ECG rhythm recognition and conduction blocks

This page teaches what each rhythm and block looks like, how to tell it from its mimics, and which guideline row the finding triggers. ACC/AHA 2018 recommends a 12-lead ECG in suspected bradycardia or conduction disorder, to document rhythm, rate and conduction and to screen for structural heart disease or systemic illness (COR I, LOE B-NR).^[2] ESC 2022 calls the 12-lead ECG an important tool for diagnosing underlying disease, for risk stratification in selected populations, and for diagnosing the ventricular arrhythmia subtype, if captured.^[5]

• Pacing modes and devices: Bradycardia and pacing indications.
• Ablation and long-term drugs for SVT: Supraventricular tachycardia: AVNRT and AVRT.
• VT causes and ICDs: Ventricular tachycardia.
• AF management: Atrial fibrillation.

Reading a rhythm: rate, QRS width and regularity

Start with the rate. ANZCOR gives the normal heart rate as usually between 60 and 100 beats per minute.^[9] The heart may beat excessively fast or excessively slow, in a regular or an irregular pattern, and the irregular pattern is commonly atrial fibrillation.^[9]

Next, decide whether the patient is stable. Whilst assessing the patient, ANZCOR asks for a 12-lead ECG if one has not been done, without delaying treatment.^[9] In a tachyarrhythmia with no adverse features, ANZCOR then classifies the QRS complexes as narrow (normal duration) or broad (0.12 s or longer).^[9]

ESC 2019 sets the line slightly differently, in milliseconds: a narrow QRS tachycardia has a QRS duration of 120 ms or less, and a wide QRS tachycardia one above 120 ms.^[4] So a QRS of exactly 120 ms (0.12 s) is broad for ANZCOR but narrow for ESC 2019.^[9][4] Outside tachycardia, the 2009 AHA/ACCF/HRS statement recommends that, for the present, a QRS duration above 110 ms be regarded as abnormal in people older than 16 years.^[3]

Differential diagnosis of narrow and wide QRS tachycardias (ESC 2019 Table 6)

^[4]

One footnote is worth remembering: ESC 2019 notes that AF with a very fast ventricular response may occasionally appear to resemble a regular narrow QRS tachycardia.^[4] ESC 2019 adds that when AF has rapid ventricular rates, the irregularity is less easily detected and can be misdiagnosed as a regular SVT.^[4]

^{[9] [4]}

Who has these rhythms

• ESC 2019: in the general population, SVT prevalence is 2.25/1000 persons and incidence 35/100 000 person-years; women have twice the risk of men, and people aged 65 years or more have more than five times the risk of younger people.^[4]
• ESC 2019: women are more likely than men to have AVNRT (ratio about 70:30), while the converse is true for AVRT (45:55).^[4]
• ESC 2019: the proportion of patients with AVRT decreases with age, whereas the proportion with AVNRT and AT increases with age.^[4]
• ESC 2019: a WPW pattern on the surface ECG is present in 0.15–0.25% of the general population, rising to 0.55% among first-degree relatives of affected patients; not all develop SVT, and intermittent pre-excitation is not rare.^[4]
• ESC 2024: atrial flutter has an overall incidence of 88 per 100 000 person-years, rising to 317 per 100 000 person-years in people over 50 years; more than half of patients with flutter will develop AF.^[6]
• ESC 2019: of wide QRS tachycardias, reported proportions are 80% VT, 15% SVT conducting with BBB aberration and 5% antegrade conduction over an accessory pathway.^[4]
• ANZCOR: most (about 80%) cardiac arrests are related to fast rhythms arising in the ventricles (ventricular tachycardia and fibrillation).^[9]

Sinus node dysfunction

The ECG findings in sinus node dysfunction are varied.^[2] ESC 2021 says SND, also known as sick sinus syndrome, ranges from sinus bradycardia, sinoatrial block and sinus arrest to bradycardia–tachycardia syndrome.^[1] It adds chronotropic incompetence, an inadequate chronotropic response to exercise, as a further manifestation.^[1]

• ACC/AHA 2018: the diagnosis of SND may be considered with sinus bradycardia, atrial depolarisation from a subsidiary pacemaker other than the sinus node (ectopic atrial rhythm, junctional rhythm or ventricular escape), intermittent sinus pauses, or a blunted heart rate response with exercise.^[2]
• ACC/AHA 2018 chose a sinus rate below 50 bpm and/or a sinus pause above 3 seconds as potential components of the definitions of SND, but says sinus bradycardia or a pause above 3 seconds alone should not be used to diagnose SND.^[2]
• ACC/AHA 2018: the degenerative fibrosis behind SND also produces atrial arrhythmias, which can coexist with sinus node disease; the combination is often called tachy-brady syndrome.^[2]
• Chronotropic incompetence (ESC 2021): an inability to increase the heart rate commensurate with the increased metabolic demands of physical activity; exercise testing can be used to diagnose symptomatic chronotropic incompetence.^[1]
• ACC/AHA 2018: the most commonly used definition in the literature has been failure to reach 80% of the expected heart rate reserve, the difference between the age-predicted maximal heart rate (220 – age) and the resting heart rate.^[2]

A slow sinus rate can be normal.^[1] ESC 2021 says sinus bradycardia of 40–50 b.p.m. at rest, or as slow as 30 b.p.m. while sleeping, particularly in trained athletes, could be accepted as a physiological finding that does not require cardiac pacing.^[1] ACC/AHA 2018 notes that the NIH defines bradycardia as a heart rate below 60 bpm in adults other than well-trained athletes, while population studies frequently use 50 bpm.^[2] With rare exceptions, the sole reason for considering any treatment for SND is the presence of symptoms (ACC/AHA 2018).^[2]

SND: what the ECG finding triggers (selected rows)

^{[1] [2]}

AV block: the degrees

Every definition of AV block asks what happens to each P wave.^[2] ACC/AHA 2018 adopted its definitions of AV block and conduction tissue disorders from the 2009 AHA/ACCF/HRS recommendations for the standardisation of ECG measurements.^[2]

Degrees of AV block

^{[2] [1] [2] [1]}

Three ways the ECG misleads

• Losing the 1:1 P:QRS relationship (ACC/AHA 2018): a 1:1 relationship between P waves and QRS complexes may be absent when the atrial and ventricular rates are similar (isorhythmic dissociation), or when the atrial rate is slower than the ventricular rate (sinus bradycardia with an accelerated junctional rhythm without consistent retrograde VA conduction).^[2]
• AF (ACC/AHA 2018): complete AV block may be imputed when the ventricular response is slow (below 50 bpm) and regular, although a junctional rhythm with AV conduction abnormalities may be associated with the same finding.^[2]
• Sleep (ACC/AHA 2018): vagally mediated AV block during sleep can be recognised by concomitant sinus node slowing (P-P prolongation).^[2]

Where is the block? Nodal or infranodal

ACC/AHA 2018 describes the normal conduction axis as the sinus node, atrial muscle, AV node, His bundle, bundle branches, fascicles, Purkinje fibres and ventricular muscle.^[2] The His bundle divides into left and right bundle branches, and the left bundle divides into anterior and posterior fascicles.^[2]

For Mobitz I block, the level of block shapes the outlook.^[1] ESC 2021 says supranodal block has a benign course, with a low risk of progression to type II or a higher degree of AV block.^[1] It adds that small, retrospective studies have suggested a higher long-term risk of death in patients aged 45 years or more without a pacemaker.^[1] Infranodal block, rare in this form, carries a high risk of progression to complete heart block, syncope and sudden death, and warrants pacing even in the absence of symptoms.^[1]

• ACC/AHA 2018: the AV node is more likely the site of block with Mobitz I block and a narrow QRS, or with severe first-degree block (above 0.30 s) and a narrow QRS.^[2]
• ACC/AHA 2018: high-degree AV block is generally considered to be intra- or infra-Hisian and treated with pacing; in unusual circumstances (at night, with accompanying sinus slowing) a vagal aetiology may be considered, especially when the QRS is narrow.^[2]
• ACC/AHA 2018: 2:1 block with bundle branch block is frequently assumed to be infranodal, but 15% to 20% of these patients can have block in the AV node.^[2]
• ESC 2021: in asymptomatic patients with incidental 2:1 block, the decision to implant should be made case by case, including the distinction between nodal and infranodal block, which may be based on PR or PP prolongation before the block, the effect of exercise on AV conduction, and an EPS.^[1]
• ESC 2021, paroxysmal AV block: infranodal block documented at EPS, or initiation of the block by atrial or ventricular premature beats, by an increased heart rate (tachy-dependent) or by a decreased heart rate (brady-dependent), supports a diagnosis of intrinsic infranodal AV block.^[1]

Exercise may help locate the block.^[2] ACC/AHA 2018 says an exercise treadmill test may help differentiate whether 2:1 AV block is Mobitz type I or II, or identify infranodal disease.^[2] Exercise causes vagal withdrawal and increased sympathetic tone, which improves AV nodal conduction.^[2] If the baseline block is infranodal, it will not resolve and will likely worsen as the sinus rate increases.^[2]

ESC 2021 adds that tachycardia-related, exercise-induced second-degree and complete AV block has been shown to be located distal to the AV node and to predict progression to permanent AV block.^[1]

Exercise testing: exertional symptoms and the level of block

^{[1] [2] [2]}

AV block: symptoms and what the finding triggers

• ESC 2021: first-degree AV block is usually asymptomatic; syncope and dizziness are mainly observed in high-degree and complete block, especially in the paroxysmal forms.^[1]
• ACC/AHA 2018: profound first-degree block can cause fatigue or exertional intolerance when the PR interval is long enough to lose AV synchrony (often called pseudo pacemaker syndrome, which may occur with a PR interval above 300 ms).^[2]
• ESC 2021: there is weak evidence that marked PR prolongation (300 ms or more), particularly when it persists or is prolonged during exercise, can lead to symptoms similar to pacemaker syndrome and/or that these can improve with pacing.^[1]
• ESC 2021: in first-degree block the prognosis is usually good in the absence of structural heart disease, and progression to high-degree block is uncommon.^[1]
• ACC/AHA 2018: first-degree and Mobitz I block (or 2:1 block at the AV node) are typically benign in that they do not progress suddenly to complete heart block.^[2]
• ESC 2021: death in untreated AV block is due to heart failure from low cardiac output, and also to sudden cardiac death from prolonged asystole or bradycardia-triggered ventricular tachyarrhythmia.^[1]
• ESC 2021: the indications for pacing are the same for paroxysmal as for permanent AV block, after ruling out a reversible cause and recognising reflex forms, which may not need pacing.^[1]

AV block rows (selected; pacing mode choice is in the bradycardia topic)

^{[1] [2]}

Notice where the two documents agree and where they differ. Both put Mobitz II (second-degree type 2), high-grade and third-degree block in their top class regardless of symptoms: ESC 2021 in sinus rhythm (Class I, Level C), and ACC/AHA 2018 when acquired and not attributable to reversible or physiologic causes (COR I, LOE B-NR).^[1][2] For 2:1 block, ESC 2021 names infranodal 2:1 in its Class I row, while ACC/AHA 2018 says permanent pacing should not be performed for asymptomatic 2:1 block believed to be at the AV node (COR III: Harm, LOE C-LD).^[1][2]

Bundle branch and fascicular blocks: the criteria

ESC 2021 discusses bundle branch and fascicular blocks with 1:1 AV conduction separately from AV block.^[1] It describes them as QRS abnormalities caused by delayed or blocked conduction of the His–Purkinje system: BBB, fascicular block alone or with BBB, and non-specific intraventricular delay.^[1] ACC/AHA 2018 uses the 2009 AHA/ACCF/HRS definitions, although some have argued that stricter criteria are required for LBBB.^[2]

Bundle branch and fascicular block criteria in adults

^[3]

The 2009 statement defines R-wave peak time as the interval from QRS onset to the peak of the R wave, in leads without a small initial R wave, in preference to the term intrinsicoid deflection.^[3] In adults the normal QRS axis is considered to be within −30° and 90°.^[3] It describes marked left-axis deviation (−45° to −90°) as often associated with LAFB, and marked right-axis deviation (120° to 180°) as often associated with LPFB.^[3]

The 2009 statement says the incomplete RBBB pattern may be present without heart disease, particularly when V1 is recorded higher than or to the right of normal and r′ is less than 20 ms.^[3]

^[3]

Bifascicular, trifascicular and alternating block

• ESC 2021: bifascicular block is defined as LBBB, or RBBB combined with left anterior or posterior fascicular block.^[1]
• ACC/AHA 2018 gives the same combination: RBBB with one of the left bundle’s fascicles is denoted bifascicular block, which also includes LBBB.^[2]
• The 2009 statement does not recommend the terms atypical LBBB, bilateral bundle-branch block, bifascicular block and trifascicular block, because of the great variation in anatomy and pathology producing such patterns; it asks for each defect to be described by the structures involved.^[3]
• ESC 2021: alternating BBB is a rare condition with clear ECG evidence for block in all three fascicles on successive ECGs, such as LBBB and RBBB on successive ECGs, or RBBB with LAFB on one ECG and LPFB on another.^[1]
• ACC/AHA 2018: true alternating BBB is evidence for significant infranodal disease and a high likelihood of sudden complete heart block with a slow or absent ventricular escape rate.^[2]

What a bundle branch block means for the patient

Most isolated blocks cause no symptoms, but some carry information.^[2][1] ESC 2021 says isolated fascicular block and BBB are rarely associated with symptoms, but their presence may be a marker for underlying structural heart disease.^[1] ACC/AHA 2018 adds that cardiac dyssynchrony from LBBB may cause symptoms, particularly when left ventricular function is reduced.^[2]

• ACC/AHA 2018: cohort studies have generally shown an association between LBBB, but not RBBB, and the development of coronary disease and heart failure.^[2]
• ACC/AHA 2018: LBBB on the ECG markedly increases the likelihood that left ventricular systolic dysfunction will be diagnosed by echocardiogram.^[2]
• ACC/AHA 2018: most studies have reported higher mortality with LBBB than with other conduction disorders.^[2]
• ACC/AHA 2018: progression of LBBB and bifascicular block to AV block and bradycardia is low, approximately 1% per year.^[2]
• ESC 2021: only a minority of patients with BBB without symptoms will develop AV block (1–2% per year).^[1]
• ACC/AHA 2018: the threshold for stress testing is lower with LBBB and concern for ischaemia, but with LBBB ischaemic ECG changes are more difficult to interpret, and an imaging component is necessary.^[2]

Syncope with a bundle branch block changes the work-up.^[1][2] ESC 2021 says that in syncope with bifascicular block, an HV of 70 ms or more, or of 100 ms or more after pharmacological stress, or induced second- or third-degree block, identifies a group at higher risk of developing AV block.^[1] In unexplained syncope with bifascicular block, a negative EPS cannot rule out intermittent or paroxysmal AV block as the cause of syncope: ESC 2021 reports intermittent or stable AV block documented by implantable loop recorder in about 50% of patients with a negative EPS.^[1]

Bundle branch block and bradycardia work-up rows (selected)

^{[2] [1]}

Acute bradycardia: the ANZCOR approach

ANZCOR defines bradyarrhythmia conventionally as a heart rate below 60/min, while noting that such rates may be entirely physiological for some people or situations.^[9] Patients with a slow heart beat who do not experience symptoms usually do not require emergency therapy.^[9]

• ANZCOR: atropine is the initial treatment, 500–600 mcg intravenously, repeated as necessary every 3–5 min up to a total dose of 3 mg (Level of evidence III-2).^[9]

• ANZCOR: patients who fail to respond to drug therapy, or who are at high risk of asystole, may require electrical pacing, internal or external.^[9]

• ANZCOR: do not give atropine after cardiac transplant; the heart is denervated and will not respond to vagal blockade, and there is some risk of inducing paradoxical AV block.^[9]

• Temporary pacing and second-line drugs: Bradycardia and pacing indications.

Supraventricular tachycardia: classification and history

ESC 2019 notes that SVT has traditionally been used to describe all kinds of tachycardias apart from VT and AF, and so has included tachycardias such as AV re-entry due to accessory connections, which is not, in essence, a supraventricular rhythm.^[4] ESC 2019 Table 5 gives a conventional classification of supraventricular tachycardias; QRS width is the basis of Table 6, shown above.^[4]

^[4]

Clues in the history

• ESC 2019: a sudden onset more likely points to AVNRT or AVRT, although an AT may also present in this way.^[4]
• ESC 2019: clear descriptions of pounding in the neck (the so-called frog sign) or shirt flapping would point to the possible competing influences of atrial and ventricular contraction on the tricuspid valve, and to AVNRT as a likely cause.^[4]

Narrow QRS tachycardia: naming the rhythm

A narrow QRS means the ventricles are being activated quickly through the His–Purkinje system.^[4] ESC 2019 says this suggests the arrhythmia arises above or within the His bundle.^[4] High septal VT can also activate the His bundle early, giving relatively narrow QRS complexes of 110–140 ms.^[4]

Narrow QRS tachycardias: the ECG definitions

^[4]

Clues on the 12-lead ECG

• ESC 2019: an ECG recorded during tachycardia is ideal; patients should be encouraged to seek recording of their ECG during episodes.^[4]
• Sinus rhythm ECG (ESC 2019): pre-excitation with a history of regular paroxysmal palpitations is generally suggestive of AVRT, but its absence does not rule AVRT out (concealed or atypical pathways).^[4]
• Onset (ESC 2019): sudden PR prolongation after an atrial ectopic beat occurs in typical AVNRT; automatic focal AT shows warm-up acceleration and cool-down deceleration.^[4]
• Regularity (ESC 2019): re-entrant tachycardias are usually regular; irregular tachycardias may be focal or multifocal AT, focal AF or flutter with varying AV conduction, and multifocal AT typically shows variable P-wave morphologies with varying PP, RR and PR intervals.^[4]
• Cycle length (ESC 2019): RR alternans may be seen in AVNRT but is below 15% of the tachycardia cycle length; if irregularity exceeds 15%, a focal arrhythmia is much more likely.^[4]
• ESC 2019: a fixed VA interval in the presence of variable RR intervals excludes AT.^[4]
• RP interval (ESC 2019): short-RP SVTs have an RP shorter than half the tachycardia RR interval, and long-RP SVTs display RP equal to or longer than PR.^[4]
• ESC 2019: on EPS a VA interval of 70 ms or less usually indicates typical AVNRT, less commonly focal AT, and has also been reported in AVRT; on the surface ECG a 90 ms cut-off has been shown to be useful if P waves are visible, but data are scarce.^[4]
• P-wave shape (ESC 2019): P waves like sinus rhythm suggest sinus tachycardia, sinus nodal re-entry or focal AT near the sinus node; different P waves with a PR equal to or longer than in sinus rhythm are typically seen in focal AT.^[4]
• Rate about 150 b.p.m. (ESC 2019): consider atrial flutter with 2:1 conduction, as the atrial activity is usually 250–330 b.p.m.^[4]
• ESC 2019: when retrograde conduction is delayed enough for retrograde P waves to be identified, a pseudo r deflection in V1 and a pseudo S wave in the inferior leads are more common in typical AVNRT than in AVRT or AT; these criteria are specific (91–100%) but modestly sensitive (58% and 14%).^[4]
• ESC 2019: AV block or dissociation during narrow QRS tachycardia is not often seen, but it rules out AVRT, because both atria and ventricles are parts of the circuit.^[4]

What vagal manoeuvres and adenosine show

Possible responses of narrow QRS tachycardia to vagal manoeuvres and adenosine

^[4]

• ESC 2019: termination with a P wave after the last QRS is very unlikely in AT and most common in AVRT and typical AVNRT; termination with a QRS is often seen in AT, and possibly in atypical AVNRT.^[4]
• ESC 2019: adenosine does not interrupt macro-re-entrant ATs.^[4]
• ESC 2019: fascicular VTs are verapamil- but not adenosine-sensitive.^[4]

Narrow QRS tachycardia: acute rows

Acute management of narrow QRS tachycardia in the absence of an established diagnosis (ESC 2019)

^[4]

The table footnote matters: i.v. beta-blockers are contraindicated in decompensated heart failure, and i.v. verapamil and diltiazem are contraindicated with hypotension or HFrEF.^[4] ESC 2019 text sets adenosine dosing as incremental, starting at 6 mg in adults followed by 12 mg, with an 18 mg dose then considered according to tolerability.^[4]

• ANZCOR, regular narrow-complex tachycardia, unstable with adverse signs caused by the arrhythmia (other than sinus tachycardia): attempt synchronised electrical cardioversion with sedation as required; adenosine is reasonable while cardioversion is prepared, but do not delay cardioversion if it fails.^[9]
• ANZCOR, regular narrow-complex tachycardia without adverse features: start with vagal manoeuvres; if the arrhythmia persists and is not atrial flutter, give adenosine 6 mg as a rapid i.v. bolus with at least a 20 ml flush, then 12 mg (which may be repeated) if there is no response.^[9]
• ANZCOR: if the rate slows transiently but the arrhythmia persists, look for atrial flutter or another atrial tachycardia.^[9]
• ANZCOR: if adenosine is contraindicated or fails to terminate a regular narrow-complex tachycardia without showing flutter, give a calcium channel blocker (for example verapamil 2.5–5 mg i.v. over 2 min, or diltiazem 15–20 mg over 2 min).^[9]

Wide QRS tachycardia: VT until proven otherwise

Most wide QRS tachycardias are VT.^[4] ESC 2019 reports proportions of 80% VT, 15% SVT with BBB aberration and 5% conduction over an accessory pathway.^[4] Misdiagnosis, with drugs usually used for SVT, can harm patients in VT, so ESC 2019 makes VT the default diagnosis until proven otherwise.^[4]

ANZCOR reaches the same place by a different route.^[9] In the peri-arrest setting it says to assume broad-complex tachycardias are ventricular in origin, and notes that treating SVT as VT is less likely to cause deterioration than treating VT as SVT.^[9]

• ESC 2019 differential 1: SVT with BBB, which may arise from pre-existing BBB or from aberrancy during tachycardia (phase 3 block), more commonly, although not invariably, an RBBB pattern.^[4]
• ESC 2019 differential 2: pre-excited SVT, with antegrade conduction over a pathway that is part of the circuit (antidromic AVRT) or a bystander during AF, focal AT/flutter or AVNRT.^[4]
• ESC 2019 differential 3: QRS widening from drugs or electrolyte disturbance; class IA, IC and III drugs can produce atypical BBB morphologies during SVT that mimic VT.^[4]
• ESC 2019 differential 4: pacemaker-related endless loop tachycardia and artefacts, which can also mimic VT.^[4]
• ESC 2019: typical flutter may also frequently occur during class IC drug or amiodarone treatment for AF, when the flutter rate may fall below 200 b.p.m. and allow 1:1 AV conduction, sometimes as a wide QRS tachycardia.^[4]

Definitions of ventricular arrhythmias (ESC 2022)

ESC 2022 definitions

^[5]

ECG features that favour VT

If a sinus rhythm ECG is available, compare it: ESC 2019 says it can provide useful diagnostic information.^[4] ESC 2019 says that if the QRS morphology is identical in sinus rhythm and tachycardia, the arrhythmia is most likely not VT, although bundle branch re-entrant and high septal VTs can look similar.^[4] A contralateral BBB pattern in sinus rhythm is more indicative of VT.^[4]

Key ECG criteria that suggest VT rather than SVT in wide complex tachycardia (ESC 2019 Table 9)

^{[4] [4]}

• ESC 2019: AV dissociation or capture/fusion beats on the 12-lead ECG are key diagnostic features of VT; P waves are often hidden, and are usually more prominent in the inferior leads and Lewis lead.^[4]
• ESC 2019: most SVTs have a 1:1 or greater atrial to ventricular relationship; VA conduction can be found in up to 50% of VT, but most VTs have more QRS complexes than P waves.^[4]
• ESC 2019: a QRS above 140 ms with RBBB or above 160 ms with LBBB pattern suggests VT; these criteria are not helpful in settings such as pre-excited SVT or when class IC or IA drugs are given.^[4]
• ESC 2019: in SVT with aberrancy the axis is confined between −60° and +120°; extreme axis deviation (−90° to ±180°) is strongly indicative of VT.^[4]
• ESC 2019: negative chest lead concordance is almost diagnostic of VT (specificity above 90%) but is present in only 20% of VTs; positive concordance can mean VT or antidromic tachycardia over a left posterior or left lateral pathway.^[4]
• ESC 2019: typical RBBB aberrancy has a small initial r′ (rSR′, rSr′ or rR′ in V1), because in RBBB the high septum is activated primarily from the left septal bundle.^[4]
• ESC 2019: in true LBBB there is no Q wave in the lateral precordial leads, so any Q or QS wave in V6 favours VT.^[4]

No criterion is perfect.^[4] ESC 2019 notes that the morphology criteria are not fulfilled in any lead in 4% of SVTs and 6% of VTs, and in one-third of cases V1 and V6 point to opposite diagnoses.^[4] Several independent studies found that various ECG-based methods have specificities of 40–80% and accuracies of about 75%; a similar accuracy would be achieved by calling every wide QRS tachycardia VT, because only 25–30% are SVTs.^[4]

Wide QRS tachycardia: acute rows

Two ESC documents cover this ground; the newer one frames its rows around the acute management of sustained VT, most of them specifying sustained monomorphic VT (SMVT).^[4][5] ESC 2022 says documenting any haemodynamically tolerated wide QRS tachycardia on a 12-lead ECG is important.^[5]

ESC 2019 against ESC 2022 for wide QRS tachycardia (a dash means no matching row in that table)

^{[4] [5]}

In the newer ESC 2022 table, vagal manoeuvres appear only in a Class IIa row, where adenosine or vagal manoeuvres should be considered for a regular, tolerated wide QRS tachycardia suspected for SVT.^[5] In haemodynamically stable patients with wide QRS tachycardia and no established diagnosis, ESC 2019 recommends vagal manoeuvres, preferably supine with leg elevation (Class I).^[4] The ESC 2022 procainamide row is limited to tolerated SMVT with known or suspected structural heart disease.^[5]

• ESC 2019: drugs such as verapamil can cause severe haemodynamic deterioration in a previously stable VT, so they should only be used when the diagnosis of SVT is fully established and secure.^[4]
• ESC 2019: adenosine may help diagnose or interrupt an adenosine-sensitive VT, but must be avoided if pre-excitation on the resting ECG suggests a pre-excited tachycardia.^[4]
• ESC 2019: if the mechanism is not fully understood, the arrhythmia should be treated as VT.^[4]
• ANZCOR: verapamil and diltiazem should not be used to terminate wide-QRS tachycardia of unknown origin, especially with a history of myocardial dysfunction (ANZCOR Class B, Level of Evidence IV).^[9]

^{[4] [5] [9]}

Irregular tachycardias: AF, flutter and pre-excited AF

ESC 2024 describes AF on the surface ECG as the absence of discernible and regular P waves, with irregular activation of the ventricles.^[6] This results in no specific pattern to RR intervals, in the absence of AV block.^[6] ANZCOR calls the hallmark of AF an irregularly irregular heart rhythm.^[9]

• ESC 2024: a standard 12-lead ECG measures 10 s, while 30 s or more on single- or multiple-lead ECG devices has generally been the consensus for monitoring devices, albeit with limited evidence.^[6]
• ESC 2024: ECG confirmation does not include non-ECG wearables and other devices that typically use photoplethysmography.^[6]
• ANZCOR: irregular narrow-complex tachycardia is most commonly AF or sometimes atrial flutter with variable AV conduction (variable block).^[9]
• ANZCOR: atrial flutter is a related but distinct arrhythmia caused by re-entry within the atria, and may be managed similarly to AF in the emergency setting.^[9]
• ESC 2019: the differential of an irregular wide QRS tachycardia is pre-excited AF, polymorphic VT, or AT with variable block and aberrancy.^[4]
• ANZCOR: an irregular broad complex tachycardia is most likely AF with bundle branch block; other causes are AF with ventricular pre-excitation (WPW) and polymorphic VT (e.g. torsades de pointes).^[9]

Pre-excited AF on the ECG

ESC 2019 describes pre-excited AF as irregular, with a varying QRS morphology and a rapid ventricular rate owing to the short refractory period of the pathway.^[4] The changing QRS reflects varying fusion between conduction over the pathway and the AV node, with variable delta wave width.^[4] ESC 2022 calls this the FBI pattern (fast, broad, irregular), which may mimic VT.^[5]

Pre-excitation and WPW

^{[4] [3]}

• ESC 2019: pre-excitation on the surface ECG can be intermittent and can even disappear permanently (in up to 35% of cases) over time.^[4]
• ESC 2019, antidromic AVRT: a wide, fully pre-excited QRS, with an RP that is difficult to assess because the retrograde P wave is usually within the ST-T segment.^[4]
• ESC 2019: paroxysmal AF has been found in 50% of patients with WPW; AF with a fast ventricular response over a pathway with a short anterograde refractory period is potentially life-threatening, because of potential degeneration into VF.^[4]
• ESC 2024: patients with WPW and AF are at risk of fast ventricular rates from rapid conduction over the accessory pathway, potentially leading to VF and sudden death.^[6]

Pre-excited AF: acute rows (ACC/AHA 2023 Section 10.6 also recommends catheter ablation of accessory pathways in pre-excited AF, COR 1, LOE B-NR)

^{[7] [4]}

ESC 2019 places a further row in its AVRT table under chronic therapy: digoxin, beta-blockers, diltiazem, verapamil and amiodarone are not recommended and are potentially harmful in patients with pre-excited AF (Class III, Level B).^[4]

The newer US guideline recommends pharmacological cardioversion with i.v. ibutilide or procainamide in haemodynamically stable pre-excited AF, as an alternative to elective cardioversion (ACC/AHA 2023, COR 1, LOE C-LD).^[7] For haemodynamically stable patients with pre-excited AF, ESC 2019 says ibutilide or procainamide (i.v.) should be considered (Class IIa, Level B).^[4] ESC 2024 AF text says immediate electrical cardioversion is needed for haemodynamically compromised pre-excited AF and that AV node-modulating drugs should be avoided.^[6] It adds that pharmacological cardioversion can be attempted with ibutilide or flecainide, that propafenone should be used with caution, and that amiodarone should be avoided because of its delayed action.^[6]

ANZCOR says to avoid adenosine, digoxin, verapamil and diltiazem if pre-excited AF or flutter is suspected, because they block the AV node and cause a relative increase in pre-excitation.^[9] ANZCOR adds that electrical cardioversion is usually the safest option.^[9]

The ESC 2019 pre-excited AF table footnote says i.v. ibutilide is contraindicated with a prolonged QTc, and i.v. flecainide and propafenone with ischaemic or structural heart disease.^[4] Risk stratification and ablation of pathways are taught in Supraventricular tachycardia: AVNRT and AVRT.

Complications and pitfalls

• Treatment can make the rhythm worse: ANZCOR says all anti-arrhythmic treatments (physical manoeuvres, drugs, cardioversion, pacing) have the potential to cause clinical deterioration.^[9]
• Calling VT an SVT: drugs usually used for SVT can be harmful in VT (ESC 2019), and ANZCOR says verapamil and diltiazem should not be used to terminate wide-QRS tachycardia of unknown origin, especially with a history of myocardial dysfunction (ANZCOR Class B).^[4][9]
• Adenosine with pre-excitation: ESC 2019 says it must be avoided if the resting ECG suggests a pre-excited tachycardia.^[4]
• A regular-looking AF: occasionally, very fast AF may appear to resemble a regular narrow QRS tachycardia (ESC 2019).^[4]
• Missing 2:1 flutter: consider it when the ventricular rate is about 150 b.p.m. (ESC 2019).^[4]
• Pacing a physiological bradycardia: ACC/AHA 2018 says permanent pacing should not be performed in asymptomatic individuals with sinus bradycardia or sinus pauses secondary to physiologically elevated parasympathetic tone (COR III: Harm, LOE C-LD).^[2]
• Reading ischaemia through LBBB: ischaemic ECG changes are more difficult to interpret, and stress testing needs an imaging component (ACC/AHA 2018).^[2]
• Labelling incomplete RBBB from a high V1: the pattern may be present without heart disease, particularly when V1 is recorded higher than or to the right of normal and r′ is less than 20 ms (2009 statement).^[3]
• Misreading AV block: ACC/AHA 2018 says careful ECG evaluation is required to diagnose AV block; a 1:1 P:QRS relationship may be absent with isorhythmic dissociation or when the atrial rate is slower than the ventricular rate.^[2]

Prognosis

• First-degree block: usually a good prognosis in the absence of structural heart disease (ESC 2021).^[1]
• Mobitz I: ESC 2021 says small retrospective studies have suggested a higher long-term risk of death in patients aged 45 years or more without a pacemaker.^[1]
• Untreated AV block: death from heart failure due to low cardiac output, and sudden death from asystole or bradycardia-triggered ventricular tachyarrhythmia (ESC 2021).^[1]
• LBBB: higher mortality than other conduction disorders in most studies (ACC/AHA 2018).^[2]
• Alternating BBB: ESC 2021 says there is general consensus that patients will progress rapidly toward AV block.^[1]
• Pre-excited AF: potential degeneration into VF (ESC 2019).^[4]

Special populations

Athletes and sleep

• ESC 2021: asymptomatic bradycardia from sinus pauses or AV block episodes is not uncommon; in healthy subjects pauses above 2.5 s are uncommon but do not necessarily constitute a disorder, and asymptomatic bradyarrhythmias are common in athletes.^[1]
• ESC 2021: sinus bradycardia of 40–50 b.p.m. at rest or 30 b.p.m. asleep, particularly in trained athletes, could be accepted as physiological.^[1]
• ACC/AHA 2018: vagally mediated AV block during sleep can be recognised by concomitant sinus node slowing (P-P prolongation).^[2]

Children

• 2009 statement: a QRS duration of 90 ms or more is prolonged under 4 years of age, and 100 ms or more is prolonged at 4 to 16 years.^[3]
• 2009 statement: the complete RBBB and LBBB QRS thresholds are above 100 ms at 4 to 16 years and above 90 ms under 4 years.^[3]
• 2009 statement: the LPFB axis criterion should be applied to children up to 16 years only when a distinct rightward change in axis is documented.^[3]
• 2009 statement: in children, an rsr′ pattern in V1 and V2 with a normal QRS duration is a normal variant.^[3]

Older people

• ESC 2019: people aged 65 years or more have more than five times the risk of developing SVT than younger people.^[4]
• ESC 2019: in older patients SVT symptoms may be more extreme, with dizziness, presyncope and syncope, and blood pressure drops are usually immediate and tend to recover.^[4]

Pregnancy

Pregnancy rows (ESC 2025)

^[8]

ESC 2025 says Mobitz type I AV block is common in pregnant women and rarely progresses during pregnancy.^[8] In acute, life-threatening settings bradycardia should be treated as in non-pregnancy, and pacing indications do not differ between pregnant and non-pregnant women.^[8]

Heart transplant

• ANZCOR: do not give atropine to patients with a cardiac transplant; the denervated heart will not respond to vagal blockade, and there is some risk of paradoxical AV block.^[9]
• ESC 2019: perceived bradycardia risk in denervated heart transplant recipients, in whom SVT is common, prompted a relative contraindication to adenosine, but more recent evidence supports its use with no particular cautions.^[4]

Evidence, guidelines and regional differences

Where the documents differ (selected rows)

^{[1] [2] [9] [4] [5] [7]}

No NHFA/CSANZ guideline on arrhythmia or conduction disease newer than the ESC and ACC/AHA documents was found when this topic was built, so the ANZ voice here is ANZCOR Guideline 11.9. ANZCOR grades its own recommendations by class (Class A, B or C) with levels of evidence, a scheme different from ESC classes and ACC/AHA COR.^[9]

Where the evidence is thin

• ESC 2019: the 90 ms surface RP cut-off is a rather arbitrary number based on limited data, and data on RP measurements during various SVTs are scarce.^[4]
• ESC 2019: ECG-based methods for wide QRS tachycardia have specificities of 40–80% and accuracies of about 75%.^[4]
• ESC 2021: the evidence is weak that marked PR prolongation (300 ms or more), particularly when it persists or is prolonged during exercise, can lead to symptoms similar to pacemaker syndrome and/or that these can improve with pacing.^[1]
• ESC 2024: the time period of AF needed for diagnosis on monitoring devices is not clear cut, and the 30 s consensus has limited evidence.^[6]
• ACC/AHA 2018: some have argued that stricter criteria are required for LBBB than the 2009 definitions it adopts.^[2]

Exam pearls

• First-degree AV block is a misnomer: each P wave is conducted, so ACC/AHA 2018 prefers first-degree AV delay.^[2]
• High-grade block: two or more consecutive non-conducted P waves at a normal rate, without complete loss of AV conduction (ACC/AHA 2018), or a P:QRS ratio of 3:1 or higher (ESC 2021).^[2][1]
• Fascicular block criteria include: LAFB, axis −45° to −90°, qR in aVL, R peak time in aVL of 45 ms or more and QRS below 120 ms, none of which apply in congenital heart disease with left-axis deviation present in infancy; LPFB, axis 90° to 180° in adults, rS in I and aVL, qR in III and aVF and QRS below 120 ms (2009 statement).^[3]
• The 2009 statement does not recommend the term bifascicular block, but ESC 2021 and ACC/AHA 2018 both define it (LBBB, or RBBB with a left fascicular block).^[3][1][2]
• Alternating BBB: pacing indicated with or without symptoms (ESC 2021, Class I, Level C).^[1]
• Wide QRS tachycardia: VT is the default diagnosis until proven otherwise (ESC 2019); about 80% are VT.^[4]
• Negative concordance: specificity above 90% for VT but present in only 20% of VTs (ESC 2019).^[4]
• R wave peak time in lead II of 50 ms or more favours VT (ESC 2019 Table 9).^[4]
• Fascicular VT is verapamil-sensitive but not adenosine-sensitive (ESC 2019).^[4]
• Pre-excited AF looks fast, broad and irregular, and may mimic VT (ESC 2022).^[5]

References9ShowHide

1. [1]Glikson M, et al. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Eur Heart J, 2021.PMID 34455430
2. [2]Kusumoto FM, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol, 2019.PMID 30412709
3. [3]Surawicz B, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part III: intraventricular conduction disturbances: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol, 2009.PMID 19281930
4. [4]Brugada J, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J, 2020.PMID 31504425
5. [5]Zeppenfeld K, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J, 2022.PMID 36017572
6. [6]Van Gelder IC, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J, 2024.PMID 39210723
7. [7]Joglar JA, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 2024.PMID 38033089
8. [8]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
9. [9]Australian and New Zealand Committee on Resuscitation Guideline 11.9 – Managing Acute Dysrhythmias ANZCOR, 2026.Source