The document provides guidance on interpreting 12-lead electrocardiograms (ECGs). It discusses evaluating the rate, rhythm, axis, signs of hypertrophy, and evidence of infarction on ECGs. Key steps include determining the heart rate using a "300, 150, 100" counting method and identifying abnormalities in rate, rhythm, conduction, hypertrophy, or signs of injury or necrosis. Interpreting ECGs involves analyzing the P wave, QRS complex, T wave, and ST segment to evaluate for conditions like myocardial infarction, bundle branch blocks, ventricular hypertrophy, and more.

1. Rapid 12-Lead ECG Interpretation
Dr.Ashutosh Kawade, MD[Medicine]
08/01/14 05:34

2. INTRODUCTION
 Rate
 Rhythm
 Axis
 Hypertrophy
 Infarction
 Other Clinical Aspects
08/01/14 05:34

3. ECG Interpretation
• Electrocardiography (ECG or EKG) is a
transthoracic interpretation of the
electrical activity of the heart over time
captured and externally recorded by skin
electrodes. It is a noninvasive recording
produced by an electrocardiographic
device.

4. 1smallbox=1mm=0.1mV
5 Large squares = 1 second
Time
1 Large square = 0.2 second1 Small square = 0.04 second
2 Large squares = 1 cm
6.1
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Horizontal axis - 1 and 3 sec marks
1 small box = 1 mm = 0.04 sec.
Every 5 lines (boxes) are bolded
Verticalaxis-voltage
ECG Graph Paper

5. RATE
• Our main objective is to rapidly determine the heart
rate from the ECG.
• First: Find a specific R wave that peaks on a heavy black
line (our "start" line).
• Next: Count off "300, 150, 100" for every thick line that
follows the start line, naming each line as shown.
Remember these numbers; we will use them
throughout our career.
• Then: Count off the next three lines after "300, 150,
100" as "75, 60, 50."
• Now: Memorize these ‘Triplets’ & make certain that we
can say the triplets without using the picture.
• Where the next R wave falls, determines the rate. It's
that simple!
08/01/14 05:34

6. Rate
Determine Rate by Observation
Using the triplets:
Name the lines following the “Start” line.
Fine division/rate association: reference
300
250
214
187
167
“75” “60” “50”
150
136
125
115
100
94
88
83
79
75
71
68
65
62
60
107
May be calculated:
1500
= RATE
mm. between similar waves
Bradycardia (slow rates)
• Cycles/6 second strip ✕ 10 = Rate
• When there are 10 large squares between similar waves, the rate is 30/minute.
Sinus Rhythm: origin is the SA Node (“Sinus Node”),normal sinus rate is 60 to 100/minute.
• Rate more than 100/min. = Sinus Tachycardia
• Rate less than 60/min. = Sinus Bradycardia
Determine any co-existing, independent (atrial/ventricular) rates:
• Dissociated Rhythms:
A Sinus Rhythm (or atrial rhythms) may co-exist with an independent rhythm
from an automaticity focus of a lower level. Determine rate of each.
Irregular Rhythms:
• With Irregular Rhythms (such as Atrial Fibrillation) always note the general
(average) ventricular rate (QRS’s per 6-sec. strip ✕ 10) or take the patient’spulse.
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7. NORMAL ECG WAVES
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8. Rhythm
★ Identify basic rhythm…
…then scan entire tracing for pauses, premature beats,
irregularity, and abnormal waves.
★ Always:
• Check for: P before each QRS.QRS after each P.
• Check: PR intervals (for AV Blocks).QRS interval (for BBB).
• Has QRS vector shifted outside normal range? (to rule out Hemiblock).
Irregular Rhythms
Sinus Arrhythmia
Irregular rhythm that varies
with respiration.
All P waves are identical.
Considered normal.
Wandering Pacemaker
Irregular rhythm. P waves
change shape as
pacemaker location varies.
Rate under 100/minute…
…but if the rate exceeds
100/minute, then it is called
Multifocal Atrial Tachycardia
Atrial Fibrillation
Irregular ventricular rhythm.
Erratic atrial spikes
(no P waves) from
multiple atrial automaticity
foci. Atrial discharges
may be difficult to see.
08/01/14 05:34

9. Rhythm continued
Escape The heart’s response to a pause in pacing
pause
Atrial
Escape Beat
or
Junctional
Escape Beat
Then…
the SA Node
usally resumes
pacing.
or
Ventricular
Escape Beat
Atrial
Escape Rhythm
Rate 60-80/min.
or
Junctional
Escape Rhythm
Rate 40-60/min.
or
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(“idiojunctional rhythm”)
Ventricular
Escape Rhythm
Rate 20-40/min.
(“idioventricular rhythm”)
Premature Beats From an irritable automaticity focus
Premature Atrial Beat
Premature Junctional Beat
Premature Ventricular Contraction
PVC’s may be:
multiple, multifocal, in runs, or
coupled with normal cycles.
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10. PVC’s
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11. Rhythm continued
Tachyarrhythmias
150 250
“focus” = automaticity focus
350 450
Rates: Paroxysmal
Tachycardia
Flutter Fibrillation
multiple foci discharging
Paroxysmal (sudden) Tachycardia …rate: 150-250/min.
Paroxysmal Atrial Tachycardia
An irritable atrial focus discharging at
150-250/min. produces a normal wave
sequence, if P' waves are visible.
• P.A.T. with block
Same as P.A.T. but only every
second (or more) P' wave
produces a QRS.
Paroxysmal Junctional Tachycardia
AV Junctional focus produces a rapid
sequence of QRS-T cycles at 150-250/min.
QRS may be slightly widened.
Paroxysmal Ventricular Tachycardia
Ventricular focus produces a rapid
(150-250/min.) sequence of (PVC-like)
wide ventricular complexes.
Flutter …rate: 250-350/min.
Atrial Flutter
A continuous (“saw tooth”) rapid sequence
of atrial complexes from a single rapid-firing
atrial focus. Many flutter waves needed to
produce a ventricular response.
Ventricular Flutter also see “Torsades de Pointes”
A rapid series of smooth sine waves from a
single rapid-firing ventricular focus; usually in
a short burst leading to Ventricular Fibrillation.
Fibrillation …erratic (multifocal) rapid discharges at 350 to 450/min.
Atrial Fibrillation
Multiple atrial foci rapidly discharging
produce a jagged baseline of tiny spikes.
Ventricular (QRS) response is irregular.
Ventricular Fibrillation
Multiple ventricular foci rapidly discharging
produce a totally erratic ventricular rhythm
without identifiable waves. Needs immediate
treatment.
08/01/14 05:34
fusion

12. Rhythm: (“heart”) blocks
Sinus (SA) Block
the Sinus Node usually resumes pacing, but
the pause may evoke an “escape” responsefrom an automaticity focus.
An unhealthy Sinus (SA) Node misses one or more cycles (sinus pause)…
AV Block
Blocks that delay or prevent atrial impulses from reaching the ventricles.
1° AV Block
2° AV Block
…prolonged PR interval
PR interval is prolonged to greater
than .2 sec (one large square).
… some P waves without QRS response
cycle until the last P wave in the
series does not produce a QRS.
Wenckebach …PR gradually lengthens with each
Mobitz …some P waves don’t produce a QRS
response. If “intermittent,” an
occasional QRS is droped.
More advanced Mobitz block may
produce a 3:1 (AV) pattern or even
higher AV ratio
2:1 AV Block …may be Mobitz or Wenckebach.
PR length and QRS width or
vagal maneuvers help differentiate.
3° (“complete”) AV Block …no P wave produces a QRS response
3° Block: P waves—SA Node origin.
QRS’s—if narrow, and if the
ventricular rate is 40 to 60 per min.,
then origin is a Junctional focus.
P waves—SA Node origin.
QRS’s—if PVC-like, and if the
ventricular rate is 20 to 40 per min.,
then origin is a Ventricular focus.
3° Block:
Bundle Branch Block
Right BBB
★ Always Check:
• is QRS within
3 tiny squares?
R R'
…find R,R' in right or left chest leads
With Bundle Branch
Block the criteria for
ventricular hypertrophy
are unreliable.
Left BBB
R R' Caution:
With Left BBB
infarction is difficult
to determine on EKG.QRS in V1 or V2 QRS in V5 or V6
Hemiblock
★ Always Check:
• has Axis shifted
outside Normal
range?
…block of Anterior or Posterior fascicle of the Left Bundle Branch.
Anterior Hemiblock
Axis shifts Leftward ➞ L.A.D.
look for Q1S3
Posterior Hemiblock
Axis shifts Rightward ➞ R.A.D.
look for S1Q3
08/01/14 05:34
 “WILLIAM MORROW”
William: ‘W’ in V1 & ‘M’ in V6: LBBB
Morrow: ‘M’ in V1 & ‘W’ in V6: RBBB

13. Axis
General Determination of Electrical Axis
Is QRS Positive ( ) or Negative ( ) in leads I and AVF?
First Determine Axis Quadrant
I
I
Is Axis Normal?
QRS in lead I
…if the QRS is Positive (mainly above
baseline), then the Vector points to
positive (patient’s left) side.
Lead I
AVF L. AVF
Normal:
{ QRS upright in I and AVF
“two thumbs-up” sign
I
Ex.R.A.D
QRS in lead AVF
Lead AVF
…if the QRS is mainly Positive, then
the Vector must point downward to
positive half of the sphere.
R.A.D. Normal
I
AVFAVF
Axis in Degrees (Frontal Plane)
After locating Axis Quadrant, find limb lead where QRS is most isoelectric:
Extreme Right Axis Deviation
lead Axis
I –90° -150
AVL –120°
III –150°
AVF –180°
-180 o
-90o
-120o
-90o
-60o
o
. L.
A.
D.
0o
0o
-30o
Left Axis Deviation
lead Axis
I –90°
AVR –60°
II –30°
AVF 0°
Normal Range
lead Axis
AVF 0°
III +30°
AVL +60°
I +90°
Right Axis Deviation
lead Axis
AVF +180°
II +150°
AVR +120°
I +90°
+180o
+150o A.
D.
+120o
+90o +90o
+30o
+60o
R.
Axis Rotation (left/right) in the Horizontal Plane
Find transitional (isoelectric) QRS in a chest lead.
transitional QRS is “isoelectric”
Patient’s
Right
V1
Rotation
n
Rightwards Leftwards
Normal Range
Patient’s
Left
V2 V3 V4 V5
V6
08/01/14 05:34
Normal
Ex.R.A.D

14. Axis
 Axis refers to the Mean Frontal Plane QRS axis (or vector) during ventricular depolarization. As we recall when
the ventricles depolarize (in a normal heart) the direction of current flows leftward and downward because most of
the ventricular mass is in the left ventricle. We like to know the QRS axis because an abnormal axis can suggest
disease such as pulmonary hypertension from a pulmonary embolism.
 Abnormalities of axis can hint at: Ventricular enlargement Conduction blocks (i.e. hemiblocks)
Determining the Axis:
• The Quadrant Approach
• The Equiphasic Approach
08/01/14 05:34
Predominantly
Positive
Predominantl
y Negative
Equiphasic
Leads I and aVF
LEFT Axis Deviation
LVH
LBBB
WPW
High diaphram, pregnancy
WNL – obese, elderly
RIGHT Axis Deviation
RVH
RBBB
LV PVCs
Pulmonary- emphysema, PE
WNL – thin, young
Determine which lead contains theDetermine which lead contains the
most equiphasic QRS complex.most equiphasic QRS complex.
The fact that the QRS complexThe fact that the QRS complex
in this lead is equally positivein this lead is equally positive
and negative indicates that theand negative indicates that the
net electrical vector (i.e. overallnet electrical vector (i.e. overall
QRS axis) is perpendicular toQRS axis) is perpendicular to
the axis of this particular lead.the axis of this particular lead.
Examine the QRS complex inExamine the QRS complex in
whichever lead lies 90° awaywhichever lead lies 90° away
from the lead identified in stepfrom the lead identified in step
1. If the QRS complex in this1. If the QRS complex in this
second lead is predominantlysecond lead is predominantly
positive, than the axis of thispositive, than the axis of this
lead is approximately the samelead is approximately the same
as the net QRS axis. If theas the net QRS axis. If the
QRS complex is predominantlyQRS complex is predominantly
negative, than the net QRS axisnegative, than the net QRS axis
lies 180° from the axis of thislies 180° from the axis of this
lead.lead.

15. Hypertrophy
Atrial Hypertrophy
Right Atrial Hypertrophy
• large, diphasic P wave with tall initial component
Initial component
Left Atrial Hypertrophy
• large, diphasic P wave with wide terminal component
terminal component
Ventricular Hypertrophy
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.
• R.A.D. with slightly widened QRS.
• Rightward rotation in the horizontal plane.
Left Ventricular Hypertrophy
S wave in V1 (in mm.)
+ R wave in V5 (in mm.)
Sum in mm. is more than 35 mm. with L.V.H.
• L.A.D. with slightly widened QRS.
• Leftward rotation in the horizontal plane.
Inverted T wave:
slants downward
gradually,
but up rapidly.
08/01/14 05:34
‘P’ PULMONALE
‘P’ MITRALE

16. LVH
08/01/14 05:34
Several Criteria for
determining LVH
Sokolow-Lyon
indices — There
are two criteria
with these
widely used
indices:1) Sum
of S wave in V1
and R wave in
V5 or V6 3.5 mV
(35 mm)and/or
2) R wave in aVL
1.1 mV (11 mm)

17. • LAD
• V1,2 deep S and
V5,6 tall R >35mm
• aVL “R” > 12mm
• Secondary ST depress
• Most frequently seen with
hypertension
• RAD
• V1 R + V6 S >10mm
• V1 rSr’ (incomplete RBBB)
• Secondary ST depress
• Usually will be seen with pulmonary
pathology
HYPERTROPHY
LVH RVH
08/01/14 05:34

18. Q wave = Necrosis
• Significant Q wave is one millimeter (one small square)
wide, which is .04 sec. in duration…
… or is a Q wave 1/3 the amplitude (or more)
of the QRS complex.
• Note those leads (omit AVR) where significant Q’s are present
… see next page to determine infarct location, and to identify
the coronary vessel involved.
• Old infarcts: significant Q waves (like infarct damage) remain
for a lifetime. To determine if an infarct is acute, see below.
Q
ST (segment) elevation = (acute) Injury (also Depression)
• Signifies an acute process, ST segment returns to
baseline with time.
• ST elevation associated with significant Q waves
indicates an acute (or recent) infarct.
• A tiny “non-Q wave infarction” appears as significant
ST segment elevation without associated Q’s. Locate by
identifying leads in which ST elevation occurs (next page).
elevation
• ST depression (persistent) may represent “subendocardial
infarction,” which involves a small, shallow area just beneath
the endocardium lining the left ventricle. This is also a variety
of “non-Q wave infarction.” Locate in the same manner as for
infarction location (next page).
T wave inversion = Ischemia
• Inverted T wave (of ischemia) is symmetrical (left half
and right half are mirror images). Normally T wave is
upright when QRS is upright, and vice versa.
T
• Usually in the same leads that demonstrate signs of
acute infarction (Q waves and ST elevation).
note those leads where T wave inversion occurs, then
identify which coronary vessel is narrowed (next page).
inversion • Isolated (non-infarction) ischemia may also be located;
NOTE: Always obtain patient’s previous ECG’s for comparison!08/01/14 05:34
Infarction

19. Infarction Location & Coronary Vessel Involvement
Coronary Artery Anatomy
Right Coronary
Artery
Left Coronary
Artery
circumflex
Anterior
descending
Infarction Location/Coronary Vessel Involvement
Posterior
• large R with
ST depression in V1 & V2
• mirror test or reversed
transillumination test
(Right Coronary Artery)
Lateral
Q’s in lateral leads I and AVL
(Circumflex Coronary Artery)
Inferior
(diaphragmatic)
Q’s in inferior leads
II, III, and AVF
(R. or L. Coronary Artery)
Anterior
Q’s in V1, V2, V3, and V4
(Anterior Descending
Coronary Artery)
08/01/14 05:34
Right Ventricular
Infarction

20. Infarct Location
• On ECG the QRS complex represents ventricular contraction. The Q
wave is the first downward wave of the QRS complex, and it is
followed by an upward R wave, however the Q wave is often absent
on ECG. Necrosis (death) of an area of the heart muscle produces a Q
wave on ECG.
• The Q wave makes the diagnosis of infarction.
• If there are Q waves in lead I and lead AVL, there is a lateral infarction.
• Inferior ("diaphragmatic") infarction is diagnosed by the presence of Q
waves in II, III, and AVF.
• Q waves in chest leads V1, V2, V3, or V4 signify an anterior infarction.
• It is common practice to determine the general location of an
infarction, but with a little anatomical knowledge of the heart's
coronary blood supply*, we can make a far more sophisticated
diagnosis.
• A lateral infarction is caused by an occlusion of the Circumflex branch
of the Left Coronary Artery. An anterior infarction is due to an
occlusion of the Anterior Descending branch of the Left Coronary
Artery.
• The base of the left ventricle receives its blood supply from branches
of either the Right or the Left Coronary Artery, depending on which
artery is "dominant.“
“Septal / Anterior Infarct.“ 
08/01/14 05:34

21. Other Clinically Significant Aspects
Pulmonary Embolism • S1Q3T3 – wide S in I, large Q and inverted T in III
• Acute Right BBB (transient, often incomplete)
• R.A.D. and rightward rotation (horizontal plane)
• Inverted T waves V1 V4 and ST depression in II➞Artificial Pacemakers
Modern artificial pacemakers have sensing capabilities and also provide a
regular pacing stimulus. This electrical stimulus records on ECG as a tiny
vertical spike that appears just before the “captured” cardiac response.
• are “triggered” (activated) when
the patient’s own rhythm ceases
or slows markedly.
sinus rhythm ceases
pacemaker spikes
• are “inhibited” (cease pacing)
if the patient’s own rhythm
resumes at a reasonable rate.
PVC stops pacemaker, but…• will “reset” pacing
(at same rate) to
synchronize with a
premature beat.
▼ ▼ ▼ ✕
Pacemaker Impulse ▲
(delivery modes)
pacemaker resumes in step
with premature beat.
▲ ▲
Ventricular Pacemaker (electrode in Right Ventricle)
(Asynchronous) Epicardial Pacemaker
Ventricular impulse not linked to atrial activity.
Atrial pacemaker
Atrial Synchronous Pacemaker
P wave sensed, then after a brief delay,
ventricular impulse is delivered.
Dual Chamber (AV sequential) Pacemaker
External Non-invasive Pacemaker
08/01/14 05:34

22. Electrolytes
Potassium wide,
flat P
peaked T
no P
Increased K+ (hyperkalemia)
wide QRS QRS widens
moderate extreme
prominent
U wave
Decreased K+ (hypokalemia)
flat T
moderate extreme
++
Calcium Hyper Ca ++
Hypo Ca
short QT prolonged QT
Digitalis
ECG appearance with digitalis (“digitalis effect”)
•Remember Salvador Dali.• T waves depressed or inverted.
• QT interval shortened.Digitalis Excess
(blocks)
• SA Block
• P.A.T. with Block
• AV Blocks
• AV Dissociation
Digitalis Toxicity
(irritable foci firing rapidly)
• Atrial Fibrillation
• Junctional or Ventricular Tachycardia
• multiple P.V.C.’s
• Ventricular Fibrillation
Quinidine Effects
Quinidine wide,
notched
P
wide QRS
U
• ECG appearance with quinidine ST
long QT interval
• Excess quinidine or other medications
that block potassium channels (or even
low serum potassium) may initiateTorsades de Pointes
Other Clinically Significant Aspects
08/01/14 05:34
Digitalis causes a gradual down-sloping of the ST segment, to
give it the appearance of Salvador Dali's moustache.
Type of VT known as “twisting of the points.”
Usually seen in those with prolonged QT intervals

23. Other Clinically Significant Aspects
08/01/14 05:34

24. Say “300, 150, 100” …“75, 60, 50”
• but for bradycardia:
1. RATE
rate = cycles/6 sec. strip ✕ 10
2. RHYTHM
Identify the basic rhythm, then scan tracing for prematurity,
pauses, irregularity, and abnormal waves.
• Check for: P before each QRS.QRS after each P.
• Check: PR intervals (for AV Blocks).QRS interval (for BBB).
• If Axis Deviation, rule out Hemiblock.
3. AXIS • QRS above or below baseline for Axis Quadrant(for Normal vs. R. or L. Axis Deviation).
For Axis in degrees, find isoelectric QRS in a limb lead
of Axis Quadrant using the “Axis in Degrees” chart.
• Axis rotation in the horizontal plane: (chest leads)
find “transitional” (isoelectric) QRS.
4. HYPERTROPHY
Check V1
{
P wave for atrial hypertrophy.
R wave for Right Ventricular Hypertrophy.
S wave depth in V1…+ R wave height in V5 for Left Ventricular Hypertrophy.
5. INFARCTION
Scan all leads for:
• Q waves
• Inverted T waves
• ST segment elevation or depression
Find the location of the pathology (in the Left ventricle),
and then identify the occluded coronary artery.
Summary
08/01/14 05:34

25. Important Precautions
 Must be Performed & Interpreted by the treating physician
 Correct Lead placement and good contact
 Proper earth connection, avoid other gadgets
 Deep inspiration record of III,aVF
 Compare serial ECGs if available
 Relate the changes to Age, Sex, Clinical history
 Consider the co-morbidities that may effect ECG
 Make a xerox copy of the record for future use
 Interpret systematically to avoid errors
08/01/14 05:34

26. Be’ware of Normal ECG
 Normal Resting ECG – cannot exclude disease
 Ischemia may be covert – supply / demand equation
 Changes of MI take some time to develop in ECG
 Mild Ventricular hypertrophy - not detectable in ECG
 Some of the ECG abnormalities are non specific
 Single ECG cannot give progress – Need serial ECGs
 ECG changes may not co-relate with Angio results
 Paroxysmal event may be missed in single ECG
08/01/14 05:34

27. Life Preserving Syndromes
• Regardless of our expertise and level of education, we
should look for the following - easily identified -
electrocardiographic signs of impending (life-
threatening!) problems, even in apparently healthy
persons.
• The atria contract, pumping blood into the ventricles just
before ventricular contraction. The electrical current
("depolarization") that causes atrial contraction is
conducted very slowly to the ventricles to allow time for
blood to fill the ventricles.
• The AV Node, the only electrical connection between the
atria and the ventricles, conducts the depolarization
impulse (from the contracting atria to the ventricles)
very slowly. This provides a brief pause for ventricular
filling after atrial contraction. On ECG, the P wave
(representing atrial contraction) is normally followed by
a short span of level baseline (pause) before the QRS
complex (ventricular contraction).
08/01/14 05:34

28. Wolff-Parkinson-White Syndrome [WPW]
• In some people, an anomalous conduction pathway, the "Kent
bundle," connects the atria and the ventricles, short-circuiting
the AV Node. The anomalous conduction pathway allows rapid
conduction to the ventricles without the normal delay. This
produces Wolff Parkinson White (WPW) syndrome, which is
characterized by conduction of the atrial depolarization current
to the ventricles immediately after atrial contraction
• On the ECG of patients with WPW syndrome, the usual short
span of baseline following the P wave is replaced by a curving
"delta wave," representing too-early stimulation ("pre-
excitation") of a portion of the ventricles. This is easy to detect
in most leads as a gentle upward curve that connects the P
wave and the QRS complex.
• Pre-excitation of the ventricles, per se, is not serious, but it may
lead to rapid ventricular rhythms that are dangerous,
particularly in elderly persons or those with heart conditions.
WPW is easily treatable; the Kent bundle can be ablated
(destroyed) using a radio frequency intra-cardiac catheter.
Therefore, early detection of delta waves on ECG can allow
these patients to enjoy a normal life span.
08/01/14 05:34

29. Brugada Syndrome
• Brugada syndrome is a recognized cause of sudden death in
apparently healthy individuals. It is responsible for about one-
half of sudden deaths in young persons without structural
heart disease, therefore early detection is critical. This familial
condition is due to malfunctioning sodium (Na+) channels in
the heart cells.
• Although the deadly arrhythmias (abnormal rhythms) that
victims experience cannot be prevented, they can be
successfully treated with an Implantable Cardioverter-
Defibrillator (ICD), which corrects the arrhythmia immediately
upon its occurrence. But persons with this syndrome must be
identified in order to provide this life-saving treatment.
• In Brugada syndrome, the QRS is widened and has two
upward peaks in (chest) leads V1 and V2, and the ST segment
is elevated. The ST segment begins at the second peak of the
widened QRS then slopes gradually downward. In Brugada
syndrome, lead V3 also has a wide QRS and ST elevation that
is stereotypical for this condition. All medical personnel who
frequently observe cardiac monitors or ECG strips should
make a mental note of this ECG pattern.
• If we keep a mental reference of the ECG morphology of
Brugada syndrome in leads V1, V2, and V3, perhaps we can
prevent an untimely death, since lead MCL1, which is a
variation of leads V1 and V2, is the most common lead used
for cardiac monitoring.
08/01/14 05:34
On the standard ECG, there is usually a short
segment of level baseline ("ST segment")
immediately following the (normally narrow) QRS
complex. The ST segment is normally level with
the baseline in all ECG leads.

30. Wellen’s Syndrome
• Rarely are we warned of an impending myocardial infarction long
before it occurs. However, in patients with Wellens syndrome,
stenosis (narrowing) of the Anterior Descending (the most
important) branch of the Left Coronary Artery is revealed on ECG
in patients with negligible or even absent symptoms. Therefore it
is important that all medical personnel be ever-vigilant for the
tell-a-tale signs of this important syndrome.
• On normal ECG's the T wave (which follows the ST segment) is
usually upright or somewhat flattened in leads V2 and V3.
However, in the ECG of some patients with stenosis of the
Anterior Descending coronary artery, the T waves are markedly
inverted (upside down) long before symptoms are present. For
those patients with Wellens syndrome , this easily detected ECG
sign is life-saving only if the person observing the ECG are savvy
enough to recognize this important problem. Be that person!
• Stenosis of the Anterior Descending coronary artery is very
treatable, and it is important that treatment be initiated before
the artery is totally occluded causing myocardial infarction... even
death. Using a special expandable catheter placed in the stenosed
artery, the narrowed area can be dilated by a cardiologist using a
procedure known as "angioplasty.“
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Currently, most angioplasty procedures employ
the implantation of a metal mesh tube known a
"stent" inside the artery, to keep it open and
prevent re-stenosis of this vital artery.
Intervention using angioplasty with stenting can
indeed be life saving, but our recognition of
Wellens syndrome is the critical link.

31. Long-QT Syndromes
• There is a group of familial syndromes collectively known as Long QT
syndrome . There are at least six different forms of Long QT syndrome
thought to be caused by dysfunctional ion channels; they all can produce
dangerous or deadly ventricular arrhythmias. Early treatment with proper
medications should be instituted as soon as this syndrome is detected, ideally
during childhood. There are, however, perhaps many thousands of people
with undetected Long QT syndrome who require treatment.
• Although the heart rate varies somewhat (in response to physiological needs),
the QT interval (measured on ECG from the beginning of the QRS to the end of
the T wave) always remains less than one-half of the cardiac cycle.
• With Long QT syndrome the QT interval is longer than one-half the length of
the cardiac cycle (usually measured from R wave to R wave). A quick glance at
any lead will reveal the lengthened QT interval.
• Lengthening of the QT interval can be caused by a variety of medications that
block ion channels (usually K+ channels). Certain types of cardiac pathology or
metabolic conditions can also lengthen the QT, but in general, lengthening of
the QT interval, regardless of the etiology, predisposes the patient to
Torsades de Pointes, and other dangerous arrhythmias. Don't overlook it!
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32. THANKS !
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33. Q-T Interval & QTc
Definition: Time interval between beginning of QRS complex to the end of T wave.
– measurement of the refractory period or the time during which the myocardium would not
respond to a second impulse; measured from the beginning of the QRS complex to the end of the T
wave
– Best leads to measure the QT are V2 or V3
– Q-T interval should be roughly less than half the preceding R-R interval
Tip: Instead of calculating the QTc, a quick way to estimate if the QT interval long is to use the following rule:
A QT > half of the RR interval is probably long.
– It is longer with slower rates and shorter with faster rates
Normally: At normal HR: QT ≤ 11mm (0.44 sec)
• QT interval varies based on heart rate
Abnormalities:
1. Prolonged QT interval: hypocalcemia and congenital long QT syndrome.
2. Short QT interval: hypercalcemia.
3. The duration of the QT interval is proportionate to the heart rate. The faster the heart beats, the
faster the ventricles repolarize so the shorter the QT interval. Therefore what is a “normal” QT varies
with the heart rate. For each heart rate you need to calculate an adjusted QT interval, called the
“corrected QT” (QTc):
 The Q-T interval can be corrected for heart rate using Basset's formula:
 Normal QTc interval = 0.39 ± 0.04 sec
 A prolonged QT can be very dangerous. It may predispose an individual to a type of
ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte
abnormalities, CNS disease, post-MI, and congenital heart disease.08/01/14 05:34

34. Sick Sinus Syndrome
• SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node
automaticity and SA conduction.
• Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor,
trauma and congenital disease.
• With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms
• Bradycardia-tachycardia syndrome
ECG Recognition:
1. Sinus bradycardia, ≤40 bpm;
2. Sinus arrest > 3s
3. Type II SAB
4. Non-sinus tachyarrhythmia ( SVT, AF or Af).
5. SNRT > 1530ms, SNRTc > 525ms
6. Instinct heart rate < 80bmp
Therapy:
1. Treat the etiology
2. Treat with drugs: anti-bradycardia agents, the effect of drug therapy is not good.
3. Artificial cardiac pacing.

35. Sick Sinus Syndrome
Sinoatrial block (note the pause
is twice the P-P interval)
Sinus arrest with pause of 4.4 s
before generation and conduction
of a junctional escape beat
Severe sinus bradycardia
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36. Bifascicular/ Trifascicular Blocks
• RBBB with either left anterior or left posterior fascicular block
• Diagnostic criteria
• 1.Prolongation of the QRS duration to 0.12 second or longer
• 2.RSR’ pattern in lead V1,with the R’ being broad and slurred
• 3.Wide,slurred S wave in leads I,V5 and V6
• 4.Left axis or right axis deviation
Trifascicular
• The combination of RBBB, LAFB and long PR interval
• Implies that conduction is delayed in the third fascicle
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Bifascicular

37. Cardiac Pacemakers
• Indications For Implantation of
Permanent Pacing in Acquired AV Blocks
• 1.Third-degree AV block, Bradycardia with
symptoms
• Asystole
• e.Neuromuscular diseases with AV block
(Myotonic muscular dystrophy)
• 2.Second-degree AV block with symptomatic
bradycardia
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38. Cardiac Pacemakers
• Definition
– Delivers artificial stimulus to heart
– Causes depolarization and contraction
• Uses
– Bradyarrhythmias
– Asystole
– Tachyarrhythmias (overdrive pacing)
• Types
– Fixed
• Fires at constant rate
• Can discharge on T-wave
• Very rare
– Demand
• Senses patient’s rhythm
• Fires only if no activity sensed after preset
interval (escape interval)
– Transcutaneous vs Transvenous vs Implanted
• Demand Pacemaker Types
– Ventricular
• Fires ventricles
– Atrial
• Fires atria
• Atria fire ventricles
• Requires intact AV conduction
• Demand Pacemaker Types
– Atrial Synchronous
• Senses atria
• Fires ventricles
– AV Sequential
• Two electrodes
• Fires atria/ventricles in sequence
• Problems
– Failure to capture
• No response to pacemaker artifact
• Bradycardia may result
• Cause: high “threshold”
• Management
– Increase amps on temporary pacemaker
– Treat as symptomatic bradycardia
– Failure to sense
• Spike follows QRS within escape interval
• May cause R-on-T phenomenon
• Management
– Increase sensitivity
– Attempt to override permanent pacer with
temporary
– Be prepared to manage VF
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39. Implanted Defibrillators
• AICD
– Automated Implanted Cardio-Defibrillator
• Uses
– Tachyarrhythmias
– Malignant arrhythmias
• VT
• VF
• Programmed at insertion to deliver predetermined therapies
with a set order and number of therapies including:
– pacing
– overdrive pacing
– cardioversion with increasing energies
– defibrillation with increasing energies
– standby mode
• Effect of standby mode on Paramedic treatments
• Potential Complications
– Fails to deliver therapies as intended
• worst complication
• requires Paramedic intervention
– Delivers therapies when NOT appropriate
• broken or malfunctioning lead
• parameters for delivery are not specific enough
– Continues to deliver shocks
• parameters for delivery are not specific enough and
device senses a reset
• may be shut off (not standby mode) with donut-magnet
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40. ECG Monitoring
• Einthoven’s Triangle
• The positioning for leads I, II,
and III were first given by
Einthoven. Form the basis
of Einthoven’s triangle.
– Each lead “looks” from a
different perspective
– Can determine the
direction of electrical
impulses
– Upright electrical recording
indicates electricity flowing
towards the + electrode
• positive deflection
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1901 - Dr. William Einthoven invented the
ECG machine

41. • Unipolar Leads
– 1 positive electrode
– 1 negative “reference point”
• calculated by using summation
of 2 negative leads
– Augmented Limb Leads
• aVR, aVF, aVL
• vertical plane
– Precordial or Chest Leads
• V1-V6
• horizontal plane
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42. • Bipolar Leads
– 1 positive and 1 negative
electrode
• RA always negative
• LL always positive
– Traditional limb leads are
examples of these
• Lead I
• Lead II
• Lead III
– Provide a view from a
vertical plane
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