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.

2017 9-24b with arrows.jpg

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.)


EKG of the Week 2017 9-10

A 52 y/o male with a history of HTN presents to the ED complaining of palpitations on and off x 2 days. He reports he has been drinking a lot of caffeinated beverages. He now feels palpitations which begin abruptly, last 1-2 hours, then resolve. They have been recurring over the last couple of days.  His EKG is below.

2017 9-10.JPG

1.    What is the rhythm?

2.    How would you manage this patient?



The rhythm is sinus rhythm with non-conducted PAC’s

Non-conducted PAC’s are benign and usually require no treatment. The main point is to recognize this is NOT 2nd degree AV block and the patient does not need a pacemaker.


The EKG demonstrates P waves followed by QRS complexes. However, the rhythm is not completely regular. Beats 3 and 10 come early. These are premature atrial contractions (AKA PAC’s). We also see pauses on the EKG (after beats 5 and 7). At the beginning of those pauses, we see P waves buried in the preceding T waves. (Look at the notching in those T waves and compare them to the other T waves in the rhythm strip.) These P waves come earlier than expected and therefore also represent PAC’s. However, note that there is no QRS complex following these P waves. This happens because the P wave comes so early, at a time when the ventricles are still refractory. So, they do not conduct. These are called non-conducted PAC’s.

Non-conducted PAC’s may appear like a 2o AV block. You see P waves with no QRS complex following them and a pause on the rhythm strip. This is usually typical of 2nd degree AV block. However, to call something 2nd degree AV block, the P waves must come on time (i.e. the P-P interval must be regular). On our EKG, the P waves come early (i.e. the P-P interval is irregular). So, the reason the ventricles do not conduct is NOT because there is a block in the AV node. It is because the P wave came too early and the ventricles are not ready to contract yet. So, this patient does not have AV node disease and does not need a pacemaker.

Non-conducted PAC’s are a very common cause of pauses on EKG. Whenever you encounter a pause, look back at the preceding T wave before the pause to see if there is a P wave buried in there.

Pauses on EKG can be caused by 3 things: Non-conducted PAC’s, SA node disease (SA block and SA arrest), and AV block. The following algorithm may be useful to diagnose pauses:

Algorithm Pauses.jpg

EKG of the Week 2017 8-27

This EKG comes courtesy of Dr. Khodorkovsky.

An 88 y/o male with a history of CHF presents after a syncopal episode. He is currently awake and alert with a normal mental status.

 Vital signs are: Pulse – 30, Respirations 16, BP 110/70.

His EKG is below:

2017 8-27.jpg

1.       What is the rhythm?

2.       How would you manage this patient?



The rhythm is a ventricular escape rhythm

The patient is hemodynamically stable. Atropine can be attempted. Pacing pads should be placed and the patient should be monitored closely.


The EKG shows a bradycardic rhythm with absent P waves, a regular rhythm, with wide QRS complexes and a rate slightly less than 30. This is consistent with a ventricular escape rhythm.

When the SA node fails, the heart has two back-up systems that can temporarily maintain a heart beat. One is the AV node (also known as the junction) which can produce a junctional escape rhythm. Another is the ventricles which can produce a ventricular escape rhythm (also known as an idioventricular rhythm).

Both rhythms present with absent P waves and a regular rhythm. A junctional escape rhythm produces narrow QRS complexes at a rate of 45-60. A ventricular escape rhythm produces wide QRS complexes at a rate of 30-45.

Treatment of a ventricular escape rhythm depends on the patient’s stability. If the patient is asymptomatic and stable, no emergent treatment is needed. Pacing pads should be placed on the chest in case the patient deteriorates.

If the patient is symptomatic or unstable, they should be treated. Atropine is the first line treatment but it may not be successful. If it is unsuccessful, the patient should be paced (transcutaneous initially followed by transvenous).

This patient was stable so pacing pads were placed and he was monitored. He was admitted to a monitored setting and had a permanent pacemaker placed.

The following algorithm may be helpful in diagnosing bradycardias:

Bradycardia algorithm.jpg