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.

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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:

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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

Epiglottitis and Awake Intubation

Mikhail Podlog, DO                Anna Van Tuyl, MD

Let's start with a case..

HPI:  41 year old male with no PMH presents to ED for sore throat and fever measured at home for 3 days. Patent was seen at urgent care yesterday and was prescribed azithromycin and prednisone for pharyngitis. Today patient started complaining of swelling in his throat and difficulty breathing so came to the emergency department for evaluation. No cough, chest pain, abdominal pain, nausea, or vomiting. No allergies, new food, or new medication.

Vital signs:       T 100.6 Oral     HR 103    RR 26    BP 170/87    SaO2 95% on RA

Physical Exam:  “Erythematous pharynx with elongation of the uvula. Muffled voice. Tender anterior cervical adenopathy”. Otherwise unremarkable exam.

Progress Notes:  ENT called to bedside for laryngoscopy. Patient found to have swollen and beefy red epiglottis with tight airway. Recommendation made for prophylactic intubation

Diagnosis:  Epiglottitis

Management: Treatment consists of three parts: airway, antibiotics, steroids.


The first priority is protecting the airway. The swelling can cause airway obstruction; therefore prophylactic intubation is frequently performed. Because intubation can be difficult, the safest approach is to perform it in the operating room with surgery on standby if an emergency surgical airway is needed. If this is not an option, the safest approach is to perform an awake intubation. During an awake intubation, the patient is consciously sedation but because they are not paralyzed they maintain their respiratory drive. Therefore, if the intubation is unsuccessful, they can continue to maintain their respiratory drive.

Awake intubation steps

  1. Dry the oropharynx - This not only helps with better visualization during intubation but allows the numbing medication to work better
    1. Glycopyrrolate 0.2 mg IV push - anticholinergic agent without CNS effect, takes about 10-20 minutes to take effect
    2. Use gauze in patients mouth to dry it as much as possible
  2. Blunt gag reflex
    1. Zofran 4-8 mg IV push
  3. Numb the oropharynx - once mucosa is dry
    1. Nebulized lidocaine
      1. 5 cc of 2-4% lidocaine
      2. Can use 2% lidocaine with epinephrine to vasoconstrict mucosa and decrease swelling
    2. Viscous lidocaine
      1. Draw up 3-5 cc of 2% viscous lidocaine in syringe and use plastic angiocath to drip down back of tongue
      2. Can alternatively place 3-5 cc of 2% viscous lidocaine on tongue depressor and place upside down on tongue and let drip down
    3. Mucosal atomization device
      1. Advance blade into pharynx slowly and spray about 5 cc of 2-4% lidocaine as you progress towards the vallecula, epiglottis, and cords
  4. Sedate
    1. Similar to procedural sedation
    2. Can use ketamine alone
      1. Start with 10-20 mg IV and push an additional 5-10 mg every minute or so as needed
    3. Ketafol (ketamine with propofol in a 1:1 to a 3:1 ratio)
      1. If using a 10 mg/mL concentration of both sedatives, mix in desired ration and place mixture in 10 cc syringe
      2. Start with 1-2 mL IV and push an additional 5-10 mg every minute or so as needed
    4. Other options include midazolam with fentanyl, or dexmedetomidine
  5. Oxygenation
    1. Preoxygenate with NRB or CPAP (with NC)
    2. Optimally position for oxygenation
    3. Maintain NC at 15L/min for entire procedure
  6. Intubation
    1. Option 1 - Video laryngoscopy
      1. Use buogie and then place endotracheal tube over bougie
    2. Option 2 - Nasal fiberoptic intubation - if you have a fiberoptic scope you can use this route
      1. Spray nasal phenylephrine prior to sedation
      2. Use nasal trumpte coated with viscous lidocaine during preoxygenation to numb nasal cavity, then remove when ready to intubate
      3. Preload endotracheal tube onto fiberoptic cable and nasally intubate
      4. Preloading the endotracheal tube allows you to confirm that it is inserted past the vocal cord by visualizing them as you withdraw the fiberoptic cable
    3. Confirm tube placement!
  7. Sedate

Patient should then be started on empiric combination therapy with a third generation cephalosporin (ceftrimraxone, cefotaxime) and staphylococcal coverage with strong consideration for MRSA coverage (clindamycin, vancomycin).  Corticosteroids such as dexamethasone are frequently administered and have been show to decrease length of stay in the ICU and overall.

Back to the case..

Patient's course: Awake intubation was attempted in the emergency department by the ED attending. Below is a short clip of what was seen on video laryngoscopy.

Even after multiple attempts, awake intubation was unsuccessful so patient was taken to the operating room for fiberoptic intubation with surgery on standby. The patient was successfully intubated and started on Clindamycin, vancomycin, and Decadron. The patient was successfully extubated 2 days later, down graded to a regular floor, and discharged home 2 days later on oral antibiotics. Patient was doing well at one month follow up.

EKG of the Week 2017 8-13

This EKG comes courtesy of Dr. Zhong and Dr. Zhi.

A 72 year old male with a history of schizoaffective disorder presents from a psychiatric center for lethargy and hypoxia.

Vital signs: Pulse 60, Respirations – 18, Blood Pressure – 107/76, O2 sat 80% on room air, Temp - 88.9.

His EKG is below.

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Because you have an awesome EKG tech, you are also presented with an old EKG on the patient (below).

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1.       What does the current EKG demonstrate?

2.       What is the clinical significance of this finding?



The EKG demonstrates Osborn waves (best seen in leads V4-V6)

Osborn waves are seen in hypothermia.


The EKG shows a widened QRS complex with positive deflections at the end of the QRS complex in leads V4-V6. These deflections are called Osborn waves or J waves.

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The EKG also shows ST elevations in leads V2 andV3. However, these were already present on the old EKG.

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 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.


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


EKG of the Week 2017 7-30

This EKG comes courtesy of Dr. Gupta and Dr. Giovanni.

A 31 year old female with a history of congestive heart failure presents to the ED lethargic and tachycardic. Her EKG is below.


1) what is the rhythm?

2) what is this rhythm suggestive of?

3) what is the treatment?


The rhythm is Bidirectional V-tach

The rhythm is suggestive of Digitalis toxicity

The treatment is Digoxin  Fab Fragments


The EKG demonstrates a wide complex tachycardia which is consistent with ventricular tachycardia. However, when you look at the rhythm strip, the QRS complexes appear to go in different directions. This is called bidirectional v-tach and is very suggestive of digoxin toxicity.

Dig toxicity can cause many EKG changes including PVC’s, high grade AV block, and AV block with increased automaticity. Bidirectional ventricular tachycardia is nearly diagnostic, although it may also occur with poisoning by aconitine and other uncommon xenobiotics (Thank you Dr. Kessler!!!).

Dig toxicity is treated with Digoxin Fab Fragments (Digibind). This binds to the digoxin and prevents it from causing further poisoning.