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...) 

Does this young man really need to go to the hospital?!

Case Study

You are dispatched to a 32-year-old male who experienced a syncopal episode while grocery shopping. Upon arrival, you find an awake, alert, and oriented adult male. He apologizes profusely for disturbing you and tells you he is fine. He denies having chest pain, shortness of breath, or unexplained sweating. He states that he skipped breakfast earlier in the day and had quite a bit of alcohol the night before. You explain the importance of checking his vital signs and blood sugar and he agrees to let you check them. His vital signs are: blood pressure 124/74, pulse 62, respirations 18, SpO₂ 99%, blood sugar 90 mg/dL. His lung sounds are clear, skin cool, dry and pink, abdomen soft and non-tender. Your partner explains the importance of acquiring an ECG and the patient agrees.

12-Lead ECG

§  What is your interpretation?

§  Do you see anything life-threatening?

§  What is your next course of action?

§  Does this patient need to be transported to the hospital?

Case Study Summary

The ECG reveals a sinus rhythm. There are no signs of chamber enlargement, axis deviation, or myocardial ischemia. Close inspection of leads V₁-V₂ reveals an incomplete right bundle branch block (rSR’ pattern), ST segment elevation, and T wave inversion, consistent with Brugada Syndrome.

Brugada Syndrome is a genetic condition involving a sodium channel abnormality in the heart’s cells. The disease causes ventricular tachydysrhythmias that may lead to syncope or sudden death. The disease primarily affects males and is most commonly discovered in the third or fourth decade of life. Brugada Syndrome is reported to cause 5% of all sudden cardiac arrest cases.

This patient should be transported to the emergency department for further evaluation. Treatment for Brugada Syndrome includes electrophysiologic testing and placement of an automated implantable cardioverter-defibrillator.

Clinical Pearls

§  Never dismiss syncope in the prehospital setting.

§  Acquire a 12-Lead ECG on all patients presenting with presyncope or syncope and scrutinize the tracing for changes consistent with life-threatening diseases.

§  Brugada Syndrome is characterized by:

§  An incomplete right bundle branch block (rSR’ pattern in leads V₁-V₂).

§  ST segment elevation in leads V₁-V_2.

§  T wave inversion in leads V₁-V_2.

Suggested Readings

Syncope–http://emedicine.medscape.com/article/811669-overview

Brugada Syndrome–http://emedicine.medscape.com/article/163751-overview

A Serial Case

An elderly male patient is transported to the emergency department following a syncopal episode. The patient reported feeling lightheaded, and experienced two witnessed syncopal episodes lasting for several minutes. Symptoms were made worse when standing up. The patient denied chest pain and reported some mild dyspnea. The patient had been in his usual state of health. The patient's medical history is significant for a tibial fracture several months prior.

Vitals:

Afebrile

BP: 72/P

P: 100

R: 24

Sp02: 92%, poor waveform, on NRB

Physical exam:

Pt is diaphoretic and alert.

Lungs are clear bilaterally.

The patient's abdomen is soft and non tender.
No evidence of lower extremity edema.

(Prehospital) 12 lead ECG:

Upon arrival at the hospital, large bore IV access was secured. A FAST (Focused Assessment with Sonography for Trauma) exam revealed no obvious free fluid and no obvious pericardial effusion. The abdominal aorta appeared grossly normal. The patient remained alert and responded to a bolus of IV crystalloid. A repeat ECG was obtained following another pre-syncopal event in the emergency department.

12 Lead ECG Interpretation and Discussion

On the repeat ECG, a sinus rhythm is present. The electrical axis is physiologic. Artifact interferes with the tracing in the inferior limb leads. ST segment elevation is present in aVR, V1, and V2. The ST segments appear horizontal in shape. That particular morphology is concerning for ischemia. While some mild ST segment depression is present in lead I, there are no clear cut reciprocal changes. The evolving changes suggest a septal wall myocardial infarction.

Final Interpretation

Sinus tachycardia, septal ST segment elevation myocardial infarction

(WRONG!)

Case Conclusion

The patient was transported emergently to the cardiac catheterization lab. The patient's coronary arteries were CLEAN and without evidence of disease. An emergent echocardiogram showed a severely dilated right ventricle with concurrent diastolic dysfunction. The clean coronary arteries and echocardiograpghic findings combined point to a massive pulmonary embolism as the cause of the patient's symptoms. Another subtle clue to this diagnosis was the hypoxia that persisted with high flow oxygen administration.

Though not all that elevates is a STEMI, field providers should nevertheless focus on identifying worrisome ST segment changes. The patient's initial ECG was somewhat non-specific. Though close inspection can reveal some slight ST segment elevation of less than 1mm in aVR and V1, it certainly did not meet standardized criteria for STEMI. The second ECG, however, represents a clear-cut evolution. ST segments have become more pronounced (elevated) in the septal leads. The increase in elevation combined with the horizontal plateau of the ST segments in leads V1-V2 suggest an evolving myocardial infarction- or an alternative diagnosis.

The patient presented with a syncopal episode and profound hypotension. Any number of emergent medical conditions can present with those complaints. Pulmonary embolism, internal bleeding, and aortic dissection must be considered in the initial assessment of the hypotensive patient. Unfortunately, there are no "classic" electrocardiographic findings associated with a large PE. That said, the following features can be seen in the setting of a pulmonary embolism.

PULMONARY EMBOLISM ECG FINDINGS

• Sinus tachycardia
• Right bundle branch block or incomplete right bundle branch block
• Deep S wave in lead I, Q wave in lead III, and an interveted T wave in lead III (S1, Q3, T3)
• T wave inversions
• Right axis deviation
• ST segment deviation (depression and elevation)

Sinus tachycardia and right bundle branch block may suggest "heart strain." These are electrical manifestations caused by the right ventricle that is pumping against a greatly increased pulmonary resistance.

aVR Rears its Ugly Elevation

A cardiologist's office calls 911 for an elderly patient who suffered a syncopal episode. The patient presented to the physician's office for a few weeks of bilateral arm pain and fatigue. The patient experienced mild dyspnea on exertion and was undergoing a chemical stress test when he experienced a brief syncopal episode. The patient was pain free at the time of EMS arrival. The patient was awake and alert. Vital signs:
BP: 104/70
P: 100
R: 22/non labored
Sp02: 96%

The cardiologist suggested transport to a facility capable of percutaneous coronary intervention. Why was the cardiologist so concerned (aside from the presence of an elderly patient with syncope in his office)? What's going on with this ECG?

12 lead ECG

12 Lead Interpretation and Discussion

The patient's rhythm is a borderline sinus tachycardia. ST segment elevation is present in leads aVR and V1. Diffuse ST segment elevation is present in the inferior and lateral leads. Though ST segment elevation in lead aVR isn't typically considered a "STEMI," there is sufficient evidence in the emergency cardiology literature that it should be considered as a "STEMI equivalent." ST segment elevation of > 1 mm (or > 0.5 mm in some studies) is associated with obstruction of the left main coronary artery. Furthermore, these patients are more likely to require surgical revascularization (CABG) or experience congestive heart failure. The skilled paramedic will easily recognize the widespread and diffuse ST segment abnormalities. This patient requires evaluation at a facility capable of percutaneous coronary intervention.

Final 12 lead ECG Interpretation

Sinus rhythm, ST segment elevation in leads aVR and V1. Probable acute obstruction of the left main coronary artery. Diffuse ST segment depression in the inferior (II, III, aVF), anterior (V4-V6), and lateral (I, aVL) leads.

Suggested Readings

• Rokos IC, French WJ, Mattu A et al. Appropriate cath lab activation: optimizing electrocardiogram interpretation and clinical decision making for acute ST elevation myocardial infarction. Am Heart Journ. Dec 2010;160(6):995-1003

• Barrabes JA, Figueras J, Moure C, et al. Prognostic value of lead aVR in patients with a first non ST segment elevation acute myocardial infarction. Circulation. 2003;108(81):814-819

• Williamson K, Mattu A, Plautz CU. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006;24:864-874