ST Segment Elevation - University of Mississippi Medical Center

ST Segment Elevation Nothing is ever as hard (or easy) as it looks

Cameron Guild, MD

Division of Cardiology

University of Mississippi Medical Center

February 17, 2012

1. Describe the electrical changes within the myocardium that lead to ST elevation on ECG.

2. Demonstrate groups of ECG leads effected by various regions of myocardial ischemia.

3. Review examples of ECG’s showing STEMI and show the corresponding coronary angiograms.

4. Identify non-ischemic causes of ST elevation that mimic STEMI.

Objectives

Review of Important Terms

J point

Intervals include waves

Segments are distances between waves

PR segment- time between atrial depolarization and ventricular depolarization

ST segment- time between ventricular depolarization and repolarization

TP segment- time where all of heart is repolarized and awaiting next depolarization

J point- the “junction” of the QRS with the ST segment

PR segment ST segment TP segment

PR interval QRS interval

QT interval

Why is there “ST elevation” in STEMI?

“isoelectric” points are where the action potential is zero (no “flow” of current). ST segment- all cells of LV are depolarized

TP segment- all cells of LV are polarized

Injured myocytes cannot produce energy to maintain electrical gradients (repolarize); thus, in constant state of full/partial depol.

Thus, the only isoelectric point in an ischemic heart is the ST segment where all cells are depolarizing. Technically, that means the ST segment is really the baseline with TP and PR

depression… not ST elevation!

0-30 min 0-12 hrs 1-12 hrs 1-5 days wks-mths

Evolution of “Current of Injury”

• Highly variable timing of above (not all stages every time)

• Reperfusion usually accelerates evolution of changes

ECG while CP free

ECG within 2 min of CP onset

Hyperacute T waves

ECG baseline & 2 hours later

5/10 CP on arrival

10/10 CP 1hr later

ECG during bad & worse chest pain

Post PCI

aVR

I

II III aVF

aVL

Coronary Artery

LV wall supplied ECG leads

LAD Anterior V1-V4 (± I, aVL, V5-V6)

LCx Lateral (± inferior, posterior)

V5-V6 (±I, aVL, or II, III, aVF)

RCA Inferior (± posterior) II, III, aVF

Coronary Territory & ECG Leads

Anterior STEMI

ST V2-V4 (±V5,V6)

• ST V1 if proximal to first septal perforator.

• ST in I, aVL if proximal to first diagonal

Occlusion of proximal LAD

Lateral STEMI

Occlusion of proximal LCx

(or 1st obtuse marginal or diagonal branch)

ST I, aVL (±V5,V6)

Inferior STEMI

Occlusion of PDA

ST II, III, aVF • Due to occlusion of the PDA

- PDA can be supplied by RCA ~85%, LCx ~15%, or even the terminal LAD (<5%)

• Can involve “posterior” wall - Due to occlusion of posterolateral branches - ST in V1-V3 (or ST in V7-V9)

• Consider RV infarction - Lead V4R (≥0.5mm ST)

RCA LCx

Anterior STEMI

Inferior STEMI

Anterior STEMI (with IVCD)

Anterior STEMI

Silent LCx

Lateral STEMI

Anterior STEMI

1) Myocardial injury (Acute MI)

2) Coronary Spasm (Prinzmetal’s)

3) Pericarditis

4) Myocarditis

5) Normal variant (young ♂)

6) Early Repolarization

7) LVH (V1-V3)

8) LBBB (V1-V3), ventricular pacing

9) Ventricular Aneurysm

10) Hyperkalemia (usually V1-V3)

11) Hypercalcemia (usually V1/V2)

12) Hypocalcemia

13) Hypothermia (Osbourne waves)- exposure, EtOH, sepsis, DKA, etc.

14) Pulmonary Embolism (V1/V2 +/-inferior leads)

15) CNS events (e.g.- SAH, tumors)

16) Type 1C Antiarrhythmics

17) Tricyclic Antidepressant Overdose

18) Brugada Syndrome

19) ARVD

20) Post Transthoracic DCCV

21) Chagas Dz (Osborne type waves)

22) Hypothyroidism

23) Other??

Causes of ST Elevation

Brady WJ et al. An Emerg Med 2001

Retrospective review of 902 adult pt’s c/o CP.

1) LVH with repolarization abnormality (25%)

2) LBBB with repolarization abnormality (15%)

3) Acute MI (15%)

4) Early repolarization (12%)

5) “undefined” BBB (5%)

6) LV aneurysm (3%)

7) Ventricular paced rhythm (1%)

8) Pericarditis (1%)

9) Other/Undefined (1%)

Statistics of ST in the ER

Condition ECG findings

Normal 1-2 mm concave ST V1-V3 (most in V2) Present in ~90% of healthy, young males

STEMI (Prinzmetal’s)

Convex ST with Reciprocal ST Corresponds to coronary region Evolves over time

Early repolarization

Concave ST, mostly precordial leads (most in V4) “Notch” at J point, resolves with exercise (HR) Usually tall R and T waves

Pericarditis Diffuse concave ST (usually just 1-3mm), PR (ST in aVR; V1 usually isoelectric) T waves don’t invert until ST’s back to baseline

LVH “with strain” V1-V2 with deep S waves, concave ST Other features of LVH (e.g. voltage)

Differentiating Causes of ST Elevation

• Clinical scenario

• Reciprocal ST depression

• Evolution over time (minutes)

• Wall motion on echo

Early Repol

Concave ST “notch” at J point Tall R’s and T’s

2006

2008

Still just Early Repol 2006

2006

2006 2006

Pericarditis

Diffuse, concave, ST (ST aVR)

PR

No loss of R waves (T’s don’t invert until ST’s at baseline)

LVH with “strain”

Concave ST in V1-V3 (assoc. with deep S wave)

Essentially opposite V4-V6 with tall R’s & ST

STEMI vs. Hyperkalemia

STEMI

K+

STEMI: T’s are broad, rounded, minimal ST segment

Hyperkalemia: T’s are narrow, pointy, discrete ST segment

STEMI with IVCD vs. Hyperkalemia

STEMI

K+

Clinical setting, QRS complexes of K+ run into each other

There are many causes of ST The majority are not STEMI’s

ECG’s are neither 100% sensitive nor specific for STEMI You will miss some STEMI’s, you will cath some normals

Sometimes your best just isn’t good enough

The clinical setting is the most important factor Common sense often rules the day

Symptoms, risk factors for CAD

ECG morphology can also be helpful, but not foolproof!! ST with STEMI is usually convex, regional, recip ST, dynamic

Beware subtle inferior STEMI’s!

Serial ECG’s can help keep you out of trouble

Summary