Relevant

EKG Pattern Types Characteristics EKG

Information

P wave is upright in leads 2, 3, and

Sinus Rhythm aVF

Regular QRS

Just a SLOW rate but everything is

Sinus Bradycardia Normal in athletes

normal

can be due to exercise, fever,

Sinus Tachycardia anxiety, MI. Can be asx

Just a FAST rate but all is normal

Asystole May not be shockable flat line

Umbrella term for all

Supraventricular tachyarrhythmias that originate

Rapid, Regular Rate
Narrow QRS

Tachycardia (SVT) above the ventricles. 1st line tx is

Adenosine, CCB, BB
Absent/abnormal P waves

Regular; 120-250

Atrial Tachycardia
Atrial depolarization not from SA
PR interval may be short (<0.12s in
node

rapid rates)

Multifocal Atrial some etiologies include: Lung Dz,

Irregular; 100-180
At least 3 different P wave

Tachycardia Hypoxia, pHTN

morphologies

Sawtooth Appearance[Flutter(F)
waves]

Tx: Ablation. Also, it is generally usually stable ratios from 2:1 to

Atrial Flutter easier to cardiovert than Afib. Re- 5:1

entry circuit in RA. P waves present

Atrial rate 240-340

Paroxysmal: comes and goes MC sustained arrythmia. Random

(<7days)
depolarizations occurring in
many spots in R and L atria. Can

Persistent: > 7days have a wide spectrum of sx. The Atrial rate of 350-600

Long standing Persistent: >12 AV Refractory Period determines fibrillatory waves (f waves)
Atrial Fibrillation months the HR. Can be caused by binge no true P wave

Permanent: Stop further drinking (Holiday Heart) and RR intervals not the same
rheumatic heart dz. IRREGULARLY IRREGULAR

attempts to stop it
Subclinical: asx

Lone AF: w/o structural heart dz

Tx includes rate or rhythm control,
anticoag; cardioversion

AVRT

This is when the ventricles are

depolarized through the NORMAL

pathway and it loops through the

ABNORMAL

Normal QRS Duration

No delta wave
Orthodromic

P waves may be buried in QRS or

retrograde?

This is when the ventricles are

depolarized from the ABNORMAL

pathway and reenters through the

NORMAL
Wide QRS Complex with delta

wave

Antidromic P wave rarely seen. If it is seen it

is retrograde and just before the

QRS

Type of AVRT? Involves an

accessory pathway (Bundle of

Kent) that cause the conduction of

impulses to be faster than

normal. The accessory pathway

connects to the ventricular Short PR intervals (<0.12s)

Widened QRS (>.12s)

Wolff-Parkinson myocardium
delta wave

White secondary ST changes opposite the

QRS vector

Involves an accessory pathway

that cause the conduction of

impulses to be faster than

normal. The accessory pathway

connects distally to the normal

conduction pathway
Short PR intervals
Lown-Ganong-

Levine Syndrome
NO delta wave
NO widened QRS

Dual Pathways in the AV node

(slow and fast) combined with a

PAC can cause this. Pathway is

Fast-slow
too long, the refractory time is
P wave AFTER QRS because of the
too short, and spread of

AVNRT Slow Fast excitation is too slow. Tx is

retrograde signal from the AV node
Rate 160-220

Slow-slow carotid massage and vagal

maneuvers.

Ebstein Disorder: Accessory

pathway b/n Atria and Ventricles

Can be normal. Can be caused by

fibrosis/sclerosis, structural heart Typically 2 R waves (R and R') that

Right Bundle dz, right heart failure. Usually in form "bunny ears"
older adults. It does not interfere normal PR interval

Branch Block with the diagnosis of LVH or Q QRS prolonged (>12ms)

wave MI. Pts can be V1 IS POSITIVE

Asymptomatic

always abnormal. Can be caused

by fibrosis/sclerosis, structural
normal PR interval
Prolonged QRS (>12ms)

Left Bundle Branch heart dz, Prior MI, V1 IS NEGATIVE

Block cardiomyopathy. Usually in older You may see ST elevation and a

adults. Interferes with dx of LVH peaked T wave (meaning it can

and acute MI. Patients can be asx mask ischemia)

Left Axis Deviation

qR complex in leads 1 and aVL
Left Anterior

Fascicular Block
rS complex in leads 3 and aVF
normal or slightly prolonged QRS

(0.08-0.1s)

Left Posterior Right Axis Deviation

normal or slightly prolonged QRS

Fascicular Block qR complex in lead 3

(FYI) rS complex in lead 1

Wide QRS but not RBBB/LBBB

Intraventricular

Conduction Delay
abnormal notching of QRS w/o
notching

This applies to ALL Heart Blocks:

Associated with drugs like BBs

and CCBs, high vagal tone (as
Prolongation of PR interval

AV Heart Block 1st seen in athletes), and

(>200ms)
degree fibrosis/sclerosis of conduction

system
ALL P waves conducted

This one is an AV node Problem

AV Heart Block 2nd

degree

PROGRESSIVELY longer PR
intervals followed by a DROPPED

Mobitz 1/Wenckebach
AV node [Link] with beat
exertion Grouped beating

RR intervals NOT regular

REGULARLY IRREGULAR

Prolonged PR interval (not

progressive)

His-Purkinje Problem. Patient

not all P waves are conducted
Mobitz 2 may need a Pacemaker.

Symptomatic
in other words: failed conduction

following constant PR interval

NO impulse conducted from P

His-Purkinji Problem. Atrial rate is

waves, some other pacemaker is
depolarizing ventricles.
AV Heart Block 3rd faster than the ventricular rate.

degree Requires a pacemaker. Can be

You can differentiate this from
Mobitz 1 because this has

caused by Lyme dz
REGULAR RR intervals and PP

intervals
P wave comes early and so it can

be almost merged with the T

wave. The QRS is also earlier than

PAC
occurs when another part of the
the normal pattern.
atria depolarizes before SA node

Normal Sinus rhythm besides this

one beat

Something stimulated the

ventricles to contract on its own.

May be because of certain drugs,

Premature beat
cardiomyopathies, ischemia, or

PVCs random. Can be a sign of CAD.

QRS is widened
compensatory pause

You see risk in hospital pts with

high catecholamine states. Many

pts may be asx

Usually 170-180 bpm

Bizarre Widened QRS

unclear P wave that are not

This is an umbrella term for all

consistent
Ventricular tachyarrhythmias that originate in

the ventricles. Due to ventricular

Evidence of AV dissociation.
Tachycardia ectopic beating. Cardiovert if they

are unstable.
Signs that favor VTACH include:
Fusion beats, Capture beats,

Josephson sign, Brugada's sign,

positive or negative concordance

Autosomal Dominant inherited

Brugada Syndrome
SCN5A mutation which encodes
for the alpha subunit of the
QRS > 100ms
ST elevation

sodium channel leading to loss of "coved ST" or "saddleback" shape

their function. Tx is ICD

One foci in the ventricles may

start firing and driving the up to 350 bpm

Ventricular flutter ventricles, thus affecting their No P wave, Wide QRS

ability to fill properly

probably the result of a flutter

rhythm and the inability of the

ventricular muscle to sustain the

Ventricular rapid rate dropping the CO

causing system wide ischemia. So
No real rhythm
change of shape and amplitude

fibrillation then the foci multiply and this with each wave
pattern occurs. If not tx

immediately, can lead to asystole

and death

specific form of

polymorphonuclear ventricular
It looks like it is twisting around a
tachycardia (PVT). Caused by a

Torsade's de combo of frequent PVCs with an

isoelectric line

Pointes "R on T" and Long QT intervals.

Can also be caused by drug

long QT (type of ventricular
fibrillation)

toxicities or electrolyte
abnormalities.

What you need to know: Bifid P

wave in Lead 2 and Biphasic P

wave in Lead V1

FYI (if you want more detail):

Lead 2:

Bifid P wave with >40 ms between

two peaks
Left Atrial Bigger 2nd 1/2 where LA part of

Enlargement the P wave is

total duration of P wave is >110 ms

Lead V1:
Biphasic P wave with terminal

negative portion that is longer than

40 ms and deeper than 1 mm

Peaked P waves that are greater

Right Atrial

Enlargement
Bigger 1st 1/2 where the RA part
of the P wave is
then 2.5 mm in inferior leads (2, 3,
and aVF) and are more than 1.55

mm in V1 and V2

The sum of the R wave in aVL and

Left Ventricular This is following the Cornell the S wave in V3:

Hypertrophy
criteria which is the most
accurate
>28 mm Males
>20 mm Female

In other words: LARGE R

Right Axis Deviation

Right Ventricular Dominant R wave in V1

Hypertrophy Dominant S wave in V5 or V6

QRS<120 ms (large)

A junctional pacemaker originates

Junctional escape in the AV node and depending on

Rate <60
Usually inverted P waves (in
where in the AV node it is

Junctional Premature Junctional Complex

located, it can create either an
example) , but they can be absent
Rhythms Accelerated Junctional short PR Interval (<120ms) if they

Junctional Tachy
inverted P wave (most common),
a P wave within the ST segment,
are present

or have no P wave.
QRS on wider end of normal

Paced Rhythm Small spike before every P wave

Steps to EKG reading:

1. P waves
a. Regular: Sinus Rhythm or Rare stuff
b. Irregular: Sinus Rhythm w/ PACs, Multifocal atrial Tachycardia or sinus w/ 2nd or 3rd AV block
c. No P waves: Afib, A-flutter, rare stuff
2. QRS Complex
a. Narrow: His-Purkinjee works, no BBB
b. Wide: BBB
negative V1=LBBB
positive V1=RBBB
3. Check intervals/segments
a. PR
Prolonged: AV block, athletes, drugs
Shorter: Exercise
[Link]
Prolonged: decrease in Ca
Shorter: increase in Ca
c. T wave
Peaked: Ischemia, HYPERkalemia
Flat, U wave: HYPOkalemia
4. Check ST
a. ST depression: Subendocardial Ischemia
b. ST elevation: Transmural Ischemia

Practice :[Link]

Determining Axis: (Fletcher)

1. Look at leads 1 and aVF:
If they are both positive then it is a normal axis

MBZ liesminoverlap

If aVF is positive, but lead 1 is negative = RAD

Kini

If aVF is negative, but lead 1 is positive

look at lead 2
negative: LAD
positive: most likely normal

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[Link] [Link]