NavEP · The diagnostic EP study
EP study workflow The basic study, step by step, and why each step is done.
Read this as a mentor talking you through your first studies. Every step has the same parts: the question it answers and why we do it, then tabs for what you do, where to look, what it looks like on a tracing, what is normal and what is not, a worked case, what to do when it goes wrong, the common traps, and a check before you move on. Tabs marked Further go beyond what you need for your first studies. Pick a step from the picture below, or switch to the whole page to read or print everything. Every statement is paraphrased from a cited source; the number after each point (e.g. BASHIR) opens its source. Labs differ, and your own lab’s protocol and the current guidelines take precedence.
Step 1
Before the lab: know the question
The question this step answersWhy is this patient here, and what result would change their management?
By the end of this step you can state the clinical question, read the ECG clues, and prepare and consent the patient.
Why we do it
An EP study records the heart’s electrical activity from catheters at fixed sites and paces from them. Each study should be shaped to answer the specific question for that patient, but it should still be done in the same systematic order every time. BASHIR A checklist approach is what protects against misdiagnosis and an inappropriate ablation. BASHIR
The usual reasons for a study
- Narrow-complex tachycardia: find the mechanism, usually as the first half of an ablation. This is the commonest reason. BASHIR
- Broad-complex tachycardia: tell SVT from VT and from pre-excited tachycardia, so the right treatment can be chosen. BASHIR
- Risk stratification for sudden death, for example after myocardial infarction, in Brugada syndrome or in WPW syndrome. BASHIR
- Bradycardia or unexplained syncope (less often now). Ambulatory monitoring has reduced the need; the study is mainly an adjunct when syncope with suspected bradycardia stays unexplained after non-invasive tests. ESCP
- Ventricular arrhythmia: programmed stimulation is now used mainly to confirm VT and to induce mappable VT for ablation. Patients with heart failure and LVEF ≤35% usually have an ICD indication anyway, so induction before implantation is not needed. ESCVA
Bring the ECGs: the study starts before you scrub
Review every ECG you can find beforehand. It often tells you what to look for in the lab. BASHIR
- The 12-lead ECG in sinus rhythm: is there pre-excitation (a delta wave)? It points towards AVRT, but no delta wave does not rule out a pathway. BASHIR
- The 12-lead ECG during tachycardia: where are the P waves, and how do they relate to the QRS? BASHIR
- Rhythm strips showing how episodes start and stop, and the response to vagal manoeuvres or adenosine. BASHIR
- The SVT page explains what each of these clues means.
Consent: the risks to explain
The handbook groups complications into four categories M:
| Category | Examples and approximate rates given |
|---|---|
| Vascular | Marked bruising or palpable haematoma in about 1–5%. Serious problems (venous thrombosis, arterial occlusion, fistula, false aneurysm) in under 1%. |
| Major but treatable | Pneumothorax or tamponade: should not occur in much more than 1%. |
| EP-specific | AV block needing a pacemaker: about 1% with slow-pathway ablation and 2–3% with septal accessory-pathway ablation. AF complicates up to 10% of SVT studies. Sustained VT/VF is common during programmed ventricular stimulation. |
| Life-threatening | Death, MI or stroke: up to 0.5% overall, highest with structural heart disease, multiple targets and older age. Radiation risk should also be mentioned. |
Discuss the AV-block risk before the study, so the operator already knows whether the patient would accept ablation near the AV node once the diagnosis is made. M
Preparation
- If you need the arrhythmia to be inducible, stop antiarrhythmic drugs about 4–5 half-lives beforehand. Amiodarone either has to stop 6 weeks or more ahead or is simply continued. Warn the patient that stopping a drug may bring on their arrhythmia. BASHIR M
- Fast the patient for at least 6 hours. BASHIR
- Most studies can be done under conscious sedation; general anaesthesia may make the arrhythmia harder to induce. BASHIR
- Peripheral IV access, blood pressure, oxygen saturation and defibrillator pads. The 12-lead ECG runs continuously through the recording system, with radiolucent electrodes so they don’t block the fluoroscopy. BASHIR
Worked case: Ms C.D.
- A 34-year-old woman with recurrent sustained palpitations. A 12-lead ECG shows a regular narrow-complex tachycardia at 168 bpm, ended by adenosine in the emergency department. She is still symptomatic on verapamil.
- Her sinus-rhythm ECG: PR 148 ms, narrow QRS, no delta wave.
- Reading the clues: adenosine ending the tachycardia points to a circuit that uses the AV node, so AVNRT or AVRT. BASHIR No delta wave does not rule out a concealed pathway. BASHIR
- The question: what is the mechanism, and can it be cured by ablation today?
- Before the lab: verapamil stopped beforehand; consent includes the roughly 1% risk of AV block needing a pacemaker with slow-pathway ablation. M
When it goes wrong
- The antiarrhythmic can’t be stopped
- Amiodarone needs 6 weeks or more off, otherwise it is simply continued; decide case by case when symptoms are severe off drugs. Warn the patient that stopping a drug may bring on the arrhythmia. BASHIR M
- A woman who could be pregnant
- The possibility of pregnancy must be checked specifically before a procedure using X-rays. BASHIR
Common traps
- An antiarrhythmic not stopped (or deep sedation) can leave the tachycardia non-inducible, and the whole study answers nothing. BASHIR
Before you move on, you should be able to say
- The clinical question, in one sentence.
- What the ECGs suggest the mechanism might be.
- That antiarrhythmics are stopped, and consent covers AV block.
Step 2
Set up: access and the four catheters
The question this step answersIs each catheter where I think it is, and does it show the signals I expect?
By the end of this step you can place the four catheters, confirm each one by its signals, and spot a misplaced CS or His catheter.
Why we do it
Each catheter is a listening post at a known landmark. Because you know where it sits, the order in which the posts “hear” activation tells you where the impulse started and how it travelled. The standard study uses four of them. BASHIR BASHIR
What you do
- Femoral venous access by the Seldinger technique, usually two or three catheters per vein. BASHIR Upper-body access is used for the CS catheter in some labs, or when the femoral route fails. M
- Place the four catheters under fluoroscopy (table below), and check each one’s signals on the recording system as you go. BASHIR
- Find the pacing threshold at each pacing site; pace at twice the diastolic threshold. BASHIR
The four catheters: where, why, and how you know
| Catheter | Where it sits | Why you need it | How you know it is right |
|---|---|---|---|
| HRA | High posterolateral right atrium at the SVC junction, near the sinus node exit. BASHIR | Its atrial signal is close to the start of the P wave in sinus rhythm, and you pace the atrium from it. BASHIR Without it a right free-wall pathway can be missed. BASHIR | Stable capture with no phrenic nerve stimulation; reposition if either fails. BASHIR |
| His | Across the antero-superior tricuspid annulus. Withdraw it slowly with clockwise torque; in LAO the tip is near 1–2 o’clock on the annulus. BASHIR | It records the low septal atrium, the His bundle and the septal ventricle, so it gives you the AH and HV. It also marks the His, which must be protected during ablation near the septum. BASHIR | Three signals: A, a sharp H and V. No A means it is too far into the ventricle and is probably recording the right bundle. BASHIR |
| CS | Decapolar catheter along the mitral annulus, with the proximal poles just inside the CS ostium. BASHIR In PA, the proximal bipole over the lateral border of the spine roughly marks the os. M | Records left atrium and left ventricle along the mitral annulus, so it shows left-sided activation and the direction it travels. BASHIR | Both A and V signals. A pure V signal with the tip pointing down means it has entered a ventricular branch. BASHIR |
| RV | Right ventricular apex (the outflow tract in a few cases). BASHIR | You pace the ventricle from it; its signal comes close to the start of the QRS. BASHIR | Stable capture without troublesome ectopy. BASHIR |
Practise these positions in RAO and LAO in the catheter explorer, then test yourself in the quiz.
From catheter to channel
The recording system
- His and most intracardiac signals are best seen with filters of about 30–40 Hz high-pass and 400–500 Hz low-pass. Filter too much and you lose parts of the signal; filter too little and noise can hide small signals such as the His. BASHIR
- For bipolar signals, the timing is what matters; their shape is generally unhelpful. BASHIR
Worked case: Ms C.D.
- Right femoral vein. Catheters: His, decapolar CS and RV apex, with the ablation catheter added later. There is no separate HRA catheter, so the atrium is paced from the CS.
- Why that is acceptable: a three-catheter study is common, with the CS catheter used to record and pace the atrium. It gives fewer signals, which makes it harder for a learner to read, and more catheters can be added if something unexpected appears. BASHIR
- Checks: the His catheter shows A, H and V; the CS shows A and V on all poles, with the proximal pair at the os.
When it goes wrong
- Vasovagal reaction during access
- Common during instrumentation, which is why IV access should be secured before the patient arrives in the lab. M
- Arterial puncture by mistake
- Usually from aiming too lateral at the groin crease. Get haemostasis before going for the vein, to lower the risk of an AV fistula. BASHIR
- The CS won’t go in, or keeps falling out
- Switch to a superior (jugular or subclavian) approach, or use a support sheath from the groin; occasionally a steerable ablation catheter is used to enter the CS and the sheath is then railroaded over it. BASHIR
- The His signal is unstable
- Repositioning is often needed; a pre-shaped catheter may be more stable than a standard curve. BASHIR
- The HRA catheter captures the phrenic nerve
- Reposition it. BASHIR
- A new bundle branch block, or AV block, as catheters move
- Catheter trauma commonly causes a constant right bundle branch block during the study. BASHIR With an existing LBBB, a catheter in the RV can cause transient complete AV block: the device-implant guide advises having pacing ready. IMPL
Common traps
- The CS catheter only partly in, with the proximal poles in the right atrium. Activation then looks earliest in the middle poles and mimics a posteroseptal pathway. Check the position on fluoroscopy before diagnosing one. BASHIR
- Losing the His signal during the study: assume the catheter has moved. BASHIR
- Pacing from the CS and capturing the ventricle (a broad QRS) instead of the atrium, because the tip has slipped into a ventricular branch. BASHIR
Before you move on, you should be able to say
- Each catheter is stable and shows the expected signals.
- The His catheter shows A, H and V.
- You know the pacing threshold at each site.
Step 3
Baseline: read the sinus beat
The question this step answersIs conduction normal at rest, and is there any pre-excitation?
By the end of this step you can measure the AH and HV correctly and recognise pre-excitation.
Why we do it
The PR interval is three journeys added together: across the atrium (PA), through the AV node (AH) and down the His–Purkinje system (HV). The His catheter lets you time each one separately, so you can say where any delay is. BASHIR
What you do
- Record in sinus rhythm at a stable rate, and note the cycle length, because the AH changes with rate. M
- Measure the AH on the His catheter: from the first sharp part of the atrial signal to the start of the His. BASHIR
- Measure the HV: from the start of the His to the earliest ventricular activation in any lead, usually the surface QRS onset. Check every lead to find it. BASHIR M
- Look at the order of atrial activation in sinus rhythm. BASHIR
On the tracing
Practise on new tracings: AH and HV
What normal looks like
- HRA is the earliest atrial signal; the His catheter atrial signal and the CS come later, and the CS activates from proximal to distal (the left atrium is activated from the septum outwards). BASHIR
- The His signal comes clearly before the earliest ventricular activity. BASHIR
| Interval | Bashir et al. | Murgatroyd et al. | Moulton & Moulton |
|---|---|---|---|
| PA | 25–55 BASHIR | 25–55 M | — |
| AH | 55–125 BASHIR | 55–125 M | 50–140 (upper limit “probably” 105–110) ELD1 |
| HV | 35–55 BASHIR | 35–55 M | 35–55 ELD1 |
What abnormal looks like
| Finding | What it suggests |
|---|---|
| Short or negative HV | Pre-excitation over an accessory pathway. BASHIR ELD1 |
| Early local V on the distal CS poles | Latent pre-excitation from a left-sided pathway. BASHIR |
| Long AH | Often vagal tone from sedation; sedation and beta-blockers lengthen the AH, and atropine or isoprenaline shorten it. BASHIR M |
| Long HV | Disease in the His–Purkinje system; it almost always comes with a bundle branch block. ELD1 Guideline thresholds for pacing are in step 7. |
Worked case: Ms C.D.
- Sinus rhythm. AH 78 ms, HV 42 ms.
- Reading it: both are inside the reference ranges (AH 55–125, HV 35–55 ms), so resting AV-node and His–Purkinje conduction are normal. BASHIR No pre-excitation.
When it goes wrong
Common traps
Before you move on, you should be able to say
- Cycle length, AH and HV, written down.
- Whether sinus activation is normal.
- Whether there is pre-excitation, manifest or latent.
Step 4
Pace the ventricle: retrograde conduction
The question this step answersCan the ventricle activate the atrium, and does it do it through the AV node or an accessory pathway?
By the end of this step you can tell retrograde conduction through the AV node from conduction over an accessory pathway.
Why we do it
Many operators do this before atrial pacing. It finds an accessory pathway early, and it is less likely to set off AF. BASHIR M It also narrows the diagnosis fast: with VA block or VA Wenckebach, AVRT is very unlikely; if VA conduction is still absent after isoprenaline, AVNRT and AVRT are both very unlikely and an atrial tachycardia becomes the probable diagnosis. BASHIR
What you do
- Ventricular extrastimuli (the retrograde curve): an 8-beat drive from the RV at 600 ms (and 400 ms), then one early beat (S2). Bring S2 in by 20 ms at a time down to 300 ms, then by 10 ms until the ventricle no longer captures. BASHIR
- Keep going right down to refractoriness, so you don’t miss a “gap”. If there is VA block or Wenckebach at baseline, repeat on isoprenaline. BASHIR
- Incremental ventricular pacing from just faster than sinus rate down to VA Wenckebach, or to 300 ms. M Shorten the cycle length by 10–20 ms every 8–10 beats. ELD2
Where to look
- Which atrial signal is first? His, proximal CS, distal CS or HRA. BASHIR
- Does the VA time lengthen as S2 gets earlier? The AV node slows with prematurity; most pathways do not. BASHIR
On the tracing
Normal or not
| What you see | What it means |
|---|---|
| Earliest A on the His catheter (or the proximal CS), CS activating proximal to distal, HRA later. VA lengthens as S2 gets earlier. | Normal: conduction up the AV node. Bashir et al. call this “midline” activation, and note that “concentric” is a misleading name for it. BASHIR The earliest A is at the proximal CS in 30–40% of normal people. BASHIR |
| No VA conduction, or VA Wenckebach | Can be normal. BASHIR It makes AVRT very unlikely (above). |
| VA <150 ms with the earliest A at the His | Retrograde fast pathway. ELD2 |
| VA >150 ms with the earliest A at the CS os | Retrograde slow pathway. ELD2 |
| VA that does not lengthen as S2 gets earlier | Suggests an accessory pathway. BASHIR |
| Eccentric activation: distal CS first, or HRA first | A left free-wall or right free-wall pathway respectively. BASHIR |
| A sudden jump in VA time | A switch of route: from a pathway to the AV node, or from the fast to the slow pathway. BASHIR BASHIR |
If activation is midline and you still suspect a septal pathway: para-Hisian pacing
Pace the RV septum next to the His at high output (His captured, narrow QRS), then lower the output until His capture is lost (broad, LBBB-like QRS). With conduction only through the AV node, losing His capture lengthens the stimulus-to-A time, typically by more than 50 ms. With a septal pathway it barely changes. BASHIR M It does not need the tachycardia to be induced. BASHIR
Worked case: Ms C.D.
- RV pacing and extrastimuli: VA conduction is present, the earliest A is on the His catheter, the CS activates proximal to distal, and the VA lengthens as S2 gets earlier.
- Reading it: midline and decremental, which is conduction up the AV node. BASHIR No sign of a retrograde pathway so far, but a septal pathway is not excluded yet. BASHIR
When it goes wrong
Common traps
Before you move on, you should be able to say
- Whether there is VA conduction.
- Whether it is midline and decremental.
- Where the earliest atrial signal is.
- Whether you suspect an accessory pathway.
Test yourself: Retrograde conduction and para-Hisian questions
Step 5
Pace the atrium: antegrade conduction
The question this step answersDoes the AV node conduct forward over one pathway or two, and is a pathway conducting forward?
By the end of this step you can recognise smooth decrement, an AH jump, an echo beat and forward pre-excitation.
Why we do it
The AV node slows down as impulses arrive earlier (decremental conduction); atrium, ventricle and His–Purkinje tissue barely do, and most accessory pathways don’t (about 8% do). BASHIR So when you pace the atrium earlier and earlier, a smoothly lengthening AH is normal, a sudden jump suggests a second (slow) AV-node pathway, and a ventricle that is reached early without any slowing suggests an accessory pathway. BASHIR
What you do
- Atrial extrastimuli (the antegrade curve): an 8-beat drive from the HRA at 600 ms (and 400 ms), then S2, brought in by 20 ms to 300 ms and then by 10 ms until the atrium no longer captures. BASHIR
- Measure the coupling as A1A2 on the His catheter, not S1S2: at short coupling the atrium itself delays the impulse. BASHIR
- Incremental atrial pacing from 400 ms, 10 ms shorter each step, until 1:1 AV conduction is lost: the AV Wenckebach point. BASHIR
Where to look
The His channel, which must show A, H and V clearly: you are watching the AH and the HV. ELD4
On the tracing
Practise on new tracings: the antegrade curve
Normal or not
| What you see | What it means |
|---|---|
| AH lengthens smoothly, HV stays constant, then the A is not followed by an H | Normal decremental AV-node conduction, ending at the AV-node effective refractory period. BASHIR BASHIR |
| AV Wenckebach point | Normally under 450 ms. BASHIR |
| A jump: A2H2 (or H1H2) increases by ≥50 ms when the coupling shortens by 10 ms | Dual AV-node pathways: the fast pathway has blocked and conduction has switched to the slow one. BASHIR The 50 ms cut-off is a convention rather than a proven threshold. ELD4 |
| A jump followed by an atrial echo beat (midline, HRA last) | Very likely AVNRT (over 90%), but you still need to induce the tachycardia to prove it. BASHIR |
| PR longer than the RR at just above the Wenckebach point (Kay’s sign) | Suggests conduction down a slow pathway. BASHIR |
| Pre-excitation growing, HV shortening or becoming negative | An accessory pathway conducting forward. BASHIR |
| HV lengthens, or an A and H with no V | Delay or block in the His–Purkinje system, below the AV node. BASHIR |
If the question is bradycardia: sinus node recovery time
Pace the HRA for 30 seconds, stop, and time the return of the first sinus beat. Repeat at several cycle lengths. A guide is a maximum recovery time under 1500 ms, or under 550 ms once the sinus cycle length before pacing is subtracted. BASHIR M These tests support ambulatory monitoring rather than replace it. M
Worked case: Ms C.D.
- Atrial extrastimuli at 600 ms: at S1S2 600/320 ms the AH jumps by 70 ms, followed by a single echo beat.
- Reading it: a jump of ≥50 ms means dual AV-node pathways; with an echo, AVNRT becomes very likely, but the tachycardia still has to be induced. BASHIR
When it goes wrong
- AF starts and doesn’t stop
- It may stop on its own. If not: internal cardioversion (15–30 J through a catheter passed to the pulmonary artery), or external cardioversion with deeper sedation. Small doses of flecainide (typically 30 mg at first) can keep sinus rhythm long enough to finish, but may make the tachycardia harder to induce and can block pathways. BASHIR
- The jump is hidden
- Repeat with a faster drive, double extrastimuli, incremental pacing (look for Kay’s sign), or after isoprenaline with or without atropine. BASHIR
Common traps
Before you move on, you should be able to say
- The AV-node ERP and the Wenckebach point.
- Whether there is a jump, and whether there are echoes.
- Whether any pathway conducts forward.
Step 6
Induce the tachycardia, then prove the mechanism
The question this step answersIs the tachycardia in the lab the patient’s tachycardia, and what is its mechanism?
By the end of this step you can induce the tachycardia, then use six observations and two manoeuvres to name its mechanism.
Why we do it
Finding a substrate in steps 4 and 5 is not a diagnosis: a slow pathway or an accessory pathway can be a bystander, and more than one substrate is present in a significant minority. Inducing the sustained tachycardia is an absolute requirement before ablation, with a few exceptions. BASHIR BASHIR
What you do
- Tachycardia often starts during the curves or incremental pacing. If not, add isoprenaline (with or without atropine), double extrastimuli, burst pacing or another pacing site. BASHIR
- Once it starts, record a 12-lead ECG and compare it with the clinical one, especially the P-wave axis and where the P sits relative to the QRS. BASHIR
- Work through the six observations below, then the manoeuvres. Pacing the ventricle during the tachycardia is worth doing even when you feel confident. BASHIR
Six things to look at during the tachycardia
| Look at | What it tells you |
|---|---|
| 1. A:V ratio | More A than V usually means an atrial tachycardia; the main exception is AVNRT with 2:1 block below the node. BASHIR |
| 2. Atrial activation sequence | Midline (His or proximal CS first) fits AVNRT, a septal pathway or a septal atrial tachycardia. Eccentric (distal CS first) usually excludes AVNRT. HRA first fits a right-sided pathway or a right atrial tachycardia. BASHIR |
| 3. Septal VA time (earliest V to earliest A on the His or proximal CS) | Under 70 ms is classic typical AVNRT and excludes AVRT, because a pathway circuit needs at least 70 ms to reach the atrium. Over 70 ms fits AVRT, slow–slow AVNRT or atrial tachycardia. BASHIR The SVT page gives the guideline’s wording. |
| 4. How it starts and stops | Atrial tachycardias don’t need the AV node, so they usually end with a conducted V. A tachycardia that keeps ending with an A is unlikely to be atrial. BASHIR |
| 5. Cycle-length wobble | If changes in the HH interval come first and the AA follows, the AV node is in the circuit (AVNRT or AVRT). If the AA changes first, it is an atrial tachycardia. BASHIR |
| 6. Bundle branch block | If a bundle branch block on one side lengthens the VA and the cycle length (by more than 20 ms), the tachycardia is AVRT using a pathway on that side. BASHIR |
Manoeuvres during tachycardia
- His-synchronous ventricular premature beat
- Deliver a single RV beat at the moment the His fires, when the His and AV node are refractory. If the next atrial signal still comes early, an accessory pathway exists (though it may be a bystander). If the beat ends the tachycardia without reaching the atrium, the ventricle is part of the circuit: AVRT. BASHIR M The cycle length must be stable to judge this. M
- Ventricular overdrive pacing (entrainment)
- Pace the RV 10–40 ms (usually 20 ms) faster than the tachycardia, confirm the atria speed up to the paced rate, then stop. A V–A–V response fits AVNRT or AVRT; a V–A–A–V response means atrial tachycardia. After AVRT the return cycle (adjusted post-pacing interval) is usually within 115 ms of the tachycardia cycle length; after AVNRT it is usually more than 115 ms longer. BASHIR EHRA
- Entrainment, the principle
- Pacing slightly faster than a re-entrant tachycardia continuously resets it; proving entrainment proves re-entry with an excitable gap. M
The SVT page takes each of these findings further, with practice questions.
On the tracing
Practise on new tracings: the tachycardia and entrainment
If nothing can be induced
Try harder first: atrial extrastimuli (single, double, triple) and burst pacing from more than one site, isoprenaline, atropine, and occasionally a beta-blocker. BASHIR If it still won’t start, whether to ablate depends on what the study found and on the clinical history, and pathways close to the AV node need a clear mandate first. BASHIR
Programmed ventricular stimulation for VT
- Pace the RV apex with an 8-beat drive at 600 ms, then add S2 at shorter and shorter coupling until VT is induced or the ventricle is refractory.
- Add S3, with S2 held just above refractoriness.
- Repeat singles and doubles with a 400 ms drive.
- Give triple extrastimuli after 600 and 400 ms drives. M §7.1
- The ESC 2022 guideline describes typical protocols as 2 RV sites, 2–3 drive cycle lengths, up to 3 extrastimuli, and isoprenaline. ESC VA 2022
- Sustained monomorphic VT is a specific finding however it was induced. Polymorphic VT or VF from triple or quadruple extrastimuli may be non-specific. Adding sites or isoproterenol raises sensitivity but lowers specificity. M §7.2 ESC VA 2022
- When sustained monomorphic VT is induced, record a full 12-lead ECG straight away, even while preparing to cardiovert, so it can be compared with the clinical VT. M §7.3
Worked case: Ms C.D.
- An atrial extrastimulus at 280 ms induces a regular narrow-complex tachycardia: cycle length 330 ms, A:V 1:1, earliest A at the His, septal VA 45 ms.
- Six observations: 1:1, midline, VA under 70 ms. That is classic typical AVNRT and excludes AVRT. BASHIR
- Manoeuvres: RV overdrive pacing gives a V–A–V response with PPI − TCL 140 ms, so not atrial tachycardia, and the ventricle is not in the circuit. A His-synchronous ventricular beat does not advance the atrium, so a septal pathway is unlikely. BASHIR
- Diagnosis: typical (slow–fast) AVNRT.
When it goes wrong
- Sustained VT that drops the blood pressure
- Synchronised DC cardioversion. If tolerated, try pace termination: burst or ramp pacing starting just shorter than the VT cycle length; this can accelerate the VT and need cardioversion. BASHIR
- VF or polymorphic VT
- Urgent defibrillation: pads should be on before ventricular stimulation starts. BASHIR
- Adenosine side effects
- High doses can occasionally provoke AF or even ventricular arrhythmias; failure to block the AV node may simply mean too low a dose (it may need more than 12 mg). BASHIR BASHIR
- Pacing keeps terminating the tachycardia
- Re-induce and repeat. If ventricular pacing consistently ends it without capturing the atrium, it is very unlikely to be an atrial tachycardia. BASHIR
- Hypotension with a still cardiac silhouette
- Suspect tamponade: confirm with echocardiography and treat with emergency pericardiocentesis. A vagal reaction is the differential. IMPL
Common traps
- Calling a V–A–A–V response without checking that the atria really were entrained to the pacing rate. BASHIR
- A “pseudo V–A–A–V” in typical AVNRT or a long-RP tachycardia: look for a His signal between the two A signals, and check whether the A–A interval equals the pacing interval. BASHIR EHRA
- Two mechanisms in one patient (5–10% of cases). Account for every unexpected finding before ablating. BASHIR
Before you move on, you should be able to say
- That the induced tachycardia matches the clinical ECG.
- The mechanism, and the observations that support it.
- What, if anything, still doesn’t fit.
Step 7
Decide: what the findings mean for management
The question this step answersWhat do we do with the answer: ablate, pace, implant, or stop?
By the end of this step you can link the diagnosis to the treatment the guidelines recommend, and its risks.
Why we do it
The study is only worth doing if its answer changes what happens next. Ablation follows a firm diagnosis, which is why steps 4–6 matter so much; near the AV node, the risk to normal conduction is weighed with the patient before ablating. BASHIR BASHIR
Conduction disease and syncope ESC pacing 2021
| Recommendation | Class / level |
|---|---|
| Syncope with bifascicular block: an EP study should be considered when syncope remains unexplained after non-invasive evaluation, or when a pacing decision is needed urgently, unless empirical pacing is preferred (e.g. elderly or frail patients). | IIa / B |
| Syncope with sinus bradycardia: an EP study may be considered when non-invasive tests haven’t linked symptoms to bradycardia. | IIb / B |
| Unexplained syncope with bifascicular block: a pacemaker is indicated if the baseline HV is ≥70 ms, there is second- or third-degree intra- or infra-Hisian block during incremental atrial pacing, or the response to pharmacological challenge is abnormal. | I / B |
Ventricular arrhythmia ESC VA 2022
- After a previous STEMI, programmed stimulation is indicated when syncope remains unexplained after non-invasive evaluation.
- In structural heart disease with mildly reduced or preserved LVEF and unexplained syncope, induced sustained monomorphic VT helps identify the cause and predict events. Induced polymorphic VT or VF is generally non-specific.
- In primary electrical diseases, programmed stimulation has no prognostic value (some evidence supports its use in Brugada syndrome).
Going on to ablation: AVNRT example
- The slow-pathway connection runs between the tricuspid annulus and the CS ostium. Lesions higher on the septum carry more risk to the AV node and are used only if lower sites fail. EHRA case 63 In the explorer, set the ablation catheter to “Slow pathway region”.
- A junctional rhythm during RF is a common but non-specific sign of an effective lesion. If the junctional beats stop conducting to the atrium, stop energy at once, because the fast pathway is at risk. EHRA case 29
- The ideal endpoint: dual physiology, echoes and AVNRT all present before ablation and none after. Often AVNRT becomes non-inducible while dual physiology remains. If it stays non-inducible even on isoproterenol, it may be reasonable to stop and observe. M §8.3
- With pulsed field ablation, slow-pathway modification has been reported with high acute success, but in one 40-patient study 17.5% had transient complete heart block. The 2026 HRS/EHRA statement makes no formal recommendation on PFA for AVNRT. PFA 2026 §SVT
Guideline indications for SVT ablation
- The 2019 ESC guideline recommends catheter ablation (class I) for symptomatic, recurrent AVNRT; for symptomatic, recurrent AVRT; for recurrent focal atrial tachycardia, especially if incessant or causing tachycardiomyopathy; and for symptomatic, recurrent CTI-dependent flutter. ESC SVT 2019
- In asymptomatic pre-excitation, an EP study with isoprenaline is recommended to risk-stratify people with high-risk occupations or hobbies and competitive athletes, and ablation is recommended when it finds high-risk properties. ESC SVT 2019
- The full table, with success and complication figures, is on the SVT page.
Anticoagulation around AF ablation
This applies to left atrial ablation for atrial fibrillation. The same-day discharge consensus (step 8) only says to hand over a prescription; the regimen comes from the 2024 ESC AF guideline.
- Before: start oral anticoagulation at least 3 weeks before catheter ablation in patients at elevated thromboembolic risk (class I, level C). ESC AF 2024
- During: uninterrupted oral anticoagulation is recommended (class I, level A). Trials show comparable safety and efficacy with minimally interrupted anticoagulation, where the morning DOAC dose is withheld on the day of the procedure. Heparin during the procedure is common practice. ESC AF 2024 §7.2.6
- After: continue the DOAC at its usual dose once haemostasis has been achieved, and keep every patient anticoagulated for at least 2 months, whatever their thromboembolic risk or rhythm outcome (class I, level C). ESC AF 2024
- Beyond 2 months: continue according to the patient’s CHA₂DS₂-VA score, not the perceived success of the ablation (class I, level A). ESC AF 2024
Worked case: Ms C.D.
- Symptomatic, recurrent AVNRT: catheter ablation is the class I recommendation. ESCSVT
- Slow-pathway modification low in the septum, between the CS os and the tricuspid annulus. EHRA Junctional beats appear during RF, with VA conduction preserved; energy is stopped at once if the junctional beats lose VA conduction. EHRA
- Endpoint: no AVNRT inducible on isoprenaline, a single echo beat remains, and AV conduction is intact. M
When it goes wrong
- The target is close to the AV node
- With a parahisian pathway, many operators stop and discuss with the patient before ablating. BASHIR
- Junctional beats lose VA conduction during slow-pathway RF
- Stop energy at once: the fast pathway is at risk. EHRA
- AF during slow-pathway ablation
- Slow-pathway modification is usually not done during AF, because you can’t judge the junctional rhythm or see VA block. BASHIR
Common traps
- Reading a negative study as reassurance in syncope: in the cited data about a third of patients with a negative study who later had a loop recorder developed AV block. ESCP
Before you move on, you should be able to say
- The diagnosis, and the treatment it points to.
- The guideline recommendation and its class behind that treatment.
- The risks you will discuss with the patient.
To be written
- Ablation of AF and VT, which are beyond the scope of a diagnostic study.
Step 8
Finish safely: observation and discharge
The question this step answersIs the patient safe to go home, and do they know what to watch for?
By the end of this step you can judge whether the patient is ready to go home and teach the warning signs.
Why we do it
Most problems after an EP study show up at the access site, and a significant pericardial effusion usually appears during or shortly after the procedure. So the end of the study is a check, not a formality. SDD
Many EP and device procedures can now be day cases. The 2026 EHRA/ACNAP consensus says the decision to send someone home the same day should be shared between the patient, the physician and the allied health team. It should weigh comorbidities such as heart failure or lung disease, procedural risk such as bleeding risk, and social factors such as distance from the hospital and support at home. SDD Advice 3
Who may go home the same day SDD Advice 1
- May be appropriate: SVT ablation, including with transseptal access, which carries less risk than AF or VT ablation. PVC ablation without structural heart disease. Straightforward AF ablation, especially single-shot cryoballoon or pulsed field ablation, when standardised screening and a local protocol are in place.
- May be appropriate (devices): generator changes, pacemaker implants in patients without complete heart block, and primary-prevention ICD or CRT in stable heart failure. Also subcutaneous ICD and leadless pacemaker implants. Data for conduction system pacing are still limited.
- Area of uncertainty: planned VT ablation in structural heart disease or reduced ejection fraction, complete heart block, secondary-prevention ICDs, and lead extraction.
The access site
- Access-site problems are the most common adverse events after EP procedures. SDD §Post-procedure
- By expert consensus, the minimum bed rest is 1–3 h after a figure-of-eight suture and 1 h after a vascular closure device. In one cited study, manual pressure for at least 10 minutes and up to 3 h of bed rest let 79% go home the same day, with 0.3% bleeding. SDD §Post-procedure
- Before discharge, inspect, palpate and listen over the site. A new bruit may mean a pseudoaneurysm or an AV fistula. Ultrasound is optional but advised if anything is abnormal. Make sure a figure-of-eight suture is removed, or that its removal is arranged. SDD §Post-procedure
Effusion and other early complications
- A significant pericardial effusion usually appears during or shortly after the procedure, so every lab needs a protocol for excluding it. There are no trials comparing a routine bedside echo before discharge with a selective one (for chest pain, breathlessness, hypotension, complications or high-risk procedures). Either approach is reasonable. Intracardiac echo used during the case can serve instead. SDD §Post-procedure
- Hypotension, unexplained sinus tachycardia or chest pain afterwards calls for a prompt 12-lead ECG and echo. SDD §Complications
- After AF ablation, most acute complications show within 6 h. A 4–6 h observation window may be safe after any uneventful procedure, including transseptal and left-sided ablation, but not VT ablation. A few complications, such as atrio-oesophageal fistula or immune-mediated pericardial effusion, appear days or weeks later and can be missed even with an overnight stay. SDD §Post-procedure
- After pulsed field ablation, delayed coronary spasm and malignant arrhythmias are extremely rare. They have been reported up to 240 minutes after the procedure. Warning signs are chest pain, ST changes, haemodynamic instability, bradycardia and ventricular arrhythmia. SDD §Complications
Minimum observation periods SDD Table 6
- Ablation: 3–6 h in low-risk patients, with no effusion, no access-site complication and a neurological check.
- Devices:
- Generator change: 1–2 h.
- Pacemaker implant: 2 h.
- ICD or CRT: 2–12 h; some patients need an overnight stay.
- Leadless pacemaker: 2–6 h, and at least 6 h after femoral access by expert consensus.
- Lead extraction: 12–24 h.
- After lead implantation, the consensus advises device interrogation, a two-plane chest X-ray and a wound check before discharge. SDD §Post-procedure
Before the patient goes home SDD Tables 7–10
- Stable rhythm and vital signs, complete haemostasis, fully awake, walking, eating and passing urine. Avoid urinary catheters where possible, and check voiding if one was used.
- Written instructions with warning signs and a 24/7 contact number, an anticoagulation plan with a prescription, and a follow-up appointment already booked.
- After sedation or general anaesthesia, a responsible adult should be available for the first 24 h. SDD Advice 3
- Warning signs to teach:
- Growing bruising, swelling or bleeding at the site.
- Any sign of stroke or TIA, which means calling emergency services.
- Fever, wound redness or discharge.
- Unexplained breathlessness.
- Chest pain beyond the expected discomfort, or palpitations.
- Syncope, dizziness, ICD shocks or worsening heart failure.
- Pain that analgesia doesn't relieve.
Worked case: Ms C.D.
- Day case. Access site dry, observation complete, no new symptoms.
- Driving: no driving for at least 2 days after a successful ablation (Group 1); the DVLA need not be told. DVLA
- Clinic review at 3 months with a 12-lead ECG. Her report is in Writing the report.
When it goes wrong
- Hypotension, sinus tachycardia or chest pain afterwards
- Prompt 12-lead ECG and echo. SDD
- Bleeding from the groin at home
- The patient should lie down, press firmly just above the puncture site for 10 minutes, then call for help; sudden severe pain, swelling or loss of power in the leg is urgent. BASHIR
Common traps
Before you move on, you should be able to say
- That the access site and the observation period are satisfactory.
- That the patient knows the warning signs and whom to call.
- That follow-up is booked.
After the study
Writing the report
The question this step answersCould someone who wasn’t there rebuild what was found and what was done?
By the end of this step you can write a report that states the diagnosis, the endpoint and the pertinent negatives.
Why we do it
The report is the only lasting record of the study. A later reader looks first for the diagnosis and how it was proven, the endpoint and the evidence for it, and anything that went off plan. Writing every report on the same skeleton is how you make sure none of that is missed. This section follows NavEP’s report template; align it with your department’s format.
The skeleton every report follows
- Header: patient ID, date, operators, procedure, indication.
- Before the procedure: anticoagulation, imaging, antiarrhythmic drugs and when they were stopped.
- Set-up: consent with the specific risks quoted, sedation or anaesthesia, access, heparin and ACT if used.
- Equipment: catheters and their positions, mapping system, energy source.
- EP findings: baseline rhythm and cycle length, AH and HV, retrograde and antegrade conduction, what was induced and how, the observations and manoeuvres, the mechanism.
- Ablation (if done): target, energy and settings as numbers with units, number and duration of applications.
- Endpoint: the test that defines success and its result.
- Safety and contingencies: anything that departed from the plan and how it was handled, fluoroscopy time and dose, haemostasis.
- Conclusion and plan: a one-line outcome, drugs, anticoagulation, the specific driving restriction, follow-up.
Four rules for every report
- State the endpoint and the evidence for it explicitly.
- Record the pertinent negatives: no effusion, no AV block, no vascular complication.
- Give settings and intervals as numbers with units, not “standard settings”.
- If the endpoint was not reached, say so and give the reason you stopped.
Contingencies to document
If any of these happened, record what was found, what was done and the outcome; if not, a pertinent negative is enough.
| Event | What to record |
|---|---|
| Endpoint not reached, or procedure abandoned | The reason, what was achieved, residual conduction or inducibility, and the plan. |
| Unexpected arrhythmia or change of strategy | The mechanism and how it was proven, whether it was treated, and that consent covered it (for example AF induced during an SVT study). |
| Pericardial effusion or tamponade | When it was recognised, echo size, pericardiocentesis and volume, heparin reversal, outcome. |
| AV block | Type and timing, transient or persistent, temporary pacing, plan. |
| Vascular complication | Haematoma, pseudoaneurysm or fistula, ultrasound findings, management. |
| Sedation escalated or airway event | Conversion to anaesthesia, the reason, who was involved. |
| Patient with a pacemaker or ICD | Checks before and after, reprogramming during the case, settings restored. |
| Possible pregnancy | The test result, and how fluoroscopy was limited. |
Example: Ms C.D.’s report (fictional)
Procedure: EP study and slow-pathway ablation. Patient: Ms C.D., 34. Operator: Dr X.
Indication: recurrent sustained narrow-complex tachycardia, ECG-documented at 168 bpm, ended by adenosine; symptomatic on verapamil. Resting ECG: sinus rhythm, PR 148 ms, narrow QRS, no pre-excitation.
Procedure: written consent. Conscious sedation. Right femoral vein, three sheaths. His, decapolar CS and RV apex catheters; 4 mm irrigated RF ablation catheter. Fluoroscopy only.
EP study: AH 78 ms, HV 42 ms. Retrograde conduction midline and decremental. Atrial extrastimuli: dual AV-node physiology with a 70 ms AH jump at S1S2 600/320 ms and a single echo beat. Tachycardia induced with S2 280 ms: cycle length 330 ms, 1:1, septal VA 45 ms, earliest A at the His. RV entrainment: V–A–V, PPI − TCL 140 ms. His-synchronous ventricular beat did not advance the atrium. Diagnosis: typical slow–fast AVNRT; AVRT excluded.
Ablation: slow pathway targeted between the CS os and the tricuspid annulus. RF 30 W, 55 °C limit, flow 17 mL/min, five applications of 60 s; junctional rhythm on three, with VA conduction preserved and PR within 20 ms of baseline.
Endpoint: after 30 minutes on isoprenaline 2 µg/min, no tachycardia inducible; one echo beat at the shortest S2, accepted. AH 82 ms, AV Wenckebach 340 ms, PR 152 ms: AV conduction intact.
Safety: fluoroscopy 4.8 min, DAP 5.2 Gy·cm². No AV block, no vascular complication. Manual pressure.
Conclusion: successful slow-pathway modification for typical AVNRT, non-inducible on isoprenaline.
Plan: day-case discharge; verapamil stopped; advice on recurrence and whom to call; no driving for 2 days (Group 1); clinic at 3 months with a 12-lead ECG; no anticoagulation.
A fictional patient with illustrative values, from NavEP’s report template; the interpretation of each finding is cited in the steps above.
Common traps
- Writing “successful” without saying which endpoint was tested and how.
- Not stating that AV conduction was preserved after ablation near the node.
- “Driving advice per DVLA” with no specific period.
Before you sign, check the report has
- The diagnosis, and the findings that prove it.
- The endpoint and the evidence for it.
- The pertinent negatives, any contingency, and a specific plan.
One page
The whole study on one page
A summary of steps 1–8 to keep beside you in the lab. It adds nothing new: the sources are cited in each step.
| Step | Look at | What “all normal” looks like |
|---|---|---|
| 1. Know the question | The ECGs, the drug history, consent | A one-sentence question; drugs stopped |
| 2. Set up | Each catheter’s signals and capture | HRA, His (A-H-V), CS (A and V), RV all stable |
| 3. Baseline | AH, HV, sinus activation order | AH 55–125, HV 35–55 ms; HRA first; no pre-excitation |
| 4. Pace the ventricle | Earliest A; does VA lengthen with earlier S2? | Midline and decremental, or no VA conduction |
| 5. Pace the atrium | AH and HV on the His channel | Smooth AH lengthening, constant HV, no jump or echo |
| 6. Induce and test | A:V, sequence, VA, start/stop, wobble, BBB; then manoeuvres | A mechanism you can defend |
| 7. Decide | The diagnosis against the guideline | A treatment plan, with its risks discussed |
| 8. Finish safely | Access site, observation time, warning signs | Discharge criteria met |
Sources
All content is paraphrased; no text, tables or figures are reproduced. Consult the originals for full detail. Each number is the same on every page of the site.