Non Sustained VT: Making a Lasting Impression!

Putting on the Pressure

A 60 yo male presents to EMS with several hours of chest pressure and diaphoresis. A 12 lead ECG is obtained following a 10 beat run of non sustained ventricular tachycardia. Despite the EMT's excitement at "firing up the paddles," the paramedic administers 324 mg of aspirin and prepares for transport to the nearest facility capable of percutaneous coronary intervention. Your partner informs you that the monitor discerns the presence of a paced rhythm. The patient has no previous medical history.


12 LEAD ECG:

12 LEAD ECG Analysis:

A sinus rhythm is present and the rate is regular. Diffuse and concerning ST segment changes appear in this tracing. First, pathologic ST segment elevation occurs in leads V2, V3 and V4. Q waves also appear throughout the tracing. The monitor misinterprets the ischemic Q wave as a pacer spike. The QRS is narrow, so an interventricular conduction delay is less likely responsible for the "false pacer" call. Reciprocal changes appear in lead aVF. There is minimal J point depression in lead III and V6. The baseline is also irregular.


12 Lead ECG Interpretation: 

Sinus rhythm, anterior wall ST segment myocardial infarction.

Comments:

• It is difficult to discern the location of the anatomic lesion based upon this ECG. The large ST segment elevation in the precordial leads suggests involvement of the LAD. The findings of lateral wall ischemia could implicate the circumflex as well. 
• The run of VT was likely due to ventricular irritability. Remember that the most devastating complications of anterior wall ischemia are lethal dysrhythmia and cardiogenuc pulmonary edema 
• Pathologic Q waves generally follow a few rules: (1) larger than a third of the corresponding R wave or (2) measure in excess of 0.03 seconds. Q waves that accompany poor R wave progression are more likely to indicate ischemia. 

Where is the culprit lesion? ST segment morphology

CASE STUDY:

Medics respond to the report of someone with chest pain and shortness of breath. Vital signs are stable. Given concern for acute coronary syndrome, a 12 lead ECG is obtained.

12 LEAD ECG

12 LEAD ECG Discussion

There is a sinus rhythm. ST segment changes are widespread. The inferior leads reveal some ST segment straightening but no frank elevation. Profound ST segment elevation in present in leads V2, V3, and V4. Reciprocal change in the form of ST segment depression is present in lead aVL. ST segment morphology is linked to adverse outcomes. The ST segments in this particular case display a concerning, "straight" shape especially prominent in lead V3.

12 LEAD ECG Interpretation

Sinus rhythm, anterior wall ST elevation myocardial infarction. 

Resolution

The patient was delivered emergently to the cardiac catheterization lab. A bare metal stent was placed in the proximal left anterior descending artery. The patient was discharged without complication on hospital day 2. 

Ante up!

CASE PRESENTATION

The patient is a 40 yo male reporting a 9/10 pressure in the center of his chest. The patient appears pale and diaphoretic.

Family history is significant for early coronary artery disease. The patient felt well prior to experiencing the "pressure in his chest."

What does the 12 lead ECG show ?
Where is this patient's occlusion ?

12 LEAD ECG INTERPRETATION

Sinus rhtyhm, rate of 60, anterior lateral STEMI

A baseline sinus rhythm is present. ST segment elevation is seen in leads V1-V5. Leads I and aVL also reveal significant > 1 mm elevation of the ST segment. Reciprocal changes in the form of ST segment depression are best visualized in the inferior limb leads III and aVF.

The distribution of ST elevation across most of the precordium suggests obstruction of the left main or left anterior descending artery. The LAD supplies blood to the left ventricule. Diagnonal branches of the left coronary artery supply the lateral wall of the left ventricle. Occlusion of a diagnoal branch corresponds to ST elevation in leads I and aVL.

EMS PEARLS
Complications related to a massive anterior myocardial infarction include:
1. Dysrhythmia (VT/VF)
2. Congestive heart failure

Congestive heart failure may occur when approximately 40% of the LV muscle mass is lost to infarction.