Pin pointing the pathway !

I’m sure that for many budding cardiologists including me, diagnosing accessory pathway based on surface ECG has been herculean task. Neverthless i have seen people doing it with ease, may be fruits of their hard work

Recently i found an article mentioning pathway localisation after atrial pacing during EP study.Amazingly it works well on surface ecg .I’m yet to see if it errs.

In the study, pathway was correct in 90% compared to 63 % with arruda criteria.

Best part is that its a stepwise algorithm

  • step 1-lead V1 polarity -Right when negative and left when positive

Now you know the side, proceed down,

  • step 2-Inferior leads polarity

For right sided pathway- All 3 +ve – Think of anterior locations (RA or NH-nodohisian).If 1-2 +ve think intermediate location RL or Sometimes NH.If all negative think posteriorly RP or RPS

Similarly, for left sided pathway-All 3+ve direct hit on LL.If 1-2 +ve again straight to LPL.If all negative again think back to LPS or LPL or DCS(deep CS) locations

  • step 3 v3 polarity

For right sided only- v3 is negative for all away from septum remember APL -RA,RP AND RL.V3 +ve for septal RPS AND NH

v1/1 ratio-For left sided posterior only-see which is more positive? lead v1 or lead 1 .If ratio more than 1 LPL and less than 1 DCS or LPS.But how to find between dcs and LPS ?

  • step 4 lead 2 QRS notch

ONLY to see between DCS and LPS -If lead 2 QRS notched its DCS Otherwise go for LPS

  • Lets try some examples

ecg -1

ecg 2

Thanks to Thomas pambrun and colleagues.Now pathway localisation is gonna be fun.

See comment section to check your answers to above ecg with EP finding in above 2 patients

Good day!


Pambrun, Thomas, et al. “Maximal Pre-Excitation Based Algorithm for Localization of Manifest Accessory Pathways in Adults.” JACC: Clinical Electrophysiology (2018): 667.

ECG in Ebsteins anomaly

“Most of chd children dont look sick, but the scars on their chest are real .They are battle scars, the scars of their fight to live


Ecg is almost never normal in ebsteins anomaly of the heart.The range of anomalies include the following,The PQRST way

P wave -right atrial enlargement is almost always seen with rightward p wave axis.Such tall P waves are popular as ‘himalayan P’ waves.PR prolongation is also not uncommon(in about 50 %).

QRS-Axis may be normal or superior .rsR’ pattern with right bundle branch pattern is often seen.Deep Q waves may be seen in inferior leads(due to septal and RV fibrosis ).QRS amplitude is often low over RV leads.Pre excitation pattern of type B WPW seen in 20 % of cases and more than 1 pathway can coexist.Fragmented / splintered QRS is a normal shaped R wave followed by smaller,broader positive deflection.

Splintered QRS is a marker of greater disease severity, increased arrythmia risk and disappears post surgery

Arrythmias are common which includes AF,flutter, atrial or AV reentrant tachycardias, Mahaim fibre tachycardia and VT.Af can some times be very rapid and dangerous.

One easy clue for diagnosing ebstein is complete or incomplete RBBB with low QRS amplitude in right sided chest leads and first degree heart block.

ECG changes in VSD

Ventricular septal defects can present with a myriad of ECG changes.What matters is the size of vsd and associated anomalies

  1. Normal ecg -In a small defect,its not uncommon to find a normal ekg.
  2. LVH with left atrial abnormality-common pattern in a left to right shunt especially moderate to large
  3. RVH-Suspect raised RV pressures in large or moderate vsd or an associated double chambered RV(means obstruction between RV inflow and outflow)
  4. Katz wachtel sign-Large equiphasic qrs in midprecordial leads due to biventricular hypertrophy
  5. AV blocks -uncommon but also can be a life threatening complication of device closures.There lies the importance of rhythm monitoring post device closures (for interventionists).

An abnormal U wave !

U wave, one of the most forgotten wave in ecg. It’s often submerged beneath pqrst wave analysis even by experts.

Let’s have a glance on this small hump.Given below as points….

 The most common theories for the origin are:

  • Delayed repolarization of purkinje fibres
  • Prolonged re-polarisation of mid-myocardial M-cells
  • After-potentials resulting from mechanical forces in the ventricular wall
  • The repolarization of the papillary muscles

  • U wave if present is negative in avR and rarely in lead 3 and avf
  • It’s rare to find a u wave in lead 1,avL and avR
  • U wave amplitude increase with most of the inotropic agents and bradycardia
  • Inversion of u wave in exercise testing is a good idea to diagnose LAD stenosis
  • Prominent U waves are seen in hypokalemia and hypercalcemia
  • U wave alternans seen in Lvf and Romano ward syndrome.

Now a qn…how to make out T- U fusion versus a notched T wave?This is not uncommon.

See the comments section for the answer
That’s all folks for the day ..

Good day!

Arm lead reversal vs Dextrocardia in ecg

Reversal of arm leads is the commonest error when recording an ecg/ekg.

Negative P in lead 1 is an useful diagnostic clue.

Chest leads show normal transition with tall R in lead reversal , whereas in true mirror-image dextrocardia the QRS complex becomes smaller and displays mostly QS or rS in v4-v6.

Also as we know lead 1 v5 v6 show same polarity a they are all lateral leads.If lead 1 qrs predominantly negative while v5,6 is positive, suspect reversal.

Exercise ECG aka “TMT test”

When not to do?

Treadmill and cardiology have an evergreen affair.Treadmill is known to give the user not just an exemplary cardiac fitness ,but diagnose serious heart diseases.But what if treadmill can lead to death!! yes it can sometimes…

Exercise ecg testing is quite popular in clinical cardiology for more than 50 years.It can be a “stand alone test ” in appropriately selected patients.When properly done risk for mortality is less than 1 in 10,000 tests.

Exercise ecg can be potentially hazardous in some situations aka absolute contraindications.It include following but not limited to following conditions

  1. Acute myocardial infarction or unstable angina
  2. acute myo or pericarditis
  3. left main coronary artery stenosis
  4. second degree or third degree AV block
  5. rapid arrythmias
  6. severe valvular stenosis
  7. acute pulmonary embolism
  8. acute non cardiac illness
  9. patients with locomotor problems
  10. Heart failure

Some other scenarios where risk benefit ratio needs to be considered.Such relative contraindications include but not limited to:

  • HCM
  • significant AV blocks
  • Recent arrhythmias
  • Moderate valvular stenosis
  • Severe (> 3 mm) ST segment depression at rest
  • Severe (> 200/110 mm) arterial hypertension

American Society of Nuclear Cardiology recommend, pharmacologic stress is meaningful only if the patient is unable to achieve ≥ 85% MPHR and five METs

Last but not the least a simple stethoscope auscultation may bring out harsh ejection systolic murmur of aortic stenosis which may prevent a mishap@treadmill.

Inspired by Ref Hurst cardiology 14 th ed