Amy Gutman MD ~ EMS Medical Director

prehospitalmd@gmail.com / www.TEAEMS.com

Part I: Cardiac Anatomy Review

Part II: The Cardiac Cycle

Part III: From One Beat to Many

Part IV: Rhythm Analysis

What is an EKG really looking at?

German “Elektrokardiogramm”

Record of the heart’s electrical depolarizations & repolarizations over time Arrhythmias, ischemia, & conduction abnormalities Electrolyte disturbances Non-cardiac diseases (i.e. hypothermia, PE)

3 lead “overview” image of heart I (lateral) II (inferior) III (inferior)

Useful for checking arrhythmias

Not great for looking for ischemic changes

Leads I, II & III are “limb leads”

Leads aVR, aVL, & aVF are “augmented” limb leads

V1 - 4th ICS to right of sternumV2 - 4th ICS to left of sternum

V3 - Between V2 & V4

V4 - 5th ICS at MCLV5 - Horizontally with V4 at AAL

V6 - Horizontally with V4 & V5 at MAL

Lead II Continuous Strip

I AvR V1 V3

II AvL V2 V4

III AvF V3 V5

I AvR V1 V4

Lateral Septal Anterior

II AvL V2 V5Inferior Lateral Septal Lateral

III AvF V3 V6Inferior Inferior Anterior Lateral

Right Coronary Artery (RCA) perfuses right ventricle / inferior heart Inferior heart

Left Main Artery (LMA) divides into: Left Anterior Descending

Artery (LAD) perfuses anterior left ventricle

Left Circumflex Artery (LCX) perfuses lateral left ventricle

Each coronary artery = one part of the EKG

You must see changes in >two “contiguous” leads to diagnose ischemia

Contiguous leads = heart “territories”: Inferior, Anterior, Lateral, Septal

Right ventricle positioned downward & inferior

Innervated by vagus nerve Same nerve as stomach IMIs often present with

N/V not “chest pain”

IIInferior

III AvF Inferior Inferior

Two vessels cover large area

V2 overlaps septal & anterior areas

Septal MI is best seen in V1 & V2

V1Septal

V2Septal

Septum & anterior left ventricle are the “precordial” leads

V1 & V2 directly over cardiac septum

V2 (septal overlap), V3, V4 look at anterior heart

V3Anterior

V4Anterior

Winds around lateral heart & left ventricle

LMA “Widow Maker”: Divides into LAD & LCX,

perfuses left ventricle LMA occlusion causes

massive antero-lateral MI

I Lateral

AvL V5 Lateral Lateral

V6 Lateral

I AvR V1 V4

Lateral Septal Anterior

LMA, LCX RCA, LAD LAD

II AvL V2 V5

Inferior Lateral Septal Lateral

RCA LMA, LCX RCA, LAD LMA, LCX

III AvF V3 V6

Inferior Inferior Anterior Lateral

RCA RCA LAD LMA, LCX

Contiguous Leads

I, AvL, V5, V6

II, III, AvF

V1, V2

(V2, V3)

V3, V4

The heart is nothing more than a mechanical pump running on electricity

The heart is a mechanical pump running on electrical energy

Electrical energy pathways determine how well the heart functions

Changes in electricity = changes in heart function

Sinoatrial Node Atrioventricular NodeLeft Atrium

Right Atrium

Right Ventricle Left Ventricle

Bundle of His

1. SA Node

2. AV Node

3. Bundle of His

4. Right & Left Ventricles

Electrical Electrical PathwayPathway

SA Node

AV Node

HisBundle

RightVentricle

Left Ventricle

One complex = one cardiac cycle

Recognizing normal means understanding abnormal

Atrial DepolarizationVentricular DepolarizationVentricular Repolarization

Width = time

Height & depth = voltage

Upward deflection = positive

Downward delection = negative

SA to AV node path causes atrial contraction

Upright in II, III, & aVF

Inverted in aVR

Variable P wave shapes suggests ectopic pacemaker

120 - 200 ms (3 to 5 small boxes) Long = 1st degree heart block Short = pre-excitation syndrome (WPW) Variable = other heart blocks

PR depression = atrial injury or pericarditis

Short PR interval <120 ms, <3 small boxes

Slurred QRS upstroke = “delta wave”

Young, healthy person with CP & palpitations

Consider with “shackalitis”

Atrial impulses conducted to ventricles via accessory pathway causing reentry

Ventricular contraction coordinated by Bundle of His & Purkinje fibers

0.06 to 0.10 sec

Duration, height & shape diagnose arrhythmias, conduction abnormalities, hypertrophy, infarction, electrolyte derangements

Short: <0.08 secs Seen in SVT

Long: >0.12 secs Often related to a

bundle branch block

Normal (physiologic) or abnormal (pathologic)

Normal: Septal depolarization Best seen in lateral leads I, aVL, V5 & V6

Qs > 1/3 R wave height, or >0.04 sec length abnormal May show infarction

0.08 - 0.12 sec

J point to beginning of T wave

Flat or depressed ST: Ischemia

ST elevation: Infarction

J Point

Ventricular repolarization

T wave usually upright Inverted: ischemia, hypertrophy, CVA Tall: hyperkalemia Flat: ischemia, hypokalemia

Beginning of QRS to end of T wave Ventricular depolarization to “resetting” the

conduction system

Normal ~ 0.40 secs Interval varies based on HR & must

be adjusted (Corrected QT / QTc)

• The heart takes too long to repolarize leaving it vulnerable to aberrant electrical impulses

• Torsades de pointes, VT, VF

Prolonged QT interval Alcohol abuse Hypomagnesemia, hypokalemia

May have a pulse, but are never “stable”

RX: magnesium bolus

Not always seen, typically small, follows T wave

Purkinje fiber repolarization

Hypokalemia, hypercalcemia, hypothermia, CVA, or thyroid disease

Inverted U wave: ischemia, volume overload

Putting it together…

1 small block = 1 mm² = 0.04 s = 40 ms

5 small blocks = 1 large block = 0.20 s = 200 ms

5 large blocks = 1 second

Each large black line = 300 150 100 75 60 50

If there is an P wave before each QRS & both are upright, then the rhythm is “sinus” From sino-atrial / SA node

P wave round, not peaked & unidirectional except in V1 & V2 (often biphasic)

Normal axis leads I & AVF are positive (upright)

When heart enlarges / hypertrophies or normal pathways are re-routed, the “axis” changes

Anything more beyond the scope of this lecture

Right Ventricular Hypertrophy R wave >S in V1, becomes

progressively smaller S wave in V5,V6 RAD with wide QRS

Left Ventricular Hypertrophy S in V1 + R in V5 (in mm) = 35mm LA with wide QRS

Why is this important for prehospital providers?

Anywhere in conduction system

Ectopic beats generated from foci other than usual sites of electrical activity Some ectopic beats in a healthy persons normal Persistent ectopic beats become “blocks” / conduction dz

Conduction disorders manifest as slowed conduction (1st degree), intermittent conduction failure (2nd degree), or complete conduction failure (3rd degree)

Slowed electrical signal not travelling through atrial tissue at normal speed resulting in long P-R PR > 0.20 sec Always a P waves before QRS P-R interval consistent

May be due to ischemia or infarct

Progressive delay AV conduction, until impulse completely blocked Occurs because impulse arrives during absolute refractory

period, so no conduction no QRS P-P intervals shorten until pause occurs Next P wave occurs & the cycle begins again

P-P interval following pause greater than P-P interval before pause

Block usually located in AV node, so QRS narrow

Multiple constant PR intervals before blocked P wave

Ventricular rate always les than atrial rate, depends on number of impulses conducted through AV node Atrial & ventricular rates irregular P waves present in 2, 3 or 4:1 conduction with QRS PR interval constant for each P wave prior to QRS

Type II AV block is almost always located in bundle branches so QRS is wide

Atria & ventricles controlled by separate pacemakers

Narrow QRS suggests AV block with junctional escape

Wide QRS suggests AV node or bundle branch block block with ventricular escape (“idioventricular”)

•40 – 60 BPM

•“Junction” between atria & ventricles

•P wave “flipped” as beat originates below SA node

LBBBLBBB• RBBB

• QRS >0.12

• “M” shaped QRS in V1 or V2

• R = 1st peak

• Ischemia, infarction, electrolyte abnormalities, meds, CNS disease

LBBB QRS >0.1-0.12s• Wide & “Peaked” QRS in V6• R Prime = 2nd peak

Stage I: Ischemia

Stage 2: Injury

Stage 3: Infarction

Stage 4: Resolution

Look in all leads for:Q waves

Inverted T wavesST segment elevation or depression

• Normal T wave upright when QRS upright

• If T wave inverted, then = ischemia

• Try and compare with old EKG to determine if inversion is new or old

• ST elevation + Q waves = acute infarction

• “Non-Q” MI = infarct without Q waves

• ST often returns to baseline in time

6 hours from lumen blocked by clot to start of tissue death appears as ST elevation

6 hour period is when must start TPA (“clot busters”) to salvage heart tissue

“Time is Muscle!”

Qs represent progression of injury to infarction

Pathologic Qs = QRS (-) deflection after PR interval & >1/3 size of QRS

If ST elevations & Qs at same time, STEMI evolving from injury to necrosis

Development of scar tissue in infarcted area occurs roughly 2 weeks after necrosis

Affected part of heart may show EKG changes forever

Be careful – flipped T waves can also mean pt having new ischemia!

Persistent ST depression may indicate “Non-Q” MI

Pacemakers Atrial or ventricular

or both

Looks like “spikes” on the ECG

Be wary of the patient with a pacer who has no spikes

Some EKG lead groups are electrical “mirrors”

ST elevations in one group appear as depressions in the other group in two specific areas: Inferior and Lateral Septal & Posterior

Elevations always come first If there are ST elevations on EKG, ST depressions on the

same EKG might be reciprocal instead of ischemic

There are no true posterior leads on a standard EKG

Septal leads look at anterior & posterior heart & “mirror” an infero-posterior infarction

Remember the RCA perfuses inferior & posterior areas: ST elevations in II, III,

aVF? ST depressed in V1, V2?

II

III

V1

V2

Most prominent feature are peaked-T waves

“Sine waves” also seen

Changes seen across ALL leads, not in a single coronary artery pattern Common with all

electrolyte / metabolic abnormalities

Anatomy plus electricity equals rhythm

SA node origin

Rate 60 – 100 beats/ minute > 100 = sinus tachycardia < 60 = sinus bradycardia

If irregular, rate determined by both a “ventricular” & “atrial” rate

Normal variant

Irregular rhythm varies with respiration

All P waves look identical

Intrinsic rate for SA node: 60 - 100bpm

Causes: Inferior MI (RCA lesion) Sedation

Rhythm originates in the SA node P wave for every QRS Rate > 100 / minute

Increased cardiac stress from systemic process: Hypovolemia / Hypotension Hypoxia Anxiety Drugs (i.e. cocaine) Exercise

Rate 60 – 90 bpm

Occasional “escape” ectopic beats

Also known as “PACs”

Atrial reentry from a circular conductive pathway

Single ectopic pacemakerMay have inverted P-waves

Two or more asynchronous cardiac pacemakers

The hallmark of this form of SVT is multiple P-wave morphologies (one from each pacemaker)

Absence of p-waves before each QRS

Irregularly irregular from ectopic foci with re-entry

Rate ~ 200-300bpm

No True P Waves

Multiple sawtooth edged P waves before each QRS

Many ectopic pacemakers Unstable rhythm May progress to atrial fibrillation

• No P waves or atrial activity

• Normal QRS • Ventricles generating slow escape rate (20-40 BPM)

“Accelerated” IVR faster than expected rate (>60) Ventricular pacemakers speed up & capture as pacers

are faster than the underlying rhythm

SVT: Generated above

ventricle P waves present Narrow

VT: Generated in

ventricles No P waves Wide

Generated above ventricles so narrow complex with P waves

May be normal in bursts in young, healthy individuals

Often difficult to differentiate from VT

•Wide QRS (>140 ms) without atrial activity / P waves

•ANY wide tachycardia is VT until proven otherwise

•Often caused by ischemic / infarcted conductive ventricular tissue causing a reentry tachycardia

SVT

Rhythm - Regular Rate - 140-220 BPM QRS Duration - normal P Wave - Buried in preceding

T wave P-R Interval - Depends on site

of supraventricular pacemaker

Impulses stimulating heart are not generated by sinus node, instead from a collection of tissue around the AV node

VT

Rhythm - Regular Rate - 180-190 BPM QRS Duration - Prolonged P Wave - Not seen Abnormal ventricular

tissues generating a rapid & irregular heart rhythm & poor cardiac output is

Wide and slow No P waves as rhythm starts below atria

<6 in a minute = Normal >6 in a row= Ventricular Tachycardia

Multiple ventricular areas contract without coordination

Quivering results in loss of cardiac output & death

Cure for VF is electrical defibrillation

Alan Lindsey ECG Learning Center in Cyberspace

Dubin’s Guide to ECGs London Ambulance Sercice Unoffical

ECG Guide Brady’s, Mosby’s, Caroline’s

Prehospital Provider Textbooks www.TheMDSite.com Wikipedia, Google The ECG Guide (Iphone App)

“Almost” everything you need to know: Part I: Cardiac Anatomy Review Part II: The Cardiac Cycle Part III: From One Beat to Many Part IV: Basic Rhythm Analysis

Is this everything you truly need to know?

Look at every strip, ECG & rhythm you can…you need to know “normal” before you can know “abnormal”