Amy Gutman MD ~ EMS Medical Director
prehospitalmd@gmail.com / www.TEAEMS.com
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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 sternum
 V2 - 4th ICS to left of sternum


V3 - Between V2 & V4
V4 - 5th ICS at MCL
V5 - Horizontally with V4 at AAL


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V6 - Horizontally with V4 & V5 at MAL
I
AvR
V1
V3
II
AvL
V2
V4
III
AvF
V3
V5
Lead II Continuous Strip
I
AvR
Lateral
V1
Septal
V4
Anterior
II
AvL
V2
V5
Inferior
Lateral
Septal
Lateral
III
AvF
V3
V6
Inferior
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”
II
Inferior
III
AvF
Inferior
Inferior

Two vessels cover large
area

V2 overlaps septal &
anterior areas

Septal MI is best seen in
V1 & V2
V1
Septal
V2
Septal

Septum & anterior left
ventricle are the
“precordial” leads

V1 & V2 directly over
cardiac septum

V2 (septal overlap), V3, V4
look at anterior heart
V4
Anterior
V3
Anterior

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
Contiguous Leads
I, AvL, V5, V6
II, III, AvF
V1, V2
(V2, V3)
V3, V4
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
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
Left Atrium
Sinoatrial Node Atrioventricular Node
Bundle of His
Right Atrium
Right Ventricle
Left Ventricle
Electrical
Pathway
SA Node
AV Node
1.
SA Node
2.
AV Node
3.
Bundle of His
4.
Right & Left
Ventricles
Right
Ventricle
His
Bundle
Left
Ventricle

One complex = one
cardiac cycle

Recognizing normal
means understanding
abnormal
Atrial Depolarization
Ventricular Depolarization
Ventricular 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
J Point

0.08 - 0.12 sec

J point to beginning of T wave

Flat or depressed ST:
 Ischemia

ST elevation:
 Infarction

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
LBBB
•
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 waves
ST 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

V1
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:
V2
 ST elevations in II, III, aVF?
 ST depressed in V1, V2?
II
III

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 pacemaker

May have inverted P-waves

Two or more asynchronous cardiac pacemakers

The hallmark of this form of SVT is multiple Pwave 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)

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“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”