arrhythmias.

Brugada syndrome

Right Axis Deviation

Right Axis Deviation Definition

QRS axis between + 90 and + 180 degrees

Right axis deviation: +90 to +180 degrees

How to recognise right axis deviation

QRS is positive (dominant R wave) in leads III and aVF QRS is negative (dominant S wave) in leads I and aVL

Right axis deviation: leads III and aVF are positive; leads I and aVL are negative Causes

Left posterior fascicular block Lateral myocardial infarction Right ventricular hypertrophy Acute lung disease (e.g. PE) Chronic lung disease (e.g. COPD) Ventricular ectopy Hyperkalaemia Sodium-channel blocker toxicity WPW syndrome Normal in children or thin adults with a horizontally positioned heart

Right Atrial Enlargement

AKA: Right atrial hypertrophy, right atrial abnormality

Attention! Before reading this page, check out our introduction to the P wave for an explanation of the basics of atrial enlargement. Electrocardiographic Criteria Right atrial enlargement produces a peaked P wave (P pulmonale) with amplitude:

> 2.5 mm in the inferior leads (II, III and AVF) > 1.5 mm in V1 and V2

Causes The principal cause is pulmonary hypertension due to:

Chronic lung disease (cor pulmonale) Tricuspid stenosis Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot) Primary pulmonary hypertension

Examples

Right atrial enlargement: P wave amplitude > 2.5mm in leads II, III and aVF

Right atrial enlargement: P wave amplitude > 1.5 mm in V2

Interventricular Conduction Delay (QRS widening)

Definition

QRS duration > 100 ms in the presence of a supraventricular rhythm. Most commonly due to bundle branch block or left ventricular hypertrophy. The most important life-threatening causes of QRS widening are hyperkalaemia and tricyclic antidepressant poisoning.

Causes Follow the links to read more about each condition. Fascicular and bundle-branch blocks

Left anterior fascicular block Left posterior fascicular block Left bundle branch block Right bundle branch block Bifascicular block Trifascicular block

Ventricular hypertrophy and dilatation

Left ventricular hypertrophy Right ventricular hypertrophy Biventricular enlargement Dilated cardiomyopathy

Electrolyte abnormalities

Hyperkalaemia

Toxins

Sodium-channel blocker toxicity (e.g. TCA overdose) - wide QRS plus positive R wave in aVR.

Pre-excitation

Wolff-Parkinson-White syndrome wide QRS plus delta waves.

Arrhythmogenic cardiac conditions

Brugada syndrome - localised QRS widening in V1-2 with RBBB morphology. Arrhythmogenic right ventricular dysplasia (AVRD) - localised QRS widening in V1-2 plus epsilon waves and variable signs of right ventricular hypertrophy.

Non-specific IVCD

Not due to any of the causes above Before making this diagnosis, be sure to check the serum potassium level and scrutinise the ECG for any signs of TCA toxicity.

Differential Diagnosis Ventricular Rhythms

Ventricular tachycardia Accelerated idioventricular rhythm Ventricular escape rhythm Ventricular-paced rhythm

Pre-excitation Syndromes
Wolff-Parkinson-White Syndrome

First described in 1930 by Louis Wolff, John Parkinson and Paul Dudley White. Wolff-Parkinson-White (WPW) Syndrome is a combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia. Incidence 0.1 3.0 per 1000. Associated with a small risk of sudden cardiac death.

Pre-Excitation & Accessory Pathways

Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway. Accessory pathways, also known as bypass tracts, are abnormal conduction pathways formed during cardiac development and can exist in a variety of anatomical locations and in some patients there may be multiple pathways In WPW the accessory pathway is often referred to as the Bundle of Kent, or atrioventricular bypass tract. An accessory pathway can conduct impulses either anterograde, towards the ventricle, retrograde, away from the ventricle, or in both directions. The majority of pathways allow conduction in both directions, with retrograde only conduction occurring in 15% of cases, and antegrade only conduction rarely seen. The direction of conduction affects the appearance of the ECG in sinus rhythm and during tachyarrhythmias. Tachyarrythmia can be facilitated by the formation of a reentry circuit involving the accessory pathway, termed atrioventricular reentry tachycardias (AVRT). Tachyarrythmia may also be facilitated by direct conduction from the atria to the ventricles via the accessory pathway, bypassing the AV node, seen with atrial fibrillation or atrial flutter in conjunction with WPW

Re-entry circuit during AVRT (retrograde conduction via Bundle of Kent) ECG in Sinus Rhythm

The presence of a pre-excitation pathway results in a number of changes to the ECG in sinus rhythm. ECG features of WPW in sinus rhythm are:

PR interval <120ms Delta wave slurring slow rise of initial portion of the QRS QRS prolongation >110ms ST Segment and T wave discordant changes i.e. in the opposite direction to the major component of the QRS complex Pseudo-infarction pattern can be seen in up to 70% of patients due to negatively deflected delta waves in the inferior / anterior leads (pseudo-Q waves), or as a prominent R wave in V1-3 (mimicking posterior infarction).

The features of pre-excitation may be subtle, or present only intermittently. Pre-excitation may be more pronounced with increased vagal tone e.g. during Valsalva manoeuvres, or with AV blockade e.g. drug therapy WPW may be described as type A or B. o Type A has a positive delta wave in all precordial leads with R/S > 1 in V1 o Type B has a negative delta wave in leads V1 and V2 In patients with retrograde-only accessory conduction all antegrade conduction occurs via the AV node, thus no features of WPW are seen on the ECG in sinus rhythm (as no pre-excitation occurs). This is termed a concealed pathway. Patients with a concealed pathway can experience tachyarrythmias as the pathway can still form part of a re-entry circuit

Atrioventricular Reentry Tachycardias (AVRT)

AVRT is a form of paroxysmal supraventricular tachycardia. A reentry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement. During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit. AVRT often triggered by premature atrial or premature ventricular beats. AVRT are further divided in to orthodromic or antidromic conduction based on direction of reentry conduction and ECG morphology.

AVRT with orthodromic (left ) and antidromic (right) AV nodal conduction AVRT with Orthodromic Conduction In orthodromic AVRT antegrade conduction occurs via the AV node with retrograde conduction occurring via the accessory pathway. This can occur in patients with a concealed pathway. ECG features of AVRT with orthodromic conduction are:

Rate usually 200 300 bpm P waves may be buried in QRS complex or retrograde QRS Complex usually <120 ms unless pre-existing bundle branch block, or raterelated aberrant conduction QRS Alternans phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished from electrical alternans by a normal QRS amplitude T wave inversion common

ST segment depression

Treatment of orthodromic AVRT

Treatment of AVRT is based on the presence of haemodynamic instability e.g. hypotension, altered mental state, or pulmonary oedema. In patients who are haemodynamically stable vagal manoeuvres may be successful, followed by adenosine or calcium-channel blockers, and DC cardioversion may be considered if non-repsonsive to medical therapy. In a haemodynamically unstable patient urgent synchronised DC cardioversion is required.

AVRT with Antidromic Conduction In antidromic AVRT antegrade conduction occurs via the accessory pathway with retrograde conduction via the AV node. Much less common than orthodromic AVRT occuring in ~5% of patients with WPW. ECG features of AVRT with antidromic conduction are:

Rate usually 200 300 bpm. Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway.

Treatment of antidromic AVRT

AVRT with Orthodromic Conduction results in a wide complex tachycardia which may be mistaken for Ventricular Tachycardia. For discussion on differentiating wide complex tachycardias see here, here, and here. Stable patients may respond to drug therapy including amiodarone, procainamide or ibutilide, but may require DC cardioversion In a haemodynamically unstable patient urgent synchronised DC cardioversion is required. If in doubt treat as VT

Atrial Fibrillation & Atrial Flutter in WPW

Atrial fibrillation can occur in up to 20% of patients with WPW. Atrial flutter can occur in up to 7% of patients with WPW. The accessory pathway allows for rapid conduction directly to the ventricles bypassing the AV node. Rapid ventricular rates may result in degeneration to VT or VF.

ECG features of Atrial Fibrillation in WPW are:

Rate > 200 bpm Irregular rhythm Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway QRS Complexes change in shape and morphology Axis remains stable unlike Polymorphic VT

Atrial Flutter results in the same features as AF in WPW expect the rhythm is regular may be mistaken for VT. Treatment of AF with WPW

Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel blockers, beta-blockers may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into VT or VF In a haemodynamically unstable patient urgent synchronised DC cardioversion is required. Medical treatment options in a stable patient include procainamide or ibutilide, although DC cardioversion may be preferred.

Other Pre-Excitation Syndromes / Accessory Pathways Lown-Ganong-Levine (LGL) Syndrome

Proposed pre-excitation syndrome Accessory pathway composed of James fibres ECG features: o PR interval <120ms o Normal QRS morphology The term should not be used in the absence of paroxysmal tachycardia Existence is disputed and may not exist

Mahaim-Type Pre-excitation

Right sided accessory pathways connecting either AV node to ventricles, fascicles to ventricles, or atria to fascicles ECG features: o Sinus rhythm ECG may be normal o May result in variation in ventricular morphology o Reentry tachycardia typically has LBBB morphology

ECG Examples Sinus Rhythm Type A Pattern Example 1

Sinus rhythm with a very short PR interval (< 120 ms). Broad QRS complexes with a slurred upstroke to the QRS complex the delta wave. Dominant R wave in V1 this pattern is known as Type A WPW and is associated with a left-sided accessory pathway. Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy these changes are due to WPW and do not indicate underlying RVH. Negative delta wave in aVL simulating the Q waves of lateral infarction this is referred to as the pseudo-infarction pattern.

Example 2

Another example of the Type A WPW pattern with dominant R wave in V1 and right precordial T-wave inversions simulating RVH.

Sinus rhythm Type B Pattern Example 3

Sinus rhythm with very short PR interval (< 120 ms) Broad QRS complexes with a slurred upstroke to the QRS complexes the delta wave. Dominant S wave in V1 this pattern is known as Type B WPW and indicates a right-sided accessory pathway. Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular hypertrophy again, this is due to WPW and does not indicate underlying LVH.

Example 4

Another example of WPW Type B:

Negative delta waves in leads III and aVF simulate the Q waves of prior inferior MI (= pseudo-infarction pattern)

Sinus Rhythm Paediatric ECGs Example 5

An example of WPW in a 5-year old boy the ECG changes are more subtle than in adults:

The PR interval is short even allowing for the patients age. The QRS complexes do not appear particularly broad however, there is definite slurring of the upstroke of each R wave, most obvious in leads II, III, aVF and V4 (= delta waves). The RSR pattern with T wave inversion in V1-2 is a normal variant in children of this age; this is still a Type B pattern due to absence of a dominant R wave in V1. There are pseudo-infarction Q waves in lead aVL simulating lateral infarction.

For more information on interpretation of the paediatric ECG, check out our Guide to Paediatric ECG Interpretation.

Example 6

Another example of paediatric WPW, this time in a 7-year old child:

Slight QRS widening and delta waves are more evident in the older child. Again, there are pseudo-infarction Q waves in aVL. It is difficult to categorise this ECG as type A or B given that a dominant R wave in V1 is normal for the childs age.

Dysrhythmias Orthodromic atrioventricular re-entry tachycardia (AVRT) Example 7

Regular, narrow complex tachycardia at 225 bpm. No discernible P-waves. The QRS complexes are narrow because impulses are being transmitted in an orthodromic direction (A -> V) via the AV node. This rhythm is indistinguishable from AV-nodal re-entry tachycardia (AVNRT).

NB. Widespread ST depression (rate-related change) is present; this in common in SVT and does not necessarily indicate myocardial ischaemia. See what happened when this patient was given adenosine Example 8

Narrow complex tachycardia at 180 bpm with no discernible P waves this is another example of orthodromic AVRT.

See what happened when this patient was given adenosine Antidromic atrioventricular re-entry tachycardia (AVRT) Example 9

Antidromic AVRT in a 5-year old boy with WPW:

There is a regular, broad complex tachycardia at ~280 bpm; this would be very difficult to distinguish from VT. However, given the childs age, VT is very unlikely: > 95% of broad complex tachycardias in children are actually some form of SVT with aberrancy. This was the presenting ECG of the 5-year old boy from Example 5 (see above for his baseline ECG); the antidromic AVRT resolved with vagal manoeuvres.

Read more about differentiating VT from SVT with aberrancy.

Example 10

Another example of broad complex tachycardia due to antidromic AVRT in a 15year old boy with WPW. The AVRT resolved with vagal manoeuvres.

Atrial Fibrillation with WPW Example 11

Atrial fibrillation in a patient with WPW:

Rapid, irregular, broad complex tachycardia (overall rate ~ 200 bpm) with a LBBB morphology (dominant S wave in V1). This could easily be mistaken for AF with LBBB. However, the morphology is not typical of LBBB, the rate is too rapid (up to 300 bpm in places, i.e. too rapid to be conducted via the AV node) and there is a subtle beat-to-beat variation in the QRS width which is more typical of WPW (LBBB usually has fixed width QRS complexes).

Example 12

Another example of AF with WPW resulting in a very rapid (up to 300 bpm in places), irregular broad-complex tachycardia with varying QRS width. There are two narrow complexes (in V1-3), where the atrial impulses are presumably conducted via the AV node instead of via the AP. This rhythm is extremely difficult to differentiate from polymorphic VT; however it does not demonstrate the twisting morphology characteristic of torsades de pointes.

NB. Regardless of the aetiology, the most appropriate treatment for this rhythm (if sustained) would be immediate electrical cardioversion. Intermittent WPW Example 13

AF with WPW showing intermittent pre-excitation:

Some of the impulses are transmitted via the AP (= pre-excited beats), producing characteristic delta waves. Other impulses are transmitted via the AV node, producing narrow QRS complexes.

Example 14

Another example of AF with WPW with intermittent pre-excitation characteristic delta waves are best seen in V2.

Lown-Ganong-Levine Syndrome Example 15

This is a possible example of LGL syndrome:

Very short PR interval. Narrow QRS complexes. No evidence of delta waves.

Low QRS Voltage

Definition The QRS is said to be low voltage when:

The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or The amplitudes of all the QRS complexes in the precordial leads are < 10 mm

Low QRS voltage due to myxoedema Mechanisms Low voltage is produced by:

The damping effect of increased layers of fluid, fat or air between the heart and the recording electrode Loss of viable myocardium Diffuse infiltration or myxoedematous involvement of the heart

Causes Specific causes of low voltage include:

Pericardial effusion Pleural effusion Obesity Emphysema Pneumothorax Contrictive pericarditidis

Previous massive MI End-stage dilated cardiomyopathy Infiltrative myocardial diseases i.e. restrictive cardiomyopathy due to amyloidosis, sarcoidosis, haemochromatosis Scleroderma Myxoedema

The most important cause is massive pericardial effusion / tamponade, which produces a triad of:

Low voltage Tachycardia Electrical alternans

ECG Examples Example 1

Massive Pericardial Effusion:

Note the presence of electrical alternans.

Example 2

Prior Massive Anterior MI:

Low QRS voltage in V1-6. This ECG also demonstrates biphasic anterior T waves (Wellens syndrome) indicating acute anterior ischaemia.

ST Elevation in aVR LMCA occlusion?

This ECG demonstrates the classical pattern of left main coronary artery (LMCA) occlusion:

Widespread horizontal ST depression, most prominent in leads I, II and V4-6 ST elevation in aVR 1mm ST elevation in aVR V1

However, ST elevation in aVR is not entirely specific to LMCA occlusion. It may also be seen with:

Proximal left anterior descending artery (LAD) occlusion Severe triple-vessel disease (3VD)

Mechanism of STE in aVR

Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR. Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum; infarction in this area could theoretically produce ST elevation in aVR.

ST elevation is aVR is thought to result from two possible mechanisms:

Diffuse subendocardial ischaemia (producing reciprocal change in aVR)

Transmural ischaemia / infarction of the basal interventricular septum (e.g. due to a proximal occlusion within the left coronary system)

NB. The basal septum is supplied by the first septal perforator artery (a very proximal branch of the LAD), so ischaemia/infarction of the basal septum would imply involvement of the proximal LAD or LMCA.

Predictive Value of STE in aVR In the context of widespread ST depression + symptoms of myocardial ischaemia:

STE in aVR 1mm indicates proximal LAD / LMCA occlusion or severe 3VD STE in aVR 1mm predicts the need for CABG STE in aVR V1 differentiates LMCA from proximal LAD occlusion Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion

In the context of anterior STEMI:

STE in aVR 1mm is highly specific for LAD occlusion proximal to the first septal branch

In patients undergoing exercise stress testing:

STE of 1mm in aVR during exercise stress testing predicts LMCA or ostial LAD stenosis

Magnitude of ST elevation in aVR is correlated with mortality in patients with acute coronary syndromes:

STE in aVR 0.5mm was associated with a 4-fold increase in mortality STE in aVR 1mm was associated with a 6- to 7-fold increase in mortality STE in aVR 1.5mm has been associated with mortalities ranging from 20-75%

For a more in-depth look at the literature on aVR, click here More ECG Examples Example 2 LMCA occlusion

Another typical example of LMCA occlusion:

Widespread ST depression, most prominent in the lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR ST elevation in aVR V1

Example 3 LMCA occlusion

The ECG shows:

Marked ST elevation in aVR >> V1 ST depression in mulitple leads (V2-6, I, II, aVL, aVF), to some extent masked by a non-specific interventricular conduction delay

This patient presented to our ED recently with severe ischaemic chest pain, vomiting, syncope (due to runs of VT) and cardiogenic shock. He was taken for emergent angiography and found to have a complete ostial occlusion of his left main coronary artery.

Example 4 Proximal LAD occlusion

This ECG shows:

ST elevation in aVR and V1 of similar magnitude. Widespread ST depression (V3-6, I, II, III, aVF)

This patient had a severe ostial LAD thrombus that was close to the left main. (This ECG is reproduced from Dr Smiths ECG Blog click here to see the ECG in its original context)

Example 5 Severe Multi-Vessel Disease

This ECG shows:

ST elevation in aVR and V1, of similar magnitude ST depression in multiple leads (V5-6, I, II, aVL, aVF) Evidence of anteroseptal STEMI ST elevation with Q wave formation in V1-3

It would be reasonable to suspect a proximal LAD occlusion based on this ECG. However, this patient actually had severe multi-vessel disease. Angiography demonstrated a chronic total occlusion of his circumflex artery, with critical stenoses of his proximal LAD, RCA and ramus intermedius. Surprisingly, in this case the culprit vessel was thought to be the RCA, which had been collateralising his chronically occluded circumflex.

Implications for therapy in acute coronary syndromes Given the ability of STE in aVR to predict critical coronary lesions and death, this ECG pattern is increasingly being recognised as a STEMI equivalent that requires emergent reperfusion therapy to prevent cardiogenic shock and death. Furthermore, the presence or absence of STE in aVR may potentially inform the decision to give thienopyridine platelet inhibitors (e.g. clopidogrel, prasugrel) during an acute coronary syndrome:

Clopidogrel treatment 7 days before CABG is associated with an increase in major bleeding, haemorrhage-related complications, and transfusion requirements. Prasugrel is associated with even more bleeding than clopidogrel. If urgent CABG (within 7 days) is likely, then there is an argument for omitting thienopyridines during the initial management of an acute coronary syndrome (or at least using clopidogrel instead of prasugrel).

In the recent study by Kosuge et al. (2011)

STE in aVR 1 mm was a strong predictor of severe LMCA / 3VD requiring CABG. Conversely, patients with < 1mm ST elevation in aVR had a negligible risk of severe LMCA / 3VD requiring CABG.

Based on this data:

Patients with < 1mm STE in aVR may safely receive clopidogrel/prasugrel during the initial treatment of their ACS as they are unlikely to proceed to urgent CABG. Patients with 1 mm STE in aVR may potentially require early CABG; therefore these patients should ideally be discussed with the interventional cardiologist ( cardiac surgeon) before thienopyridines are given.

Left Bundle Branch Block

Left Bundle Branch Block Background

Normally the septum is activated from left to right, producing small Q waves in the lateral leads. In LBBB, the normal direction of septal depolarisation is reversed (becomes right to left), as the impulse spreads first to the RV via the right bundle branch and then to the LV via the septum. This sequence of activation extends the QRS duration to > 120 ms and eliminates the normal septal Q waves in the lateral leads. The overall direction of depolarisation (from right to left) produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3), and usually leads to left axis deviation. As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (M-shaped) R wave in the lateral leads.

Dominant S wave in V1 with broad, notched ('M'-shaped) R wave in V6 Diagnostic Criteria

QRS duration of 120 ms Dominant S wave in V1 Broad monophasic R wave in lateral leads (I, aVL, V5-V6) Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL) Prolonged R wave peak time > 60ms in left precordial leads (V5-6)

Associated Features

Appropriate discordance: the ST segments and T waves always go in the opposite direction to the main vector of the QRS complex Poor R wave progression in the chest leads Left axis deviation

QRS Morphology in the Lateral Leads

The R wave in the lateral leads may be either:

M-shaped Notched Monophasic RS complex

'M'-shaped QRS complex

Notched R wave

Monophasic R wave

RS complex QRS Morphology in V1 The QRS complex in V1 may be either:

rS complex (small R wave, deep S wave) QS complex (deep Q/S wave with no preceding R wave)

Typical appearance of LBBB in V1 with rS complex (tiny R wave, deep S wave) and appropriate discordance (ST elevation and upright T wave) Causes

Aortic stenosis Ischaemic heart disease Hypertension Dilated cardiomyopathy Anterior MI Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease) Hyperkalaemia Digoxin toxicity

NB. It is unusual for left bundle branch block to exist in the absence of organic disease. Incomplete LBBB

Incomplete LBBB is diagnosed when typical LBBB morphology is associated with a QRS duration < 120ms.

Incomplete LBBB (QRS duration 110ms) Differential Diagnosis

Left ventricular hypertrophy may produce a similar appearance to LBBB, with QRS widening and ST depression / T-wave inversion in the lateral leads.

More Examples of LBBB

Left Bundle Branch Block

Left Bundle Branch Block

AF with LBBB

Sgarbossa Criteria
Background

In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG is difficult. The baseline ST segments and T waves tend to be shifted in a discordant direction (appropriate discordance), which can mask or mimic acute myocardial infarction. However, serial ECGs may show dynamic ST segment changes during ischemia. A new LBBB is always pathological and can be a sign of myocardial infarction.

Electrocardiographic Criteria The three criteria used to diagnose infarction in patients with LBBB are:

Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5) Concordant ST depression > 1 mm in V1-V3 (score 3) Excessively discordant ST elevation > 5 mm in leads with a negative QRS complex (score 2). This criterium is sensitive, but not specific for ischemia in LBBB. It is however associated with a worse prognosis, when present in LBBB during ischemia.

A total score of 3 has a specificity of 90% for diagnosing myocardial infarction.

During right ventricular pacing the ECG also shows left bundle brach block and the above rules also apply for the diagnosis of myocardial infarction during pacing, however they are less specific. In the GUSTO-1 trial the ECG criterion with a high specificity and statistical significance for the diagnosis of an acute MI was:

Excessively discordant ST segment elevation 5 mm (in leads with a negative QRS complex).

Two other criteria with acceptable specificity were:

Concordant ST elevation 1 mm in leads with positive QRS Concordant ST depression 1 mm in leads V1, V2, or, V3

ECG Example

Positive Sgarbossa criteria in a patient with LBBB and troponin-positive myocardial infarction:

This patient presented with chest pain and had elevated cardiac enzymes. Baseline ECG showed typical LBBB. There is 1mm concordant ST elevation in aVL (= 5 points). Other features on this ECG that are abnormal in the context of LBBB (but not considered positive Sgarbossa criteria) are the pathological Q wave in lead I and the concordant ST depression in the inferior leads III and aVF. This constellation of abnormalities suggests to me that the patient was having a high lateral infarction.

Right Ventricular Infarction

Clinical Significance

Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon. Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents. Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.

The ECG changes of RV infarction are subtle and easily missed! How to spot right ventricular infarction The first step to spotting RV infarction is to suspect it in all patients with inferior STEMI! In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:

ST elevation in V1 - the only standard ECG lead that looks directly at the right ventricle. ST elevation in lead III > lead II - because lead III is more rightward facing than lead II and hence more sensitive to the injury current produced by the right ventricle.

Other useful tips for spotting right ventricular MI (as described by Amal Mattu and William Brady in ECGs for the Emergency Physician):

If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2. If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed. NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.

Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided leads (V3R-V6R). Right-sided leads There are several different approaches to recording a right-sided ECG:

A complete set of right-sided leads is obtained by placing leads V1-6 in a mirrorimage position on the right side of the chest (see diagram, below). It may be simpler to leave V1 and V2 in their usual positions and just transfer leads V3-6 to the right side of the chest (i.e. V3R to V6R). The most useful lead is V4R, which is obtained by placing the V4 electrode in the 5th right intercostal space in the midclavicular line. ST elevation in V4R has a

sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% in the diagnosis of RV MI.

Reproduced from Morris and Brady, 2002. Click image for link to original reference. NB. ST elevation in the right-sided leads is a transient phenomenon, lasting less than 10 hours in 50% of patients with RV infarction. Example ECGs Example 1a

Inferior STEMI. Right ventricular infarction is suggested by:

ST elevation in V1 ST elevation in lead III > lead II

Example 1b

Repeat ECG of the same patient with V4R electrode position:

There is ST elevation in V4R consistent with RV infarction

Example 2

Another example of right ventricular MI:

There is an inferior STEMI with ST elevation in lead III > lead II. There is subtle ST elevation in V1 with ST depression in V2. There is ST elevation in V4R.

Example 3

This ECG shows a full set of right-sided leads (V3R-V6R), with V1 and V2 in their original positions. RV infarction is diagnosed based on the following findings:

There is an inferior STEMI with ST elevation in lead III > lead II. V1 is isoelectric while V2 is significantly depressed. There is ST elevation throughout the right-sided leads V3R-V6R.

Short QT Syndrome

Image reproduced from Schimpf et al. (See references below for link) Description

Short QT syndrome is a recently-discovered arrhythmogenic disease associated with paroxysmal atrial and ventricular fibrillation, syncope and sudden cardiac death. It is a genetically-inherited cardiac channelopathy on the same spectrum as other familial arrhythmogenic diseases such as Long QT Syndrome (LQTS), Brugada Syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT). Patients are typically young and healthy, with no structural heart abnormalities; age at first presentation ranges from a few months to the sixth decade of life (median age = 30 years).

The most common initial presenting symptom is cardiac arrest (in one-third of cases); other patients may present with palpitations or syncope due to rapid atrial fibrillation or self-terminating ventricular arrhythmias. Witnessed cardiac arrest within the first year of life and unexplained infant deaths have been observed in patients and families with SQTS, making it a possible cause of sudden infant death syndrome (SIDS). SQTS is still a relatively new disease: It was first described in 2000, and elucidation of the genetic, electrophysiological and clinical abnormalities associated with the disease has only taken place over the past few years.

Mechanism Arrhythmogenesis in SQTS is thought to result from:

Extremely short atrial and ventricular refractory periods (manifest on the ECG as a short QT interval). Transmural dispersion of repolarisation, i.e., the different layers of the myocardium (endocardium, epicardium and the mid-myocardial M-cells) repolarise at different rates.

Both these repolarisation abnormalities convey an increased susceptibility to re-entrant atrial and ventricular arrhythmias. Genetic Basis

SQTS is a genetically heterogenous disease, with multiple mutations producing a similar clinical picture. Five mutations have been characterised so far, all of which seem to be inherited in an autosomal dominant fashion. SQTS genotypes 1-3 are produced by a gain-of-function mutation in myocardial potassium channels (the opposite to LQTS), with increased potassium efflux during various stages of the action potential leading to more rapid atrial and ventricular repolarisation with marked shortening of the QT interval (<320 ms). SQTS genotypes 4 and 5 are produced by a loss-of-function mutation in the L-type cardiac channel, with reduced influx of calcium during the plateau phase of the action potential leading to modest shortening of the QT interval (<360ms) associated with a Brugada-syndrome-like QRS complex morphology.

Potassium fluxes in SQTS 1-3

A. Schematic representation of the normal action potential and the flux of ions. B. With gain-offunction mutations in any of 3 different potassium channels (SQTS 1-3), the cardiac action potential shortens and the QT interval decreases. (Reproduced from Brugada et al)

Classification of SQTS according to genotype

Classification of SQTS according to genotype. (Reproduced from Moreno-Reviriego & Merino)

Diagnosis At present, there are no diagnostic criteria for SQTS. The diagnosis is based upon the patients symptoms (e.g. syncope, palpitations), family history (of syncope, sudden death or atrial fibrillation at an early age) and characteristic findings on the 12-lead ECG.

Clinical features So far, there have only been a handful of cases of SQTS reported in the literature. The true prevalence of the disease is unknown. The largest case series to date reported on 29 patients with the disease:

The most common presenting symptom was cardiac arrest (in one-third of cases). Cardiac arrest occurred in the first months of life in two patients. Syncope was the presenting symptom in 24% of cases, thought to be secondary to self-terminating episodes of ventricular fibrillation. Up to 31% of patients complained of palpitations, and 80% of patients had documented episodes ofatrial fibrillation. All patients had a QT < 320ms and a QTc < 340ms with no evidence of structural heart disease(NB. This case series did not include the more recentlydescribed SQTS genotypes 4 & 5)

ECG features The main electrocardiographic abnormalities seen in SQTS are:

Short QT interval Lack of the normal changes in QT interval with heart rate Peaked T waves, particularly in the precordial leads Short or absent ST segments Episodes of atrial or ventricular fibrillation

QT, ST and T-wave changes in SQTS Short QT interval, peaked T waves and short ST segments in two patients with SQTS 1.

Reproduced from Crotti et al. Short QT interval There is currently no universally accepted lower limit of normal for the QT interval that can be used to diagnose SQTS.

Known patients with SQTS genotypes 1-3 all had QTc intervals < 300-320 ms Known patients with SQTS genotypes 4 & 5 all had QTc intervals < 360 ms

A recent review by Viskin suggested the following approach:

QTc intervals < 330 ms in males or < 340 ms in females should be considered diagnostic of SQTS QTc intervals < 360 ms in males or < 370 ms in females should only be considered diagnostic of SQTS when supported by symptoms or family history

A QT interval scale for diagnosing SQTS and LQTS

A 'QT interval scale' for diagnosing SQTS and LQTS. (Reproduced from Viskin) Lack of the normal changes in QT with heart rate

Patients with SQTS demonstrate fixed QT intervals which remain constant over a range of heart rates. At fast heart rates, the calculated QTc may appear normal (= pseudonormal QTc) However, as the heart rate slows, the QTc typically fails to prolong. Serial ECGs or Holter monitoring at rest may be used to try and capture short QT intervals during periods of relative bradycardia (heart rate 60-80bpm). Exercise testing may demonstrate lack of adaptation of QT interval with different heart rates.

Fixed QT interval seen on Holter monitoring in a patient with SQTS

Holter strip from a patient with SQTS at heart rates of 68 and 119 bpm. QT interval of 280 ms remains constant at both heart rates. (Reproduced from Short QT Syndrome.org)

Electrophysiological Studies Electrophysiological studies in SQTS demonstrate:

Extremely short atrial and ventricular refractory periods High rates of inducible atrial and ventricular fibrillation Marked vulnerability to mechanical induction of ventricular fibrillation

The role of EP studies in diagnosing and risk-stratifying patients with SQTS has not yet been established. Treatment Options

At present, the only effective treatment is implantation of an ICD. The main problem with this is T-wave oversensing and inappropriate shocks due to the tall, narrow T waves seen in SQTS. Efforts to find a suitable pharmacological treatment have focused on potassium blocking anti-arrhythmic agents (classes Ia and III). Class III agents ibutilide and sotalol, while having theoretical benefits in prolonging QT and suppressing arrhythmias, have been shown to be ineffective due to reduced drug binding to mutated potassium channels. Class Ia agents quinidine and disopyramide have shown more promising effects. Quinidine is currently the agent of choice, having been shown in SQTS 1 patients to markedly prolong both the QT interval and ventricular refractory period, with normalisation of ST segments and T waves and prevention of VF induction.

ST Elevation in aVR LMCA occlusion?

This ECG demonstrates the classical pattern of left main coronary artery (LMCA) occlusion:

Widespread horizontal ST depression, most prominent in leads I, II and V4-6 ST elevation in aVR 1mm ST elevation in aVR V1

However, ST elevation in aVR is not entirely specific to LMCA occlusion. It may also be seen with:

Proximal left anterior descending artery (LAD) occlusion Severe triple-vessel disease (3VD)

Mechanism of STE in aVR

Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR.

Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum; infarction in this area could theoretically produce ST elevation in aVR.

ST elevation is aVR is thought to result from two possible mechanisms:

Diffuse subendocardial ischaemia (producing reciprocal change in aVR) Transmural ischaemia / infarction of the basal interventricular septum (e.g. due to a proximal occlusion within the left coronary system)

NB. The basal septum is supplied by the first septal perforator artery (a very proximal branch of the LAD), so ischaemia/infarction of the basal septum would imply involvement of the proximal LAD or LMCA.

Predictive Value of STE in aVR In the context of widespread ST depression + symptoms of myocardial ischaemia:

STE in aVR 1mm indicates proximal LAD / LMCA occlusion or severe 3VD STE in aVR 1mm predicts the need for CABG STE in aVR V1 differentiates LMCA from proximal LAD occlusion Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion

In the context of anterior STEMI:

STE in aVR 1mm is highly specific for LAD occlusion proximal to the first septal branch

In patients undergoing exercise stress testing:

STE of 1mm in aVR during exercise stress testing predicts LMCA or ostial LAD stenosis

Magnitude of ST elevation in aVR is correlated with mortality in patients with acute coronary syndromes:

STE in aVR 0.5mm was associated with a 4-fold increase in mortality STE in aVR 1mm was associated with a 6- to 7-fold increase in mortality STE in aVR 1.5mm has been associated with mortalities ranging from 20-75%

For a more in-depth look at the literature on aVR, click here

More ECG Examples Example 2 LMCA occlusion

Another typical example of LMCA occlusion:

Widespread ST depression, most prominent in the lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR ST elevation in aVR V1

Example 3 LMCA occlusion

The ECG shows:

Marked ST elevation in aVR >> V1 ST depression in mulitple leads (V2-6, I, II, aVL, aVF), to some extent masked by a non-specific interventricular conduction delay

This patient presented to our ED recently with severe ischaemic chest pain, vomiting, syncope (due to runs of VT) and cardiogenic shock. He was taken for emergent angiography and found to have a complete ostial occlusion of his left main coronary artery.

Example 4 Proximal LAD occlusion

This ECG shows:

ST elevation in aVR and V1 of similar magnitude. Widespread ST depression (V3-6, I, II, III, aVF)

This patient had a severe ostial LAD thrombus that was close to the left main. (This ECG is reproduced from Dr Smiths ECG Blog click here to see the ECG in its original context)

Example 5 Severe Multi-Vessel Disease

This ECG shows:

ST elevation in aVR and V1, of similar magnitude ST depression in multiple leads (V5-6, I, II, aVL, aVF) Evidence of anteroseptal STEMI ST elevation with Q wave formation in V1-3

It would be reasonable to suspect a proximal LAD occlusion based on this ECG. However, this patient actually had severe multi-vessel disease. Angiography demonstrated a chronic total occlusion of his circumflex artery, with critical stenoses of his proximal LAD, RCA and ramus intermedius. Surprisingly, in this case the culprit vessel was thought to be the RCA, which had been collateralising his chronically occluded circumflex.

Implications for therapy in acute coronary syndromes Given the ability of STE in aVR to predict critical coronary lesions and death, this ECG pattern is increasingly being recognised as a STEMI equivalent that requires emergent reperfusion therapy to prevent cardiogenic shock and death. Furthermore, the presence or absence of STE in aVR may potentially inform the decision to give thienopyridine platelet inhibitors (e.g. clopidogrel, prasugrel) during an acute coronary syndrome:

Clopidogrel treatment 7 days before CABG is associated with an increase in major bleeding, haemorrhage-related complications, and transfusion requirements. Prasugrel is associated with even more bleeding than clopidogrel. If urgent CABG (within 7 days) is likely, then there is an argument for omitting thienopyridines during the initial management of an acute coronary syndrome (or at least using clopidogrel instead of prasugrel).

In the recent study by Kosuge et al. (2011)

STE in aVR 1 mm was a strong predictor of severe LMCA / 3VD requiring CABG. Conversely, patients with < 1mm ST elevation in aVR had a negligible risk of severe LMCA / 3VD requiring CABG.

Based on this data:

Patients with < 1mm STE in aVR may safely receive clopidogrel/prasugrel during the initial treatment of their ACS as they are unlikely to proceed to urgent CABG. Patients with 1 mm STE in aVR may potentially require early CABG; therefore these patients should ideally be discussed with the interventional cardiologist ( cardiac surgeon) before thienopyridines are given.

Supraventricular Tachycardia (SVT)

Background

The term supraventricular tachycardia (SVT), whilst often used synonymously with AV nodal re-entry tachycardia (AVNRT), can be used to refer to any tachydysrhythmia arising from above the level of the Bundle of His. Different types of SVT arise from or are propagated by the atria or AV node, typically producing a narrow-complex tachycardia (unless aberrant conduction is present). Paroxysmal SVT (pSVT) describes an SVT with abrupt onset and offset characteristically seen with re-entrant tachycardias involving the AV node such as AVNRT or atrioventricular re-entry tachycardia (AVRT).

Supraventricular tachycardia Classification

SVTs can be classified based on site of origin (atria or AV node) or regularity (regular or irregular). Classification based on QRS width is unhelpful as this is also influenced by the presence of pre-existing bundle branch block, rate-related aberrant conduction or presence of accessory pathways.

Classification of SVT by site of origin and regularity Regular Sinus tachycardia Atrial tachycardia Atrial flutter Inappropriate sinus tachycardia Sinus node re-entrant tachycardia

Atrial

Irregular Atrial fibrillation Atrial flutter with variable block Multifocal atrial tachycardia

Atrioventricular

Atrioventricular reentry tachycardia (AVRT) AV nodal re-entry tachycardia (AVNRT) Automatic junctional tachycardia

AV Nodal Re-entry Tachycardia (AVNRT)

This is the commonest cause of palpitations in patients with structurally normal hearts. AVNRT is typically paroxysmal and may occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines). It is more common in women than men (~ 75% of cases occurring in women) and may occur in young and healthy patients as well as those suffering chronic heart disease. Patients will typically complain of the sudden onset of rapid, regular palpitations. The patient may experience a brief fall in blood pressure causing presyncope or occasionally syncope. If the patient has underlying coronary artery disease the patient may experience chest pain similar to angina (tight band around the chest radiating to left arm or left jaw). The patient may complain of shortness of breath, anxiety and occasionally polyuria due to elevated atrial pressure releasing atrial natriuretic peptide. The tachycardia typically ranges between 140-280 bpm and is regular in nature. It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought. The condition is generally well tolerated and is rarely life threatening in patients with pre-existing heart disease.

Pathophysiology

In comparison to AVRT, which involves an anatomical re-entry circuit (Bundle of Kent), in AVNRT there is a functional re-entry circuit within the AV node.

Different types of re-entry loops: Functional circuit in AVNRT (left), anatomical circuit in AVRT (right) Functional pathways within the AV node

In AVNRT, there are two pathways within the AV node:

The slow pathway (alpha): a slowly-conducting pathway with a short refractory period. The fast pathway (beta): a rapidly-conducting pathway with a long refractory period.

Mechanism of re-entry in "slow-fast" AVNRT (ERP = effective refractory period) Initiation of re-entry

During sinus rhythm, electrical impulses travel down both pathways simultaneously. The impulse transmitted down the fast pathway enters the distal end of the slow pathway and the two impulses cancel each other out. However, if a premature atrial contraction (PAC) arrives while the fast pathway is still refractory, the electrical impulse will be directed solely down the slow pathway (1). By the time the premature impulse reaches the end of the slow pathway, the fast pathway is no longer refractory (2) hence the impulse is permitted to recycle retrogradely up the fast pathway. This creates a circus movement whereby the impulse continually cycles around the two pathways, activating the Bundle of His anterogradely and the atria retrogradely (3). The short cycle length is responsible for the rapid heart rate. This is the most common type of re-entrant circuit and is termed Slow-Fast AVNRT. Similar mechanisms exist for the other types of AVNRT.

Electrocardiographic Features General Features of AVNRT

Regular tachycardia ~140-280 bpm. QRS complexes usually narrow (< 120 ms) unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction. ST-segment depression may be seen with or without underlying coronary artery disease. QRS alternans phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished from electrical alternans by a normal QRS amplitude. P waves if visible exhibit retrograde conduction with P-wave inversion in leads II, III, aVF. P waves may be buried in the QRS complex, visible after the QRS complex, or very rarely visible before the QRS complex.

Subtypes of AVNRT Different subtypes vary in terms of the dominant pathway and the R-P interval. The RP interval represents the time between anterograde ventricular activation (R wave) and retrograde atrial activation (P wave). 1. Slow-Fast AVNRT (common type)

Accounts for 80-90% of AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction. The retrograde P wave is obscured in the corresponding QRS or occurs at the end of the QRS complex as pseudo r or S waves

ECG features:

P waves are often hidden being embedded in the QRS complexes. Pseudo R wave may be seen in V1 or V2. Pseudo S waves may be seen in leads II, III or aVF. In most cases this results in a typical SVT appearance with absent P waves and tachycardia

Cardiac rhythm strips demonstrating (top) sinus rhythm and (bottom) paroxysmal SVT. The P wave is seen as a pseudo-R wave (circled in bottom strip) in lead V1 during tachycardia. By contrast, the pseudo-R wave is not seen during sinus rhythm (it is absent from circled area in top strip). This very short ventriculo-atrial time is frequently seen in typical Slow-Fast AVNRT. 2. Fast-Slow AVNRT (Uncommon AVNRT)

Accounts for 10% of AVNRT Associated with Fast AV nodal pathway for anterograde conduction and Slow AV nodal pathway for retrograde conduction. Due to the relatively long ventriculo-atrial interval, the retrograde P wave is more likely to be visible after the corresponding QRS.

ECG features:

QRS-P-T complexes. Retrograde P waves are visible between the QRS and T wave.

3. Slow-Slow AVNRT (Atypical AVNRT)

1-5% AVNRT Associated with Slow AV nodal pathway for anterograde conduction and Slow left atrial fibres as the pathway for retrograde conduction.

ECG features:

Tachycardia with a P-wave seen in mid-diastole effectively appearing before the QRS complex. Confusing as a P wave appearing before the QRS complex in the face of a tachycardia might be read as a sinus tachycardia.

Summary of AVNRT subtypes

No visible P waves? > Slow-Fast P waves visible after the QRS complexes? > Fast-Slow P waves visible before the QRS complexes? > Slow-Slow

Management of AVNRT

May respond to vagal maneuvers with reversion to sinus rhythm. The mainstay of treatment is adenosine. Other agents which may be used include calcium-channel blockers, beta-blockers and amiodarone. DC cardioversion is rarely required. Catheter ablation may be considered in recurrent episodes not amenable to medical treatment.

Other types of SVT Most of the other types of SVT are discussed elsewhere (follow links in table above). Two lesscommon types are discussed below. Inappropriate Sinus Tachycardia

Typically seen in young healthy female adults. Sinus rate persistently elevated above 100 bpm in absence of physiological stressor. Exaggerated rate response to minimal exercise. ECG indistinguishable from sinus tachycardia.

Sinus Node Reentrant Tachycardia (SNRT)

Caused by reentry circuit close to or within the sinus node. Abrupt onset and termination. P wave morphology is normal. Rate usually 100 150 bpm.

May terminate with vagal manoeuvres.

ECG Examples Example 1a

Slow-Fast (Typical) AVNRT:

Narrow complex tachycardia at ~ 150 bpm. No visible P waves. There are pseudo R waves in V1-2.

Pseudo R' waves in V1-2 Example 1b

The same patient following resolution of the AVNRT:

Sinus rhythm. The pseudo R waves have now disappeared.

Pseudo R' waves in V1-2 have resolved Example 2a

Slow-Fast AVNRT:

Narrow complex tachycardia ~ 220 bpm. No visible P waves. Subtle notching of the terminal QRS in V1 (= pseudo R wave). Widespread ST depression this is a common electrocardiographic finding in AVNRT and does not necessarily indicate myocardial ischaemia, provided the changes resolve once the patient is in sinus rhythm.

Example 2b

The same patient following resolution of the AVNRT:

Sinus rhythm. Pseudo R waves have disappeared. There is residual ST depression in the inferior and lateral leads (most evident in V4-6), indicating that the patient did indeed have rate-related myocardial ischaemia ( NSTEMI).

Example 3

Patient with Slow-Fast AVNRT undergoing treatment with adenosine:

The top section of the rhythm strip shows AVNRT with absent P waves and pseudo R waves clearly visible. The middle portion of the strip shows adenosine acting on the AV node to suppress AV conduction there are several broad complex beats which may be aberrantly-conducted supraventricular impulses or ventricular escape beats (this is extremely common during administration of adenosine for AVNRT). The bottom section shows reversion to sinus rhythm; the pseudo R waves have resolved.

Example 4a

Fast-Slow (Uncommon) AVNRT:

Narrow complex tachycardia ~ 120 bpm. Retrograde P waves are visible after each QRS complex most evident in V2-3.

Retrograde P waves Example 4b

The same patient following resolution of the AVNRT:

Now in sinus rhythm. The retrograde P waves have disappeared.

Retrograde P waves resolved Example 5a

Fast-Slow AVNRT:

Narrow complex tachycardia ~ 135 bpm. Retrograde P waves following each QRS complex upright in aVR and V1; inverted in II, III and aVL.

Upright retrograde P waves in aVR

Inverted retrograde P waves lead II Example 5b

The same patient following resolution of the AVNRT:

Sinus rhythm. The retrograde P waves have disappeared.

Retrograde P waves in aVR resolved

Retrograde P waves in lead II resolved Example 6a

Fast-Slow AVNRT:

Narrow complex tachycardia at ~ 125 bpm. Retrograde P waves follow each QRS complex: upright in V1-3; inverted in II, III and aVF.

Upright retrograde P waves in V2

Inverted retrograde P waves in lead II Example 6b

The same patient following resolution of the AVNRT:

Sinus rhythm. Retrograde P waves have disappeared.

Retrograde P waves in V2 have resolved

Retrograde P waves in lead II have resolved Example 7

SVT with QRS Alternans:

Narrow complex tachycardia ~ 215 bpm. Retrograde P waves are visible preceding each QRS complex (upright in V1, inverted in lead II). There is a beat-to-beat variation in the QRS amplitude without evidence of low voltage (= QRS alternans). The PR interval is ~ 120 ms, so this could be either a low atrial tachycardia or possibly an AVNRT with a long RP interval (i.e. either Fast-Slow or Slow-Slow varieties).