EKG of the Week 2019 9-8

This EKG comes courtesy of Dr. Litvak.


An 83 year old female with a history of COPD and CAD presents to the ED with a brief episode of right sided chest pain associated with palpitations. Patient denies syncope. No nausea or vomiting. No SOB.

Vital signs: Pulse – 80, R – 18, BP - 144/92, O2 sat 98%.

Her EKG is attached.

2019 9-8.jpg

1.     What is the rhythm?

2.     How would you manage this patient?


Sinus rhythm with non-conducted PAC’s

 Non-conducted PAC’s are treated the same as patients with PAC’s – look for a cause, check electrolytes, usually no emergent intervention needed.


The EKG demonstrates a sinus rhythm at a rate of approximately 80. After beats #4, 7 and 11, there are P waves with no QRS complex following them.

2019 9-8b.jpg

However this is NOT 2nd degree AV block. If you map out the P waves, the “dropped” P waves come earlier than expected. In fact, they come right after the preceding T wave. Since the P waves come so early, the ventricles are still refractory so they do not conduct.

The way we know this is not AV block is because the P waves come earlier than expected. This patient needs no emergent intervention and should not have a pacemaker placed.

Non-conducted PAC’s may appear like a 2nd degree AV block. You see P waves with no QRS complex following them and a pause on the rhythm strip. However, to call something 2nd degree AV block, the P waves must come on time (i.e. the P-P interval must be regular). So, whenever you diagnose AV block, measure the P-P intervals and make sure they are regular. If the “dropped” P wave comes early, it is likely a non-conducted PAC and not AV block.

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 2019 8-25

This EKG comes courtesy of Dr. Conor Russell.


58 year old male with PMHx of HTN presented to the ED for diffuse chest pain, 8/10, associated with nausea. Onset 20 minutes prior to arrival while he was mowing the lawn. The patient was given 2 sublingual nitro’s by EMS with no symptomatic relief.

 VS T 98.4, HR 70, BP 149/92, RR 20, SpO2 99%

 Patient was ill appearing, diaphoretic and clutching his chest. 


His EKG is below.

2019 8-25.jpg

1.     What does the EKG demonstrate?

2.     How would you manage this patient?


The EKG shows slight ST depressions with tall T waves in the anterior leads. This is known as deWinter’s T waves.

 This pattern should be recognized as a STEMI equivalent and the patient should have urgent reperfusion.


Hyperacute T waves have long been described as an early finding in acute MI’s. This finding typically evolves into ST elevations.

In 2008 deWinter described an EKG pattern similar to hyperacute T waves that often persisted and never evolved into frank ST elevations. The pattern was noted in 2% of patients with anterior wall MI’s who were found to have 100% LAD occlusions on cath.  The EKG pattern they noticed was, “1-3 mm upsloping ST segment depression at the J point in leads V1-V6 that continues into tall positive symmetrical T waves” (de Winter et al. N Engl J Med 2008;359:2071). There was often associated 1-2mm ST elevations in lead aVR. They recommend that, “Ambulance staff, emergency physicians, cardiologists and other caregivers involved in STEMI networks should familiarize themselves with these sometimes subtle ECG changes. …practitioners should not miss the important finding of the ECG pattern described above to avoid potential delay in treatment” (de Winter et al. Journal of Electrocardiology. 2016; 49:76–80).

 Our patient’s EKG demonstrates slight ST depressions in leads V2-V6 with tall T waves in these leads. (There are also slight ST depressions in leads II, III and aVF). There is slight ST elevation in lead aVR. At the insistence of the brand new ED attending Dr. Russell, the patient was taken to the cath lab and found to have a 100% proximal LAD occlusion. Stents were placed.

Hyperacute T waves from acute ischemia can be difficult to distinguish from peaked T waves seen in hyperkalemia. One article suggests that hyperacute T waves are “asymmetric with a broad base” (Brady et al. J Accid Emerg Med 2000;17:40–45). However, peaked T waves in hyperkalemia are, “tall, narrow, and peaked with a prominent or sharp apex, and are symmetrical” (Brady et al. J Accid Emerg Med 2000;17:40–45).


EKG of the Week 2019 8-12

This EKG comes courtesy of Dr. Mohammed Hassan, Dr. Savarese and PA Vitulli.

A 79 y/o female complained of weakness and dyspnea. She had a past medical history of COPD, CHF, and CLL. She was started on a new chemotherapy drug (venetoclax) one day prior to arrival. 


V/S: P 119, BP 72/39, RR 14, T 97.1 F

Her EKG is below:

2019 8-12.jpg

 1.     What does the EKG demonstrate? 

2.     What is this diagnostic of?

3.     How would you manage this patient?


The EKG demonstrates a sine wave pattern

This is diagnostic of hyperkalemia.

 The patient should be treated immediately with calcium. Other measures for hyperkalemia should be initiated as well.




The EKG demonstrates a sine wave pattern. It looks almost like v-tach but it is slower. This is diagnostic of hyperkalemia. Whenever you see something that looks like “slow v-tach” think about hyperkalemia.

Hyperkalemia causes a series of changes to the EKG. An early sign is peaked T waves. This is followed by flattening of P waves, widening of the QRS complex and ultimately a sine wave.

A sine wave pattern on EKG represents life threatening hyperkalemia. This first step in treatment should be IV calcium. This stabilizes the cardiac membrane against the effects of the hyperkalemia. It does not lower the potassium level. You should start to see the effects of the calcium on the EKG within minutes. The QRS should start to narrow and ultimately return to normal. To fix the potassium level, give insulin (with glucose to prevent hypoglycemia), albuterol, perhaps bicarb and ultimately dialysis.

This patient had a potassium level of 9.7. She also had a uric acid level of 33.9, and a Phosphorus of 18.5. She was found to be in tumor lysis syndrome due to her chemo drug (venetoclax).


The patient required multiple doses of IV calcium. She also received IV insulin, D50, bicarb, and nebulized albuterol. She then went for emergent dialysis.

EKG of the Week 2019 7-28

This EKG comes courtesy of Dr. Khodorkovsky.

A 91 year old female with a history of HTN and a pacemaker, presented for chest pain x 45 minutes. It was described a s “It feels like somebody is sitting on my chest”.

The EKG is below:

2019 7-28.jpg

The patient’s previous EKG is below:

2019 7-28 previous EKG.jpg

1.      What does the current EKG demonstrate?

2.      How would you manage this patient?


The EKG shows a paced rhythm with concordant ST elevations in lead aVL and possibly lead I, and concordant ST depressions in leads V3, V6, III and aVF.

 This EKG is concerning for an acute coronary occlusion. The patient should be sent to the cath lab.



Identifying STEMI in the setting of a paced rhythm can be very challenging. Sgarbossa described criteria which are specific for the early diagnosis of MI (Sgarbossa et al. Am J Cardiol. 1996 Feb 15;77(5):423-4; Sgarbossa et al. NEJM 1996;34:481-7). These criteria are:

Sgarbossa's criteria.jpg

In a normal paced rhythm or a “normal” left bundle branch block, there are “normal” ST depressions and ST elevations. However, the ST elevations typically go in opposite direction to the QRS complex. These are called discordant changes. For example, in the patient’s old EKG, leads V1-V6 demonstrate negative QRS complexes with ST elevations. Leads I and aVL demonstrate positive QRS complexes with ST depressions.

However, our patient’s current EKG demonstrates concordant ST elevations in lead aVL and possibly I. The QRS complex is positive and the ST segments are elevated. This is consistent with Sgarbossa’s first criterion. There are also concordant ST depressions in leads V3, V6, III and aVF. The QRS complexes are negative and the ST segments are depressed. Although the depressions in leads V6, III and aVF are not one of the Sgarbossa criteria, they likely represent a reciprocal change. The concordant ST depression in lead V3 meets the second Sgarbossa criterion. This EKG is clearly changed from the patient’s previous EKG which demonstrated a normal paced morphology.

Our patient’s initial troponin was negative. The second troponin was 3.4. This EKG represents an acute MI in the presence of a paced rhythm.

EKG of the Week 2019 7-14

A 42 year old female with a history of a partial thyroidectomy 20 years ago, presents for abrupt onset palpitations. She has had similar symptoms in the past but they have always been brief. This time it is not going away. She recently flew to New York from Texas. She denies excesses caffeine use, cocaine, amphetamines.

Vital signs: Pulse - 180, R – 20, BP 140/70.

Her EKG is below.

2019 7-14.jpg

1.      What does the EKG demonstrate?

2.      How would you manage this patient?


The EKG demonstrates SVT.

The patient is stable. She can be managed with modified vagal maneuver, adenosine, or other AV nodal blockers.



The EKG shows a narrow QRS complex regular tachycardia with absent P waves and no flutter waves. This is consistent with SVT.

Modified vagal maneuver was attempted which was unsuccessful. The patient then received adenosine 6 mg IV. The EKG below shows what happened during adenosine administration.

2019 7-14b.jpg

The EKG below is after the patient converted.

2019 7-14c.jpg

SVT is caused by a reentry circuit that involves the AV node. So AV nodal blockers are the treatment of choice. Options include adenosine, calcium channel blockers and beta blockers.

SVT can be brought on by many different things. In our patient the recent travel history should raise a suspicion for pulmonary embolism. Our patient had a D-dimer sent which was negative.

The following algorithm can be useful in diagnosing tachyarrhythmias:

tachycardia algorithm.jpg

EKG of the Week 2019 6-16

This EKG comes courtesy of Paramedics Howie Kafka and Jay Teitelbaum.


A 64 year old male with a history of high cholesterol complained of sudden onset 10/10 left sided chest pain with no radiation. Pain began at rest.

Vital signs: BP 184/121, HR 84.

Physical exam: Diaphoretic and ill appearing.

His EKG is below.

2019 6-16.jpg

1.     What does the EKG demonstrate?

2.     What parts of the heart are involved?


The EKG demonstrates ST elevations in leads II, III, aVF, V4-V6, with R waves and ST depressions in leads V1-V3.

This represents an inferoposterolateral STEMI.


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.


When there are both ST elevations and ST depressions on the same EKG, the pathology is where the elevations are. The depressions are only a reciprocal change.


This EKG shows ST elevations in leads II, III, aVF, V4-V6. This represents an inferolateral STEMI. There are also R waves and ST depressions in leads V1-V3. This represents a posterior wall MI.

Remember that the heart is a 3 dimensional structure. That means that it has an entire posterior side as well. Just as the anterior wall, the lateral wall, and the inferior wall can infarct, the posterior wall can infarct as well. Most of the time, the posterior wall does not infarct by itself. It usually occurs together with an inferior wall or infero-lateral MI as in this EKG. However, infarctions of the posterior wall alone can occur in up to 4% of MI’s. In these cases, the other walls of the heart will be normal. None of the standard 12 leads look directly at the posterior wall. So, how can we recognize a posterior wall MI on a 12 lead EKG? We have to infer the presence of a posterior wall MI based on reciprocal changes.

ST depressions can be a sign of primary ischemia, or they can be a reciprocal change of ST elevations in the opposite wall of the heart. Reciprocal ST depressions occur in the leads opposite the wall with the ST elevations. ST depressions in leads V1-V3 are a reciprocal change of ST elevations in the “opposite wall”. The opposite wall of the antero-septum is the posterior wall. ST depressions with R waves in leads V1-V3 are seen in a posterior wall MI.

Imagine a mirror situated between the posterior wall and the anterior wall. If an acute MI occurs in the posterior wall, it would cause ST elevations and Q waves.  Since we can’t see the posterior wall on a standard 12 lead EKG, we can only see the “mirror image” of the posterior wall in the antero-septal leads. The mirror image of ST elevations and Q waves is ST depressions and R waves. So, when we see ST depressions and R waves in leads V1-V3, that indicates a posterior wall MI.

Some people will actually take this EKG and turn it upside down and backwards, and look at leads V1-V3 through the back of the page. If you do that, you will see ST elevations and Q waves.

In the setting of an infero-posterior or infero-postero-lateral STEMI, such as in our EKG, there is no need to confirm the presence of posterior wall involvement as it does not change patient management in any way. However, if the only finding on the EKG suggests an isolated posterior wall MI, you can confirm the presence of a posterior wall MI by doing posterior leads. Place leads V8 and V9 on the left back. They are placed at the same intercostal space as lead V6. Lead V8 is placed in the midscapular line. Lead V9 is placed at the left spinal border. Now run the EKG again and look for ST elevations in leads V8 and V9. If they are present, that is diagnostic of a posterior wall MI.

Our patient went to the cath lab and was found to have a 100% circumflex occlusion.

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.

2019 6-2b.jpg

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.)