Introduction to EKG for non-EKG
Techs
By: Adam Arseneault CCT
Many Slides Courtesy of :
Mícheál P. Macken MD MRCPI
And Roneil Malkani MD
The Run Down

Understanding heart conduction

Neurological studies of interest

What rhythms to worry about


Commonly seen rhythms and conduction
abnormalities
Question time
Cardiac Conduction
(Marquette Electronics, 1996 )
Sinoatrial (SA) Node


The Sinoatrial Node is the hearts pacemaker
Found in the wall of the right atrium at the
junction with the superior vena cava

Rich vagal and parasympathetic innervation

Intrinsic range of firing is 60-100 bpm
(French, 2006)
Atrioventricular (AV) Node




Back-up Pacemaker
Located in the wall of the right atrium next to the
tricuspid valve
Responsible for slowing down conduction from the
atria to the ventricles so atrial contraction can occur
This slowing lets the atria slightly overfill the ventricles
to increase cardiac output and the ventricular pump

Rich vagal and parasympathetic innervation

Intrinsic rate is 40-60 bpm
(French, 2006)
Bundle of His (AKA HIS Bundle)




Starts just at the bottom of the AV Node to
where the Left and Right Bundle Branches fork
Located in the right atrium and inter-ventricular
septum
It is the route of communication between the
atria and ventricles
Intrinsic rate of 40-45 bpm
(French, 2006)
Right and Left Bundle Branches

Left Bundle Branches


Right Bundle Branch


Conducts to the left ventricle
Conducts to the right ventricle
Intrinsic rate is 40-45 bpm
(French, 2006)
Purkinje System


Made up of individual cells just beneath the
endocardium
These cells initiate the ventricular depolarization
cycle

Located in the ventricles

Intrinsic rate 20-40 bpm
(French, 2006)
Cardiac Conduction
(Marquette Electronics, 1996 )
Conduction in Motion
What is an EKG?


Basics: Waveforms are representations of the electrical activity created by
depolarization of the atria and ventricles
With an EKG we can measure the rate and regularity of heartbeats, as well as the
size and position of the chambers, the presence of any damage to the heart, and the
effects of drugs or devices used to regulate the heart, such as a pacemaker.
What is an EKG?






12-lead ECG
- 10 electrodes required to produce 12lead ECG.
- – Electrodes on all 4 limbs (RA, LA,
RL, LL)
- – Electrodes on precordium (V1–6)
- Monitors 12 leads (V1–6), (I, II, III)
and (aVR, aVF, aVL)
- Allows interpretation of specific areas
of the heart

- – Inferior (II, III, aVF)

- – Lateral (I, aVL, V5, V6)

- – Anterior (V1–4)
What is an EKG?
What is an EKG?



P Wave (Atrial
Depolarization)
QRS Complex (Rapid
Ventricular Depolarization)
T Wave (Ventricular
Repolarization)
(Wagner, 2006)
Depolarization and Repolarization


Depolarization when a cell membrane's charge
becomes positive in order to generate an action
potential. Caused by positive sodium and
calcium ions going into the cell (concentration
gradient)
Repolarization (re-negative) when a cell
membrane's charge returns to negative after
depolarization. Caused by positive potassium
ions moving out of the cell.
What is an EKG?

1mm (small square) = 40 ms

5mm (big square) = 200 ms

Methods for measuring heart rate



For regular rhythms: Rate = 300 / number of large squares in between each
consecutive R wave
For very fast rhythms: Rate = 1500 / number of small squares in between each
consecutive R wave
For slow or irregular rhythms: Rate = number of complexes on the rhythm strip x 6
(this gives the average rate over a ten-second period)
What is an EKG?

PR Interval

QRS Interval

QT Interval
Interval Norms
P-Wave

PR Interval

Time from beginning of the P wave to the
beginning of the QRS complex (onset of
ventricular depolarization) Normal range is from
120 ms – 200 ms

Atrial contraction begins in the middle of the P
wave and continues throughout the PR interval

Corresponds to the delay necessary for the
ventricles to fill after atrial contraction

The atrial repolarization wave (electrical impulse)
is usually hidden by the QRS complex
QRS Complex

Time it takes for the depolarization of the
ventricles

Norms – 40 ms to 120 ms measured from the
initial deflection of the QRS from the
isoelectric line to the end of the QRS complex.

R-wave point when half of the ventricular
myocardium has been depolarized

RS line activation of the posteriobasal portion
of the ventricles
Ventricular Depolarization



Ventricular depolarization requires normal function of
the right and left bundle branches. A block in either
the right or left bundle branch delays depolarization
of the ventricles, resulting in widening QRS
Ventricular contraction begins at about half-way
through the QRS complex and continues to the end
of the T-wave.
Pumping of blood begins when ventricular pressure
exceeds aortic pressure, causing the semi lunar
valves to open. This is normally at the end of the
QRS complex and start of ST segment.
(Molson Medical Informatics Project, 2000)
ST Segment



Period from the end of ventricular depolarization to the
beginning of ventricular repolarization
Although the ST segment is isoelectric, the ventricles
are actually contracting
Elevated or depressed is a hallmark sign of ischemia,
CAD or impending MI (STEMI)
Norm 80 ms to 120 ms
(Molson Medical Informatics Project, 2000)
QT Interval

Normally 340 ms to 430 ms

Measure from the beginning of the Q wave to the end of the T wave

Represents the total duration of electrical activity of the ventricles

Prolonged QT is associated with an increased risk of ventricular arrhythmias,
especially torsades de pointes

QTc is prolonged if > 440ms in men or > 460ms in women

QTc > 500 is associated with increased risk of torsades de pointes

QTc is abnormally short if < 350ms

A useful rule of thumb is that a normal QT is less than half the preceding RR interval
T Wave

Corresponds to the rapid ventricular repolarization

Normally rounded and positive

Most labile wave in the EKG
U Wave



Thought to represent repolarization of the
purkinje fibers
Not always seen
Prominent U waves are most often seen in
hypokalemia, but may be present in
hypercalcemia, thyrotoxicosis, or exposure to
digitalis, or epinephrine
Telemetry Monitoring

Rate per minute

Examine R to R regularity

Check P waves

Measure PR Interval

Determine if each P wave is followed by a QRS
complex

Examine the QRS

Examine the QT Interval
(Wagner, 2006)
Normal Cardiac Rhythm

Rate: 60-100 bpm

Regular rate and rhythm

PR Interval between 120-200 ms

QRS Interval between 40-120 ms

QT Interval between 340-430 ms
Sinus Rhythm

Rate: 60-100 bpm

Regularity: Regular

P-Waves: Regular and 1:1 ratio with QRS

PR Interval: PR 120-200 ms
Sinus Bradycardia

Rate: <60 bpm

Regularity: Regular

P-Waves: Regular and 1:1 ratio with QRS

PR Interval: PR 120-200 ms
Sinus Tachycardia

Rate: >100 bpm; usually under 170 bpm

Regularity: Regular

P-Waves: Regular and 1:1 ratio with QRS

PR Interval: PR 120-200 ms
Sinus Arrhythmia

Rate: Any sinus rate

Regularity: Irregular

P-Waves: Regular and 1:1 ratio with QRS

PR Interval: PR 120-200 ms
EKG Abnormalities During Partial Seizures
in Refractory Epilepsy


Fifty-one seizures in 43 patients with intractable partial epilepsy
Cardiac rhythm and conduction abnormalities are common during
seizures, particularly if they are prolonged or generalized, in
intractable epilepsy. These abnormalities may contribute to SUDEP.
Nei et al, Epilepsia, 2000
EEG and ECG in Sudden Unexplained
Death in Epilepsy



21 patients with SUDEP compared with previous study of
43 patients with refractory partial epilepsy – studied ECG
changes
Ictal max HR was significantly higher in SUDEP patients
than in controls (mean 149 bpm vs 126 bpm)
Ictal cardiac repolarization or rhythm abnormalities 56% in
SUDEP vs 39% in controls: not significant
Nei et al, Epilepsia, 2004
 Ictal asystole (IA) =preventable cause of sudden unexplained death in
Epilepsy
 Compared heart rate (HR) characteristics of IA patients to a group of
patients with vasovagal (benign, not seizure-related) asystole.
 IA was seen in 8 patients, all with temporal lobe epilepsy.
 No statistical difference was found in:
– duration of asystole, bradycardia, and baseline HR characteristics
 Only significant difference: higher HR acceleration post-asystole in
the controls.
Schuele et al, Epilepsia, 2008
Arrhythmias Encountered in Neurological
Conditions (Stroke, Seizures, etc.)
Atrial




Ventricular
Bradycardia
•
Supraventricular
tachycardias
Ectopic ventricular
beats
•
Multifocal ventricular
tachycardias
•
Torsades de pointes
•
Ventricular fibrillation
Atrial flutter
Atrial fibrillation
Possible Mechanisms:

Altered parasympathetic/vagal activity

Altered sympathetic activity


Imbalance between these two arms of the
autonomic nervous system
Increased circulating catecolamines
Premature Atrial Contractions



These complexes originate in the atria
They often originate from ectopic pacemaker
sites within the atria which results in an
abnormal P wave
The complex occurs before the normal beat is
expected, and followed by a pause
Premature Atrial Contractions

Rate: Underlying rhythm

Regularity: Irregular with PAC's; Compensatory Pause

P-Waves: Ectopic P-wave; Differs from Sinus P wave

PR Interval: Differs from underlying Sinus P wave
Supraventricular Tachycardia

Regularity: Regular

Rate: 140 – 220 bpm

P-Waves: Usually blocked by preceding T wave

QRS: Generally normal

Usually starts and stops suddenly
Atrial Flutter




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Rate: Atrial: 240-440 bpm; Ventricular varies
Regularity: Atrial rate regular; Ventricular rate from 2:1 to
8:1
Atrial flutter is characterized by "sawtooth" atrial activity
and a conduction ratio to the ventricles of 2:1 to 8:1
Caused by a reentry circuit located in the right atrium
Check patients cardiac history, if any
Atrial Fibrillation

Rate: Can vary

Regularity: Irregular

P-Waves: No discernible P-wave present



This is the most common sustained cardiac arrhythmia
Characterized by an undulating baseline replacing P
waves and an irregularly irregular ventricular response
Check patients cardiac history, if any
Premature Ventricular Contraction

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A PVC is a depolarization that arises in either ventricle
before the next expected sinus beat altering the normal
sequence of depolarization
The two ventricles depolarize sequentially instead of
simultaneously
Conduction moves slowly and this results in a widened
QRS complex (greater than 120 ms)
Three or more PVC's in a row is considered a run of
Ventricular Tachycardia
If it lasts for more than 30 seconds it is designated
sustained VT
(French, 2006)
Premature Ventricular Contraction

Rate: Underlying rhythm

Regularity: Irregular

P-Waves: Underlying rhythm

PR Interval: Underlying rhythm

QRS: Severely different from other beats, >120 ms
Ventricular Tachycardia

Rate: >100 bpm to <220 bpm

Regularity: Generally Regular; Can be Irregular

QRS Interval: >120 ms


Treatment: If patient is sleeping – wake them up and see if they
are responsive and whether rhythm terminates. Also check
whether pt. has AICD
If neither – call Code!
Torsades de Pointes
Torsades de Pointes



Polymorphic ventricular tachycardia (PVT) is a form of
ventricular tachycardia in which there are multiple ventricular
foci with the resultant QRS complexes varying in amplitude,
axis and duration. The most common cause of PVT is
myocardial ischaemia.
Torsades de pointes (TdP) is a specific form of polymorphic
ventricular tachycardia occurring in the context of QT
prolongation; it has a characteristic morphology in which the
QRS complexes “twist” around the isoelectric line.
For TdP to be diagnosed, the patient has to have evidence of
both PVT and QT prolongation.
Ventricular Fibrillation



Rate: Very Rapid; too unorganized to count
Regularity: Irregular; No normal QRS;
Waveform varies in size and shape; No Pwaves; No T-waves
Treatment is always immediate unsynchronized
defibrillation
Ventricular Fibrillation


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Ventricular Fibrillation is a rhythm in which multiple areas
within the ventricles are erratically depolarizing and
repolarizing
There is no organized depolarization, therefore the
ventricles do not contract as a unit
The myocardium is quivering - There is no cardiac output
This is the most common arrhythmia seen in cardiac arrest
from ischemia or infarction.
The rhythm is described as coarse or fine VF. Coarse VF
indicates recent onset of VF. Prolonged delay without
defibrillation results in fine VF and eventually asystole
Treatment is always immediate unsynchronized
defibrillation
Asystole

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
No Conduction
Asystole represents the total absence of ventricular
electrical activity
Since depolarization does not occur, there is no
ventricular contraction
This may occur as a primary event in cardiac arrest, or
it may follow VF or pulseless electrical activity (PEA).
Treatment: Immediate
Transient Asystole

Asystole can also be transient, a few seconds
up to 1 minute or longer, due to vagal
hyperactivity

Sleep apnea/Snoring during sleep

Valsalva maneuver

During seizures : Ictal asystole

Medullary centers in brainstrem

Valsalva reflex

Other causes
Ancillary Information
• Junctional Rhythms/beats
• AV Blocks
•
First, Mobitz I and II, Third degree
• WPW
• Brugada
• Electronic Pacer
Junctional Escape Rhythm

Rate: 40-60 bpm

Regularity: Regular


P-Waves: They will be inverted, and may appear before or
after the QRS complex, or they may be absent, hidden by
the QRS
PR Interval: If Present PR <120 ms
Premature Junctional Contraction

Rate: Underlying rhythm

Regularity: Irregular


P-Waves: They will be inverted, and may appear before or
after the QRS complex, or they may be absent, hidden by
the QRS
PR Interval: If Present PR <120 ms
First Degree AV-Block

Regularity: Regular

Rate: Underlying rhythm

P-Waves: Regular and 1:1 ratio with QRS

PR Interval: Constant and prolonged PR
Interval, >0.20 sec
Second Degree AV-Block;
Type 1Wenckebach

Regularity: Irregular

Rate: Underlying rhythm

P-Waves: Regular


PR Interval: PR gradually elongates until a dropped beat
which leads to a reset
This is usually benign and due to increased vagal activity
Second Degree AV-Block;
Mobitz Type 2

Rate: Underlying rhythm

Regularity: Irregular

P-Waves: Regular

PR Interval: P-waves march but not all conducted


This block is bad because it originates below the AV node, the
escape rhythm is too slow
Treatment is a pacemaker
Third Degree AV-Block; Complete
Heart Block





Rate: Underlying rhythm
P-Waves: Regular but not related to QRS
A total lack of conduction through the AV node
This conduction defect is dangerous and may progress to
ventricular standstill
Treatment is an artificial pacemaker
Wolff-Parkinson-White Syndrome

Short PR interval (< 120ms)

Broad QRS (> 100ms)



A slurred upstroke to the QRS complex (the delta
wave)
Pre-excitation refers to early activation of the
ventricles due to impulses bypassing the AV node via
an accessory pathway
In WPW the accessory pathway is often referred to as
the Bundle of Kent, or atrioventricular bypass tract
Lifeinthefastlane.com

Can cause tachyarrhythmia
Wolff-Parkinson-White Syndrome
Bundle of Kent
Accessory
Pathway
Brugada Syndrome


Note the pattern resembling a right bundle branch block,
the P-R prolongation and the ST elevation in leads V1-V3
Brugada is a recently found arrhythmia that can lead to
ventricular fibrillation, also may be inherited.
Brugada.org
Pacemaker Rhythms



If a patient has a pacemaker you may see spikes
representing the electrical activity from the pacemaker
You could see a “spike” preceding a wide QRS when
ventricular pacing
Or a “spike” preceding P wave when atrial pacing
Ventricular Pacemaker Rhythm
Atrial Pacemaker Rhythm
Atrial and Ventricular Pacing
Left-sided Brain Hemorrhage
Causing ST Segment Elevation
Introduction to EKG for non-EKG
Techs
By: Adam Arseneault CCT
Many Slides Courtesy of :
Mícheál P. Macken MD MRCPI
And Roneil Malkani MD