EKG of the Week 2019 3-3

This EKG comes courtesy of Dr. Mohammad Hassan and Dr. Husain.

A 30 Year old male with a history of panic attacks presented to the ED complaining of palpitations and SOB. He states it began after drinking iced tea and coffee. He did not syncopize. He denied chest pain, nausea, vomiting.

He appears lethargic with a waxing and waning mental status.

Vital signs: Pulse – 230, Respirations – 20, BP – 90/50.

His EKG is below.

2019 3-3.jpeg

 

1.     What does the EKG demonstrate?

 2.     How would you manage this patient?

ANSWER:

The EKG shows a wide complex tachycardia.

The patient is unstable. The appropriate treatment is electrical synchronized cardioversion.

 

The EKG shows a wide complex tachycardia. That should be treated as v-tach until proven otherwise. In this case, the rhythm is irregular. V-tach should be regular. When you see a very fast irregular wide complex tachycardia, it raises the concern for a-fib with underlying WPW.

The patient was unstable so he was treated with electrical cardioversion. His post-cardioversion EKG is below. It shows a sinus rhythm with a short PR interval and a delta wave consistent with WPW.

2019 3-3b.jpg

It was later discovered that the patient had a history of WPW and had a previous ablation.

WPW puts patients at risk for tachyarrhythmias. SVT is the most common arrhythmia in WPW. A-fib is the most dangerous arrhythmia in WPW. It can lead to unopposed conduction down the accessory pathway which can lead to V fib. 

Patients with a-fib in WPW who are unstable should be treated with electrical cardioversion. Patients who are stable should be treated with procainamide.

Our patient was treated with cardioversion and he converted to sinus rhythm. He became more stable. He was admitted to telemetry and had an ablation performed.

EKG of the Week 2019 2-17

This EKG comes courtesy of Dr. Ross Hardy.

 

A 62 year old male with a history of diabetes presents for generalized weakness for a few days. He also reports nausea and vomiting. He has no fever. No chest pain. Mild shortness of breath.

Vital signs: Pulse – 50, Respirations – 22, BP 160/90, O2 sat 99%, blood glucose 110.

His EKG is below.

2019 2-17.jpeg

1.      What does the EKG demonstrate?

2.      How would you manage this patient?

ANSWER:

The EKG demonstrates bradycardia with peaked T waves, loss of P waves, and a widening of the QRS complex. This is consistent with hyperkalemia. 

The patient should be treated with calcium for myocardial protection. A potassium level should be checked and other medications to lower the potassium should be administered.

 

 

The EKG shows sinus bradycardia with a PAC. There are peaked T waves, loss of P waves, and a widening of the QRS complex.

Labs revealed BUN 90, Creatinine 9, potassium 8.1.

The patient was treated with calcium which improved the EKG. He also was given glucose/insulin and albuterol and was sent for emergent dialysis.

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. Whenever you see a wide QRS complex with a bizarre rhythm or what looks like “slow V-tach”, think about hyperkalemia.

 

 

EKG of the Week 2019 2-3

An 83 year old male with a history of CHF presents complaining of intermittent dizziness. He has no chest pain. He did not pass out.

Vital signs: Pulse 90, Respirations 18, BP 160/90.

His EKG is below.

2019 2-3.jpg

1.       What does the EKG demonstrate?

2.       How would you manage this patient?

ANSWER:

The EKG shows a sinus rhythm with runs of ventricular tachycardia.

The patient is stable. He has runs of v-tach which are making him symptomatic. He can be managed with anti-arrhythmic medications such as amiodarone.

 

 

The EKG shows an underlying sinus rhythm with runs of v-tach (one at the very beginning of the EKG and another towards the end) at a rate of approximately 200. The V-tach is what is causing the patient’s intermittent dizziness.

The treatment of ventricular tachycardia depends on the stability of the patient.

If the patient is in cardiac arrest (i.e. v-tach without a pulse), the patient should be treated like a v-fib cardiac arrest with defibrillation, CPR, and anti-arrhythmic medication.

If the patient is not in cardiac arrest (i.e. v-tach with a pulse) and the patient is unstable, the patient should be treated with electrical cardioversion.

If the patient is not in cardiac arrest (i.e. v-tach with a pulse) and the patient is stable, the patient should be treated with anti-arrhythmic medications. Options include amiodarone lidocaine and procainamide.

Our patient was not in cardiac arrest and was stable. He was treated with amiodarone with food results. He was admitted to the CCU.

 

EKG of the Week 2019 1-20

This EKG comes courtesy of Dr. Khodorkovsky.

An 88 y/o male with a history of CHF presents after a syncopal episode. He does not remember the event. He is currently awake and alert. BP 130/80.

His EKG is below:

2019 1-20.jpg

1.       What does the EKG demonstrate?

2.       How would you manage this patient?

ANSWER:

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. If no reversible cause is identified the patient will need a pacemaker.

 

The EKG shows a bradycardic rhythm with absent P waves, a regular rhythm, with wide QRS complexes and a rate 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 or ventricular escape 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 symptomatic in that he had a syncopal episode. He had a normal potassium and was not on any medications that can cause bradycardia. A transvenous pacemaker was placed.

The following algorithm may be helpful in diagnosing bradycardias:

 

Bradycardia algorithm.jpg

EKG of the Week 2019 1-6

This EKG comes courtesy of Dr. Ann Giovanni.

A 63 year old male, with a history of HTN and DM, was teaching computer class when he had a syncopal episode. EMS was called and he had a second syncopal episode while on the EMS monitor. The rhythm strip is below.

2019 1-6 EMS strip.JPG

He woke up on his own prior to being shocked by EMS. He arrived in the ED with no chest pain and no shortness of breath but feeling like he was going to pass out.

His ED EKG is below.

2019 1-6.jpg

1.    What does the EKG demonstrate?

2.    How would you manage this patient?

ANSWER:

The rhythm strip demonstrates ventricular fibrillation. The EKG shows downsloping ST segments in leads V1-V3 consistent with Brugada syndrome.

Patients with Brugada syndrome require placement of an ICD.

 

Evaluating patients after syncope can be challenging. In the absence of a clear history suggesting a particular cause (i.e. subarachnoid hemorrhage, pulmonary embolism), we are often left wondering whether the patient had a cardiac arrhythmia as the cause of their syncope or was it a more benign cause. The only way to know for sure is to have the patient on an EKG machine at the time of the syncope which usually doesn’t happen. Otherwise we are left with looking at an EKG taken after the syncope to see if it gives us clues that the patient may have had an arrhythmia as the cause of their syncope (i.e. prolonged QT, WPW, Brugada, ARVD).

In this case Dr. Giovanni’s team was fortunate that EMS had the patient on a monitor at the time of a syncopal episode and was able to capture the ventricular fibrillation. Now we know that the patient’s syncope was certainly due to a dangerous arrhythmia. The next question becomes why did the patient have spontaneous v-fib? The EKG gives us the answer.

The EKG demonstrates a sinus rhythm with a 1st degree AV block and PVC’s. There are also downsloping ST segments in leads V1-V3 leading into inverted T waves. There is no isoelectric separation between the QRS complex and the T wave. This is consistent with Brugada syndrome.

Brugada syndrome is a genetic (autosomal dominant) sodium channel defect. It predominantly affects males (90%). Patients with Brugada syndrome are at risk for ventricular arrhythmias such as polymorphic V-tach and v-fib. Patients who had a syncopal episode who have an EKG pattern consistent with Brugada syndrome likely had a ventricular arrhythmia. There is no specific treatment for Brugada syndrome. So, these patients require placement of an ICD to manage their ventricular arrhythmias.

 

It's 2019, let's chat....

Created by the Division of Diversity & Inclusion

Happy new year to all! Every year that goes by, I marvel at how quickly the year has passed. Nevertheless, 2019 is here and, with it, comes a chance to learn and grow. Late last year, I became increasingly aware of an issue that affects all of us. The issue is that of the disturbing rate of physician mental health issues and, specifically how it relates to physician suicide. I know, not the most uplifting topic for the first post in the new year, but an important one to be aware of. However, what’s more important than recognizing that physician suicide is a thing, albeit an unfortunately prevalent one if we read or listen to the news, is the larger issue of how we treat physician mental health issues. Slowly, but surely, the conversation is starting to shift towards understanding that marginalizing mental health issues among healthcare providers, specifically those of us who deal with frontline traumatic cases, is detrimental to all. It is no longer acceptable to hide the fact that issues like depression and anxiety affect many of us. The fear of being stigmatized by our colleagues and medical boards is a large reason that many physicians do not seek the appropriate care they need. The time has come for this to stop. Maybe 2019 will be the year that we can change this.

Check out this recent article published in ACEPNow about one physician’s struggle to retain her medical license to practice after appropriately seeking care for her mental health issues.

Also, here’s an article I recently wrote for FemInEM about physician suicide. Look out soon for a FemInEM podcast I also recently had the pleasure of doing about this very topic. It was educational for me and, hopefully, will be for all of you who listen.

EKG of the Week 2018 12-23

A 34 y/o female presents to the ED complaining of palpitations.

The EKG is below.

2018 12-23.JPG
  1. What finding does this EKG demonstrate?

  2. What is the next step?

ANSWER:

The EKG demonstrates limb lead reversal of the right arm and left arm.

Repeat the EKG with appropriate lead placement.

 

The EKG appears to demonstrate T wave inversions in leads II, III and aVF and can be mistaken for inferior wall ischemia. However, a closer look at the EKG reveals that in lead I the P wave is inverted, the QRS complex is predominantly negative, and the T wave is inverted. In lead aVR, the P wave is upright, the QRS complex is predominantly positive, and the T wave is upright. This is the opposite of what you expect to see in a normal EKG. This clues you in that the right and left arm leads have been reversed. With limb lead reversal, T wave inversions may appear that are not really signs of ischemia.

The findings on EKG in reversal of right and left arm leads are:

  1. inverted P-QRS-T waves in lead I

  2. upright P-QRS-T in lead aVR (as opposed to the expected inversion of these waves in a normal EKG)

  3. QRS vector in lead I does not match that of lead V6

 

Inversion of the P-QRS-T complex in lead I can also occur with dextrocardia. However, with dextrocardia, there will be a lack of normal precordial R-wave progression from leads V1–V6. In reversal of the arm electrodes, the precordial leads will not be affected so R wave progression should be normal.

Reversal of the right leg and left leg leads usually causes no change on the EKG because the right leg lead is only a ground and does not record any electrical activity.

(Harrigan et al. Electrocardiographic Electrode Misplacement, Misconnection, and Artifact. J Emerg Med. 2012;43(6):1038-1044.)