EKG of the Week Answer 2018 8-12

An 82 y/o female presents for syncope. While sitting at home she felt light-headed then passed out. A few minutes later she had a second syncopal episode. There was no seizure activity. She had no chest pain or shortness of breath.

Past medical history: Pacemaker placed 2 weeks prior for pauses.

V/S: Pulse 30, R 18, BP 110/70. She was awake and alert with a normal mental status.

Her EKG is below.

2018 8-12.jpg

1.       What does the EKG demonstrate?

2.       What are the possible causes of this problem?

 

ANSWER:

The EKG demonstrates intermittent pacemaker failure to capture.

Failure to capture can be caused by lead fracture, lead displacement, electrolyte abnormalities and ischemia.

 

The EKG shows intermittent pacemaker failure to capture. Some pacer spikes are followed by QRS complexes and some spikes are not. This is the cause of the patient’s syncope. When the pacemaker does not capture the patient reverts to her native rhythm (sinus bradycardia with pauses) and then passes out.

Causes of pacemaker failure early after placement include lead fracture and lead displacement. Lead displacement is the most common cause. It is most likely to occur in the first month after placement. Lead fracture typically occurs at the site of attachment to the pulse generator or at abrupt angulations. Chest X-ray is very useful to assess for these complications (Rosen’s Emergency Medicine 7th Ed. Ch. 78). Look for fractures of the leads. Also look to make sure the lead tip is in the proper position. Comparing this X-ray to an X-ray taken after pacemaker placement will be very helpful.

Blood tests can assess for electrolyte abnormalities and ischemia.

Next, your EP consultant or the representative from the device company can assess the device. To determine the cause of the failure, measure the lead impedance and the threshold. The chart below is useful.

2018 8-12 chart.jpg

                 Indian Pacing Electrophysiol J. 2003 Oct-Dec; 3(4): 231–238.

 

Our patient had a very high threshold for capture. The output was increased to 8 Volts with a pause of 1 second to achieve capture. At this setting the patient remained with 100% capture.

She was admitted to telemetry and EP was consulted. She was found to have dislodgement of the ventricular lead. The lead was replaced and the patient did well.

 

 

EKG of the Week 2018 7-29

An 82 year old female presents for light-headedness. She states she feels weak and feels like she will pass out. No chest pain, no SOB.

Vital signs: Pulse – 45, BP 100/70, Respirations – 16.

Her EKG is below.

2018 7-29.jpg

1.       What does the EKG demonstrate?

2.       How would you manage this patient?

 

ANSWER:

The EKG shows 3rd degree AV block.

Pacing pads should be placed on the patient’s chest. Causes of the AV block should be sought and corrected.

 

The EKG shows a bradycardia, with the presence of P waves and some dropped P waves (i.e. P waves without a QRS following it).

2018 7-29 dropped P waves.jpg

This can be caused by 2nd degree or 3rd degree AV block. Differentiating these can sometimes be difficult. First, measure the R-R intervals. If they are irregular, you are likely dealing with a 2nd degree AV block (likely type I). If the R-R intervals are regular, you should then measure the P-R intervals. If the R-R intervals are regular and the P-R intervals are also regular, you are again dealing with a 2nd degree AV block (likely type II). If the R-R intervals are regular and the P-R intervals are irregular, that is consistent with 3rd degree AV block.

On this EKG, the R-R intervals are regular…

2018 7-29 R-R intervals are regular.jpg

…and the P-R intervals are irregular:

2018 7-29 P-R interals are different.jpg

This is consistent with 3rd degree AV block.

The algorithm below may be helpful:

Algorithm 2nd degree vs 3rd degree AV block.jpg

The management of 3rd degree AV block depends on the patient’s stability and symptoms.

First look for correctable causes such as medication toxicity (beta blockers, calcium channel blockers, digoxin), or electrolyte abnormalities (hyperkalemia). If none of these exist and the patient is unstable they should have an emergent pacemaker placed. If the patient is stable, pacing pads should be placed on the chest in case the patient deteriorates and you need to start pacing them quickly. Otherwise they can then be observed until a permanent pacemaker can be placed.

EKG of the Week 2018 7-8

A 72 y/o female with history of a-fib, MI, complains of chest pressure, onset at rest, non-radiating, associated with SOB. The pain was worsened by taking a deep breath. There was no tearing sensation and no back pain. She had no recent travel, immobilization or surgery.

Her EKG is below.

2018 7-8.jpg

1.     What does the EKG demonstrate?

2.     What is the differential diagnosis for this EKG pattern?

3.     How would you work up this patient?

 

ANSWER:

The EKG shows a-fib with 2 PVC’s and T wave inversions most pronounced in leads V2-V4.

This EKG pattern of T wave inversions in the anteroseptal leads can be seen in anterior wall ischemia, pulmonary embolism, aortic dissection, and intracranial hemorrhage.

Our patient received cardiac enzymes and a D-dimer. Tn was 0.06. D-dimer was 1173. CT showed Right main pulmonary artery embolism extending to right-sided segmental and subsegmental branches.

 

T wave inversions in the anteroseptal leads is abnormal and can be seen in several disease processes. Putting this finding in the context of the patient’s symptoms is very important. For example, if this is seen in a patient with head trauma, it is likely due to intracranial hemorrhage.

Our patient presented with chest pain. She had a previous MI. However, she said this pain was exacerbated by breathing. When asked, she also said this pain was different then her previous MI pain. That prompted the concern for pulmonary embolism which was confirmed by CT.

This patient actually had a chest CT two weeks prior which was negative for PE.

Several EKG patterns have been described in pulmonary embolism including sinus tachycardia, S1Q3T3, S1S2S3, incomplete or complete right bundle branch block, and T wave inversions V1-V4.

Remember to consider a broad differential in patients with chest pain and in patients with anteroseptal T wave inversions.

EKG of the Week 2018 6-24

This EKG comes courtesy of Dr. Lukasz Cygan.

A 43 year old male with no past medical history presented with lightheadedness. He thought the symptoms were worsened by a sour patch candy. He had no chest pain or palpitations.

His vital signs were normal. His EKG is below.

2018 6-24.jpg

1.       What does the EKG demonstrate?

2.       What is the management of this condition?

 

ANSWER:

The EKG shows high take off ST elevations in leads V1 and V2 with a gradually descending ST segment. This is consistent with Brugada type II.

Brugada syndrome is managed with ICD placement. There is no direct treatment for Brugada syndrome.

 

The EKG shows high take off ST elevations in leads V1 and V2 with a gradually descending ST segment. This is sometimes referred to as a “saddle back configuration”. This is consistent with Brugada type II.

Brugada syndrome is a genetic (autosomal dominant) sodium channel defect. It predominantly affects males (90%). Patients with Brugada syndrome are at risk for polymorphic V-tach. Patients who had a syncopal or near-syncopal episode who have an EKG pattern consistent with Brugada syndrome must be suspected of having had an episode of V-tach.

Brugada type I presents with downsloping, or “coved”, ST elevations in leads V1 and V2 leading into inverted T waves. There is no isoelectric separation between the QRS complex and the T wave.

There is no specific treatment for Brugada syndrome. So, these patients require placement of an ICD to manage their ventricular arrhythmias.

Our patient went to the EP lab and the diagnosis of Brugada was confirmed. He had an ICD placed and is doing well. The sour patch candy was likely a red herring.

 

 

 

EKG of the Week 2018-6-10

This EKG comes courtesy of Dr. Kong.

A 60 y/o male with hx of HTN, presented for palpitations.

V/S: P - 140, BP 180/90, R - 18.

Two EKG's are below. EKG a was the first EKG.

2018 6-10a.png

EKG b was taken after the patient was given diltiazem.

2018 6-10b.png

1.       What rhythm is demonstrated in EKG a?

2.       What other pattern is demonstrated in EKG a?

3.       What happened to the QRS complexes between EKG a and EKG b?

 

ANSWER:

The rhythm is atrial fibrillation with a rapid ventricular response. 

There is a left bundle branch block

The bundle branch block went away. This is known as a rate related bundle branch block.

 

The first EKG shows rapid a-fib with a left bundle branch block. The patient was treated with diltiazem with resultant control of the heart rate. When that happened the bundle branch block disappeared and the QRS narrowed. This is known as a rate related bundle branch block.

As the heart rate increases, the cardiac cycle shortens. Eventually the next beat arrives when one bundle is still refractory. So it conducts down the other bundle and then across the heart, the same as in a regular bundle branch block. However, when the heart rate slows, the cardiac cycle lengthens and the bundle recovers. When the bundle recovers the bundle branch block disappears.

No specific treatment is needed for a rate-related bundle branch block.

EKG of the Week 2018 5-27

This EKG comes courtesy of Dr. Litvak and Dr. Calabro.

A 59 y/o male with no significant past medical history presented to the ED complaining of weakness and shortness of breath. He had been fatigued for several weeks. He presents drowsy.

V/S: Pulse 120, Respirations 28, BP 180/90.

His EKG is below.

2018 5-27.jpg
  1. What does the EKG demonstrate?
  2. How would you manage this patient?

 

ANSWER:

The EKG shows a wide QRS complex with an irregular rhythm.

This EKG is concerning for hyperkalemia. This patient’s Potassium was 9.9. He was treated with calcium, insulin, glucose, albuterol, bicarb and 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.

This patient was given calcium. The repeat EKG below shows some improvement in the rhythm but the QRS remained wide.

2018 5-27b.jpg

The patient was found to have AKI with BUN 225 and Cr 25. Blood gas showed pH 6.95, pCO2 16, HCO3 4. A foley was placed and the patient was anuric.

The patient was sent for emergent dialysis. After dialysis the EKG (below) shows a normal sinus rhythm with a narrow QRS complex.

2018 5-27c.jpg