EKG of the Week 2017 12-3

This EKG comes courtesy of Dr. Kevin Tavangarian.


A 17 year old female with no past medical history presents to the ED S/P cardiac arrest. Her father heard her fall in her room and came in to find her “jerking all extremities” then became unresponsive. She was found by EMS in v-fib. She was defibrillated once with ROSC. She presented to the ED with a pulse, intubated and sedated. Her EKG on presentation to the ED is below.

2017 12-3.jpg

1.    What does the EKG demonstrate?

2.    How would you manage this patient?



The EKG shows significant QT prolongation.

Electrolytes should be checked. A medication and drug history should be obtained. If all those are negative, the patient will likely need an ICD.


The EKG shows a sinus rhythm with significant QT prolongation (the T wave goes into the next P wave).

QT prolongation can be congenital. It can also be caused by many medications, as well as electrolyte abnormalities including hypocalcemia and hypokalemia.

In our patient, the K was 3.2. All the remaining labs were normal. She was not on any medications. As far as the team was able to elicit, there was no history of drug use.

QT prolongation puts patients at risk for ventricular arrhythmias such as ventricular tachycardia, Torsade de Pointes, and ventricular fibrillation. This is likely what happened in our patient.


EKG of the Week 2017 11-19

This EKG comes courtesy of Dr. Elias Youssef.

A 51 year old male with no past medical history complains of chest pain. The pain woke him from sleep. It is right sided, described as sharp. It radiates to the mid back. It is associated with shortness of breath and the pain is worse when he takes a deep breath. There is no nausea or vomiting.

The EKG is below.

2017 11-19.jpg

1.    What does the EKG demonstrate?

2.    How would you manage this patient?



The EKG shows hyperacute T waves in leads V2-V4.

Hyperacute T waves can be an early sign of an STEMI. Serial EKG’s should be performed as the ST elevations may develop. Even if the ST elevations do not develop, urgent cardiology consultation should be sought as these patients may have a proximal LAD occlusion and may need urgent PCI.


The EKG demonstrates tall symmetric T waves in leads V2-V4. This can be an early sign of a STEMI. Serial EKG’s may evolve and start to show ST elevations in those same leads.

However, in some patients this T wave pattern persists and ST elevations never develop. Nevertheless these patients are found at cath to have proximal LAD occlusions. These are referred to as deWinter’s T waves. The EKG shows 1- to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continue into tall, positive symmetrical T waves. In most patients in the deWinter article there was a 1- to 2-mm ST-elevation in lead aVR.

It is difficult to differentiate these T waves from the peaked T wave seen in hyperkalemia. When you see this T wave pattern, both hyperkalemia and acute coronary syndrome should be considered in the differential.

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

REFERENCE: de Winter et al. A New ECG Sign of Proximal LAD Occlusion. N Engl J Med 2008:359;19.

EKG of the Week 2017 11-5

This EKG comes courtesy of Dr. Eric Golike.

A 47 year old male with a history of HTN and high cholesterol was awoken from sleep with chest pressure through his mid chest. The pain is non-radiating. It began two hours prior to arrival in the ED and has been constant.

The EKG is below.

2017 11-5.jpg

1.       What does the EKG demonstrate?

2.       How should this patient be managed?



The EKG shows ST elevations in leads V2-V5, I and aVL with reciprocal depressions in leads II, III and aVF. There is an underlying right bundle branch block.

This EKG meets STEMI criteria. The patient should go to the cath lab for emergent PCI.


The EKG shows an underlying right bundle branch block (RBBB). The criteria for a RBBB are:

1.       Widened QRS complex

2.       RSR’ pattern in leads V1-V3

3.       Deep terminal S waves in leads V5, V6, I and aVL

4.       Secondary ST/T changes in leads V1-V3

In addition, there are ST elevations in leads V2, V3, V4, V5, I and aVL with reciprocal depressions in leads II, III and aVF. This represents an anterolateral acute MI.

A left bundle branch block can mimic ST elevations and can mask the presence of an MI. So, ST elevations in a left bundle branch block may not signify an acute MI. Sgarbossa’s criteria are needed to determine if the ST elevations represent an acute MI. However, a right bundle branch block does NOT mask ST elevations. So, if you see ST elevations in the presence of a right bundle branch block, it is indicative of an MI.

This patient was seen at a community hospital which does not have PCI capabilities. He was transferred to the University Hospital and went straight to the cath lab where he was found to have a 100% proximal LAD occlusion.

2017 11-5 cath pre PCI.jpg

Two stents were placed and flow was restored:

2017 11-5 cath post PCI.jpg

EKG of the Week 2017 10-8

A 70 y/o male with a long standing history of hypertension presents to the ED complaining of chest pain. Vital signs are: Pulse 60, BP 200/110, Respirations 18. His EKG is below.

2017 10-8.jpg

1.       What does the EKG show?

2.       What is the significance of these findings?



The EKG shows evidence of Left Ventricular Hypertrophy (LVH) with ST depressions in leads V4-V6. This is known as “LVH with strain”.

This pattern indicates strain on the left ventricle, and represents a patient at increased risk for coronary artery disease.


The EKG shows a sinus rhythm with a PAC (beat #2).

There is large voltage on the EKG. The S wave in lead V1 is approximately 30 mm. The S wave in lead V2 is approximately 25 mm. The R wave in aVL is approximately 20 mm. This is consistent with Left Ventricular Hypertrophy (LVH). LVH is a common complication of long standing hypertension. There are several different diagnostic criteria for LVH on EKG. Some are:

1.       R wave in lead V5 or V6 > 25 mm

2.       S wave in lead V1 or V2 > 25 mm

3.       R wave in lead V5 or V6 + the S wave in lead V1 > 35 mm

When the LVH pattern is accompanied by ST depressions and T wave inversions in the lateral precordial leads (as in this EKG), this is referred to as “LVH with strain”. Similar to right ventricular strain in the setting of pulmonary embolism, this finding represents left ventricular strain. It is caused by delayed repolarization of the left ventricle so the spread of repolarization is reversed. This EKG finding is not very sensitive but it is pretty specific for LVH with strain (specificity 90-100%). It indicates some degree of systolic dysfunction. Patients with LVH with strain have an increased risk for coronary artery disease, MI and ventricular arrhythmias.

LVH with strain on an EKG represents a poor long term prognostic factor.



(Wagner, Marriott’s Practical Electrocardiography, 10th Ed. pp. 84, 91)

(Ogah et al. Cardiovasc J Afr 2008; 19: 39–45.)

Case 55

70 yoF with PMH of CHF, HTN, HLD, DM2 presents to the ED with abdominal bloating and discomfort for 3 weeks. Denies N/V/D, fever, chills, urinary symptoms, bloody stool, CP, SOB. Last seen by PMD 5 years ago.

T 98.8 (R), BP 180/100, HR 97, RR 16, O2 99% RA

EXAM: Head atraumatic, PERRLA, ears clear BL, throat midline. Heart RRR no MRG. Lungs CTAB. Abd with mild periumbilical discomfort. Extremities warm, well perfused.

Images obtained by ultrasound are seen below. 


1.     What do you see?
2.     What are the normal dimensions of the aorta?
3.     What are the different views and landmarks needed to identify the aorta by ultrasound?
4.     What are the next steps in the management of this patient?
5.     Where are 95% of abdominal aortic aneurysms located?


  1. Saccular abdominal aortic aneurysm
  2. The aorta should measure less than 3.0 cm in diameter, and iliac arteries should measure less than 1.5 cm in diameter, measured from outer wall to outer wall.
  3. Proximal aorta: “sea gull” sign which is created by the celiac trunk/axis splitting into the common hepatic artery and splenic artery. The left gastric artery is also part of the celiac axis, but is not visualized during the transabdominal bedside ultrasound scan.
    Middle aorta: “mantle clock” sign created by the superior mesenteric artery and the hyperechoic fat surrounding the vessel.  The splenic vein runs superior to the SMA and the left renal vein runs inferior to the SMA and superior to the aorta.   
    Distal aorta: located just proximal to the iliac bifurcation.
  4. Consult vascular surgery. Medical optimization of blood pressure.
  5. 95% of abdominal aortic aneurysms are located in the infrarenal portion of the aorta.

EKG of the Week 2017 9-24

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 148, R 28, BP 85/59

The EKG is below.

2017 9-24.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 is below.

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It 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.

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 put 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.)