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...) 

Simply a Sinus STEMI? No!

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Paramedics respond to a 55 yo female with chest pain and shortness of breath. The patient is alert and hypertensive. The peripheral pulse is irregular.

12 lead ECG: 

12 Lead ECG Interpretation:

The underlying rhythm is most definitely not sinus. A rhythm strip is not included in the LifeNet transmission. Though the first visualized QRS complex in leads I, II, and III APPEARS to be conducted, there is PR interval is excessively long (> 0.2seconds). Furthermore, the P to P intervals appear constant. There is a "p" hiding in the ST segment of the next QRS complex. The constant P to P interval suggests a third degree heart block. ST segment elevation is present in the inferior leads. Reciprocal change is evident in the anterior-septal (V1-V6) and lateral (I, aVL) leads. Recall that ST depression in the septal leads (V1-V2) could indicate posterior involvement. Posterior wall changes generally exhibit tall R waves in leads V1-V3 which are absent in this particular tracing. 

Third degree heart block, inferior wall ST segment myocardial infarction with possible posterior extension. 

12 lead ECG Case Discussion:

This case highlights the importance of a rhythm strip. If there is any question about the presence or absence of an underlying conduction problem, always obtain a rhythm strip. LifeNet provides just a few seconds of rhythm analysis; this interval is occasionally inadequate for proper rhythm determination. Inferior wall changes, coupled with the heart block, suggest injury to the SA node. This patient would benefit from the prophylactic application of pacing pads. Avoid nitrogylcerin in the presence of inferior wall changes and an underlying heart block. 

The "buried P wave" and constant P to P interval: 

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The Deceptive Ears of a Rabbit

This particular ECG resulted in a great deal of discussion. Though I don't have the actual details of the patient encounter, its clear that the ECG machine, the paramedic student, the preceptor, and the emergency physician all contest the actual interpretation of the following tracing. ECGs like this one represent fantastic learning opportunities. When confronted with a bunch of squiggly lines and conflicting information, it is imperative to stay focused and proceed through the ECG interpretation in a stepwise fashion. Judging from all of the hashmarks, pen marks, and circles, there wasn't any resolution by the time the paramedics had cleaned their stretcher and left for their station!

1) What's the rate?
2) What's the rhythm?
3) Are concerning ST/T segment changes present?
4) Where are my defibrillator / pacer pads?

12 lead ECG

12 lead ECG interpretation and discussion

The ECG tracing reveals a regular rhythm. Before getting distracted by rabbit ears or conduction delays, it is important to discern whether or not a sinus rhythm is present. P waves are occasionally visualized, but there is simply no fixed PR ratio. The absence of a fixed PR suggests that a high grade block is present. Considering the widened QRS, it is likely that the tracing represents a third degree heart block. Further corroborating that interpretation is the relatively fixed R to R interval. Putting this together: wide QRS + fixed R to R + varied PR interval  = third degree heart block. By definition, a right bundle branch block or left bundle branch block CANNOT be diagnosed in the absence of a sinus rhythm.

The ST/T segments are grossly abnormal. The large QS wave present in leads III and aVF suggest a prior inferior wall myocardial infarction. In addition, there is poor R wave progression across the precordial leads. The R wave is still of decreased amplitude in lead V4. Recall that the R wave should transition to a mostly positive deflection by lead V4. There is minimal ST segment elevation in the inferior leads as well. Though this patient may be suffering from acute ischemia, the presence of a third degree block is requires aggressive management and expeditious transport. This rhythm, in the presence of anginal symptoms, warrants chemical or electrical therapy. Transport to an interventional facility, patient stability permitting, is a good strategy.

Fix the rate first!

Final interpretation

Probable third degree heart block, probable inferior wall myocardial infarction, old anterior wall myocardial infarction