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

Transcription

1 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

2 Objectives 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.

3 Review of Important Terms 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 J point PR segment ST segment TP segment PR interval QRS interval QT interval

4 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!

5 Evolution of Current of Injury 0-30 min 0-12 hrs 1-12 hrs 1-5 days wks-mths Highly variable timing of above (not all stages every time) Reperfusion usually accelerates evolution of changes

6 Hyperacute T waves ECG while CP free ECG within 2 min of CP onset

7 ECG baseline & 2 hours later

8 5/10 CP on arrival ECG during bad & worse chest pain Post PCI 10/10 CP 1hr later

9 Coronary Territory & ECG Leads 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 avr avl I III avf II

10 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

11 Lateral STEMI ST I, avl (±V5,V6) Occlusion of proximal LCx (or 1 st obtuse marginal or diagonal branch)

12 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 ) LCx RCA

13 Anterior STEMI

14 Inferior STEMI

15 Anterior STEMI (with IVCD)

16 Anterior STEMI

17 Silent LCx

18 Lateral STEMI

19 Anterior STEMI

20 Causes of ST Elevation 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??

21 Statistics of ST in the ER 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%) Brady WJ et al. An Emerg Med 2001

22 Differentiating Causes of ST Elevation Condition ECG findings Normal 1-2 mm concave ST V1-V3 (most in V2) Present in ~90% of healthy, young males STEMI (Prinzmetal s) Early repolarization Pericarditis LVH with strain Convex ST with Reciprocal ST Corresponds to coronary region Evolves over time Concave ST, mostly precordial leads (most in V4) Notch at J point, resolves with exercise ( HR) Usually tall R and T waves 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 V1-V2 with deep S waves, concave ST Other features of LVH (e.g. voltage) Clinical scenario Reciprocal ST depression Evolution over time (minutes) Wall motion on echo

23 Early Repol Concave ST notch at J point Tall R s and T s

24 Still just Early Repol

25 Pericarditis Diffuse, concave, ST (ST avr) PR No loss of R waves (T s don t invert until ST s at baseline)

26 LVH with strain Concave ST in V1-V3 (assoc. with deep S wave) Essentially opposite V4- V6 with tall R s & ST

27 STEMI vs. Hyperkalemia STEMI K + STEMI: T s are broad, rounded, minimal ST segment Hyperkalemia: T s are narrow, pointy, discrete ST segment

28 STEMI with IVCD vs. Hyperkalemia STEMI K + Clinical setting, QRS complexes of K + run into each other

29 Summary 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