EKG of the Week 2019 6-2

This EKG comes courtesy of Dr. Pilat.


A 5 month old boy presented to the ED with intermittent fast heart rate observed by the mother. No change in the level of activity or alertness, normal feeding, no SOB or any other additional complaints. No recent illness. Physical exam revealed a well-appearing, well-nourished baby boy, smiling, playful, active, good eye contact, normal work of breathing, no retractions, lungs CTA b/l, tachycardia, abdomen soft NT/ND, normal skin color and temperature, no cyanosis, capillary refill<2 sec.

V/S: P – recorded at triage as 148, R 28, BP 85/59

The EKG is below.

2019 6-2.jpg

1.     What does the EKG demonstrate?

2.     How would you manage this baby?


The EKG demonstrates a regular narrow complex tachycardia at a rate of approximately 220 with absent P waves. This is consistent with SVT.

 Infants in SVT can be managed with vagal maneuvers. If they are unsuccessful, give adenosine 0.1 mg/kg.


This patient received 3 doses of adenosine (0.1, 0.2, 0.2) and then converted.

The post-conversion EKG (below) shows a sinus rhythm with tall P waves (best seen in leads II, III, aVF, V1 and V2) consistent with right atrial enlargement. There is also a short PR interval with a delta wave (best seen in leads V4-V6) consistent with pre-excitation.

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This patient had Ebstein’s anomaly. This is a congenital malformation of the tricuspid valve where the valve is located “too low” in the right ventricle. This results in the upper portion of the right ventricle effectively becoming part of the right atrium (known as “atrialization of the right ventricle”). The functional portion of the right ventricle is very small. Most patients with Ebstein’s anomaly also have tricuspid regurgitation and an atrial septal defect.

Patients with Ebstein’s anomaly often present with cyanosis and signs of right-sided heart failure. They are also at risk for arrhythmias including narrow complex SVT, wide complex tachycardia, a-flutter, a-fib, v-tach and sudden cardiac death.

The abnormal tricuspid valve results in direct muscle connection from the right atrium to the right ventricle. This can serve as an accessory pathway which puts the patient at risk for pre-excitation arrhythmias (WPW). 10-25% of patients with Ebstein’s anomaly will have WPW.

Management of arrhythmias in patients with Ebstein’s anomaly is the same as in the general population.


This patient was admitted to the hospital and seen by pediatric cardiology. Her echo showed mild to moderate tricuspid regurgitation, normal RV pressure, dilated right atrium.

She was started on propranolol and discharged home.



(Attenhofer Jost, et al. Ebstein’s Anomaly. Circulation. 2007;115:277-285)

(Loomba et al, Association of Atrial Tachycarrhythmias with Atrial Septal Defect, Ebstein’s Anomaly and Fontan Patients. Expert Review of Cardiovascular Therapy 2011;9:887.)

EKG of the Week 2019 5-19

This EKG comes courtesy of Dr. Joseph Basile.

A 50 y/o male police officer complains of “agita”. He reports heartburn sensation on and off x 3 days. He had another episode today. He has been taking Tums and Nexium which have been relieving his symptoms.

His EKG is below.

2019 5-19.jpg

1.      What does the EKG demonstrate?

2.      How would you manage this patient?


The EKG demonstrates ventricular bigeminy with an evolving anterior wall STEMI.

The patient should be managed as a STEMI with antiplatelet agents and emergent revascularization.


The EKG shows a sinus rhythm with ventricular bigeminy (every second beat is a PVC). When PVC’s are present on an EKG, it can make the diagnosis of MI difficult because the PVC’s must be ignored and the native beats must be examined for signs of MI.

On this EKG, the native beats in leads V1-V3 show ST elevations with Q waves. There are also mild ST elevations in the native beats of leads V4-V6, I and aVL. There are reciprocal ST depressions in the native beats in leads II, III and aVF. (See arrows below.)

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When faced with an EKG with PVC’s or PAC’s, look at only the native beats to determine the rhythm and to see if there are signs of MI.

Our patient went to the cath lab and was found to have a 100% occlusion of the proximal LAD. A stent was placed and the patient did well.

EKG of the Week 2019 5-5

This EKG comes courtesy of Dr. Cynthia Benson.

A 34 year old male presents unresponsive. He was found by EMS lethargic, and was intubated in the field.

Vital Signs: Pulse  140, BP 80/50.

His EKG is below.

2019 5-5.JPG

1.      What does the EKG demonstrate?

2.      How would you manage this patient?


The EKG shows a widened QRS with prominent R wave in aVR consistent with TCA toxicity.

The patient should be given sodium bicarbonate, IV fluids, and will likely need pressors.



The EKG shows a tachycardia, with slight widening of the QRS, and a terminal R wave in lead aVR, with terminal S waves in lead I and aVL. This is characteristic of sodium channel blockade from tricyclic antidepressant (TCA) toxicity. This patient ingested Amitriptyline. An empty bottle was found next to him.

TCA toxicity causes sodium channel blockade so it slows phase 0 depolarization of the action potential. This results in a widened QRS complex. The right bundle branch normally has a longer refractory period than the left bundle branch. So, when the TCA slows depolarization, it slows it more in the right bundle branch than in the left. That means that after the left bundle is finished conducting the right bundle is still firing. So there is extra conduction towards the right side of the heart at the end of the QRS. It’s almost like a mini right bundle branch block. This results in a rightward shift of the terminal 40-ms of QRS axis and a right bundle branch block pattern.

On a normal EKG, the QRS in aVR looks like this:

2019 5-5 normal aVR.jpg

In our TCA EKG, aVR has a positive deflection at the end of the QRS (terminal R wave) in aVR:

2019 5-5 aVR.jpg


On a normal EKG, lead I and aVL look like this:

2019 5-5 Normal I and aVL.jpg


In our TCA EKG, we see a negative deflection (terminal S wave) in leads I and aVL: 

2019 5-5 I and aVL.jpg

Initial treatment of this patient should include resuscitation with IV fluids and pressors. The antidote for TCA toxicity is sodium bicarbonate. This accomplishes sodium loading to overcome the sodium channel blockade and also accomplishes serum alkalinization.


EKG of the Week 2019 4-21

A 73 year old male with a history of a-fib S/P ablation 3 years ago. Presented to the ED complaining of weakness and near-syncopal episodes. He had no recent changes in medication. He had no chest pain.

His monitor strip is below. This occurred several times during his ED stay.

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1.      What does the monitor show?

2.      How would you manage this patient?


The monitor strip shows a sinus rhythm with a prolonged sinus pause.

 The patient is symptomatic with prolonged pauses. He should have a transvenous pacemaker placed.


The patient presented with near syncopal episodes. He was noted to be in sinus rhythm. However, on the monitor he had multiple prolonged pauses.

Pauses on EKG can be caused by: 1) non-conducted PAC’s (most common cause); 2) sinus node disease (Sinus arrest or SA block); 3) AV block.

In a non-conducted PAC, you will see a P wave that comes earlier than expected with no QRS complex following it. This happens because the PAC occurs so early that when it hits the AV node, it is still refractory. The P wave may come so early that it is buried in the preceding T wave just before the pause. Look back at the last T wave before the pause and see if it looks different than the other T waves on the strip. If it looks different, it might be because there is a P wave buried in that T wave. These pauses are usually very brief.

In sinus node disease, you will see a pause with no P waves. In sinus arrest, the SA node takes a little vacation and doesn’t fire. So there will be a pause with no P waves and the length of the pause will be random. In SA block, the SA node continues to fire but can’t depolarize the atrium. So, again there are absent P waves, however the length of the pause will be a multiple of the normal P-P length. Meaning, if you make believe a P wave happened during the pause at it’s expected location, the next P wave will come on time.

Finally, if the pause is due to AV block (2nd or 3rd degree), there will be P waves coming on time with no QRS complex following.

In our case, the patient has a prolonged pause with no P waves and is consistent with sinus node disease.

The patient had a transvenous pacemaker placed and subsequently had a permanent pacemaker inserted.

The following algorithm is useful in diagnosing pauses:

Algorithm Pauses.jpg

EKG of the Week 2019 4-7

This EKG comes courtesy of Dr. Tony Gao.

A 68 year old male presents complaining of chest pain and SOB x 2 hour. Described as pressure-like. Non-radiating. Began with mild exertion.  Has been persistent since.

Vital signs: Pulse – 65, Respirations – 18, BP 140/90.

His EKG is below.

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1.      What does the EKG demonstrate?

2.      How would you manage this patient?


The EKG shows ST elevation in lead I and aVL consistent with a lateral wall MI.

The patient should be managed as a STEMI with antiplatelet therapy and urgent revascularization.



The EKG shows ST elevations in lead I and aVL as well as 0.5 mm ST elevations in leads V5 and V6. There are reciprocal depressions in lead III.


ST elevations represent acute injury to the myocardium. Leads II, III and aVF look at the inferior wall. Leads V1 and V2 look at the interventricular septum. Leads V3 and V4 look at the anterior wall. Leads V5, V6, I and aVL look at the lateral wall.


The most common location of a STEMI is in the inferior wall. Next is the anterior wall and the least common location is the lateral wall. Lateral wall ST elevations are often more subtle than in other walls of the heart.


Our patient went to the cath lab and was found to have a 100% occlusion of the left circumflex artery. He had a successful PCI and did well.