The History of Present (and Past) Illness

EMS responds to the home of a 69 yo male patient. The patient reports retrosternal chest pain x 3 hours. The patient has taken 2 of his own nitroglycerin without relief. The patient reports mild shortness of breath. He denies nausea or loss of consciousness. The  patient is slightly diaphoretic and states, "you know, this feels entirely similar to my previous MI's." The patient has a history of coronary artery disease, HTN, and placement of three metal stents.

Vital signs:
BP: 180/100
P: 90
R: 22

Sp02: 94%

12 Lead ECG:

12 Lead ECG Interpretation and Discussion:

There is a baseline sinus rhythm. The rate is approximately 80 beats per minute. There is ST segment elevation in lead I. In addition, ST segment elevation is present in leads V2-V4. There are no reciprocal changes in the inferior wall leads. There are non specific ST segment changes (flattening) present in leads V5-V6.  The QRS axis is difficult to determine but the slightly positive complex in lead aVF and the positive complex in lead I put the mean vector at about 0 degrees, or within the physiologically "normal" range. (17 degrees according to the all knowing interpretation software..)
Incidentally, the QRS is decreased in amplitude. Low voltage QRS is concerning in the setting of patients who present in extremis or with hypotension. Low voltages can indicate serious underlying conditions such as pericardial effusion and tamponade. The patient is hypertensive and a bit tachypneic (RR>18). Remain vigilant for the development of pulmonary edema.



The distribution of the ST segment elevation suggests an acute infarction of the heart's septal and anterior walls. Lead I STE may indicate some lateral involement as well. Patients with anterior wall STEMI are at risk for the development of dysrhythmia and congestive heart failure. The routine administration of morphine sulfate, contrary to many established protocols, has not been associated with improved patient outcome. Administer aspirin, nitroglycerin, and transport to a facility capable of percutaneous coronary intervention.

As mentioned in previous cases, ST segment elevation in leads aVR or even V1 may be predictive of a left main coronary artery occlusion. The anterior wall injury pattern, as seen in this ECG, may be due to acute occlusion of the left anterior descending artery or one of its branches. It is challenging to reliably identify the culprit lesion; anatomy is always better defined during the cardiac catheterizaton.

Final ECG Interpretation:
Sinus rhythm, rate of 90, anterior wall STEMI. Probable acute lateral wall ischemia  Low voltage QRS.  

***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