How to Read an EKG Strip

EKG paper is a grid where time is

measured along the horizontal axis.
Each small square is 1 mm in length and
represents 0.04 seconds.
Each larger square is 5 mm in length and
represents 0.2 seconds.

Voltage is measured along the vertical

axis.
10 mm is equal to 1mV in voltage.

Instant Feedback:
On a typical EKG grid, 5 small squares, or
1 large square, represent 0.20 seconds of
time.
()True
()False

Normal Components of the

EKG Waveform

P wave
Indicates atrial depolarization, or contraction of
the atrium.
Normal duration is not longer than 0.11 seconds
(less than 3 small squares)
Amplitude (height) is no more than 3 mm
No notching or peaking
The relationship between P waves and QRS
complexes helps distinguish various cardiac
arrhythmias.
The shape and duration of the P waves may
indicate atrial enlargement.

QRS complex
Indicates ventricular depolarization, or
contraction of the ventricles.
Normally not longer than .10 seconds in
duration
Amplitude is not less than 5 mm in lead II
or 9 mm in V3 and V4
R waves are deflected positively and the
Q and S waves are negative

 Q -- first downward deflection

R -- first upright deflection
S -- second downward deflection
& return to baseline

 The duration, amplitude, and morphology of the QRS

complex is useful in diagnosing cardiac arrhythmias,
conduction abnormalities, ventricular hypertrophy,
myocardial infarction, electrolyte derangements, and
other disease states.
Q waves can be normal (physiological) or pathological.
Normal Q waves, when present, represent
depolarization of the interventricular septum. For this
reason, they are referred to as septal Q waves, and can
be appreciated in the lateral leads I, aVL, V5 and V6.
Q waves greater than 1/3 the height of the R wave,
greater than 0.04 sec (40 ms) in duration, or in the right
precordial leads are considered to be abnormal, and
may represent myocardial infarction.

T wave
Indicates ventricular repolarization
Not more that 5 mm in amplitude in
standard leads and 10 mm in precordial
leads
Rounded and asymmetrical

 Inverted (or negative) T waves can be a sign of

coronary ischemia, left ventricular hypertrophy, or
CNS disorder.
Tall or "tented" symmetrical T waves may indicate
hyperkalemia. Flat T waves may indicate coronary
ischemia or hypokalemia.
The earliest electrocardiographic finding of acute
myocardial infarction is sometimes the hyperacute T
wave, which can be distinguished from hyperkalemia
by the broad base and slight asymmetry.
When a conduction abnormality (e.g., bundle branch
block, paced rhythm) is present, the T wave should be
deflected opposite the terminal deflection of the QRS
complex. This is known as appropriate T wave
discordance.

 ST segment
Indicates early ventricular repolarization
Normally not depressed more than 0.5
mm
May be elevated slightly in some leads (no
more than 1 mm)

 The normal ST segment has a slight

upward concavity.
Flat, downsloping, or depressed ST
segments may indicate coronary
ischemia.
ST segment elevation may indicate
myocardial infarction.

 J-point is the point at

which the QRS complex
meets the ST wave.
Although ST elevation
with an upward concavity
and J-point notching often
reflects a normal variant,
this is only true if the
patient is asymptomatic.
The same ST pattern in a
patient with chest pain is
due to acute coronary
syndrome until proven
otherwise

 PR interval
Indicates AV conduction time
Duration time is 0.12 to 0.20 seconds

 A prolonged PR interval may indicate a first

degree heart block.
A short PR interval may indicate a preexcitation syndrome via an accessory
pathway that leads to early activation of the
ventricles, such as seen in Wolff-ParkinsonWhite syndrome.

QT interval
Measured from the Q to
the end of the T.
Represents ventricular
depolarization and
repolarization (sodium
influx and potassium
efflux)
V3, V4 or lead II optimize
the T-wave.
QT usually less than half
the R-R interval
(0.32-0.40 seconds when
rate is 65-90/minute)

 QT varies with rate. Correct for rate by

dividing QT by the square root of the RR
interval.
Normal corrected is < 0.46 for women and
< 0.45 for men.

 Prolonged QT may be inherited or

acquired
(predisposes to long QT syndrome and
torsades de pointe)
Inherited - defective sodium or potassium
channels
Acquired - drugs, electrolyte imbalance or
MI
At least, 50 drugs known to affect QT
(including: quinidine, amiodarone and
dofetilide)

Instant Feedback: Normal QRS duration is

0.15 - 0.25 seconds.
() True
() False

 What is the PR interval in this ECG? A.

0.12 sec B. 0.16 sec C. 0.20 sec D. 0.28
sec E. 0.50 sec

 The correct answer is D.

You measure PR from the beginning of P
to the beginning of QRS. The normal PR
interval is 0.12 - 0.20 sec, or 120 to 200
ms. 1st degree AV block is defined by PR
intervals greater than 200 ms.

 What is the QRS duration seen here?

A. 0.04 sec B. 0.06 sec C. 0.10 sec
D. 0.12 sec E. 0.14

 The correct answer is B.

Normal QRS duration is 0.06 sec to 0.10
sec measured from the beginning to the
end of the complex. Remember, the QRS
complex represents the simultaneous
activation of the ventricles. However, most
of the QRS complex is from the larger left
ventricle.

 What is the QT interval of this ECG, and is it

normal for this heart rate?
A. 0.34 sec & no B. 0.34 sec & yes C. 0.40 sec
& no D. 0.40 sec & yes E. 0.48 sec & maybe

 The correct answer is B.

The QT interval is from the beginning of QRS to
the end of the T wave. In this case it is between
8 and 9 small boxes long (~0.34 sec.). The
upper limit of the QT is 0.40 sec @ 70 bpm. For
every 10 bpm above 70, subtract 0.02 sec. Add
0.02 sec for every 10 bpm below 70. This ECG
has a heart rate of about 80, so the upper limit of
normal is 0.38 sec.

 What is the PR interval of this ECG?

A. 0.08 sec B. 0.12 sec C. 0.22 sec D. 0.28 sec E.
80 msec

 The correct answer is C.

PR is from the beginning of P to the
beginning of QRS. This PR is slightly
prolonged.

 What is the QRS duration seen here?

A. 0.04 sec B. 0.08 sec C. 0.12 sec D. 0.14
sec E. 0.16 sec

 The correct answer is B.

Measure from the beginning to the end of
the QRS complex.

 Choose the correct QT interval for this ECG:

A. 0.34 sec B. 0.40 sec C. 0.44 sec D. 0.48
sec E. 0.20 sec

 The correct answer is A.

Measure from the beginning of the QRS
complex to the end of the T wave.

Electrode Placement and

Lead Selection

 Proper electrode placement is essential

in order to acquire accurate EKG strips.
Most EKG monitor manufacturers have a
set of placement guidelines specific to
their products.

The following are some general

guidelines.
Skin preparation:
Shave hair away from electrode
placement site.
Rub site briskly with alcohol pad.
Rub site with 2x2 gauze.
Place electrode. Be sure that the electrode
has adequate gel and is not dry.

Monitoring cable connections

Europe

Red
Yellow
Green
Black
White

Connectto:

RightArm
LeftArm
LeftLeg
RightLeg
Chest

U.S.A.

White
Black
Red
Green
Brown

Individual chest leads

White / Red
White / Yellow
White / Green
White / Brown
White / Black
White / Violet

C1/V1
C2/V2
C3/V3
C4/V4
C5/V5
C6/V6

Brown / Red
Brown / Yellow
Brown / Green
Brown / Blue
Brown / Orange
Brown / Purple

With electrodes on the

right arm (red), left arm
(yellow) and left leg
(green)
Lead I uses red and
yellow, yellow is looking
from 3 o'clock.
Lead II uses red and
green, green is looking
from 5 o'clock.
Lead III uses yellow and
green, green is looking
from 7 o'clock.

 Lead aVR is looking

from the red wire,
across to between
yellow and green, 10
o'clock.
Lead aVL is looking
from the yellow wire,
across to between red
and green, 2 o'clock.
Lead aVF is looking
from the green wire,
across to between
yellow and red, 6
o'clock.

Trouble shooting and Tips

Change the electrodes everyday.
Make sure all electrical patient care equipment is
grounded.
Be sure all the lead cables are intact. Some
manufacturers require changing the cables
periodically.
Be sure the patient's skin is clean and dry.
Make sure the leads are connected tightly to the
electrodes.
Patient movement frequently causes
interference. For example, the action of brushing
teeth may cause interference that mimics V-tach.

A "Method" of ECG
Interpretation

STEPS
1. Measurements
2. Rhythm Analysis
3. Conduction Analysis
4. Waveform Description
5. ECG Interpretation

I. Measurements (usually made

in frontal plane leads)
1. Heart rate (state atrial and ventricular, if
different)
2. PR interval (from beginning of P to beginning of
QRS)
3. QRS duration (width of most representative
QRS)
4. QT interval (from beginning of QRS to end of T)
5. QRS axis in frontal plane

Method 1
When the rhythm is regular, the heart
rate is 300 divided by the number of
large squares between the QRS
complexes.
For example, if there are 4 large
squares between regular QRS
complexes, the heart rate is 75
(300/4=75).

Method 2
The second method can be used with
an irregular rhythm to estimate the
rate. Count the number of R waves in
a 6 second strip and multiply by 10.
For example, if there are 7 R waves in a
6 second strip, the heart rate is 70
(7x10=70).

Method 3
The Cardiac Ruler Method
Place the beginning point of a cardiac
ruler over an R wave. Look at the number
on which the next R wave falls and that
becomes the heart rate for that patient.
Use the following numbers to indicate
what the heart rate is between two
successive R waves : 300, 150, 100, 75,
60, 50, 43, 37, 33, 30

Method 4
The 1500 Method
Count the number of small boxes between
two R waves and divide this number into
1500 to obtain the HR/min.
Example : If there were 12.5 small boxes
between two successive R waves, then
the heart rate would be : 1500/12.5 small
boxes = 120 bpm.

 What is the approximate heart rate of this ECG?

A. 55 bpm B. 70 bpm C. 90 bpm D. 100 bpm E.
110 bpm

 The correct answer is B.

Although the lines are hard to see, each
beat is about 4 lines apart. Beats
separated by one line would indicate a rate
of 300 bpm
2 lines...150 bpm
3 lines...100 bpm
4 lines...75 bpm
5 lines...60 bpm.

 What is the approximate heart rate?

A. 50 bpm B. 65 bpm C. 75 bpm D.
90 bpm E. 100 bpm

 The correct answer is D.

Each QRS complex is separated by about
3 1/2 big boxes. Thus the rate is between
100 and 75, or about 90 bpm.

How to Measure the QRS Axis

The frontal plane QRS axis represents
only the average direction of ventricular
activation in the frontal plane. As such this
measure can inform the ECG reader of
changes in the sequence of ventricular
activation (e.g., left anterior fascicular
block), or it can be an indicator of
myocardial damage (e.g., inferior
myocardial infarction).

 Normal Axis: Both Lead 1 and AVF are

upright. (2 thumbs up)
LAD: Lead 1 upright and AVF downward
(Left thumb up , right thumb down)
RAD: Lead 1 down and AVF upright (Left
thumb down, right thumb upright)
Extreme RAD: Both Lead 1 and AVF
downward (2 thumbs down)

 In the diagram the

normal range is
identified (-30 to
+90 ). Left axis
deviation (i.e.,
superior and leftward)
is defined from -30
to -90 , and right axis
deviation (i.e., inferior
and rightward) is
defined from +90 to
+150 .

II. Rhythm Analysis

State basic rhythm (e.g., "normal sinus
rhythm", "atrial fibrillation", etc.)
Identify additional rhythm events if
present (e.g., "PVC's", "PAC's", etc)
Consider all rhythm events from atria, AV
junction, and ventricles

Most common effect

Decreased CO

Most severe effect

Sudden cardiac
death/arrest

Most dangerous

Ventricular
dysrhythmias

Least dangerous

Atrial dysrhythmias

Sinus Dysrhythmias

Sinus Tachycardia

Rate101-160/min
P wave: sinus
QRS: normal
Conduction: normal
Rhythm: regular or slightly irregular

 The clinical significance of this

dysrhythmia depends on the underlying
cause. It may be normal.
Underlying causes include:
increased circulating catecholamines
CHF
hypoxia
PE
increased temperature
stress
response to pain

 Treatment: fluids, digitalis, beta blockers,

CCB, bed rest, O2 inhalation

Sinus Bradycardia

Rate: 40-59 bpm

P wave: sinus
QRS: normal (.06-.12)
Conduction: P-R normal or slightly
prolonged at slower rates
Rhythm: regular or slightly irregular

 This rhythm is often seen as a normal

variation in athletes, during sleep, or in
response to a vagal maneuver. If the
bradycardia becomes slower than the SA
node pacemaker, a junctional rhythm may
occur.
Treatment includes:
treat the underlying cause,
atropine,
isoproterenol, or
artificial pacing if patient is hemodynamically
compromised.

Sinus Arrhythmia

Rate: 45-100/bpm
P wave: sinus
QRS: normal
Conduction: normal
Rhythm: regularly irregular

 The rate usually increases with inspiration and

decreases with expiration.
This rhythm is most commonly seen with
breathing due to fluctuations in parasympathetic
vagal tone. During inspiration stretch receptors
in the lungs stimulate the cardioinhibitory centers
in the medulla via fibers in the vagus nerve.
The non respiratory form is present in diseased
hearts and sometimes confused with sinus
arrest (also known as "sinus pause").
Treatment is not usually required unless
symptomatic bradycardia is present.

Atrial Dysrhythmias

Premature Atrial Contractions

 Rate: normal or accelerated

P wave: usually have a different
morphology than sinus P waves because
they originate from an ectopic pacemaker
QRS: normal
Conduction: normal, however the ectopic
beats may have a different P-R interval.
Rhythm: PAC's occur early in the cycle
and they usually do not have a complete
compensatory pause

 PAC's occur normally in a non diseased

heart.
However, if they occur frequently, they
may lead to a more serious atrial
dysrhythmias.
They can also result from CHF, ischemia
and COPD.

Paroxysmal Atrial Tachycardia

 Rate: atrial 160-250/min: may conduct to

ventricles 1:1, or 2:1, 3:1, 4:1 into the
presence of a block.
P wave: morphology usually varies from
sinus
QRS: normal (unless associated with
aberrant ventricular conduction).
Conduction: P-R interval depends on the
status of AV conduction tissue and atrial
rate: may be normal, abnormal, or not
measurable.

 PAT also known as Paroxysmal Supraventricular

Tachycardia (PSVT) may occur in the normal as
well as diseased heart.
It is a common complication of Wolfe-ParkinsonWhite syndrome.
This rhythm is often transient and usually
requires no treatment.
However, it can usually be terminated with vagal
maneuvers.
Digoxin, antiarrhythmics, adenosine and
cardioversion may be used.
Frequent symptomatic episodes may require
surgical intervention. When an accessory
conduction pathway can be demonstrated,
interventional surgery to ablate the accessory
conduction pathway can be curative.

Atrial Flutter

 Rate: atrial 250-350/min; ventricular conduction

depends on the capability of the AV junction
(usually rate of 150-175 bpm).
P wave: not present; usually a "saw tooth"
pattern is present.
QRS: normal
Conduction: 2:1 atrial to ventricular most
common.
Rhythm: usually regular, but can be irregular if
the AV block varies.

 Atrial flutter almost always occurs in

diseased hearts. It frequently precipitates
CHF.
The treatment depends on the level of
hemodynamic compromise.
Cardioversion, vagal maneuvers and
verapamil are used when prompt rate
reduction is needed.
Otherwise, digoxin and other
antiarrhythmic drugs can be used.

Atrial Fibrillation

 Rate: atrial rate usually between 400650/bpm.

P wave: not present; wavy baseline is
seen instead.
QRS: normal
Conduction: variable AV conduction; if
untreated the ventricular response is
usually rapid.
Rhythm: irregularly irregular. (This is the
hallmark of this dysrhythmia).

 Atrial fibrillation may occur paroxysmally, but

it often becomes chronic. It is usually
associated with COPD, CHF or other heart
disease.
Treatment includes:
Digoxin, diltiazem, or other anti-dysrhythmic
medications to control the AV conduction rate
and assist with conversion back to normal sinus
rhythm.
Cardioversion may also be necessary to
terminate this rhythm.
Surgical Management
Chemical ablation- alcohol or phenol
Mechanical ablation use cryoprobe

- for SVT,AF, WPW syndrome

Ventricular Dysrhythmias

Premature Ventricular Contractions

 Rate: variable
P wave: usually obscured by the QRS, PST or T
wave of the PVC
QRS: wide > 0.12 seconds; morphology is
bizarre with the ST segment and the T wave
opposite in polarity. May be multifocal and
exhibit different morphologies.
Conduction: the impulse originates below the
branching portion of the Bundle of His; full
compensatory pause is characteristic.
Rhythm: irregular. PVC's may occur in singles,
couplets or triplets; or in bigeminy, trigeminy or
quadrigeminy.

 Falling on the T wave- most vulnerable

period of the cardiac cycle; if heart is
stimulated at this time it cannot respond in
an organized manner therefore
precipitating life threatening dysrhythmias

 PVCs can occur in healthy hearts. For example,

an increase in circulating catecholamines can
cause PVCs. They also occur in diseased hearts
and from drug (such as digitalis) toxicities.
Treatment is required if they are:

associated with an acute MI,

occur as couplets, bigeminy or trigeminy,
are multifocal, or
are frequent (>6/min).

 TXT: Lidocaine IV push

initial bolus dose;75-100mg then 50-100
within 10-15 minutes prn
Procainamide IV push
Bretylium

Torsade de Pointes

Rate: usually between 150 to 220/bpm,

P wave: obscured if present
QRS: wide and bizarre morphology
Conduction: as with PVCs
Rhythm: Irregular

 Paroxysmal starting and stopping

suddenly
Hallmark of this rhythm is the upward and
downward deflection of the QRS
complexes around the baseline. The term
Torsade de Pointes means "twisting
about the points."
Consider it V-tach if it doesnt respond to
antiarrythmic therapy or treatments

 Caused by:
drugs which lengthen the QT interval such as
quinidine
electrolyte imbalances, particularly hypokalemia
myocardial ischemia

Treatment:
Synchronized cardioversion is indicated when
the patient is unstable.
IV magnesium
IV Potassium to correct an electrolyte imbalance
Overdrive pacing

Ventricular Tachycardia

 Rate: usually between 100 to 220/bpm,

but can be as rapid as 250/bpm
P wave: obscured if present and are
unrelated to the QRS complexes.
QRS: wide and bizarre morphology
Conduction: as with PVCs
Rhythm:three or more ventricular beats in
a row; may be regular or irregular.

 Ventricular tachycardia almost always occurs in

diseased hearts.
Low CO leading to cerebral or myocardial
ischemia
Some common causes are:

CAD
acute MI
digitalis toxicity
CHF
ventricular aneurysms.

 Treatment:
If With pulse: Procainamide, Lidocaine.
Defibrillation if with LOC, cardioversion if
conscious
If without pulse: CPR, Epinephrine, Lidocaine
or Amniodarone

Ventricular Fibrillation

 Rate: unattainable
P wave: may be present, but obscured by
ventricular waves
QRS: not apparent
Conduction: chaotic electrical activity
Rhythm: chaotic electrical activity

 This dysrhythmia results in the absence of

cardiac output.
Almost always occurs with serious heart
disease, especially acute MI.
The course of treatment for ventricular fibrillation
includes:
immediate defibrillation 200, 300, 360J and
ACLS protocols.
Identification and treatment of the underlying
cause is also needed
Epinephrine, Lidocaine. Procainamide

Asystole/Ventricular Standstill

 Rate: none
P wave: may be seen, but there is no
ventricular response
QRS: none
Conduction: none
Rhythm: none

 Asystole occurs most commonly following the

termination of atrial, AV junctional or ventricular
tachycardias. This pause is usually insignificant.
Asystole of longer duration in the presence of
acute MI and CAD is frequently fatal.
Interventions include:

CPR, 100% oxygen,

IV
intubation
transcutaneous pacing
epinephrine 1.0 mg., IV push, q3-5 minutes
atropine

Management of Dysrhythmias
Vagal Maneuvers
Induce vagal stimulation of the cardiac
conduction system and are used to terminate
supraventricular tachycardias
Carotid Sinus Massage
Physician massages over the carotid artery for 6-8
seconds until a change in cardiac rhythm is seen

Valsalva Maneuver
Bear down or induce a gag reflex

Cardioversion

Synchronized counter shock to convert an

undesirable rhythm to a stable rhythm
Lower amount of energy is used
Defibrillator is synchronized to the R wave
to avoid discharging the shock during the T
wave
For tachycardias developing in atrial ,
junctional or ventricular tissue

Important Interventions

Sedation before the procedure

Hold digoxin 48 hours preprocedure
Stop O2
No one touches patient or bed
Post procedure
Maintain airway patency
02 inhalation

V/S
LOC
Monitor cardiac rhythm
Monitor for indications of successful
response
Conversion to sinus rhythm
Strong peripheral pulses
Adequate BP

Pacemakers - electronic device that

delivers direct stimulation to the heart,
causing electrical depolarization and
cardiac contraction
-initiates and maintains the heart rate
when the natural pacemakers of the
heart are unable to do so
- Temporary and Permanent

Noninvasive Temporary Pacemaker

Used as an emergency measure

Large electrode is placed on the chest and back
Do not take the pulse or Bp on the left side
Do not place electrode on the female breast
Do not shave the hair or apply alcohol to skin
Wash skin with soap and water before applying
electrodes

Transvenous Invasive Temporary

Pacing
Lead wire is place through antecubital,
femoral, jugular or subclavian vein into the
right atrium for atrial pacing or through the
right ventricle
Restrict client movement to prevent lead
lead wire displacement

Epicardial Invasive Temporary

Pacing
Applied by using a trans-thoracic
approach
Lead wires are threaded loosely on the
epicardial surface of the heart after
cardiac surgery

Epicardial Invasive Temporary

Pacemaker

Permanent Pacemaker
Pulse generator is internal and surgically
implanted in a subcutaneous pocket under
the clavicle or abdominal wall
Leads are passed trans-venously via the
cephalic or subclavian vein to the
endocardium on the right side of the heart
Report any fever, swelling, redness over
the insertion site

Avoid contact sports

Inform airport security of pacemaker
Wear loose clothing
Do not operate electrical appliance directly over
the pacemaker
Avoid transmitter towers or antitheft devises
When experiencing unusual feelings near
electrical devises move 5-10 feet away then
check pulse

III. Conduction Analysis

Normal" conduction
implies normal sinoatrial (SA), atrioventricular (AV), and
intraventricular (IV)
conduction

Blocks

Atrio-Ventricular Blocks
1 AV block impulse from SA node is
transmitted normally but is delayed longer
at the level of the AV node
Associated with CAD, congenital anomalies
asymptomatic, no intervention

First Degree
Atrioventricular Blocks

R
T

P
Q
Do you have a normal P wave?
Do you have a normal PR segment?
Do you have a normal PR interval?
Do you have a normal QRS-T?

Yes
No
Prolonged (> 0.20 sec)
Yes

Criteria for First Degree Heart

Block
P waves present
QRS complexes present
P waves morphology and axis usual for the
subject
QRS complexes morphology and axis usual for
the subject
One P wave to each QRS complex
P-R interval constant

P-R interval must be prolonged

( i.e. > 0.20 sec )

FIRST
FIRST DEGREE
DEGREE
AV
AV BLOCK
BLOCK
PR interval > 0.20 sec

0.28
0.28sec
sec

0.28
0.28sec
sec

0.28
0.28sec
sec

 2 AV block only some impulses are

transmitted, AV node becomes selective
about which impulses are conducted to
the ventricles

Second Degree
Atrioventricular Blocks
Do you have a normal P wave?
Yes
Do you have a normal PR segment?
No
Do you have a normal PR interval?
No
Will there be intermittent P waves not
followed by QRS complex? Yes (dropped beats)

Mobitz Type 1(Wenckebach Phenomenon)

- progressively prolonged PR interval
until no QRS complex follows P wave

SECOND
SECOND DEGREE
DEGREE AV
AV BLOCK
BLOCK
MOBITZ
MOBITZ II
Progressive lengthening
of PR interval w/ intermittent
drop beats .

0.20
0.20sec
sec

0.28
0.28sec
sec

0.20
0.20sec
sec

 Mobitz Type II
constant PR interval until suddenly a
ventricular beat is dropped
more serious because it often
progresses to a block of a higher degree and
dysrhythmias
TXT: atropine, isoproterenol,pacemaker

SECOND
SECOND DEGREE
DEGREE
AV
AV BLOCK
BLOCK
MOBITZ
MOBITZ IIII
Fixed PR interval
w/ intermittent
drop beats .

0.18
0.18sec
sec

0.18
0.18sec
sec

BLOCK AT THE
Bundle of His
Bilateral bundle
branches

Trifascicle

0.18
0.18sec
sec

 3 AV block- all impulses from the atria are

blocked
AV dissociation
TXT: pacemaker insertion, isoproterenol
ventricular standstill (Stoke Adams Attack)
- fatal complication

THIRD
THIRD DEGREE
DEGREE
AV
AV BLOCK
BLOCK

Complete atrioventricular block

Impulses originate at both SA node and at
the subsidiary pacemaker below the block
Do you have regularly occurring P waves and QRS complexes? Yes
Are the P waves related to the QRST complexes? No
Is the atrial rate < = > ventricular rate? greater
Ventricular rate = 83 BPM

Atrial
Atrialrate
rate==100
100BPM
BPM

Ventricular rate = 83 BPM

Atrial
Atrialrate
rate==100
100BPM
BPM

Atrial
Atrialrate
rate==100
100BPM
BPM

ECG Simulator.zip

Bundle Branch Block

Diagnosis is made by the appearance of
widened QRS complexes (more than .12
secs or > 3 small squares)
When a BBB is present , either the left of
the right ventricle may depolarize late,
depending on which side is blocked.

 Check chest lead V1 and V2 for the

appearance of RsR on QRS complexes
for RBBB
Check chest leads V5 and V6 for
appearance of RsR on QRS complexes
for LBBB

RBBB

 There's no specific treatment for many

cases of bundle branch block, whether it
affects the left or the right bundle branch.
In fact, in most cases people are
symptom-free and there's no need for
therapy.

Medications
Treatment of underlying conditions
may involve using medications to
reduce high blood pressure, or drugs
to reduce the effects of heart failure.

 The American Heart Association and the

American College of Cardiology
recommend treatment called reperfusion
therapy for people with left bundle branch
block who are suspected of having had a
heart attack. This treatment involves using
drugs such as streptokinase or tissue
plasminogen activator to dissolve blood
clots and increase the flow of blood to the
heart.

 Artificial pacemakers
In a minority of people with bundle
branch block, doctors may
recommend implanting an artificial
pacemaker.

IV. Waveform Description

Carefully analyze the 12-lead ECG for
abnormalities in each of the waveforms in
the order in which they appear: P-waves,
QRS complexes, ST segments, T waves,
and... Don't forget the U waves

P Waves
Right Atrial Hypertrophy
Large diphasic P wave with tall
initial component

 Left Atrial Hypertrophy

Large diphasic P wave with wide
terminal component

QRS Complex, Q Waves and ST- T

Wave Changes
Right Ventricular
Hypertrophy
R wave greater than S
in V1 but R wave gets
progressively smaller
from V1-V6
S wave persists in V5
and V6
RAD with slightly
widened QRS

 Left Ventricular
Hypertrophy
S wave in V1(in
mm) + R wave in
V6 (in mm) = more
than 35 mm
LAD with slightly
widened QRS
Inverted T wave

 Q- Wave MI - total coronary occlusion

Non Q-wave MI - subtotal coronary
occlusion
Most MI's are located in the left ventricle

Area of Myocardium
Involved
Anterior

Coronary artery supply

Posterior

RCA

Inferior

RCA

Anteroseptal

LAC/LAD branch

High lateral

Circumflex artery
marginal branch or LCA
LCA,left ant.branch or
RCA,post.descending
branch

Apical

LCA/LAD branch

Area of Myocardium
Involved

ST Segment Elevation
and Q waves on ECG

Anterior

V3 and V4

Posterior

ST segment depression
V1-V4

Inferior

II, III and AVF

Anteroseptal

V1-V4

Lateral

I, aVL,V5,V6

Zone of infarction
Zone of hypoxic injury
Zone of ischemia

Pathologic Q
Wave

 Pathological Q waves
25% or more of the height of the partner R
wave
greater than 0.04 seconds in width - one
small square
greater than 2mm (two small squares) in
depth .

Q waves are a marker of electrical

silence, which, when pathological,
implies full thickness death of
myocardium, which happened a long
time ago.

Zone of infarction
Zone of hypoxic injury

Zone of ischemia

ST Segment
Elevation

Zone of infarction
Zone of hypoxic injury
Zone of ischemia

 Usual ECG evolution of a Q-wave MI; not

all of the following patterns may be seen;
the time from onset of MI to the final
pattern is quite variable and related to the
size of MI, the rapidity of reperfusion (if
any), and the location of the MI.

A. Normal ECG prior to MI

B. Hyperacute T wave changes increased T wave amplitude and
width; may also see ST elevation
C. Marked ST elevation with
hyperacute T wave changes
(transmural injury)
D. Pathologic Q waves, less ST
elevation, terminal T wave inversion
(necrosis) (Pathologic Q waves are
usually defined as duration >0.04 s
or >25% of R-wave amplitude)
E. Pathologic Q waves, T wave
inversion (necrosis and fibrosis)

Inferior MI Family of Q-wave MI's

Pathologic Q waves and
evolving ST-T changes in
leads II, III, aVF
Q waves usually largest in
lead III, next largest in lead
aVF, and smallest in lead II

Example #1: frontal plane

leads with fully evolved
inferior MI (note Q-waves,
residual ST elevation, and T
inversion in II, III, aVF)

 Example #2: Old

inferior MI (note
largest Q in lead
III, next largest in
aVF, and smallest
in lead II)

True Posterior MI

ECG changes are seen

in anterior precordial
leads V1-3, but are the
mirror image of an
anteroseptal MI
Example #1: Acute
inferoposterior MI (note
tall R waves V1-3,
marked ST depression
V1-3, ST elevation in II,
III, aVF)

Anterior Family of Q-wave MI's

Anteroseptal MI
- Q, QS, or qrS
complexes in leads V1V3 (V4)
- Evolving ST-T changes
Example: Fully evolved
anteroseptal MI (note QS
waves in V1-2, qrS
complex in V3, plus ST-T
wave changes)

 Acute anterior or
anterolateral MI
(note Q's V2-6
plus hyperacute
ST-T changes)

 High Lateral MI
(typical MI
features seen in
leads I and/or
aVL)
note Q-wave,
slight ST
elevation, and T
inversion in lead
aVL

Non-Q Wave MI
Recognized by evolving ST-T changes over time
without the formation of pathologic Q waves (in a
patient with typical chest pain symptoms and/or
elevation in myocardial-specific enzymes)
Although it is tempting to localize the non-Q MI
by the particular leads showing ST-T changes,
this is probably only valid for the ST segment
elevation pattern

Inferior Wall Non Q Wave

Anterior Wall Non Q Wave

MI

Lateral Wall Non Q Wave

MI

Posterior Wall Non Q Wave

MI

V. ECG Interpretation
This is the conclusion of the above
analyses. Interpret the ECG as "Normal",
or "Abnormal". Occasionally the term
"borderline" is used if unsure about the
significance of certain findings. List all
abnormalities.

 Examples of "abnormal" statements are:

Inferior MI, probably acute
Old anteroseptal MI
Left anterior fascicular block (LAFB)
Left ventricular hypertrophy (LVH)
Nonspecific ST-T wave abnormalities
Any rhythm abnormalities

HR=72bpm; PR=0.16s; QRS=0.09s; QT=0.36s; QRS axis = -70o

(left axis deviation)
Normal sinus rhythm; normal SA and AV conduction; rS in leads II,
III, aVF
Interpretation: Abnormal ECG: 1) Left anterior fascicular block

Thats All for Now!!!

Thank YOU!!!

Advanced Cardiac Life

Support

CODE BLUE HINTS

1. Stay calm, check your own pulse!
Familiarize yourself with the equipment on your
ward(s) or hospital.
In preparation for a possible code blue, identify
specific roles for different members of your team
(e.g. assign one person to chest compressions,
another to establish central IV access, etc).
Remember the basics: CPR, defibrillation,
airway management (don't get caught up in
memorizing drug dosages).

2. At the start of the code, appoint specific

people to specific tasks:
Get crash cart/defibrillator/backboard.
Get information and chart.
Establish airway (bag mask, intubate).
Establish IV access, check pulse.
Perform chest compressions.
Get ABG, check labs.
Nursing (give meds, place leads, etc).
Pharmacist (deliver meds).

3. When applying monitor leads to patient,

remember: "white to the right, smoke above fire"
(white on right shoulder, black on left shoulder
and red near precordium on left).
4. If performing chest compressions:
Remember to get a backboard under the patient.
The optimal rate is 100 times a minute. Your job
when performing compressions is to circulate
the patient's blood effectively (important for
cerebral perfusion and for circulation of
medications).

5. Defibrillator/monitor:
Always check lead placement and check
asystole or a questionable rhythm in 2
leads.
When defibrillating with paddles, use 25
lbs. of pressure.
Do not shock asystole. Take time to
confirm that the rhythm is not coarse VF.
6. For tachycardia, ejection fraction guides
treatment (try to find in patient's chart).

7. Remember the five H's and the five T's

for PEA and asystole:
5 H's: hypovolemia, hypoxia, hydrogen ion
(acidosis), hyper/hypokalemia,
hypothermia.
5 T's: tablets (drugs), tamponade, tension
PTX, thrombosis (coronary), thrombosis
(PE).

8. No high dose epinephrine.

9. Don't forget to check code status prior to
starting ACLS (make sure you have the
right chart!).

CONDITIONS ASSOCIATED
WITH CARDIAC ARREST

Condition

Clinical Setting

Acidosis

Diabetes, diarrhea, drugs, Ensure adequate CPR,

oxygenation, ventilation.
toxins, prolonged
Hyperventilate.
resuscitation, renal
failure, shock/sepsis,
If pH < 7.20 consider
preexisting acidosis.
HCO3.

Hypothermia

Treatment

If severe (< 30C), limit

EtOH, burns, CNS
initial shocks for VF/VT to
disease, debilitated,
three.
homeless, or elderly pt,
drowning, drugs, toxins, Active internal warming
endocrine disease,
and resuscitation.
exposure, trauma,
Goal is to first get T >
spinal cord disease.
30C, then restart ACLS.

Hemorrhage,
Fluids, PRBC's,
diabetes, GI loss,
Hypovolemia
look for site of loss if
shock, major
applicable.
burns, trauma.
Hypoxia

Consider in all
patients with
cardiac arrest.

EtOH, diabetes,
diuretic use,
drugs, toxins,
Hypokalemia
profound GI loss,
hypomagnesemia
.

Ensure adequate
CPR, oxygenation,
ventilation, correct
ETT placement.
If < 2.5 mEq/L
and associated with
cardiac arrest, give 2
mEq/min IV up to 1015 mEq and reassess.

Hyperkalemia Renal failure,

dialysis patients,
metabolic
acidosis, drugs,
toxins,
hemolysis,
rhabdomyolysis,
massive tissue
injury.

HypoMg

10% calcium
chloride 5-10 ml IV
slow push (don't give
if hyperkalemia due to
dig toxicity).
1 amp D50 IV.
10 U regular
insulin IV.
1-2 amps of HCO3
IV.
Albuterol nebs.

EtOH, DKA,
1-2 g IV MgSO4
severe diarrhea, IV over 2 minutes.
diuretics, burns,

Myocardial
infarction

Consider in all
patients with
cardiac arrest and
especially those
with pre-existing
coronary disease or
risk factors.

Consider
thrombolytics,
emergent cardiac
catheterization, or
urgent CABG.

Cardiac
Tamponade

Hemorrhagic
diathesis, post MI,
pericarditis,
trauma, postcardiac surgery.

Administer fluids.
Obtain bedside
echo if possible.
Urgent
pericardiocentesis.
Surgical
intervention if
appropriate

Poisoning

EtOH, unusual
behavioral or
metabolic
presentation,
exposure, psychiatric
disease, classic
toxicologic
syndrome.

Send tox screen,

consult toxciologist.
Treat suspected
ingestion.
Prolonged
resuscitation may be
appropriate.

Pulmonary
Embolism

Hospitalized patient,
recent surgery,
peripartum, history
of DVT, risk factors
for DVT.

Adminster fluids,
pressors as needed
attempt to confirm
diagnosis.
Consider
thrombolytics or urgent
surgical intervention.

Tension
Placement of
Pneumothorax central line,
mechanical
ventilation,
lung disease,
thoracentesis
, trauma.

Needle
decompression: 14
gauge angiocath at
2nd ICS, MCL.
Chest tube
placement.

COMPREHENSIVE ACLS
ALGORITHM

1.

Unresponsive? Go to primary ABCD

(basic life support):

A = open airway

B = give 2 breaths

C = check pulse

D = get defibrillator

2.
Use defibrillator to check rhythm:
If VF/VT: give 3 shocks, begin CPR
If PEA or asystole: begin CPR
immediately.

3.
Go to secondary ABCD:
A = intubate the airway: endotracheal tube (ETT)
or laryngeal mask airway (LMA).
B = confirm position of ETT objectively with end
tidal CO2 and O2 saturation and secure airway
to prevent dislodgement so that patient can
breathe.
C = IV access, continue CPR, give
vasoconstrictor agent (vasopressin or
epinephrine) and then consider antiarrhythmics,
buffer, pacer for circulation, cardiovascular
support.
D = differential diagnosis: look for the reversible
causes (5 H's and 5 T's).

4.

Follow the appropriate algorithm

and switch to a different algorithm as
needed

VENTRICULAR FIBRILLATION
AND PULSELESS VT
1.

Follow the protocol: shock shock

shock (200J, 300J, 360J) drug
shock (360 J) drug shock (360J)
etc.

2.

First give vasoconstrictor agent:

Vasopressin 40 U IV x 1 if no response
give epinephrine as below.
Epinephrine 1 mg IV q 3-5 minutes.

3.
Then give antiarrhythmic agent:
First line: Amiodarone 300 mg IV rapid
push, can repeat 150 mg IV x 1.
Second line:
Lidocaine 1.0-1.5 mg/kg (70-100 mg) IV q 3-5
minutes up to a total of 3 mg/kg.
Magnesium 1-2 g IV (mainly for
hypomagnesemic state or polymorphic VT).
Procainamide 30 mg/min IV up to 17 mg/kg
total (not recommended in refractory VF).

4.
Buffer:
Bicarbonate 1-3 amps IV (first line for
hyperkalemia; less evidence for prolonged
arrest, TCA overdose, aspirin overdose).

PULSELESS ELECTRICAL
ACTIVITY (PEA)
1.

First give vasoconstrictor agent for

cardiovascular support while you search
for a cause.
Vasopressin 40 U IV x 1 or
Epinephrine 3-5 mg IV q3-5 minutes.

2.

Give atropine if the PEA rhythm is

slow:

Atropine 1 mg IV q 3-5 minutes to
total of 0.04 mg/kg (3-4 doses for most
patients)
3.

Finding a reversible cause is key.

While you are searching, follow steps #48.

4.

Correct presumed hypovolemia and

hypoxia:
Fluids, fluids, fluids wide open.
Intubate immediately.
5.
Correct presumed hyperkalemia and
acidosis:
Give 1-3 amps HCO3 IV.

6.
Consider hypothermia and overdose:
Actively warm the patient (if they are
hypothermic).
Check the chart and history for evidence of
overdose.
7.

Rule out tamponade and pneumothorax

(PTX):
Consider insertion of needle at subxiphoid
space directed at 45 degrees toward left
shoulder for tamponade.
Consider insertion of 14 gauge angiocath into
2nd intercostal space, midclavicular line on
side of PTX.

8.

Consider thrombosis (massive MI or

PE):
Consider TPA or emergency
PTCA/CABG for MI.
Consider TPA for massive PE.

ASYSTOLE
1.

Carries a poor prognosis.

2.

Review differential diagnosis just as

in PEA algorithm.

3.

First line: transcutaneous pacing

should be started immediately.

4.

Adrenergic agent: for cardiovascular

support while you search for a cause:
Epinephrine 1 mg IV q 3-5 minutes.
Atropine 1 mg IV q 3-5 minutes to total of
0.04 mg/kg (3-4 doses for most patients).

5.
If refractory:
Review quality of resuscitation.
Look for atypical clinical features
(hypothermia, drug overdose).
If > 10 minutes with adequate effort and
no atypical features consider stopping
code.

BRADYCARDIA
1. Primary then secondary survey
including 12-lead ECG.
2.
Serious signs/symptoms?
Atropine 0.5-1.0 mg IV q 3-5 minutes up to
0.04 mg/kg (3-4 doses for most patients).
Transcutaneous pacing.
Dopamine 5-20 mcg/kg/minute.
Epinephrine 2-10 mcg/minute.

3.

Is there type II second degree AV

block or third degree AV block?
Proceed to transcutaneous pacing until
transvenous pacer can be placed.

TACHYCARDIA
1.

Is the patient unstable (chest pain,

shortness of breath, altered mental status, loss
of consciousness, hypotension, congestive heart
failure, myocardial infarction)?
If unstable and HR is cause go to
cardioversion.
2.

If stable, get 12-lead ECG and classify

arrhythmia. Then treat specific rhythm as
clinically indicated.

THE END!!!!