ST Elevation MI

Introduction and Objectives

Rapid recognition of a ST elevation MI (STEMI) on electrocardiogram is of paramount

importance in the emergency department. In general, high risk patients with chest pain should
receive an EKG within 5-10 minutes of presenting to the ED. Treatment for a STEMI is medical
therapy followed by rapid revascularization: “Time equals muscle!” Overall, the quicker a
patient undergoes revascularization in general the better outcome they will have. Identifying this
condition on EKG then activating a STEMI protocol will get the patient to the cardiac
catheterization lab as early as possible for emergency PTCA or stenting.

Upon completion of this module you should be able to:

 Define a STEMI
 Give a differential diagnosis of ST elevations (it’s not always a STEMI)
 Recognize the varied clinical presentations of patients with STEMI
 Understand regional blood vessel distribution correlation on EKG

What is a STEMI?

In order to diagnose a STEMI, one must first be able to identify the ST segment on the EKG.
The ST segment is isoelectric and represents the interval between ventricular repolarization and
depolarization. It begins at the J-point and should be isoelectric to the TP and PR segments.
Classically, STEMI is diagnosed if there is >1-2mm of ST elevation in two contiguous leads on
the ECG or new LBBB with a clinical picture consistent with ischemic chest pain. Classically the
ST elevations are described as “tombstone” and concave or “upwards” in appearance. However,
other morphologies such as convex or straight elevations might be seen.

Differential diagnosis of ST elevations

The most serious cause of ST elevations on ECG is a ST elevation MI, however there are other
possible etiologies. As usual always consider the “worst first”. In borderline or atypical cases
remember that timely diagnosis of STEMI is imperative versus diagnosing a benign condition
such as early repolarization.

Pathologic ST Segment Elevation

STEMI: Most commonly caused by an acute occlusion of a coronary blood vessel secondary to
acute plaque rupture and thrombosis. However, cocaine use can also cause a STEMI due to
coronary vasospasm, rather than occlusion with thrombosis.

Pericarditis: The hallmark features of pericarditis are diffuse global concave ST elevations with
associated PR depressions. Patients with pericarditis will classically have chest pain that is worse
with laying back and improved by sitting forward. Pericarditis itself may not cause instability,
but an acute and/or large effusion may cause pericardial tamponade.

Left Bundle Branch Block(LBBB): LBBB does signify underlying heart disease but may be new
or a chronic change. LBBB is caused by blockage of the left segment of the Bundle of His and
causes ventricular depolarization to occur in a right to left direction(as opposed to the normal left
to right). This in turn causes QRS prolongation (>120 ms) and an abnormally appearing QRS
complex. Leads V1-3 will have deep S waves and V5-6 will have tall R waves. When
interpreting an ECG in a patient with LBBB, there will be discordant ST segment changes
present (i.e. deep S wave causes ST elevation). Diagnosing a patient with a STEMI in setting of
LBBB is challenging and consulting a clinical decision rule (CDR) the Sgarbossa criteria is
recommended. In general, one should look for concordant ST changes (i.e. tall R wave with ST
elevations). In the past, a new LBBB in a patient with ischemic chest pain was considered to be
an indication for a patient to undergo cardiac catheterization. However, in recent years this has
become more controversial with evidence suggesting these patients may be managed more
conservatively.
Clinical Pearls

Brugada syndrome: Brugada syndrome is a disease of the myocardial sodium channels which
may mimic STEMI on EKG. This condition is important to recognize because it can lead to
sudden cardiac death in patients. The classic “Brugada sign” is ST elevation and a partial right
bundle branch block in V1 and V2.

Common Benign Causes ST elevation

Ventricular Paced Rhythm: A paced rhythm on EKG will appear morphologically similar to
LBBB(see above) with discordant ST elevations seen. The one noticeable difference will be the
presence of pacer spikes. In general, uou cannot read ischemia in a v-paced rhythm!

Benign Early Repolarization (BER): Benign early repolarization usually represents a normal
variant most often seen in young, healthy patients. ST elevations are most prominent in the
precordial leads and there is often a “fish hook” or notching at the J-wave in lead V4. The ST
changes in early repolarization may be more prominent at slower heart rates and resolve with
tachycardia.

Left Ventricular Hypertrophy (LVH): LVH causes a similar pattern of ST elevations as LBBB
with ST elevations present in leads with deep S waves(V1-3) and ST depressions or T wave
inversions present in leads with tall R waves(I, AVL, V5-6). The ECG changes that are seen are
due to thickening of the left ventricular wall leading to prolonged depolarization.

Clinical Presentation

Patients who are experiencing an acute STEMI are classically described as presenting with
pressure or crushing chest pain associated with shortness of breath, nausea/vomiting or
diaphoresis. The chest pain might be described as radiating into the patient’s neck, left arm or
jaw. Oftentimes, they will appear visibly uncomfortable and may have a fist clutching the center
of their chest. This classic finding of angina is known as the Levine sign. It is important to
remember as noted in “The Approach to Chest Pain” module that many patients with a STEMI or
acute coronary syndrome (ACS) including: elderly, diabetic and female patients may present
more typically with an anginal equivalents such as nausea and vomiting, fatigue, and/or
shortness of breath. For all patients presenting to the emergency department with chest pain or
other symptoms concerning for ischemia an EKG should be performed rapidly after triage to
determine if ST elevations consistent with a STEMI are present. If seen an aspirin should be
given and s STEMI protocol should be activated. “Time is muscle!” The majority of STEMI
patients will undergo emergent catheterization and attempted revascularization. In some cases
when a catheterization lab is not immediately available (transfer time of over 90 minutes) or per
patient/family decision a thrombolytic such as tPA may be given.

Understanding regional blood vessel distribution correlation on EKG

Evaluating the EKG accurately for a patient presenting with a STEMI is an important skill to
learn. The leads on the EKG are divided into different regional distributions of the heart that in
turn reflect a certain coronary artery. Reciprocal changes or ST depressions may be seen in a
different regional distribution on the EKG and support the diagnosis of a STEMI. When
discussing the case with the interventional cardiologist they will want to know what region is
experiencing ischemia and if there are any other changes present on the EKG such as reciprocal
changes, arrhythmia, or in IMI right ventricular extension.
Inferior STEMI: Leads II, III and aVF represent the inferior portion of the heart that is most
commonly perfused by the right coronary artery (RCA). Reciprocal ST depressions will be seen
in aVL and possibly lead I. Inferior myocardial infarctions are common and represent 40-50% of
myocardial infarctions. However, this subgroup of STEMI patients has relatively low in-hospital
mortality when compared with other patients who experience MI.

Right Ventricular Infarct: There is a subset of IMI patients who will be experiencing extension of
their infarct into the right ventricle. These patients’s blood pressure is severely preload
dependent and they may present with hypotension. It is for this reason that nitroglycerin should
be avoided in patients who are presenting with an inferior STEMI. RV infarct is suggested if ST
elevations are also seen in V1, or if the ST elevations are larger in lead III when compared with
II. The diagnosis of RV infarct can be confirmed by doing a right-sided EKG and seeing ST
elevation seen in v4R.
 Heart Block and Bradycardia: In addition to the ST elevations on EKG one should also look for
second or third degree heart block or bradycardia. The AV node is supplied by the right coronary
artery (RCA) which makes these arrhythmias more common in patients who are experiencing an
inferior STEMI.

Anterior STEMI: Anterior STEMI is caused by occlusions in the left anterior descending artery
(LAD). This area is represented by ST segment elevation in the pre-cordial leads V1-V6 as well
as the lateral leads I and aVL. Reciprocal changes presents as ST depressions seen in III and
aVF. Anterior myocardial infarctions are generally associated with the worst outcomes due to
involvement of a large amount of muscle within the heart. In general, patients with anterior MI
have higher rates of heart failure, ventricular ectopy (Vfib/VTach) in-hospital, and overall
mortality when compared with patients with inferior MI.

Lateral STEMI: The lateral wall of the LV is supplied by branches of the LAD and left
circumflex (LCx) arteries. Infarction of the lateral wall often occurs as extension of another
territory (i.e. anterolateral MI). Lateral extension can indicate a larger area of tissue involvement
and a consequently worse prognosis. The lateral leads are V4-6, I and aVL with reciprocal ST
depressions present in III and aVF.

There are three broad categories of lateral infarction.

1. Anterolateral: caused by occlusion of the LAD.

2. Inferior-posterior-lateral: caused by occlusion of the LCx.
3. Isolated lateral infarction: due to infarction of smaller vessels such as diagonal, obtuse
marginal(OM) or ramus intermedius.

Posterior infarction: Posterior infarction complicates 15-20% of STEMIs generally occurring

with either inferior or lateral infarction, with isolated posterior infarctions being rare. Isolated
posterior infarctions are challenging to recognize as ST elevations are not seen on a conventional
EKG. Findings suggestive of this diagnosis include ST depression with upright T waves and
large broad R waves(>30 ms) in leads V1-3 and a dominant R wave in V2. This diagnosis can be
confirmed by performing a posterior EKG (leads V7-9 are placed on back). ST elevations will be
present in these posterior leads.

Clinical Pearl

Wellen’s syndrome: Wellen’s syndrome is a pattern of deeply inverted or biphasic T-waves in

V2-V3. Although this is not a true STEMI, this pattern is highly suggestive of critical stenosis of
the LAD. It is important to recognize this finding as these individuals are at increased risk for a
large anterior wall MI in the next few days or weeks.
 Conclusion

Overall, you will achieve your goals if you keep up high index of suspicion, perform serial
EKG’s, practicing EKG reading and remember the objectives!

 STEMI = 1-2 mm ST elevation in 2 contiguous leads

 Give DDX STEMI= MI vs. pericarditis, LBBB, early repol/LVH, V-paced
 Varied presentations: Classic vs. anginal equivalent (SOB, Epigastic pain)
 Regional blood vessel ischemia correlates to specific areas of the EKG