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. 

Pointy ST Segments and Abnormal Labs

Your crew responds to a local skilled nursing facility for a patient with "abnormal labs." The nurse tells you that the patient's "K was elevated." The patient reports a near syncopal episode approximately 40 minutes prior to arrival. The patient feels weak and dizzy. No chest pain, shortness of breath, or vomiting is endorsed. The patient is ill appearing but awake, alert, and oriented.

Vital signs:
BP: 82/40
P: 49
R: 16
Sp02: 86% on room air

A 12 lead ECG is obtained:

12 Lead ECG Discussion

The rhythm is sinus bradycardia. Unless this 80 year old is a marathon runner, the rate is abnormal. Furthermore, the bradycardia occurs in association with (1) near syncope and (2) abnormal vital signs. ST segment elevation is seen in leads II, III, and aVF. Reciprocal change in the form of ST segment depression is seen in lead aVL. STE is also observed in the lateral precordial leads. The R waves are tall in V2 and V3 but there is no concurrent ST segment depression to suggest involvement of the heart's posterior wall. Q waves, though not pathologic, appear in leads II, III, and aVF, and favor the diagnosis of ischemia.

12 Lead ECG Interpretation 

Sinus bradycardia, Inferior-lateral ST segment myocardial infarction. 

Case Discussion

This case presents more than a few dilemmas and teaching points. First, it emphasizes the association between dizziness, weakness, and acute coronary syndromes. Elderly patients may not present with the classic "chest pain" or "chest pressure." Dyspnea, dizziness, and weakness are well known anginal equivalents and should be aggressively investigated, especially in the setting of abnormal vital signs. The presence of peaked T waves might suggest underlying hyperkalemia. The changes associated with hyperkalemia are usually diffuse. The STE in this ECG follows an anatomic (inferior-lateral) pattern. If there is concern for "abormal labs," then the administration of calcium is probably warranted. Calcium should always be considered first line in the management of hyperkalemic emergencies.

What About the Rate? 

This patient also presents with symptomatic bradycardia. A well accepted axiom in EMS and emergency medicine is, "fix the rate FIRST." EMS protocols would probably advocate for a healthy dose of atropine. Ischemia of the SA node (caused by RCA occlusion) can certainly result in a symptomatic bradycardia, heart blocks, and other types of badness. However, be cautious when administering atropine to a patient suffering from an active MI. Atropine will increase myocardial demand and have the potential to exacerbate ischemic symptoms. A gentle fluid bolus may suffice to mitigate hypotension, and opening of an occluded RCA will make everything right as rain...

KEY POINTS:

• Fix the rate first (WITH CAUTION in cases of active ischemia!) 
• Calcium is first line in the treatment of suspected hyperkalemia and ECG changes
• Weakness, dizziness, and syncope should be regarded as anginal equivalents- especially in the elderly 
• Inferior wall myocardial infarction can produce bradycardia, heart blocks, and syncope

Special thanks to JoElyn for providing these ridiculously complex ECGs! (And best wishes as a newly minted registry medic...) 

"Abnormal ECG" and Bypass of the Closest Facility

So.. would you call this one and activate the cath lab from the prehospital ECG? The patient is a 72 year old female with severe uncontrolled hypertension. She called 911 for mild shortness of breath. Her blood pressure is over 200 mm Hg systolic. The patient is awake, alert, and oriented. The paramedic is bypassing a local facility in favor of the closest cardiac interventional center.

What's your analysis?

12 Lead ECG

 

12 Lead ECG Interpretation and Discussion

A baseline sinus rhythm is present. There is a significant amount of artifact that interferes with interpretation in the limb leads. A fusion beat is seen in the limb lead tracings. However, there is > 1mm of ST segment elevation in lead III. Lead aVF also has minimal ST segment elevation. Pathologic Q waves are present in contiguous leads (III and aVF). Though an isolated Q wave is common in limb lead III, the presence of Q waves in contiguous inferior leads (III and aVF) suggests ischemia. In addition, ST segment depression is present in the reciprocal leads of I and aVL. This finding further supports the presence of acute injury. ST segment elevations are also seen in leads aVR and V1. As discussed in a previous case, the presence of STE in leads aVR and V1 may predict obstruction of the left main coronary artery. Poor R wave progression is present across the precordial leads V2-V6. This finding  (the loss of R wave amplitude) is consistent with the machine generated diagnosis of "anterior infarct, age undetermined." These findings, when put together, reveal an inferior wall STEMI. This patient is best cared for at a facility capable of percutaneous cardiac intervention.

Final interpretation

Sinus rhythm, inferior wall STEMI. Anterior wall ischemia. Reciprocal changes in the form of ST depression present in the anterior-lateral limb leads.