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 **Unconfirmed** but I'm worried about ***MEETING ST ELEVATION MI CRITERIA!*** PART 1/2

Family members call 911 for an 80 yo male experiencing chest discomfort. The patient has a history of HTN, dementia. The patient reports chest discomfort that began "a few hours" prior to EMS arrival. The patient reports some mild shortness of breath. The patient is otherwise alert and in mild distress.

PHYSICAL ASSESSMENT
BP: 136/78
P: 60
R: 22
Sp02: 95% on RA
Lung sounds are clear.
Heart tones present, no murmur.
No leg edema.

12 LEAD ECG
















12 LEAD ECG INTERPRETATION
It appears that LifeNet has done the job for you. There are three stars on either side of the ***MEETS ST ELEVATION MI CRITERIA***. Guess there's nothing more to say.

What say you? To cath or not to cath? Treatment? Additional questions?

There's STE in V1 !

EMS responds to the report of a 77 year old male with chest pain. The patient is hypertensive, alert, and hemodynamically stable. Aspirin and nitroglycerin are administered per treatment protocol. A 12 lead ECG is obtained, and the paramedic asks about transport to the closest hospital versus a facility capable of percutaneous coronary intervention...


12 lead ECG



12 lead ECG Discussion

There is a baseline sinus rhythm. The rhythm is regular. Close scrutiny of lead II and V1 reveals the presence of p waves. The ST segments are upright in most leads with the exception of aVR. The QRS duration is slightly prolonged consistent with an interventricular conduction delay. The (1) positively deflected QRS in lead V1 and the (2) lengthened QRS duration suggests the presence of a RIGHT bundle branch block. There is a subtle slurred l S wave in V6 which further corroborates the diagnosis of a right bundle branch block.

The Slurred S Wave

12 lead ECG Interpretation

Sinus rhythm, right bundle branch block, rate of approx 80 beats/min.

Case resolution

The patient was transported to a local facility. Serial ECGs remained unchanged and cardiac enzymes were normal. The patient was discharged to home following an overnight hospital stay and a cardiac stress test.

***ACUTE MI SUSPECTED*** Abnormal ECG ***Unconfirmed***

After a mind numbing session of protocol review, your partner asks you to review a 12 lead ECG. The ECG tracing was obtained from a patient who was diaphoretic, hypotensive, and semi-conscious.

What's the underlying rhythm?
What are your treatment priorities?

Rampart, prepare to receive telemetry...

12 Lead ECG:

12 Lead ECG Interpretation and Case Discussion:
Once again, kudos to the ECG interpretation software! The ECG is absolutely, without question, ***ABNORMAL***. It looks like this tracing triggered every single lifenet alert possible. The ECG reveals, simultaneously, "inferior and lateral injury patterns" coupled with "atrial fibrillation" and an "anterior injury pattern."

FIRST, the presence of a wide complex tachycardia is easily recognized. The rhythm is wide and regular which suggests ventricular tachycardia. The ventricular rate is in excess of 200 beats per minute. The combination of a wide complex tachycardia and an unstable patient should always warrants serious consideration of electrical therapy. In this particular case, a biphasic shock of 200 or 300 joules isn't likely to produce the desired result.

Now, the patient's chest hairs are signed and you're left with the same troublesome waveform. Vital signs have not improved. This tracing is classic for a specific type of ventricular tachycardia called "sinusoidal" ventricular tachycardia. This rhythm is characterized by a rapid ventricular rate a regular appearance of the QRS complex. Sinusoidal ventricular tachycardia is often called ventricular flutter. It is typically a pre-arrest rhythm that deteriorates rapidly into the more familiar ventricular fibrillation.

Though typically caused by severe hyperkalemia, ventricular flutter may be medication induced. Sodium channel blocking anti-dysrhythmics and anti-psychotics have been linked to sinusoidal VT. Treatment therefore involves:

• Rapid administration of IV calcium (stabilizes the myocardium)
• Empiric treatment for hyperkalemia (consider bicarbonate, albuterol, etc)
• Defibrillation
• Treatment of underlying cause (emergent hemodialysis)

Administration of anti-dysrhythmics such as lidocaine are not usually effective and may even precipitate deterioration of the rhythm into ventricular fibrillation.

When confronted with the dreaded sinusoidal ventricular tachycardia, consider the patient's history if at all possible. Patients with known renal disease or complex medical comorbidities may be at risk for hyperkalemia. If local protocols permit, aggressively treat hyperkalemia. Administration of calcium may render the myocardium less resistant to electrical therapy.

The patient's potassium level was measured at over 9 mEQ/L (normal 3.5-5 mEQ/L) .

Final 12 Lead ECG Interpretation:Sinusoidal ventricular tachycardia, ventricular flutter likely secondary to severe hyperkalemia