Acute Coronary Syndromes Disclosures I work for Virginia Garcia Memorial Health Center, Beaverton, OR. Jon Tardiff, BS, PA-C OHSU Clinical Assistant Professor And I am a medical editor for Jones & Bartlett Publishing. Goals of this session Identify Acute Coronary Syndromes (STEMI vs NSTEMI) Identify old myocardial infarction Distinguish between Right and Left BBB Arabic, Somali, Mai Mai, Pashtu, Urdu, ASL, and more! 4
What a 12-Lead ECG can help you do For example: 73 y.o. male with nausea, syncope Diagnose ACS / AMI Interpret arrhythmias Identify life-threatening syndromes (WPW, LGL, Long QT synd., Wellens synd., etc) Infer electrolyte imbalances Infer hypertrophy of any chamber Infer COPD, pericarditis, drug effects, and more! 6 Acute Inferior MI What rhythm? (look at V 1 for P waves) ST elevation 7 8
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) 9 Confounder: Left Bundle Branch Block Impending AMI with normal ECG! 11 12
13 hrs later Acute Anterior MI ECG Lead Placement & Electrophysiology Review Elevated ST segments 13 14 Rapid Interpretation Tips Limb Leads I II III (standard leads) Dr. Willem Einthoven - ± 15 + 16
Leads I, II, III Normal 12-Lead ECG I II III 17 Conduction System Lead II II R P wave axis upright in L II P T U R Q S R wave axis upright in L II SA Node AV Node His Bundle BBs Purkinje Fibers Q S 20
Intervals II Limb (frontal plane) Leads PR QRS QT I II III avr (standard leads) avl PR Interval: 120 200 msec (3 5 boxes) QRS width: 60 120 msec (1 ½ 3 boxes) QT/QTc interval: 400 msec (10 boxes) 21 avf (augmented leads) 22 Augmented Leads Normal 12-Lead ECG avl avr avf 23
R 6 Frontal Plane Leads (limb leads) I II L III F - Axis Leads I II III avr* avl avf 25 26 QRS Morphology in Lead II Axis Determination II 27
Why We Care About Axis Deviations Normal axis is -20 to +110 The axis shifts towards hypertrophy & away from infarction The axis also shifts for ectopic rhythms, such as V-Tach 29 Axis Deviation Horizontal heart (0 ): obesity, 3 rd trimester pregnancy. Ascites Vertical heart (90 ): slender build Left Axis Deviation: LBBB, Anterior MI, Inferior MI, Left anterior hemiblock, LVH Right Axis Deviation: Anterior MI, Lateral MI, RBBB, COPD, RVH, Left posterior hemiblock Extreme RAD: Ectopic rhythm 30 (VT), MI How to determine Axis Easiest: the computer does it for you! I Practice: Axis 1 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 1 Normal Axis I F 1 34 2 I F 35 2 Left Axis Deviation I F 36 3
3 Right Axis Deviation 4 37 38 4 Extreme Right Axis Deviation Limb (frontal plane) Leads Chest (precordial) Leads I II III avr (standard leads) V1 V2 V3 V4 (anterior leads) avl avf V5 V6 (lateral leads) 39 (augmented leads) 40
V Lead Cutaway 41 V Lead Progression Normal 12-Lead ECG
Step-by-step method for reading a 12-Lead 45 46 Rapid Interpretation Tips Rapid Interpretation Tips Identify the rhythm. If supraventricular*, 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, betablocker, clopidogrel, statin, etc. Supraventricular rhythms Sinus rhythm Atrial fibrillation Junctional rhythm PSVT Atrial tachycardia Atrial flutter Wandering atrial pacemaker Multifocal Atrial Tachycardia
Normal 12-Lead ECG Rapid Interpretation Tips Rapid Interpretation Tips Identify the rhythm. If supraventricular, 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, betablocker, clopidogrel, statin, etc. The Problem with Bundle Branch Blocks (right-sided lead) Bundle Branch Blocks (QRS > 0.12 sec.) (left-sided lead) Dyssynchronized contraction of the ventricles Reduced cardiac output Worsened heart failure LBBB confounds the EKG interpretation LBBB makes it harder to find ACS V1 r S R Right BBB (V1, V2, MCL1: rsr pattern) I notch Left BBB (L I, V5, V6: upright QRS with a notch) 52
Bundle Branch Blocks Two QRSs Healthy ventricle Blocked bundle RBBB V 1 & V 2 V1 r R I notch I slur S 53 LBBB Practice: Bundle Branch Block V 5 V 6 (& I, avl) 56
Which Bundle Branch is Blocked? 5 Right Bundle Branch Block (Lead V1) 5 RBBB RBBB Which Bundle Branch is Blocked? LBBB 12-Lead 6 Left LBBB Bundle 12-Lead Branch Block (L I, V5, V6) 6
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 III -avr III Old 65 Rapid Interpretation Tips Rapid Interpretation Tips Identify the rhythm. If supraventricular, Rule out left bundle branch block. If no LBBB, 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, betablocker, clopidogrel, statin, etc. ST elevation, ST depression, T wave inversion, pathologic Q waves STEMI NSTEMI? Normal Ischemia Injury Infarction
Percutaneous Coronary Intervention RCA before and after stenting The Spectrum of Acute Coronary Syndromes Shock / Healthy CAD Angina Unstable Angina NSTEMI STEMI Death Patent artery ~50% ~70% >70% or 100% ~90% 100% 100% (or vasospasm) Before stenting After stenting 71 No symptoms Pain on Pain at rest; exertion relieved by NTG Constant pain
NSTEMI vs STEMI STEMI: ECG Changes ~90% NSTEMI Constant pain 100% STEMI Constant pain (normal) (w/onset cx pn) (20 minutes) (1 hour) (>1 hr) (1 week years) A. Normal ECG B. Hyperacute T wave changes - increased T wave amplitude and width; may also see ST elevation C. Marked ST elevation with hyperacute T wave changes (transmural injury) D. Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis) E. Pathologic Q waves, T wave inversion (necrosis and fibrosis) F. Pathologic Q waves, loss of R waves (fibrosis) Why Pathologic Q Waves Form MI ECG Patterns Normal q Pathologic Q NSTEMI (non Q wave MI) 75
STEMI Typical Progression Axis is shifting leftward Acute Inferior MI Acute Inferior MI#1 ST elevation 77 Qs Qs Acute Inferior MI #2 Same Patient~2 hrs later Same Patient 9 days later 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 Acute Anterior MI Page Acute Inferior MI Page 1/3 of Inferior MIs 15% of MIs Acute R Ventricle MI Page Acute Lateral MI Page
Acute Posterior MI Page Practice: Infarct Location 86 Where is the Pathology? Acute Anterior MI 7 Acute Anterior MI (ST Elevation in V1 - V4) 7 ST Elevation What is the R wave axis?
Where is the Pathology? Acute Inferior MI 8 Acute Inferior MI Acute (ST Inferior elevation MI in II, III, F) 8 Where is the Pathology? Acute Inferolateral MI 9 Acute Inferolateral Acute MI Inferolateral MI (ST elevation in II, III, F, V5, V6) 9 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? Large R waves ST Depression V1, V2, V3 Large R Waves Depressed STs 11 Acute Posterior MI Large R waves ST Depression V1, V2, V3 Large R Waves Depressed STs 11 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
Case report: 58 y.o. male c/o chest 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. HIPPA note: this is NOT Bill Clinton s actual ECG! 12 EKG follows. What treatment? Angiography reveals 90% occlusion in some coronary arteries. But he did have a CABG & became adherent to his meds! Ischemia / Impending MI no loss of R waves yet but inverted T waves 12 Excellent outcome: Pt is active, healthy, has improved diet, is compliant with meds; and has inspired thousands of Americans to go to their providers for cardiac evaluations Treatment: quadruple CABG (coronary artery bypass graft). The Bill Clinton Effect
Rhythm? Pathology? 13 Large Old Anterolateral MI 13 Ventricular aneurysm Large Qs V1 V6 109 Ventricular aneurysm 110 I also teach Arrhythmia interpretation (SVTs, heart blocks, etc.) Just Say NO to Drug Seekers and an EKG game: The Rhythm Method The Rhythm Method jontardiff@aol.com