EKG of the Week 2017 6-18

This EKG comes courtesy of Dr. Kong.

A 64 year old female presents to the ED complaining of fluttering in her chest. She has no past medical history and is on no medications.

Her vital signs are: Pulse 40, Respirations 16, BP 130/80.

Her EKG is below.

1.       What is the rhythm?

2.       How would you manage this patient?

 

ANSWER:

The rhythm is 2nd degree AV block type I (AKA Wenckebach block).

2nd degree AV block type I usually requires no specific emergency treatment.

 

The EKG shows some dropped P Waves (P waves with no QRS complexes following them). This can be caused by 2nd degree or 3rd degree AV block. 2nd degree AV block has 2 types: type I and type II. In type I 2nd degree AV block, there is progressive lengthening of the PR interval followed by a dropped P wave. Then the cycle begins again. In type II 2nd degree AV block, the PR interval is constant and there are dropped P waves.

A quick way to differentiate type I from type II 2nd degree AV block is to compare the PR intervals before and after the dropped P waves.  In type I, the PR interval before the drop will be longer than the PR interval after the drop. In type II, the PR interval before the drop and after the drop should be the same. (Note: This method is inaccurate in 2:1 AV block.)

On the EKG below, the red arrows are pointing at the dropped P waves. The PR intervals before and after the drop are circled in blue. Note that the PR interval before the drop (0.40 seconds) is longer than the PR interval after the drop (0.20 seconds). This is consistent with 2nd degree type I AV block.

An approach to interpreting a bradycardic EKG is below.

2nd degree AV block type I usually requires no specific emergency treatment. It can occur in the setting of an inferior wall MI. In that case the treatment is to treat the ischemia. If it occurs as an adverse effect of a medication, the medication should be withdrawn.

EKG of the Week 2017-5-28

This EKG comes courtesy of Dr. Khodorkovsky.

An 87 year old male with a history of HTN presents to the ED for chest pain and shortness of breath which began the night before. He vomited this morning.

V/S: Pulse 102, Respirations 16, BP 86/52.

He is ill appearing on exam.
His EKG is below.

1.       What does the EKG demonstrate?

2.       What is the diagnosis?

3.       How would you manage this patient?

ANSWER:

The EKG shows sinus tachycardia with an anterolateral ST elevation MI.

The diagnosis is Cardiogenic shock

Cardiogenic shock is managed with aspirin, anticoagulation, vasopressors, and urgent cath.

 

The EKG demonstrates ST elevations in leads V1-V6, I and aVL with reciprocal depressions in leads II, III and aVF. This is consistent with an anterolateral STEMI. It usually suggests a proximal LAD occlusion.

The patient’s clinical condition (acute MI with tachycardia and hypotension) is consistent with cardiogenic shock. Cardiogenic shock is a state of heart failure that results in inadequate cardiac output, hypoperfusion, and end-organ dysfunction. The most common cause is LV dysfunction from an acute MI. It carries a very high mortality rate (50-80%).

The acute MI should be managed as all other MI’s with aspirin and anticoagulation. To manage the shock, Dobutamine can increase cardiac output but it causes hypotension. Norepinephrine is the preferred first-line adrenergic agent.

Cardiac cath with PCI is the treatment of choice.

Our patient went to the cath lab and was found to have a 100% occlusion of the proximal left main, as well as 70% occlusion of the proximal RCA. His ejection fraction was 10%. An intra-aortic balloon pump was placed. He was treated with vasopressors. Unfortunately he expired the following day.

 

Reference: Moskovitz et al. Cardiogenic Shock. Emerg Med Clin N Am 33 (2015) 645–652.

EKG of the Week 2017 5-14

This EKG comes courtesy of Dr. Altberg.

A 17 year old male presents to the ED for a seizure. He has never had seizures before. He is currently awake and alert with normal vital signs.

His EKG is below.

1.       What does the EKG demonstrate?

2.       Does this explain the patient’s seizure?

 

ANSWER:

The EKG demonstrates WPW.

WPW can cause arrhythmias which can look like seizures.

 

The EKG demonstrates a sinus rhythm at a rate of approximately 55. The PR interval is approximately 0.10 seconds. There is a delta wave, best visualized in leads V4, V5, V6, II, and aVF. This is consistent with WPW.

WPW is a syndrome of pre-excitation of the ventricles. There is a by-pass tract connecting the atrium and the ventricle which can by-pass the AV node. Normally, when an impulse conducts down the normal conduction system, there is a delay as it passes through the AV node. When an impulse conducts down the by-pass tract, the impulse is not slowed down as it would be if it went through the AV node. So, the amount of time it takes the impulse to get from the atrium to the ventricle is shorter. This is reflected on the EKG by a short PR interval. Once the impulse leaves the bypass tract, it must travel through ventricular myocardium until it reaches normal conduction tissue. So, the impulse travels slower than normal impulses, and is reflected on the EKG by a delta wave and a wide QRS complex.

Patients with WPW are susceptible to tachyarrhythmias. SVT is the most common arrhythmia.

Arrhythmias can cause syncope with some shaking and this may mimic a seizure. So, keep arrhythmia in your differential of patients who present with seizure, especially new onset. As Dr. Reich teaches us, always do an EKG in a patient with new onset seizure.

EKG of the Week 2017 4-30

This EKG comes courtesy of Dr. Hahn.

An 82 year old female presents to the ED complaining of palpitations. She has no chest pain and denies syncope.  Her vital signs are normal.

Her EKG is below.

1.       What is the rhythm?

2.       How would you manage this patient?

 

ANSWER:

The rhythm is sinus with PAC’s. Every third beat is a PAC. This is called atrial trigeminy.

PAC’s usually require no specific management. Patients can be advised to avoid potential triggers such as sympathomimetics, caffeine, Red Bull, etc.

 

The EKG demonstrates an irregular rhythm, but there is a pattern to the irregularity (i.e. it is not irregularly irregular like a-fib). Beat #3 and beat #4 are preceded by P waves and appear to be sinus beats. Beat #5 comes earlier than expected, has a narrow QRS, and probably has a P wave buried in the T wave from beat #4. Thus, it is a PAC. Beats 6 and 7 are sinus, beat 8 is a PAC. Beats 9 and 10 are sinus and beat 11 is a PAC. This pattern continues. When every third beat is a PAC, that is known as atrial trigeminy.  (Every second beat would be bigeminy. Every fourth beat would be quadrigeminy.)

Premature beats can originate from the atria (PAC’s), the junction (i.e. the AV node – called PJC’s) or from the ventricles (PVC’s). PAC’s appear as a P wave which comes earlier than expected followed by a QRS complex that is narrow. Following the PAC, there is a non-compensatory pause. This means that the length from the P wave preceding the PAC to the P wave of the next normal beat is random. It is not related at all to the distance between the normal P waves in the normal beats. This happens because the PAC “re-sets” the SA node. This means, the PAC depolarizes the SA node, so it has to recover before it can generate the next normal beat.

++++PJCs may have a P wave before or after the QRS complex. The P wave will look different than the sinus P waves and it will often be retrograde (i.e. inverted). PJC’s are uncommon in healthy hearts. They occur in CHF, digoxin toxicity, ischemic heart disease, and AMI (especially of the inferior wall).++

PVC’s have no preceding P wave and the QRS complex is wide and bizarre. It looks distinctly different than the other QRS complexes in that lead. Following the PVC, there is a compensatory pause. This means, if you “march out” the P waves, the P waves will continue to arrive at the expected time after the PVC. This occurs because the PVC does NOT reset the SA node. As far as the SA node is concerned, the PVC never happened. So, the SA node continues to fire at its normal pattern.

PAC’s usually require no specific treatment. Patients should be advised to avoid known triggers. These include cocaine, amphetamines, caffeine, Red Bull, pseudoephedrine, etc. Stress is also a common cause of PAC’s.

 

EKG of the Week 2017 4-16

This EKG comes courtesy of Dr. Altberg.

A 19 year old male presents to the ED intoxicated. He also complains of palpitations. His EtOH level is 261. (This is equivalent to a blood alcohol content of 0.26).

His vital signs are: Pulse 140, Respirations 18, BP 120/80.

His EKG is below.

1.       What does the EKG demonstrate?

2.       How would you manage this patient?

ANSWER:

The EKG demonstrates atrial fibrillation. In the setting of acute alcohol intoxication, this is known as Holiday Heart Syndrome.

The heart rate is normal. No specific interventions are necessary. The patient should be observed on telemetry until the a-fib resolves.

 

Patients who “binge drink” are at risk for supraventricular arrhythmias, with atrial fibrillation being the most common. It can also cause atrial flutter, atrial tachycardia, and PVC’s. These patients are typically healthy with no past history of cardiac disease. When they stop drinking, the symptoms go away. This is known as Holiday Heart Syndrome. The arrhythmias can occur at the time of drinking or up to 36 hours later.

Patients with Holiday Heart Syndrome typically present with palpitations. They may also have chest pain and syncope. There are several mechanisms that have been proposed to explain why Holiday Heart occurs.

Initial treatment of patients with Holiday Heart is the same as other patients with atrial fibrillation. If they are tachycardic, their rate should be controlled with AV nodal blockers. However, they are typically at low risk for clots and usually do not require anticoagulation. Rhythm control is usually unnecessary as the arrhythmia usually resolves spontaneously within 24 hours. They should be admitted to a monitored setting.

 

(Tonelo, et al. Holiday Heart Syndrome Revisited after 34 Years. Arq Bras Cardiol. 2013 Aug; 101(2): 183–189.)

(Voskoboinik, Alcohol and Atrial Fibrillation : A Sobering Review. Journal of the American College of Cardiology. Volume 68, Issue 23, 13 December 2016, Pages 2567–2576)