FOCUS 1 ECG course Dr. Boyd SEMC

Course Objectives To fully understand a basic approach to ECG interpretation To recognize the 13 most common rhythm disturbances. To recognize acute myocardial ischemia and infarction on a 12-lead ECG.

Course outline 1. ECG basics 2. Arrhythmias 3. Acute Coronary syndromes 4. Cases and review 5. Test

Systematic approach R Roy RATE R Rogers RHYTHM I is INTERVALS A a AXIS H horseback HYPERTROPHY I icon INFARCT

Acute Coronary Syndromes Part 3: Acute Coronary Syndromes

Case History Mr. B. Skimmer, age 45, complains of chest “discomfort,” nausea, severe fatigue Past Med Hx: hypertension (poor control), 2 to 3 pack/day cigarettes, high stress job Refuses coworkers’ assistance States: “It’s just the flu” Goes to break room to rest

Should Mr. Skimmer go to ED by ALS ambulance? WHY? Case Progression One hour later a coworker finds Mr. Skimmer lethargic, pale, profusely diaphoretic Coworker offers to drive Mr. Skimmer to ED, only 3 minutes away Should Mr. Skimmer go to ED by ALS ambulance? WHY?

What should you — as the key ACLS provider — do first? Case Progression Mr. Skimmer arrives at your ED with O2 via NRB; IV LR @ KVO Received “MONA” in field; BP dropped alarmingly, near syncope Triaged as urgent Placed in ED critical care bed What should you — as the key ACLS provider — do first?

The Five Quadrads Approach to ACLS-EP 1. Primary ABCD Survey 2. Secondary ABCD Survey 3. Oxygen–IV–monitor–fluids 4. Temp–BP–HR–RR 5. Tank–tank–pump–rate

Assessment Five Quadrads Approach Primary Survey Airway: adequate Breathing: present with equal chest rise, adequate tidal volume Circulation: pulse present carotid and radial Defibrillation: not needed

Assessment Five Quadrads Approach Secondary Survey Airway: adequate Breathing: lung sounds clear Oxygen sat 97% with NRB Circulation: sinus rhythm 2-mm ST-elevation in leads II, III, aVF BP 126/84 mm Hg; IV access present Differential diagnosis: AMI. Others?

Assessment Five Quadrads Approach Oxygen–IV–monitor–fluids Started by EMS; continued in ED Vital signs T=99.1°F, BP=126/84 mm Hg, HR=74 bpm, RR=28/min Tank–tank–pump–rate Consider sources of hemodynamic compromise

What would you like to do NOW?

Immediate ED Assessments O2–IV–monitor–fluids (done by EMS) Grade chest pain: character, intensity H & P: focus on thrombolytic screening VS — frequent recordings Multilead ECG? (12, 15, or 22 leads) First set serum markers Electrolytes; coagulation studies Portable chest film

12-Lead ECG Findings 1. ST-segment elevation or new LBBB strongly suspicious for injury 2. ST-segment depression/dynamic T-wave inversion; strongly suspicious for ischemia 3. Nondiagnostic or normal ECG; chest pain strongly suspicious for ischemia

ECG 1: Interpretation?

ECG 1: elevated ST segments; inferior leads (II, III, aVF); ST depression: precordial leads V2-V5; lateral leads I, aVL Suspect occlusion — right coronary artery

Localizing Ischemia or Injury aVF inferior III inferior V3 anterior V6 lateral aVL lateral II inferior V2 septal V5 lateral aVR I lateral V1 septal V4 anterior

Coronary Artery Distribution Left Septal wall of LV Anterior and lateral walls of LV Inferior wall LV (10%) Both bundle branches Right Inferior wall of LV (90%) Posterior wall of LV AV node (90%) Right ventricle

Cardiac Anatomy in Relation to Coronary Artery Right coronary artery Septal wall V1-V2 Left anterior descending artery Anterior wall V3-V4 Left main coronary artery Circumflex artery Lateral wall I, aVL, V5-V6

Posterior View of the Heart NOTE 1: Inferior wall supplied by either the right (85% to 90% of people) or left coronary artery. NOTE 2: If there is acute injury in inferior leads (II, III, aVF), unknown whether left or right coronary artery is blocked. NOTE 3: KEY — you must obtain a RIGHT-SIDED ECG at once. Leads II, III, aVF (from left coronary artery) Lateral wall Inferior wall Right coronary artery Posterior descending artery Posterior wall Circumflex artery HOW TO GET RIGHT-SIDED ECG?

Lead Placement for a Right-sided ECG V1 V3R V4R V5R V6R V2

Right Ventricular Infarction Inferior lead changes  RV infarction? Use lead V4R (ST elevation >1 mm) Clinical significance: Increased mortality Preload dependence Vasodilators may cause severe hypotension What is management of RV infarction?

Coronary Insufficiency Insufficient blood supply to the heart due to: increased myocardial demand decreased blood flow

Major Effects of Coronary Insufficiency Ischemia Injury Infarct

ISCHEMIA Transient loss of myocyte function Subendocardial layer most susceptible Returns to normal rapidly with restoration of blood flow

INJURY Persisting myocyte damage with potential for recovery Injured myocytes do not fully depolarize Causes include Non Q wave infarct Prinzmetal’s variant angina

INFARCT Death of myocardial tissue Infarcted tissue is electrically silent

J-point J-point is the point at which the QRS complex meets the ST wave. ST segment elevation with an upward concavity is usually benign, especially when seen in healthy, asymptomatic individuals. ST segment elevation with a downward convexity is more likely to be due to acute coronary syndrome. Although ST elevation with an upward concavity and J-point notching often reflects a normal variant, this is only true if the patient is asymptomatic. The same ST pattern in a patient with chest pain is due to acute coronary syndrome until proven otherwise.

ISCHEMIA-EKG CHANGES ST straightening ST-T junction sharpening Inverted U waves ST segment depression (>1mm) ST segment down-sloping T wave inversion/symmetry

INJURY-EKG CHANGES Rapid ST elevation (>1mm) Evolving T wave inversion

INFARCT- EKG CHANGES Tall peaked (hyperacute) T waves ST elevation in area of infarct Q waves in area of infarct T wave inversion Reciprocal changes

TIMELINE OF INFARCTION Immediate Hyperacute T’s Minutes ST elevation Hours T wave depression Days Q wave

HYPERACUTE T WAVES Immediately appear Greater than 5 mm limb leads Greater than 10 mm precordial leads

Potassium summary:

ST ELEVATION Occurs within minutes Criteria for transmural injury: > 1.0mm in two or more limb leads > 2.0mm in two or more precordial leads

Q WAVES Duration more important than amplitude Significance based upon: clinical setting width >.04 seconds depth > 1/3 R wave Septal Q waves are normal

ELEVATED ST SEGMENT OTHER CAUSES

ST ELEVATION PNEUMONIC Elevated ST, think of “A PEA”

ELEVATED ST SEGMENT - PNEUMONIC A cute MI P ericarditis E arly Repolarization A neurysm

PERICARDITIS Early Diffuse concave upward ST elevation (Except AVR) No Q waves or reciprocal ST changes PR segments depressed in leads with upright P waves

PERICARDITIS Late T waves invert -usually not until ST segments return to baseline !

PERICARDITIS Can be focal: surgery trauma acute MI

EARLY REPOLARIZATION Normal variant Upward concavity- Think fish hook! J point begins with a notch or a slur

EARLY REPOLARIZATION No reciprocal ST changes If ST elevation > 30% total T height, early repol less likely

EARLY REPOLARIZATION CONTINUED ST T WAVE ST T WAVE

ANEURYSM ST elevation usually with deep Q wave or QS in same leads ST - T wave changes are stable and persist for a long period

Other causes besides ischemia DEPRESSED ST SEGMENT Other causes besides ischemia

DEPRESSED ST SEGMENT Digitalis effect LV Strain Hypokalemia Nonspecific ST changes Resolving pericarditis

DIGITALIS EFFECT “Coved” ST depression especially lateral leads Biphasic, flattened, inverted T waves Decreased QTc interval

Digitalis effect summary: In addition to a wide variety of atrial conduction defects, ventricular ectopy, and heart blocks, early digitalis toxicity manifests itself as: a shortening of the QT interval in addition to scooped-out appearing ST segments.

STRAIN PATTERNS Delayed repolarization of ventricle; results in (-) ST and T wave segments ST depression with upward convexity and T wave inversion

LVH with strain pattern Edhouse, J. et al. BMJ 2002;324:1264-1267 Copyright ©2002 BMJ Publishing Group Ltd.

STRAIN PATTERNS Lateral leads - THINK LVH Anterior leads -THINK RVH or PE

STRAIN PATTERNS ST , T wave in leads with large R ST , T wave in leads with large S

HYPOKALEMIA Prominent U waves Low voltage Trough-like ST segment depression T wave flattening, inversion or notching QT interval prolongation PR interval prolongation

NONSPECIFIC ST CHANGES Changes that don’t fit criteria for ischemia infarct or strain Most changes are normal variants

Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. 12-Lead ECG Rhythm Strip

The 12-Lead ECG The 12-Lead ECG sees the heart from 12 different views. Therefore, the 12-Lead ECG helps you see what is happening in different portions of the heart. The rhythm strip is only 1 of these 12 views.

The 12-Leads The 12-leads include: 3 Limb leads (I, II, III) 3 Augmented leads (aVR, aVL, aVF) 6 Precordial leads (V1- V6)

Views of the Heart Lateral portion of the heart Some leads get a good view of the: Anterior portion of the heart Inferior portion of the heart

ST Elevation One way to diagnose an acute MI is to look for elevation of the ST segment.

ST Elevation (cont) Elevation of the ST segment (greater than 2 small boxes) in 2 contiguous pre-cordial leads is consistent with a myocardial infarction (Greater than one small box in 2 limb leads)

Anterior View of the Heart The anterior portion of the heart is best viewed using leads V1- V4.

Anterior Myocardial Infarction If you see changes in leads V1 - V4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

Putting it all Together Do you think this person is having a myocardial infarction. If so, where?

Interpretation Yes, this person is having an acute anterior wall myocardial infarction.

Other MI Locations Now that you know where to look for an anterior wall myocardial infarction let’s look at how you would determine if the MI involves the lateral wall or the inferior wall of the heart.

Other MI Locations Lateral portion of the heart Anterior portion of the heart Lateral portion of the heart Inferior portion of the heart First, take a look again at this picture of the heart.

Other MI Locations Limb Leads Augmented Leads Precordial Leads Second, remember that the 12-leads of the ECG look at different portions of the heart. The limb and augmented leads “see” electrical activity moving inferiorly (II, III and aVF), to the left (I, aVL) and to the right (aVR). Whereas, the precordial leads “see” electrical activity in the posterior to anterior direction. Limb Leads Augmented Leads Precordial Leads

Other MI Locations Now, using these 3 diagrams let’s figure where to look for a lateral wall and inferior wall MI. Limb Leads Augmented Leads Precordial Leads

Anterior MI Remember the anterior portion of the heart is best viewed using leads V1- V4. Limb Leads Augmented Leads Precordial Leads

Lateral MI So what leads do you think the lateral portion of the heart is best viewed? Leads I, aVL, and V5- V6 Limb Leads Augmented Leads Precordial Leads

Inferior MI Leads II, III and aVF Limb Leads Augmented Leads Now how about the inferior portion of the heart? Limb Leads Augmented Leads Precordial Leads

Putting it all Together Now, where do you think this person is having a myocardial infarction?

Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF.

Putting it all Together How about now?

Anterolateral MI This person’s MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)!

ST Elevation and non-ST Elevation MIs

ST Elevation and non-ST Elevation MIs When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time. The ECG changes over time with each of these events…

ECG Changes Ways the ECG can change include: ST elevation & depression Appearance of pathologic Q-waves T-waves peaked flattened inverted

ECG Changes & the Evolving MI There are two distinct patterns of ECG change depending if the infarction is: Non-ST Elevation ST Elevation ST Elevation (Transmural or Q-wave), or Non-ST Elevation (Subendocardial or non-Q-wave)

ST Elevation Infarction The ECG changes seen with a ST elevation infarction are: Before injury Normal ECG Ischemia ST depression, peaked T-waves, then T-wave inversion Infarction ST elevation & appearance of Q-waves Fibrosis ST segments and T-waves return to normal, but Q-waves persist

ST Elevation Infarction Here’s a diagram depicting an evolving infarction: A. Normal ECG prior to MI B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves C. Infarction from ongoing ischemia results in marked ST elevation D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves

ST Elevation Infarction Here’s an ECG of an inferior MI: Look at the inferior leads (II, III, aVF). Question: What ECG changes do you see? ST elevation and Q-waves Extra credit: What is the rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!

Non-ST Elevation Infarction Here’s an ECG of an inferior MI later in time: Now what do you see in the inferior leads? ST elevation, Q-waves and T-wave inversion

Non-ST Elevation Infarction The ECG changes seen with a non-ST elevation infarction are: Before injury Normal ECG Ischemia ST depression & T-wave inversion Infarction ST depression & T-wave inversion Fibrosis ST returns to baseline, but T-wave inversion persists

Non-ST Elevation Infarction Here’s an ECG of an evolving non-ST elevation MI: Note the ST depression and T-wave inversion in leads V2-V6. Question: What area of the heart is infarcting? Anterolateral

Wellen’s warning From this EKG you can predict what will be seen on Coronary Angiography So from the beginning, we have Sinus Rhythm, left atrial enlargement from the p morphology in V1, left axis deviation due secondarily to the Massive ACUTE ST ELEVATION MI localized by the ST Elevations in v2 through v5 which would be labeled "Antero-Lateral". But what is more important to notice on this EKG is the specific ST-Twave changes in v2-v3 which are labeled "Wellens Warning" or "Wellen's Sign" which represent Left Anterior Descending (LAD) artery stenosis/thrombosis.

In Figure 1 you can see the black arrows pointing to the specific ST-T wave findings that are labeled "Wellen's Warning" or "Wellen's Sign" which are present in our patients EKG. This characteristic pattern was well reported in an article by Wellens and colleagues in 1962 in the American Heart Journal (Am Heart J 103:730, 1962) and was found to represent Critical Left Anterior Descending artery stenosis. Also found to represent impending stenosis if no ST-Elevations where present yet. When examining patients for the first time with any type of unstable angina or chest pain symptoms with no ST changes but Wellen's warning present should not be taken lightly but aggressively pursued to rule out Ischemia. Figure 2 is an example of a patient who presented with chest pain with no other EKG changes but these and went on to have a Massive MI due to a lesion of the LAD. So Even if there are no ST elevations this characteristic finding in v2 and v3 should not be over looked.                                                     

What do you see here?

Brugada syndrome

Brugada syndrome Familial autosomal dominant (But majority of cases are sporadic) St elevation V1 –V3, RBBB and T-wave inversion Patients with this condition are at increased risk for sudden cardiac death, despite having structurally normal hearts

Systematic approach R Roy RATE R Rogers RHYTHM I is INTERVALS A a AXIS H horseback HYPERTROPHY I icon INFARCT

End of part 3