Acute Coronary Syndromes Disclosures

• I work for Virginia Garcia Memorial Health Center, Beaverton, OR.

Jon Tardiff, BS, PA-C • And I am a medical editor for Jones & Bartlett Publishing. OHSU Clinical Assistant Professor

Goals of this session

• Identify Acute Coronary Syndromes (STEMI vs NSTEMI) • Identify old • Distinguish between Right and Left BBB

Arabic, Somali, Mai Mai, Pashtu, Urdu, ASL, and more! 4 For example: What a 12-Lead ECG can help you do 73 y.o. male with nausea, syncope

• Diagnose ACS / AMI • Interpret • Identify life-threatening syndromes (WPW, LGL, Long QT synd., Wellens synd., etc) • Infer electrolyte imbalances • Infer hypertrophy of any chamber • Infer COPD, , drug effects, and more!

66

What rhythm? (look at V1 for P waves) Acute Inferior MI

ST elevation

77 88 P waves Limitations of a 12-Lead ECG

• Truly useful only ~40% of the time • Each ECG is only a 10 sec. snapshot • Serial ECGs are necessary, especially for ACS • Other labs help corroborate ECG findings (cardiac markers, Cx X-ray) • Confounders must be ruled out (LBBB, LVH, WPW, digoxin, RVH, pericarditis, dissecting aneurysm)

99

Confounder: Left

Impending AMI with normal ECG!

111111 121212 ECG Lead Placement 13 hrs later — Acute Anterior MI & Electrophysiology Review

Elevated ST segments

131313 14

RapidRapid InterpretationInterpretation TipsTips

Limb Leads Dr. Willem Einthoven  I (standard  II leads)  III - ±

15 + 161616 Leads I, II, III Normal 12-Lead ECG

I

II III

17

Conduction System Lead II

P wave axis …upright in L II II R T P U R

Q S R wave axis …upright in L II SA Node AV Node His Bundle BBs Purkinje Fibers 20 Q S Intervals II Limb (frontal plane) Leads

 I (standard  PR II leads)  III QRS QT  aVR  aVL PR Interval: 120 – 200 mSec (3 – 5 boxes)  aVF QRS width: 60 – 120 mSec (1 ½ – 3 boxes) QT/QTc interval: 400 mSec (10 boxes) 21 (augmented leads) 22

Augmented Leads Normal 12-Lead ECG

aVL

aVR aVF

23 6 Frontal Plane Leads (limb leads) Axis I Leads - I II III II III L aVR* aVL F R aVF

25 26

QRS Morphology in Lead II Axis Determination

II

27 Why We Care About Axis Deviations Axis Deviation

The axis shifts towards hypertrophy Horizontal heart (0°): obesity, & away from infarction 3rd trimester pregnancy. Ascites

The axis also shifts for ectopic Vertical heart (90°): slender build rhythms, such as V-Tach Left Axis Deviation: LBBB, Anterior MI, Inferior MI, Left anterior hemiblock, LVH

Right Axis Deviation: Anterior MI, Lateral MI, RBBB, COPD, RVH, Normal axis is -20° to +110° Left posterior hemiblock

Extreme RAD: Ectopic rhythm 29 (VT), MI 30

How to determine Axis Practice: Axis 1

Easiest: the computer does it for you! I

Pretty Easy: Thumbs up / Thumbs down

A Little Harder: find the tallest R wave (if tallest is Lead II = normal axis) F

31 32 Axis Practice Normal Axis 11 2 I I

F F 333333 34

2 3 Left Axis Deviation I

F

35 36 3 4

373737 38

4 Extreme Right Axis Deviation Limb (frontal Chest (precordial) plane) Leads Leads

 I  V1 (standard   (anterior II leads) V2  III  V3 leads)  aVR  V4  aVL  V5 (lateral  aVF  V6 leads)

393939 (augmented leads) 40 V Lead Cutaway

41

Normal 12-Lead ECG V Lead Progression Step-by-step method for reading a 12-Lead

4545 46

Rapid Interpretation Tips Supraventricular rhythms • Identify the rhythm.Rapid IfInterpretation supraventricular* Tips , If no LBBB, • Sinus rhythm • Atrial fibrillation • If present, • PSVT • Rule out other confounders: WPW, pericarditis, LVH, • Atrial digoxin effect • Atrial flutter • Identify location of infarct, and consider appropriate • Wandering atrial pacemaker treatments: MONA, PCI [or fibrinolytic], nitrate • Multifocal infusion, heparin infusion, GP IIb, IIIa inhibitor, beta- blocker, clopidogrel, statin, etc. Normal 12-Lead ECG Rapid Interpretation Tips • Identify the rhythm.Rapid IfInterpretation supraventricular, Tips If no LBBB,

If present, • Rule out other confounders: WPW, pericarditis, LVH, digoxin effect • Identify location of infarct, and consider appropriate treatments: MONA, PCI [or fibrinolytic], nitrate infusion, heparin infusion, GP IIb, IIIa inhibitor, beta- blocker, clopidogrel, statin, etc.

Bundle Branch Blocks The Problem with Bundle (QRS > 0.12 sec.)

Branch Blocks (right-sided lead) (left-sided lead)

V1 R’ • Dyssynchronized contraction of the ventricles I notch • Reduced cardiac output r • Worsened • LBBB confounds the EKG interpretation S —LBBB makes it harder to find ACS Left BBB Right BBB (L I, V5, V6: (V1, V2, MCL1: upright QRS rsR’ pattern) with a notch)

52 Bundle Branch Blocks Two QRSs RBBB Blocked Healthy bundle ventricle

V1 & V2

V1 R’ I notch I slur r

S 535353

LBBB Practice: Bundle Branch Block

V5 V6

(& I, aVL)

56 Which Bundle Branch is Blocked? 5 Right Bundle Branch Block (Lead V1) 5

RBBB RBBB

Which Bundle Branch is Blocked? 6 6 LBBB 12-Lead LeftLBBB Bundle 12-Lead Branch Block (L I, V5, V6) Where is the Pathology? Right Bundle Branch Block

Left Bundle Branch Block

63 64 New 12-Lead ECG Format New 12-Lead ECG Format New

aVL II aVL II

I aVF I aVF

-aVR Old -aVR III III

65

Rapid Interpretation Tips ST elevation, ST depression, inversion, pathologic Q waves Rapid Interpretation Tips STEMI • Identify the rhythm. If supraventricular, NSTEMI? • Rule out . If no LBBB, Normal Injury Infarction • Check for: ST elevation, or ST depression with T wave inversion, and/or pathologic Q waves. If present, • Rule out other confounders: WPW, pericarditis, LVH, digoxin effect • Identify location of infarct, and consider appropriate treatments: MONA, PCI [or fibrinolytic], nitrate infusion, heparin infusion, GP IIb, IIIa inhibitor, beta- blocker, clopidogrel, statin, etc. Percutaneous Coronary Intervention

RCA before and after stenting The Spectrum of Acute Coronary Syndromes

Shock / Healthy CAD NSTEMI STEMI Death

Patent ~50% ~70% >70% or 100% ~90% 100% 100% artery (or vasospasm)

Before stenting After stenting No symptoms Pain on Pain at rest; 71 exertion relieved by NTG Constant pain NSTEMI vs STEMI STEMI: ECG Changes

NSTEMI STEMI (normal) (w/onset cx pn) A. Normal ECG B. Hyperacute T wave changes - increased T wave amplitude and width; may also see ST elevation (20 minutes) (1 hour) C. Marked ST elevation with hyperacute T wave changes (transmural injury) D. Pathologic Q waves, less ST

(>1 hr) elevation, terminal T wave (1 week – years) inversion (necrosis) E. Pathologic Q waves, T wave inversion (necrosis and fibrosis) ~90% 100% F. Pathologic Q waves, loss of R waves (fibrosis) Constant pain Constant pain

Why Pathologic Q Waves Form MIMI ECGECG PatternsPatterns

Normal q Pathologic Q NSTEMI (non Q wave MI)

75 Acute Inferior MI STEMI — Typical Progression Acute Inferior MI#1 Axis is shifting leftward…

ST elevation

77 Qs Qs

Same Patient~2 hrs later Same Patient 9 days later Acute Inferior MI #2 Acute Inferior MI #3

Permanent left axis deviation

New ST elevation But NO anterior infarct (no Qs)

Worsened ST elevation Permanent Q waves (inferior wall scar)

Qs Qs 45% of MIs 40% of MIs

AcuteAcute AAnteriornterior MMII PPageage AcuteAcute IInferiornferior MMII PPageage

1/3 of Inferior MIs 15% of MIs

AcuteAcute R VentricleVentricle MIMI PagePage AcuteAcute LateralLateral MMII PagePage AcuteAcute PPosteriorosterior MMII PPageage Practice: Infarct Location

86

Where is the Pathology? 7 Acute Anterior MI 7 Acute Anterior MI (ST Elevation in V1 - V4)

ST Elevation

What is the R wave axis? Where is the Pathology? 8 Acute Inferior MI 8 Acute Inferior MI Acute(ST Inferior elevation MI in II, III, F)

Where is the Pathology? 9 9

Acute Inferolateral MI Acute InferolateralAcute MIInferolateral MI (ST elevation in II, III, F, V5, V6)

Note the axis has not shifted and there are no loss of R waves yet, because it is early in the AMI,. Where is the Pathology? 10 Acute Inferior MI & Right Ventricle MI 10

Where is the MI? Acute Posterior MI • V1, V2, V3 11 • V1, V2, V3 11 • Large R Waves • Large R Waves Large R waves • Depressed STs Large R waves • Depressed STs ST Depression ST Depression

Normal V1 – V3 Normal V1 – V3 Where is the Pathology? Left Bundle Branch Block

LBBB LAE

LBBB

MI? What rhythm is this? Sinus Tach Acute Anteroseptal MI

Anterior MI Anterior MI

Elevated ST segments Rhythm? Pathology? Acute Inferolateral MI

Elevated STs II, III, aVF, V5, V6

MI? Rhythm? AF? Acute Anterolateral MI

Hyperacute T waves V3–V6 (early sign of AMI)

Elevated STs HIPPA note: Case report: this is NOT Bill Clinton’s 12 58 y.o. male c/o chest actual ECG! “tightness” and shortness of breath x 20 minutes, which gradually subsided. Recurrent episodes over several months. Pt thought it was “acid reflux”, but finally goes to ED. Pt is noncompliant with statin therapy, & admits to poor diet. Family Hx cardiac disease. Hx HTN. Meds: Plavix, ACE inhibitor.

EKG follows. What treatment? Angiography reveals 90% occlusion in some coronary arteries.

But he did have a CABG & became 12 adherent to Excellent outcome: his meds! Pt is active, healthy, has Ischemia / Impending MI improved diet, is compliant with meds; and has no loss of R waves yet… inspired thousands of Americans to go to their providers for cardiac …but inverted T waves evaluations…

“The Bill Clinton Effect” Treatment: quadruple CABG (coronary artery bypass graft). 13 13 Rhythm? Pathology? Ventricular aneurysm Large Old Anterolateral MI

Large Qs V1–V6

Ventricular aneurysm 10910109 11011110

I also teach…

• interpretation (SVTs, heart blocks, etc.)

• Just Say “NO” to Drug Seekers

• and an EKG game: “The Rhythm Method™”

“The Rhythm Method™”

[email protected]