CME INDIA Case Presentation by Dr. Deepak Gupta, DM cardiology, Pulse Hospital, Ranchi.

CME INDIA Case Study

Post electric shock ECG (It was a commercial electric shock during repairing)

27 yr-old-male, (previously healthy) got admitted after electrocution

What should be next steps?

CME INDIA Discussion (Inputs also from CSI-Jharkhand)

Dr S. N. Nagarajan, DM, Card., Tripur, TN:

  • Echo, cardiac bio markers and monitor him for vitals. Looks like spasm ( direct thermal effect on myocardium)

Dr D. P. Khaitan, National President-CCDSI, Gaya:

  • The pertinent findings can be grouped into two

( 1 ) Conduction disturbance

PR interval 0.22″ ( please see V4 for clarity) + RBBB

( complete ) +Left posterior hemiblock (Rt.axis deviation.)

= Trifasicular block

There is a chance of going into CHB – reassess and if needed Temporary pace maker might be placed

(2 )

* ST coving over leads 1, aVL and V1-2 including aVR which is having higher amplitude than that of V1

** There is marked ST depression over inferior leads and V3-6 possibly reciprocal.

  • The injury is possibly due coronary vasospasm – should be rechecked up by serial ECGs and in meantime should be placed on CCB drugs like Nifedipine and watch.
  • We should further also assess about pericardial injury itself.
  • Other needed investigations should be done
  • Right sided chest leads should be explored
  • ECG should. be repeated  again to reassess the rhythm  to exclude atrial flutter if any.

Dr Varun Kumar, Card, Ranchi:

  • It is myocardial injury due to shock…

Dr Anupam, DM Card, Ranchi:

  • Looks like Brugada syndrome in V1/V2. ST T changes may be post shock.

Dr Deepak Gupta:

  • ECG after few hours:

27 yr-old-male, (previously healthy) got admitted after electrocution

Dr S. N. Nagarajan, Tripur, TN:

  • Clearly due to vasospasm sir?
  • Need observation and monitoring.
  • How was the echo? To rule out apical ballooning.

Dr D. P. Khaitan, Gaya:

  • I am also in favour of coronary spasm. Post electrical shock ECG showing a slight prolongation of QTc interval. Please let us know serum electrolytes .

Dr Deepak Gupta:

  • Coronary spasm of which artery is likely? How do you explain marked ST depression in V3 to V6 and Inferior leads?
  • Electrolytes are normal . All cardiac enzymes are normal including trop T.
  • Echo-No RWMA. Normal LV function. No Pericardial Effusion  

 Dr D. P. Khaitan Gaya:

  • The significance of accompanying ST segment depends upon the leads involved. And Segment deeper over V3-6 with Inferior lead is associated with anterolateral or septal subendocardial injury from a severe lesion in LAD or the Left main coronary artery. On normalization of coronary spasm the ST depressions would also vanish.
  • There might be diffuse coronary spasm – to be considered.
  • The association of RBB and Left posterior fascicle involvement indicate that both LAD and LCX are involved – both are the offshoots of LMCA. The region of LAD involvement indicates in this case by coronary spasm and deeper ST depression over 1, aVL ,V3-6  indicate either subtotal spasm occlusion over LCX or reciprocal changes. If so, the main culprit is either coronary spasm at LAD or LMCA.

Dr Varun Kumar, Ranchi:

  • It  can be explained simply. I’ve not heard or read that all the coronary artery spasmed at the same time and it is also least likely that a 27 yrs. old person has critical atherosclerotic lesion of coronaries.

Dr Deepak Gupta, Ranchi:

  • True.
  • Coronary spasm can occur but usually of RCA because close chest wall proximity.
  • In this case ECG changes can only be explain by diffuse transient myocardial injury.
  • Myocardial injury can result from the direct effects of electric current (electrothermal conversion and electroporation), but several other mechanisms including Myocardial infarction by coronary spasm or thrombosis, myocardial contusion by cardiopulmonary resuscitation with subsequent haematoma formation in small coronary arteries, extensive catecholamine release mediated injuries and coronary blood flow reduction secondary to generalized severe hypotension compromising myocardial perfusion can occur.
  • Coronary spasm can occur but usually of RCA because close chest wall proximity.

Dr Varun Kumar / Dr Satish Kumar(Bokaro):

  • Agree.

Dr Ashish Ranjan Jha, Ranchi:

  • Nicely explained.
  • I have seen such ECG change after wasp bite. CAG  was normal but I have also seen anterior wall STEMI with critical LAD occlusion in a 21yr male .
  • Kounis syndrome.

CME INDIA Learning Points

  • The most common arrhythmias, post electric shock are:
    • Sinus tachycardia
    • Premature ventricular contractions
    • Ventricular tachycardia
    • Atrial fibrillation
  • Most arrhythmias occur soon after the electrical shock.
  • Delayed ventricular arrhythmias are noted up to 12 hours following an incident.
  • Most patients not experiencing sudden cardiac death have nonspecific ST–T-wave abnormalities that usually resolve spontaneously.
  • Patients without ECG changes on presentation are unlikely to experience life-threatening arrhythmias.
  • Electrical injury can cause transient Brugada type electrocardiographic pattern. (The Brugada syndrome is characterised by a distinct type of ST-segment elevation in right precordial leads (V1-V3), right bundle branch block (RBBB) pattern, and high incidence of sudden cardiac death (SCD) in patients with structurally normal hearts) Such patients may be at high risk of developing life threatening ventricular arrhythmias and sudden death.
  • Patients with electrocution induced Brugada type electrocardiographic pattern need close monitoring for life threatening cardiac arrhythmias.
  • Kounis syndrome is a ubiquitous disease which represents a magnificent natural paradigm and nature’s own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture. Kounis syndrome seems to be not a rare disease but an infrequently diagnosed clinical entity which has revealed that the same mediators released from the same inflammatory cells are also present and in acute coronary events of non-allergic etiology. These cells are not only present in the culprit region before plaque erosion or rupture but they release their contents just before an actual coronary event -Kounis 2016.
  • Types of Kounis Syndrome:

TypeCardiac HistoryPathological Changes
1.Normal coronary arteries No risk factors for IHDCoronary artery vasospasm
2.Inactive pre-existing atheromatous diseasePlaque erosion of rupture causes vasospasm or infarction
3.Previous coronary artery stentingStent thrombosis secondary to platelet activation


  1. Nikolaidis LA, Kounis NG, Gradman AH. Allergic angina and allergic myocardial infarction: a new twist on an old syndrome. Can J Cardiol. 2002 May;18(5):508-11 
  2. Kounis NG. Kounis syndrome (allergic angina and allergic myocardial infarction): a natural paradigm? Int J Cardiol. 2006 Jun 7;110(1):7-14 
  3. Abdelghany M, Subedi R, Shah S, Kozman H. Kounis syndrome: a review article on epidemiology, diagnostic findings, management and complications of allergic acute coronary syndrome. Int J Cardiol. 2017;232:1–4.
  4. Rangaraj R, Moorthy N, Patil SS, Manjunath C. Brugada-type electrocardiographic pattern induced by electrocution. Indian Pacing Electrophysiol J. 2009;9(1):56-59.

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