Acute Inferior MI What a 12-Lead EKG can help you do 73 y.o. male [PDF]

SLIDE 1

Jon Tardiff, BS, PA-C

OHSU Clinical Assistant Professor

Rapid 12-Lead EKG Interpretation

jontardiff@aol.com

I work for Virginia Garcia

Memorial Health Center.

And I am a medical editor for Jones & Bartlett Publishing.

Disclosures:

3

Goals for today’s ECG Review:

Determine Right vs Left bundle branch block
Diagnose Acute MI
Diagnose old MI
Location of the infarct
Other Acute Coronary Syndromes
Other ECG confounders
Determine Axis
Pfun!

What a 12-Lead EKG can help you do

Diagnose ACS / AMI
Interpret arrhythmias (computer Dx)
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!

5 5

For example: 73 y.o. male with nausea, syncope

6 6

Acute Inferior MI

ST elevation

SLIDE 2

What rhythm? (look at V1 for P waves)

Atrial flutter (w/septal MI?)

The flutter waves are invisible in Lead II

9 9

another example…

10

10 10 1

WPW with Atrial Fib

WPW Graphic
Wolff-Parkinson-White synd.
short PR
wide QRS
delta wave

12 12 2 12 2

Same pt, converted to SR

SLIDE 3

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 (dissecting

aneurysm, pericarditis, WPW, LBBB, digoxin, RVH)

14 14 14 14 4 14 14 14 14 14 4

Confounder: Left Bundle Branch Block

15 15 15 15 15 15 15 15 15 15 15 15 5 15 5 15 15 1

Impending AMI with normal ECG!

16 16 16 16 16 16 16 16 16 16 16 16 6 16 6 1

13 hrs later — Acute Anterior MI

Elevated ST segments

Pt is a 4 y.o. child w/ one episode of tachycardia and shortness of breath. WPW mimicking MI (false Q waves in Lead II, III, AVF, V1, & V3). Also mimicking LBBB.

Confounder: Wolff-Parkinson-White syndrome

“ECG Pearls”

Lead II is the easiest lead to read / most intuitive
But Lead V1 is our single best lead.
Lead V3 is best for QT interval measurement
“A Q in III is free.” (isolated Q in L III)
80% of reading an ECG is finding the P wave!
The other half is knowing where the + electrode
is. ☺

SLIDE 4

19

ECG Lead Placement & Electrophysiology Review

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I II III

Limb Leads

(standard leads)

±

+

Normal 12-Lead ECG

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Rapid Interpretation Tips

22 22 22 22 2 22 22 2 22 22 22 22 2

Rapid Int nterpretati ati ti ti i ti i ti i ti i ti ti tion n

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Tip

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Dr. Willem Einthoven

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SA Node AV Node His Bundle BBs Purkinje Fibers P Q R S T

II

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Conduction System

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Q R S P wave axis R wave axis …upright in L II …upright in L II

Lead II

SLIDE 5

25

QRS Morphology in Lead II II

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Leads I, II, III

I II III

27 27

PR

II

Intervals

PR Interval: 120 – 200 mSec (3 – 5 boxes) QRS width: 60 – 120 mSec (1½ – 3 boxes) QT/QTc interval: 400 mSec (10 boxes) QT QRS

28

300, 150, 100, 75, 60, 50 Quick, easy, sufficient

Triplicate Method:

Count PQRST

in a 6- second strip & multiply x 10

Easy, & more accurate

6-second :

300 150 100 75 60 6 seconds

Horizontal axis is time (mS); vertical axis is electrical energy (mV)

29

Normal Sinus Rhythm

What is the heart rate?

6 seconds

30

I II III aVR aVL aVF

Limb (frontal plane) Leads

(augmented leads) (standard leads)

SLIDE 6

Normal 12-Lead ECG

32

6 Frontal Plane Leads

(limb leads) I II III R L F

Axis

33

Leads

I II III aVR* aVL aVF

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34 35

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Limb (frontal plane) Leads

(augmented leads) (standard leads) (anterior leads) (lateral leads)

Chest (precordial) Leads

36

SLIDE 7

V Lead Cutaway

V Lead Progression

Normal 12-Lead ECG

Lots of ways to read EKGs…
QRSs wide or narrow?
Regular or irregular?
Fast or slow?
P waves?
Sinus rhythm or not?
If not, is it atrial fibrillation?
BBB?
MI?

Symptoms:

Syncope is bradycardia, heart blocks, or VT
Rapid heart beat is AF, SVT, or VT

41

Step-by-step method for reading a 12-Lead

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, beta- blocker, clopidogrel, statin, etc.

SLIDE 8

Supraventricular rhythms

Sinus rhythm
Atrial fibrillation
Junctional rhythm
PSVT / AVNRT
Atrial tachycardia
Atrial flutter
Wandering atrial pacemaker
MAT

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, beta- blocker, clopidogrel, statin, etc.

The Problem with Bundle Branch Blocks

Desynchronized contraction of the ventricles
Reduced cardiac output
Worsened heart failure
LBBB confounds the EKG interpretation

and makes it harder to find ACS

47

Bundle Branch Blocks

(QRS > 0.12 sec.)

Left BBB

(L I, V5, V6: upright QRS with a notch)

Right BBB

(V1, V2, MCL1: rsR’ pattern) R’ S r notch

I

V1

(left-sided lead) (right-sided lead)

48

Bundle Branch Blocks

Two QRSs

48 48 48 48 48 8 48 48 48 48 48 4

notch

I

Healthy ventricle Blocked bundle R’ S r

V1

slur

I

SLIDE 9

V1 & V2 RBBB V5 V6 (& I, aVL) LBBB

51

Practice: Bundle Branch Block

RBBB

Which Bundle Branch is Blocked?

1

RBBB

Right Bundle Branch Block (Lead V1)

1

LBBB 12-Lead

Which Bundle Branch is Blocked?

2

SLIDE 10

LBBB 12-Lead

Left Bundle Branch Block

(L I, V5, V6)

2

Where is the Pathology? Right Bundle Branch Block

58 58 58 58 58 8 58 58 58 58 58 58 5

Where is the Pathology?

59

Left Bundle Branch Block

Axis Determination

SLIDE 11

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Why We Care About Axis Deviations

The axis shifts towards hypertrophy & away from infarction

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Axis Deviation

Horizontal heart (0°): obesity, 3rd 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 (VT), MI

63

How to calculate Axis

Easiest: the computer does it for you! Easy: find the tallest R wave (if tallest is Lead II = normal axis) Even easier: (if Lead II is upright = normal axis Funnest: Thumbs up / Thumbs down

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Calculating Axis: Thumbs Up / Down Method

Lead I —Your Left thumb Lead aVF —Your Right thumb

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Practice: Axis

3

I F

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Axis Practice

1

66 66 66 66 66 66 66 66 66 66 66 66 6 66 66 66 66 66 6

Ax A is Pra ractice

1

Axis is is is is s is is s is s is is s is s Pra ra ra ra ra ra ra ra ra ra a ra ra ra ra a ra r cti Normal Axis

I F

SLIDE 12

67

4

I F

68

4

Left Axis Deviation

I F

69

5

70

5

70 70 70 70 70 70 70 70 70 70 70 70 70 70

Right Axis Deviation

71

6

72 72 72 72 72 72 72 72 7

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Extreme Right Axis Deviation

SLIDE 13

73

New 12-Lead ECG Format

aVL I

aVR

II aVF III

New 12-Lead ECG Format

aVL I

aVR

II aVF III New Old

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, beta- blocker, clopidogrel, statin, etc.

Ischemia Injury Infarction Normal

STEMI

ST elevation, ST depression, T wave inversion, pathologic Q waves

77

SLIDE 14

Percutaneous Coronary Intervention

80

RCA before and after stenting

Before stenting After stenting

STEMI: ECG Changes

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)

(w/onset cx pn) (20 minutes) (1 hour) (1 week – years) (>1 hr) (normal)

MI ECG Patterns MI E MI E MI E MI E MI E MI E MI E MI E MI E MI E MI E MI E MI E MI CG P CG P CG P CG P CG P CG P CG P CG P CG P CG P CG P CG P CG P G atte atte atte atte atte atte atte atte atte att att att att at rns rns ns rns rns s ns ns rns rns s ns ns n

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Why Pathologic Q Waves Form

Normal q Pathologic Q

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STEMI — Typical Progression

SLIDE 15

Acute Inferior MI#1

Acute Inferior MI

ST elevation Qs Qs

Axis is shifting leftward…

Acute Inferior MI #2

Same Patient~2 hrs later

Worsened ST elevation Qs Qs New ST elevation

Acute Inferior MI #3

Same Patient 9 days later

Permanent Q waves (inferior wall scar) But NO anterior infarct (no Qs)

Permanent left axis deviation Acute Anterior MI Page Acut Acut Acut Acut Acu Acu Acu Acu Acu Acu Acu Acu Acu Acu Acu Acu Acu Acu Acu A e An e An e An e An e An e An e An e An e An e An e An e An e An e An An e An e An e An e An A teri teri teri teri teri eri eri eri teri teri eri eri teri teri i teri eri teri ter er or M

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45% of MIs

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SLIDE 16

Acute Lateral MI Page Acu Acu Acu A te te t t L t L t L t Lat Lat L t Lat t L t t L t L era era eral M l M l M l M M l M l M l M l M M l M M l M l M l M M l M l M l M l I P I P I P I P P I P P I P P I P Page age e g age age age ge age ge age ge g

15% of MIs

Acute Posterior MI Page Acut Acut Acut Acut Acut Acut Acut Acut A t t A t Acut Acut Acut Acut Acu Acu Acu Ac A e Po e Po P e Po P e Po P e Po P t ster ster ster ster ster t ster ster ster t ster t ster ster t ste ior ior ior ior ior ior ior io io i MI P MI P MI P MI P MI P MI P MI P MI P MI P MI P I P MI P MI P MI P MI P MI P MI P MI P MI P MI Page age age age age age e age ge g ag ag a

93

Practice: Infarct Location

Acute Anterior MI

Where is the Pathology?

7 Acute Anterior MI

(ST Elevation in V1 - V4)

ST Elevation What is the R wave axis?

7

Acute Inferior MI

Where is the Pathology?

8

SLIDE 17

Acute Inferior MI

(ST elevation in II, III, F)

8

Acute Inferolateral MI

Where is the Pathology?

9

Acute Inferolateral MI

(ST elevation in II, III, F, V5, V6) Note the axis has not shifted yet, because it is early in the AMI, and there are no loss of R waves yet.

9

Where is the Pathology?

10

Acute Inferior & Right Ventricle MI

Acute Inferior MI & Right Ventricle MI 10

Where is the MI?

Normal V1 – V3

V1, V2, V3
Large R Waves
Depressed STs

ST Depression Large R waves

11

SLIDE 18

Acute Posterior MI

Normal V1 – V3

V1, V2, V3
Large R Waves
Depressed STs

ST Depression Large R waves

11

104

Confounders

Rapid Interpretation Tips

Identify the rhythm. If supraventricular,
Rule out left bundle branch block. 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.

WPW Graphic

Wolff-Parkinson-White synd.

Wolff-Parkinson-White synd.

Short PR, Wide QRS, “Delta” wave
Short PR

Widened QRS Delta wave

108

False Q Waves (the Delta wave)

WPW

False Q waves mimic MI

SLIDE 19

Other Confounders

110 110 110 110 110 110 110 110 110 110 110 110 110 110 10 110 110 10 110 110 11

Benign Normal Variant ST Elevation

Mild upsloping ST segments

Pericarditis

Elevated STs in multiple leads Depressed PR segments

NO loss of R waves •

Elevated STs in multiple leads Depressed PR segments

Other Confounders

Left Ventricular Hypertrophy

Tall R waves in V5, V6; deep S waves in V1, V2

Tall R waves V5, V6 Deep S waves V1, V2

“strain”

Other Confounders: Digoxin

(ST Depression)

Depressed ST segments

SLIDE 20

115

ST Depression

(a diagnostic challenge) Can be caused by:

Ischemia
Digoxin effect
Tachycardia
LVH, BBB
Hypokalemia
NSTEMI (Non Q wave MI)

Ischemic ST Depression (a positive exercise ECG)

117

Practice: Confounders

12

44 y.o. female with history of tachycardia

WPW (short PR, Wide QRS, Delta waves)

false Q waves delta waves short PR

12

120

13

30 y.o. male with positional chest pain

SLIDE 21

121 121 121 21 2

13

Pericarditis

Depressed PR segments Elevated ST segments in multiple leads

Putting it all together

Where is the Pathology?

LAE LBBB LBBB

Left Bundle Branch Block

125 125 125 125 125 125 25 25 2 1 2 6 1 2

Right Bundle Branch Block

SLIDE 22

127 27 127 127 127 127 127 27 127 27 127 127 127 127 127 27 1 128 128 128 128 128 128 128 128 128 128 128 128 128 128 128 2 12 1

6

Acute Anterior MI

Elevated ST segments

Anterior MI

MI? What rhythm is this?

Anterior MI

Sinus Tach Acute Anteroseptal MI

Elevated ST segments

Rhythm? Pathology? Acute Inferolateral MI

Elevated STs II, III, aVF, V5, V6

SLIDE 23

Anterolateral Ischemia- Junctional Rhythm Rhythm? MI? Anterolateral Ischemia- Junctional Rhythm

Junctional Rhythm; Acute Anterolateral Ischemia

P P Inverted Ts

Acute Inferolateral MI ECG

MI?

Acute Inferolateral MI ECG

Acute Inferolateral MI

137 137 137 137 137 137 137 137 37 137 137 137 137 37 37 37 3

Rhythm? Pathology?

14

138 138 138 138 138 138 138 138 138 138 138 138 8 38 38 8 138 13 3

Large Old Anterolateral MI

Large Qs V1–V6

Ventricular aneurysm

14

SLIDE 24

Case report: 58 y.o. male c/o chest “tightness” and shortness

f 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.

HIPPA note: this is not Bill Clinton’s actual ECG!

Treatment: quadruple CABG (coronary artery bypass graft). Ischemia / Impending MI

no loss of R waves yet… …but inverted T waves

But he did have CABG & became adherent to his meds…

Excellent outcome: Pt is active, healthy, has improved diet, is compliant with meds; and has inspired thousands of Americans to go to their physician for cardiac evaluations… “The Bill Clinton Effect”