Rapid ECG Interpretation - Part 2

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Rapid Emergency ECG Interpretation Part II – advanced

Agenda:

2013 changes in STEMI criteria Detecting ischemia and infarction BBB’s Sgarbossa Criteria Mimics (BER, Paced, LVH, etc.) Agenda

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What is your interpretation ?

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S.Tach at 114 bpm with Acute Inferoposterior MI with 2:1 Type 1 AV block

Have a system…:

Have a system … R ate & R hythm I ntervals & I schemia P waves for every QRS D ropped beats E lectrolyte abnormalities M yocardial Infarction Ripped EM Part I – the basics

When looking for signs of ischemia have a system…:

When looking for signs of ischemia have a system… P athologic Q-waves E levation of S-T Segment A djacent contiguous leads R eciprocal changes & R wave Progression T wave changes Neil PEART Part II – advanced Just think of…

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Continguous Leads

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Right Ventricle Left Ventricle S Posterior Wall Lateral Wall Anterior Wall V1 V2 V3 V4 V5 V6

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Continguous Leads

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An inferolateral myocardial infarction with reciprocal changes in leads I, aVL, V1, and V2

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Reciprocal changes: presence of widespread ST segment depression in the anterolateral leads strongly suggests that the subtle inferior ST segment elevation is due to acute infarction

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Poor R wave progression Definition : R wave height ≤ 3 mm in V3 . Causes : Prior anteroseptal MI Left ventricular hypertrophy Inaccurate lead placement (e.g. transposition of V1 and V3) Dilated cardiomyopathy May be a normal variant

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Poor R wave progression secondary to prior anteroseptal MI

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Poor R wave progression due to electrode misplacement (leads V1 and V3 reversed)

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New or presumed new “Left Bundle Branch Block” in isolation is no longer an indication for a STEMI 2. Providers should use Sgarbossa’s Criteria to diagnose STEMI in the presence of LBBB 3. Isolated S-T depression in V1-V4 is an indication of a posterior MI 4. Widespread S-T depression with S-T elevation in aVR is an indication of proximal LAD or LMCA occlusion. 5. Hyperacute T-waves without S-T elevation may be an early indicator of a STEMI 2013 changes in STEMI criteria

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STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis. STEMI Diagnosis

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2013 STEMI criteria Diagnostic ST elevation in the absence of left ventricular (LV) hypertrophy or left bundle-branch block (LBBB) is defined as new ST elevation at the J point in at least 2 contiguous leads of: ≥ 2 mm in men or ≥ 1.5 mm in women in leads V2–V3 and/or of ≥1 mm in other contiguous chest leads or the limb leads

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Sequence of changes seen during evolution of myocardial infarction

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The ECG sign of subendocardial ischemia is ST segment depression (A) . Depression is reversible if ischemia is only transient but depression persists if ischemia is severe enough to produce infarction. T wave inversion with or without ST segment depression (B) is sometimes seen but not ST segment elevation or Q wave. That is why subendocardial infarction is also called non-ST-elevation myocardial infarction (NSTEMI) and less commonly non-Q wave myocardial infarction. Cardiac Ischemia

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Cardiac Ischemia ST segment depression seen in subendocardial ischemia or infarction can take on different patterns: The most typical being horizontal or down-sloping depression. Up-sloping ST depression is less specific.

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Digoxin effects can mimic ST segment depression and ischemia Downsloping ST depression with a characteristic “sagging” appearance Flattened, inverted or biphasic T waves Shortened QT interval

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Cardiac Ischemia and infarction In transmural MI, ischemia in the subendocardium spreads to the epicardium and involves full thickness of the myocardium. In the acute phase, the ECG signs are ST segment elevation.

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The elevated ST segment may slope upward or be horizontal or dome-shaped. Hyperacute (tall positive) T waves may precede ST segment elevation (A) or seen at the same time with ST elevation (B) during this acute phase. Cardiac Ischemia and infarction

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Anterior myocardial infarction with S-T segment elevation (showing “ tombstone ” R waves)

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ST segment morphology in other conditions

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Cardiac Ischemia and infarction Hours to days later during the evolving phase, pathological Q waves appear, the elevated ST segments return towards baseline, and the T waves become inverted.

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A Q wave is normal if it is shallow and brief

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Pathologic Q-waves

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Pathological Q waves in inferior and anterior leads

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Hyperacute T-waves

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Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia. Peaked T-waves

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Broad, asymmetrically peaked or ‘hyperacute’ T-waves are seen in the early stages of ST-elevation MI (STEMI) and often precede the appearance of ST elevation and Q waves.

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Placement of right sided chest leads

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The Three ST-Segment and T-Wave Configurations That Can Be Identified by Lead V 4 R in Patients with Acute Inferoposterior Myocardial Infarction. Wellens HJ. N Engl J Med 1999;340:381-383.

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Isolated posterior infarction with no associated inferior changes (note ST segment depression in leads V1 to V3)

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What is your interpretation ?

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Position of V7, V8, and V9 on posterior chest wall

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ST segment elevation in posterior chest leads V8 and V9

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Typical appearance of posterior infarction in V2 V2 Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.

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V2

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Posterior MI Posterior MI is suggested by the following changes in V1-V3: Horizontal ST depression Tall, broad R waves (>30ms) Upright T waves Dominant R wave (R/S ratio > 1) in V2

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Acute inferior myocardial infarction with associated right ventricular infarction

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Acute inferior myocardial infarction with right ventricular involvement

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Long standing ST segment elevation and T wave inversion associated with a previous anterior myocardial infarction (echocardiography showed a left ventricular aneurysm)

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T wave inversion can be seen normally in III, and aVF

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What is your interpretation ?

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Right Bundle Branch Block A right bundle branch block is defined as having a QRS duration > 0.12 seconds with an rsR’ or RsR’ complex in the right precordial leads plus a slurring of the R’ in these leads in addition to an S wave in lead I.

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R obin

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Tall R' wave in V1 ("M" pattern) with wide, slurred S wave in V6 ("W" pattern)

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What is your interpretation ?

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Left Bundle Branch Block Typical complex morphology of a left bundle branch block includes a deep and wide Q or S wave in V1 (no R wave in V1) with a slurred and sometimes notched R wave in the lateral leads.

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Dominant S wave in V1 with broad, notched (‘M’-shaped) R wave in V6

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Sgarbossa’s Criteria A scoring system developed to be used to identify AMI in the presence of a LBBB on a scale of 0 to 5. A minimal score of 3 was required for a specificity of 90%.

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Sgarbossa’s Criteria

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Mimics Bundle Branch Blocks Paced Rhythms Benign early repolarization Pericarditis Hyperkalemia V.Tach LVH Ventricular aneurysm Brugada Syndrome

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Mimics Bundle Branch Blocks

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Mimics Paced Rhythms

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Mimics Benign early repolarization

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Mimics Benign early repolarization AKA: “J-point elevation” Benign early repolarization (BER) is a ECG pattern most commonly seen in young, healthy patients < 50 years of age. It produces widespread ST segment elevation that may mimic pericarditis or acute MI. Up to 10-15% of ED patients presenting with chest pain will have BER on their ECG, making it a common diagnostic challenge for clinicians. The physiological basis of BER is poorly understood. However, it is generally thought to be a normal variant that is not indicative of underlying cardiac disease. BER is less common in the over 50s, in whom ST elevation is more likely to represent myocardial ischemia. It is rare in the over 70s.

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Mimics Pericarditis

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Pericarditis Mimics

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ECG findings — which are divided into 4 stages . The easiest way to remember these sequential changes is to conceptualize these stages as follows:  Stage I — everything is UP ( ST elevation in almost all leads except perhaps leads III,aVR,V1 ) .  Stage II — transition ( = "pseudonormalization" ) .  Stage III — everything is DOWN ( inverted T waves ) .  Stage IV — normalization. Mimics

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Mimics Hyperkalemia

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Mimics Hyperkalemia

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Mimics V.Tach

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Mimics LVH

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Mimics LVH

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Mimics LVH

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Mimics Left Ventricular Hypertrophy The left ventricle hypertrophies in response to pressure overload secondary to conditions such as aortic stenosis and hypertension. This results in increased R wave amplitude in the left-sided ECG leads (I, aVL and V4-6) and increased S wave depth in the right-sided leads (III, aVR, V1-3). The thickened LV wall leads to prolonged depolarisation (increased R wave peak time) and delayed repolarisation (ST and T-wave abnormalities) in the lateral leads.

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Mimics Voltage Criteria Limb Leads R wave in lead I + S wave in lead III > 25 mm R wave in aVL > 11 mm R wave in aVF > 20 mm S wave in aVR > 14 mm Precordial Leads R wave in V4, V5 or V6  > 26 mm R wave in V5 or V6 plus S wave in V1 > 35 mm Largest R wave plus largest S wave in precordial leads > 45 mm Left Ventricular Hypertrophy

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Mimics LVH

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Mimics Ventricular aneurysm

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Mimics Ventricular aneurysm Definition : Persistent ST elevation following an acute myocardial infarction. Following an acute STEMI, the ST segments return towards baseline over a period of two weeks, while the Q waves persist and the T waves usually become flattened or inverted. However, some degree of ST elevation remains in 60% of patients with anterior STEMI and 5% of patients with inferior STEMI. The mechanism is thought to be related to incomplete reperfusion and transmural scar formation following an acute MI. This ECG pattern is associated with paradoxical movement of the ventricular wall on echocardiography (ventricular aneurysm).

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Mimics ECG Features Of LV Aneurysm: ST elevation seen > 2 weeks following an acute myocardial infarction. Most commonly seen in the precordial leads. May exhibit concave or convex morphology. Usually associated with well-formed Q- or QS waves. T-waves have a relatively small amplitude in comparison to the QRS complex (unlike the hyperacute T-waves of acute STEMI).

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What is your interpretation ?

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Brugada Syndrome

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Brugada Syndrome Brugada syndrome is due to a mutation in the cardiac sodium channel gene. This is often referred to as a sodium channelopathy. Over 60 different mutations have been described so far and at least 50% are spontaneous mutations, but familial clustering and autosomal dominant inheritance has been demonstrated. ECG changes can be transient with Brugada syndrome and can also be unmasked or augmented by multiple factors:

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Brugada Syndrome Brugada Syndrome is an ECG abnormality with a high incidence of sudden death in patients with structurally normal hearts. A consensus conference reported in 2005 that it was the second leading cause of death in males <40 (after trauma).

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Brugada Syndrome This ECG abnormality  must  be associated with one of the following  clinical criteria   to make the diagnosis: Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT). Family history of sudden cardiac death at <45 years old . Coved-type ECGs in family members. Inducibility of VT with programmed electrical stimulation . Syncope. Nocturnal agonal respiration.

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Brugada Syndrome

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Type I J wave amplitude > 2mm T wave Negative ST-T configuration Coved Type ST segment (terminal portion) Gradually Descending

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Type II J wave amplitude > 2mm T wave Positive or biphasic ST-T configuration Saddle Back ST segment (terminal portion) Elevated > 1mm V1 V2

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Type III J wave amplitude > 2mm T wave Positive ST-T configuration Saddleback ST segment (terminal portion) Elevated > 1mm V1 V2

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What is your interpretation ?

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Wellen’s Syndrome Proximal critical stenosis of LAD artery Symmetrical deeply inverted T waves in V2-3 or Biphasic in V2-3 with minimal ST elevation.

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Wellen’s Syndrome

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Wellen’s Syndrome Wellens’ syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with ischemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery. Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at  extremely high risk for extensive anterior wall MI  within the next 2-3 weeks.

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Wellen’s Syndrome There are two patterns of T-wave abnormality in Wellens’ syndrome: Type A Wellens’ T-waves are deeply and symmetrically inverted Type B Wellens’ T-waves are biphasic, with the initial deflection positive and the terminal deflection negative

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Wellens’ Type A

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Wellens’ Type B

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Mark P.Brady PA-C Dept.of Emergency Medicine Cambridge Health Alliance

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