EKG of the Week 2019 10-27

This EKG comes courtesy of Dr. Michael Kaiserian.

A 67 year old male presented to the Emergency Department complaining of generalized fatigue for two days. He was recently diagnosed with leukemia but did not start any treatment yet.

Vital signs: Pulse 40, Respirations 16, BP 130/80.

His EKG is below.

2019 10-27.JPG

1.      What is the rhythm?

2.      How would you manage this patient?


The EKG shows a junctional escape rhythm.

 The patient is stable. Atropine can be attempted. Causes for the bradycardia should be sought.


 The EKG demonstrates a bradycardia at a rate of approximately 40. There are no P waves prior to the QRS complexes. There are retrograde P waves following the QRS complexes (best seen in the rhythm strip in lead II). The rhythm is regular, and the QRS complex is relatively narrow. This is consistent with a junctional escape rhythm. Junctional escape rhythms may present with absent P waves or with retrograde P waves.

When faced with a bradycardia, the algorithm below may be helpful to diagnose the rhythm.

Bradycardia algorithm.jpg

Patients with bradycardia can be treated with atropine. If they are unstable, they should be treated with transcutaneous or transvenous pacing. In a stable patient, you have more time to analyze the rhythm and investigate potential causes.

Some potentially reversible causes include hyperkalemia, and medications such as digoxin, beta blockers and calcium channel blockers. So, obtaining a quick potassium level from a blood gas can be very useful. A medication history should be obtained as well.

This patient was found to have hyperkalemia. They were treated with IV Calcium. The repeat EKG is below:

2019 10-27b.JPG

It shows restoration of sinus rhythm. Patients with arrhythmias due to hyperkalemia should be treated with calcium followed by medications to shift potassium out of the blood.

EKG of the Week 2019 10-6

This EKG comes courtesy of Dr. Ben Chill.

A 50 y/o male with a history of adrenal insufficiency presented with altered mental status.

V/S: P – 55, R – 12, BP 90/60.

His EKG is below.

2019 10-6.jpg

1.      What does the EKG demonstrate?

2.      What is the significance of this finding?

3.      How would you manage the patient?


The EKG shows Sinus bradycardia with Osborn waves.

 It suggests hypothermia.

 The patient should be treated with rewarming.


The EKG demonstrates a widened QRS complex with positive deflections at the end of the QRS complex in leads V2-V6. These deflections are called Osborn waves or J waves. This suggests hypothermia.

Although this case occurred during this time of year, when it is not cold outside to cause environmental hypothermia, our patient had adrenal insufficiency. His core temperature was 88 degrees F.

Hypothermia causes several EKG changes including bradycardia, lengthening of all intervals (PR, QRS, QT), atrial fibrillation and Osborn waves.

 Osborn waves are deflections at the J point in the same direction as the QRS complex. The height of the Osborn wave is proportional to the degree of hypothermia. Osborn waves typically appear when the core temperature drops to approximately 87 degrees F (30.5 degrees C). The mechanism for the generation of Osborn waves is unclear, but it may be due to unequal depolarization and repolarization.

 Our patient was treated with rewarming.  Because the underlying cause was adrenal insufficiency, he was also treated with parenteral steroids. He was admitted to the ICU.


(Vassallo et al. A Prospective Evaluation of the Electrocardiographic Manifestations of Hypothermia. Acad Emerg Med 1999; 6:1121– 1126)




EKG of the Week 2019 9-22

This EKG comes courtesy of Dr. Ahad Anjum.

A 67 year old male with a history of end stage renal disease on dialysis, presented complaining of substernal crushing chest pain and bilateral shoulder pain, 5/10, associated with shortness of breath. Onset at rest.

Vital signs: Pulse – 62, BP 103/56, Respirations 20, O2 sat 98%.

His first EKG (EKG a) is below.

2019 9-22a.JPG

A second EKG (EKG b) was performed with right sided leads.

2019 9-22b.JPG

1.      What does EKG a show?

2.      What does EKG b show?

3.      What medication is contraindicated in this patient?

4.      How would you manage this patient?


EKG a shows an infero-posterior STEMI with a 2nd degree type I AV block

EKG b shows ST elevations in V3R and V4R.

 Nitroglycerin is contraindicated.

 The patient should be managed as an acute STEMI with antiplatelets, anticoagulation and urgent revascularization. Nitroglycerin should not be given.


EKG a shows ST elevations in leads II, III and aVF. There are reciprocal depressions in lead V5, V6, I and aVL. This suggests an inferior wall STEMI. There are also R waves with ST depressions in lead V2. This suggests posterior involvement as well.

The EKG also shows a 2nd degree type I AV block. The PR intervals get progressively longer and ultimately there is a dropped P wave. This type of AV block often occurs in the setting of an inferior wall MI. As the ischemia is corrected, the AV block goes away as well.

The inferior wall is typically supplied by the right coronary artery (RCA). If there is a distal occlusion of the RCA, you will get an inferior wall MI. If there is more proximal occlusion of the RCA, you will get an inferior wall MI as well as a right ventricular MI. This is important to recognize because a right ventricular MI is a contraindication to nitroglycerin. So, any time you see an inferior wall STEMI, you must do right sided leads to exclude right ventricular MI prior to giving the patient nitroglycerin.

In our patient, the right sided leads showed ST elevations in V3R and V4R consistent with right ventricular MI. Patients with inferior wall MI and right ventricular MI have decreased cardiac output as well as decreased preload. If nitroglycerin is given, venous return to the heart decreased, preload to the left ventricle will decrease and cardiac output will decrease even more. Blood pressure will plummet. So, nitroglycerin is contraindicated in right ventricular MI’s.

Our patient was sent to the cath lab and was found to have a 100% proximal RCA occlusion and an EF of 25%. A stent was placed.

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.