Localizing Infarcts On a 12-Lead EKG



Almost Everything You Need To Know About EKGs But Were Afraid To Ask

Lecture Notes (But Not ALL The Good Stuff In The Lecture)

References Mosby, Bates, Dubin’s Rapid Interpretation of EKGs, , LifeInTheFastLane, Amal Mattu, eMedicine, AmbulanceTechnicianStudy.co.uk

Three main vessels feed the heart ~ the RCA, LAD, LCX. The Right Coronary Artery (RCA) perfuses the right side / bottom of heart in inferior territory / right ventricle. The RCA Posterior Descending Artery branch (PDA) feeds the posterior heart.

The Left Main Artery (LMA) divides into Left Anterior Descending (LAD) (anterior left ventricle / LV) & Left Circumflex (LCX) (lateral left ventricle / LV). The LMA = “The Widowmaker” as a blockage there threatens LAD & LCX / entire left ventricle which is the main heart “pump”.

The heart lies with right ventricle downwards / inferiorly in the chest, perfused by the RCA. Inferior innervated partly by vagus nerve which also innervates the diaphragm. This is why patients with inferior ischemia may have NV or hiccups vs chest pain (“anginal equivalent”).

The 12 lead EKG primarily looks at the anterior heart, septal & anterior left ventricle (LV). The anterior LV (LAD): V2 (septal overlap) V3, V4. Wrapping around the heart (in latin: “circumflex”) is lateral LV territory, V5, V6, (with leads I & AVL.) Infarcting the LAD territory produces an anterior MI.

V5 and V6 are on the left side of the chest. Along with I and AVL, they reflect lateral LV territory. This part of the heart is perfused by the circumflex artery.

The LMA divides into the LAD & LCX, which perfuse most of the left ventricle. An LMA occlusion threatens both areas of the LV at the same time producing an antero-lateral MI, with EKG changes in V2-4, I, aVL, &/or V5-6.

Septal leads are in the center of the chest looking at the area between the ventricles. The septum is perfused partly by RCA, and partly by the LAD. A septal MI shows in V1 and V2.

ISCHEMIA VS INFARCT

In a “normal” EKG complex the electrical impulse originates in the SA Node, to AV node, down the ventricles past bundle of His, into each left & right bundle.

-Rhythm: Regular (R to R interval)

-Rate: Regular (60–99 beats/minute)

-P wave: upright, before every QRS complex

-QRS: narrow, not wide (0.04-0.10 seconds)

Ths EKG complex evolves as heart becomes ischemic, which is measured at the “J point”

Not depressed Depressed

STAGES OF A MYOCARDIAL INFARCTION

1st Stage: Acute Injury (Hyperacute T Waves / ST Elevations)

If clot occludes an artery lumen, infarction begins. Acute injury lasts ~6 hours & is the time between lumen blockage & the start of tissue death distal to the clot. This is the time frame within which TPA or cardiac catherization must be done save the heart muscle. This stage of infarct begins as hyperacute (peaked) T waves & ST elevation in leads that reflect whichever part of the heart being affected.

2nd Stage: Necrosis (Pathologic Q Waves)

Big Q-waves represent progression of the ST elevation MI from acute injury to necrosis. “Pathologic” q-waves are greater than a third of the total size of the QRS and appear at >6 hours.

The appearance of q-waves generally = missed “window” for clot lysis as the tissue is already dead. However, ST elevations + Q waves = evolving injury & possible indication for TPA. ST segments return to baseline / “isoelectric” line) as Qs develop.

3rd Stage: Resolution (Persistent Qs, or flipped Ts):

Development of scar tissue in infarcted area, roughly two weeks post necrotic stage. Affected part of the heart will still show EKG changes, possibly forever – ‘persistent Q-waves’, or flipped T-waves. To review:

Before MI 1st Stage Necrosis Resolution: Q remains +/- flipped T as well

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WHAT IS ELECTRICAL RECIPROCITY?

Some EKG leads “mirror each other” electrically, so ST elevations in one group show as ST depressions in the other group. This is NOT ischemia in the reciprocal “mirrored” leads. The primary heart areas that do this are inferior / lateral & septal / posterior. Inferior ST elevations in II, III & aVF can produce lateral ST depressions in I, AVL, V5 & V6. It’s a reflection, bouncing electrically across the heart from the inferior injury, showing up in reverse. Remember ST elevations always come FIRST. If there are ST elevations anywhere on an EKG, consider if ST depressions might be reciprocal rather than ischemic.

Inferior MI, Lateral Reciprocity

Identify the primary inferior ST elevations in II, III, aVF then identify ST depressions in I & AVL lateral leads. See the ST depressions in V1 & V2? What else do you need to worry about?

Right Ventricular MI

Posterior reciprocity related to coronary artery anatomy. The RCA = “culprit lesion” as it perfuses inferior & posterior heart via the PDA branch. The septal leads (front of the heart) reflect a posterior event (back of the heart) in the same way that inferior / lateral ones do, but there are no true “posterior” leads on an EKG. The way you see the posterior heart is via a right-sided EKG (place V4 on patient’s back), or by looking at leads looking at the front of the heart only backwards & upside down. ST elevation in II, III & AVF + ST depression in V1 & V2 = acute ST elevation infero-posterior MI / right ventricular MI. 50% inferior MIs affect enough RV territory to make pressure & fluid management issues difficult In a right-ventricular MI, the ventricle becomes hypokinetic instead of sending pumping effectively causing a drop in preload. These patients get liters of volume but no nitroglycerin - the opposite management of a left-sided MI. NTG causes hypotension (coronary artery vasodilator) and may cause cardiogenic shock.

OK Jedi….What’s Going On in this EKG?

Systematically: Lead I, aVL, V2-V6 ST elevation throughout lateral territory – possibly a circumflex infarct. ST depressions in aVF & III = reciprocal changes. Lateral STEMI, inferior reciprocity. V1 q-wave, with V2, V3, V4 anterior ST elevations already forming q waves = second infarct area! If there is an infarction in the lateral and anterior heart that means the culprit vessel is in the circumflex & LAD = left main lesion = Widowmaker

RHYTHM ANALYSIS

Normal Sinus Rhythm

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Rhythm Regular; Rate 60-100; QRS Duration Normal; P Wave Visible before each QRS complex; P-R Interval Normal

Sinus Bradycardia

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Heart rate 100; QRS Duration Normal; P Wave visible before each QRS complex; P-R Interval Normal

Supraventricular Tachycardia (SVT)

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Narrow complex atrial tachycardia not controlled from SA node, instead from tissue around the atrioventricular (AV) node. Rhythm Regular; Rate 140-220 beats; QRS Duration Usually normal; P Wave Often buried in preceding T wave; P-R Interval Depends on site of supraventricular pacemaker

Atrial Fibrillation

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Many atria foci generating own electrical impulses, leading to irregular impulse conduction to ventricles. Rhythm Irregularly irregular; Rate 100-160 but slower if on medication; QRS Duration Usually normal; P Wave Not distinguishable as atria are firing all over; P-R Interval Not measurable

Atrial Flutter

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Abnormal tissue generating rapid atrial heart rate, however AV node not involved. Rhythm Regular; Rate 150-300 bpm; QRS Duration Usually normal; P Wave Replaced with multiple “F” flutter waves, usually at a ratio of 2:1 (2F - 1QRS) but sometimes 3:1; P Wave rate ~300 bpm; P-R Interval Not measurable

1st Degree AV Block

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Conduction delay through AV node but all electrical signals reach the ventricles. Generally benign. Rhythm Regular; Rate Normal; QRS Duration Normal; P Wave Ratio 1:1; P Wave rate Normal; P-R Interval Prolonged

2nd Degree Block Type 1 (Wenckebach)

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Conduction block of some but not all atrial beats to the ventricles. Progressive lengthening of PR interval then failure of conduction of atrial beat with dropped QRS complex. Rhythm - Regularly irregular; Rate Normal or Slow; QRS Duration Normal; P Wave Ratio 1:1 for 2,3 or 4 cycles then 1:0.; P Wave rate Normal but faster than QRS rate; P-R Interval Progressive lengthening of P-R interval until a QRS complex is dropped

2nd Degree Block Type 2

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Electrical excitation intermittently fails to pass through AV node or bundle of His. Rhythm Regular; Rate Normal or Slow; QRS Duration Prolonged; P Wave Ratio 2:1, 3:1. P Wave rate - Normal but faster than QRS rate; P-R Interval Normal or prolonged but constant

3rd Degree Block

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Atrial contractions normal but no electrical conduction to ventricles. Ventricles generate own slow signal through an escape focus within the ventricle. Rhythm Regular; Rate Slow; QRS Duration Prolonged; P Wave Unrelated; P Wave rate Normal but faster than QRS rate; P-R Interval Variation

Bundle Branch Block

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Abnormal conduction through bundle branches causes a depolarization delay through ventricles. Rhythm Regular; Rate Normal; QRS Duration Prolonged; P Wave Ratio 1:1; P Wave rate Normal and same as QRS rate; P-R Interval Normal

Premature Ventricular Complexes

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Ventricles depolarize prematurely in response to a signal within the ventricles. Rhythm Regular; Rate Normal; QRS Duration Normal; P Wave Ratio 1:1; P Wave rate Normal and same as QRS rate; P-R Interval Normal

Junctional Rhythms

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Impulse generated below the atria. Rhythm – Regular; Rate - 40-60 Beats per minute; QRS Duration Normal; P Wave Ratio 1:1 if visible. Inverted in lead II; P Wave rate Same as QRS rate; P-R Interval - Variable

Ventricular Tachycardia (VT)

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Results from abnormal tissues in ventricles generating rapid and irregular heart rhythm. Rate 150-250 Beats per minute; QRS Duration Prolonged; P Wave Not seen

Ventricular Fibrillation (VF)

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Disorganized electrical signals cause ventricles to quiver instead of contract in a rhythmic fashion. Rhythm Irregular; Rate >300, disorganized; QRS Duration Not recognizable; P Wave Not seen

Asystole

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Rhythm Flat; Rate 0 Beats per minute; QRS Duration None; P Wave None

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