EKG of the Week 2019 5-5

This EKG comes courtesy of Dr. Cynthia Benson.

A 34 year old male presents unresponsive. He was found by EMS lethargic, and was intubated in the field.

Vital Signs: Pulse  140, BP 80/50.

His EKG is below.

2019 5-5.JPG

1.      What does the EKG demonstrate?

2.      How would you manage this patient?

ANSWER:

The EKG shows a widened QRS with prominent R wave in aVR consistent with TCA toxicity.

The patient should be given sodium bicarbonate, IV fluids, and will likely need pressors.

 

  

The EKG shows a tachycardia, with slight widening of the QRS, and a terminal R wave in lead aVR, with terminal S waves in lead I and aVL. This is characteristic of sodium channel blockade from tricyclic antidepressant (TCA) toxicity. This patient ingested Amitriptyline. An empty bottle was found next to him.

TCA toxicity causes sodium channel blockade so it slows phase 0 depolarization of the action potential. This results in a widened QRS complex. The right bundle branch normally has a longer refractory period than the left bundle branch. So, when the TCA slows depolarization, it slows it more in the right bundle branch than in the left. That means that after the left bundle is finished conducting the right bundle is still firing. So there is extra conduction towards the right side of the heart at the end of the QRS. It’s almost like a mini right bundle branch block. This results in a rightward shift of the terminal 40-ms of QRS axis and a right bundle branch block pattern.

On a normal EKG, the QRS in aVR looks like this:

2019 5-5 normal aVR.jpg

In our TCA EKG, aVR has a positive deflection at the end of the QRS (terminal R wave) in aVR:

2019 5-5 aVR.jpg

 

On a normal EKG, lead I and aVL look like this:

2019 5-5 Normal I and aVL.jpg

 

In our TCA EKG, we see a negative deflection (terminal S wave) in leads I and aVL: 

2019 5-5 I and aVL.jpg

Initial treatment of this patient should include resuscitation with IV fluids and pressors. The antidote for TCA toxicity is sodium bicarbonate. This accomplishes sodium loading to overcome the sodium channel blockade and also accomplishes serum alkalinization.

 

EKG of the Week 2019 4-21

A 73 year old male with a history of a-fib S/P ablation 3 years ago. Presented to the ED complaining of weakness and near-syncopal episodes. He had no recent changes in medication. He had no chest pain.

His monitor strip is below. This occurred several times during his ED stay.

2019 4-21.jpg

1.      What does the monitor show?

2.      How would you manage this patient?

ANSWER:

The monitor strip shows a sinus rhythm with a prolonged sinus pause.

 The patient is symptomatic with prolonged pauses. He should have a transvenous pacemaker placed.

 

The patient presented with near syncopal episodes. He was noted to be in sinus rhythm. However, on the monitor he had multiple prolonged pauses.

Pauses on EKG can be caused by: 1) non-conducted PAC’s (most common cause); 2) sinus node disease (Sinus arrest or SA block); 3) AV block.

In a non-conducted PAC, you will see a P wave that comes earlier than expected with no QRS complex following it. This happens because the PAC occurs so early that when it hits the AV node, it is still refractory. The P wave may come so early that it is buried in the preceding T wave just before the pause. Look back at the last T wave before the pause and see if it looks different than the other T waves on the strip. If it looks different, it might be because there is a P wave buried in that T wave. These pauses are usually very brief.

In sinus node disease, you will see a pause with no P waves. In sinus arrest, the SA node takes a little vacation and doesn’t fire. So there will be a pause with no P waves and the length of the pause will be random. In SA block, the SA node continues to fire but can’t depolarize the atrium. So, again there are absent P waves, however the length of the pause will be a multiple of the normal P-P length. Meaning, if you make believe a P wave happened during the pause at it’s expected location, the next P wave will come on time.

Finally, if the pause is due to AV block (2nd or 3rd degree), there will be P waves coming on time with no QRS complex following.

In our case, the patient has a prolonged pause with no P waves and is consistent with sinus node disease.

The patient had a transvenous pacemaker placed and subsequently had a permanent pacemaker inserted.

The following algorithm is useful in diagnosing pauses:

Algorithm Pauses.jpg

EKG of the Week 2019 4-7

This EKG comes courtesy of Dr. Tony Gao.

A 68 year old male presents complaining of chest pain and SOB x 2 hour. Described as pressure-like. Non-radiating. Began with mild exertion.  Has been persistent since.

Vital signs: Pulse – 65, Respirations – 18, BP 140/90.

His EKG is below.

2019 4-7.jpg

1.      What does the EKG demonstrate?

2.      How would you manage this patient?

ANSWER:

The EKG shows ST elevation in lead I and aVL consistent with a lateral wall MI.

The patient should be managed as a STEMI with antiplatelet therapy and urgent revascularization.

 

 

The EKG shows ST elevations in lead I and aVL as well as 0.5 mm ST elevations in leads V5 and V6. There are reciprocal depressions in lead III.

 

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.

 

The most common location of a STEMI is in the inferior wall. Next is the anterior wall and the least common location is the lateral wall. Lateral wall ST elevations are often more subtle than in other walls of the heart.

 

Our patient went to the cath lab and was found to have a 100% occlusion of the left circumflex artery. He had a successful PCI and did well.

EKG of the Week 2019 3-17

This EKG comes courtesy of Dr. Podlog, Dr. Zhi, and Dr. S. Hassan.

 

An 83 year old female presented to the emergency department complaining of dizziness and sob on exertion for two days. Her first EKG is below (EKG A):

2019 3-17a.jpg

She later had a second EKG (EKG B):

2019 3-17b.jpg

 

1.    What does EKG A demonstrate?

2.    What does EKGB demonstrate?

3.    How would you manage this patient?

ANSWER:

EKG A shows a 2:1 AV block with a ventricular rate of 40.

EKG B shows a 3rd degree AV block.

The patient should have a pacemaker placed.

 

The patient presented with dizziness and SOB and was found to be bradycardic. The EKG helps elucidate the type of bradycardia.

EKG a shows bradycardia with the presence of P waves but some dropped P waves. This can occur in 2nd degree or 3rd degree AV block. On EKG A, it appears that some P waves are followed by QRS complexes and others are not. This is consistent with 2nd degree AV block. Every 2nd P wave is dropped, so we can not tell if it is 2nd degree type I or 2nd degree type II.

However, on the repeat EKG, there appears to be no relationship between the P waves and the QRS complexes. The R-R intervals are regular and the PR intervals are irregular. This is consistent with 3rd degree AV block.

Patients with 2nd degree AV block can progress to 3rd degree AV block. Close monitoring is essential. Also, running a loner rhythm strip or frequently repeating the EKG can be helpful to allow you to identify higher grade AV block.

Patients with symptomatic 3rd degree AV block require pacing. Prehospital, these patients should be treated with transcutaneous pacing. In the hospital, a transvenous pacemaker should be placed.

Our patient had a transvenous pacemaker placed. EKG C is the repeat EKG after the pacemaker:

2019 3-17c.jpg

The following algorithm is helpful in diagnosing bradycardias on EKG:

Bradycardia algorithm.jpg

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.