CRITICAL CARE CARDIAC

ELECTROPHYSIOLOGY
Department of Emergency Medicine
EAST AVENUE MEDICAL CENTER
OBJECTIVES
After the module, the students will acquire the basic
knowledge in cardiac electrophysiology.
▪ Physics
▪ Anatomy
▪ Molecular biochemistry
▪ Physiology

Develop a method and sense of confidence needed in

ecg reading.
Cognitive OBJECTIVES
Describe the timely recognition and interventions
requiring an electrocardiograph to prevent morbidity
among patients.
Describe priorities and specific interventions for
patients with the utility of an electrocardiograph.
Introduction
Section I
Definition
Electrocardiograph
An instrument that records the electrical activity of
the heart
Provides information about
▪ Orientation of the heart in the chest
▪ Conduction disturbance
▪ Electrical effects of electrolytes and medications
▪ Presence of ischemic changes
Principles
Depolarization and repolarization are displayed as
waveforms
▪ Upward deflection
▪ Downward deflection
 Isoelectric line
 The baseline of the electrocardiogram, recorded in the TP
interval during rhythms with P waves
SIDENOTE
 Artifacts
 EKG deflections caused by
influences other than the heart’s
electrical activity.
 CAUSES:
▪ electrical interference
SIDENOTE

▪ muscle tremors
▪ metal objects
▪ loose electrodes
▪ ground hum
▪ varies with respiration
EINTHOVEN’S TRIANGLE

Limb leads
 PRECORDIAL LEAD
PLACEMENT
The precordial electrodes
should be placed as follows:
▪ V1 - right sternal border, fourth
intercostal space
SIDENOTE

▪ V2 - left sternal border, fourth

intercostal space;
▪ V3 - midway between V2 and V4
▪ V4 - left midclavicular line, fifth
intercostal space
▪ V5 - left anterior axillary line, same
horizontal level as V4
▪ V6 - left midaxillary line, same
horizontal level as V4 and V5
 RIGHT-SIDED LEAD
PLACEMENT
▪ The right ventricular ECG electrodes
are placed across the right side of the
chest in a mirror image of the
standard left-sided electrodes and are
labeled V1R to V6R; alternatively, RV1
SIDENOTE

to RV6 is another commonly used

nomenclature for this electrode
distribution.
 POSTERIOR LEAD
PLACEMENT
▪ The posterior electrodes V8 and V9
are placed on the patient’s back—V8
at the tip of the left scapula and V9 in
an intermediate position between
lead V8 and the left paraspinal
SIDENOTE

muscles.
▪ An additional electrode, V7, may also
be used and is placed on the
posterior axillary line equidistant from
electrode V8.
Concepts
Section II
ELECTROPHYSIOLOGY
MAJOR CELL TYPES
 Pacemaker cells
 Purkinje fibers
 Contractile cells

MAJOR CATIONS
 Sodium [Na+]
 Potassium [K+]
 Calcium [Ca+]
ELECTROPHYSIOLOGY
MAJOR CELL TYPES
 Pacemaker cells
 Purkinje fibers
 Contractile cells

MAJOR CATIONS
 Sodium [Na+]
 Potassium [K+]
 Calcium [Ca+]
PACEMAKER LOCALIZATION
SUPRAVENTRICULAR
Sino-atrial node

Atrioventricular node

Bundle of His

VENTRICULAR
Bundle Branches
(right and left)
*Purkinje fibers
1 SA node depolarizes.

2 Electrical activity goes rapidly to AV

node via intermodal pathways.

Depolarization spreads more slowly

3 across atria. Conduction slows through
AV node.

Depolarization moves rapidly through

4 ventricular conducting system to the
apex of the heart.

5 Depolarization wave spreads upward

from the apex.
REGULAR RHYTHMS

SA Node Dominant 60-100 bpm

Junctional Escape 40-60 bpm
AV node
Bundle of His (BOH)
Ventricular Escape 20-40 bpm
Bundle branch
Purkinje fibers
NOMENCLATURE
Sinus Tachycardia

*Atrial slow controlled rapid

Junctional Accelerated Tachycardia

Ventricular Idio- Accelerated Tachycardia

20 40 60 80 100
*SVT – reserved for regular SUPRAVENTRICULAR RHYTHMS with HR ≥ 150
*Agonal rhythms – rates less than 20 bpm
Age related cut-off for SVT: 180 bpm (child) 220 bpm (infant)
ECG waveform
Section III
ECG PAPER

1 small square = 0.04 sec

= 1 mm
= 0.1 mV
1 big square = 0.2 sec
5 big squares = 1 sec
300 big squares = 1 min
‘P’ wave
 Represents ATRIAL DEPOLARIZATION
 Normal characteristics:
▪ Monophasic in lead II RIGHT
ATRIUM
✓ Smooth and rounded contour
LEFT
✓ No more than 3 mm in height ATRIUM
✓ No more than <0.10 sec in duration

▪ Biphasic in lead V1
✓ Sensitive in detecting
P waves
‘P’ wave
 Relevance:
▪ Chamber enlargement (atria)
▪ Supraventricular pacemaker
 Nomenclature
▪ RAE as P pulmonale
▪ LAE as P mitrale
 STEP 2
STEP 1 QRS COMPLEX
NARROW WIDE

UPRIGHT SINUS
P WAVE

BUNDLE
SIDENOTE

BRANCH BLOCK
INVERTED
JUNCTIONAL /
NODAL
ABSENT VENTRICULAR
SIDENOTE Alternate Leads
SIDENOTE Alternate Leads
 Wandering Atrial Pacemaker
 Pacemaker site “wanders”
▪ Need at least three (3) phenotypes of P waves
 Irregular atrial rate
 If rate is > 100: Multifocal Atrial Tachycardia (MAT):
SIDENOTE

▪ Most commonly associated with COPD

▪ High mortality
 May resemble a-fib
SIDENOTE Wandering Atrial Pacemaker
SIDENOTE Multifocal Atrial Tachycardia
SIDENOTE Atrial Flutter
SIDENOTE Atrial Flutter
Thromboembolic Event
Risk Stratification
SIDENOTE Paroxysmal SVT
 Sick Sinus Syndrome
 A.K.A. “tachy-brady syndrome”
 Most patients are asymptomatic.
 More common in elderly population.
 May have recurrent supraventricular arrhythmia and
SIDENOTE

bradyarrhythmia.
 Frequently seen in patients with concomitant atrial fibrillation.
 Often chronotropically incompetent.
 May be caused by drug therapy.
‘PR’ interval
 Time for the atria to depolarize
and the delay of impulse through
the AV junction
 P wave + PR segment P wave PR
 NV: 0.12-0.20 sec segment

 Shortens as the heart rate

increases
 Relevance:
▪ Accessory conduction
pathway
▪ AV conduction abnormality
Accessory Conduction Pathways
 Also Called Pre-Excitation Syndromes (PES)
 These syndromes are characterized by an aberrant conduction SA
pathway that enters the ventricular muscle in addition to the normal
pathway. Since these aberrant pathways are shorter they cause
ventricular depolarization prior to the normal pathway.
 There are 2 pre-excitation syndromes
AV
▪ Wolff–Parkinson-White (WPW)
▪ Lown-Ganong-Levine (LGL)
 Both pathways show shortened P-R intervals of less than 0.20 sec.
 High propensity to convert to severe tachycardia. V
 Wolff –Parkinson-White (WPW)
 The aberrant pathway is the bundle of Kent which bypasses
the AV node. This gives a shortened P-R interval ( i.e. less
than 0.20 seconds)
 There is a shoulder on the R-wave of the QRS complex. This
shouldered QRS complex is called a Delta-wave and is the
SIDENOTE

result of a fused ( fusion) beat from the normal and aberrant

pathway.
 Delta Wave
 Short PR interval (< 120ms)
 Broad QRS (> 100ms)
 A slurred upstroke to the
QRS complex
SIDENOTE
SIDENOTE
 Lown-Ganong-Levine (LGL)
 The aberrant pathway is the bundle of James which joins the
normal pathway above the AV node.
 Since the abnormal pathway joins the normal pathway above
the AV node rather than within it there is no delta wave but just
a shortened PR interval (i.e. less than 0.20 seconds)
SIDENOTE
SIDENOTE
SIDENOTE
AV Conduction Defect
SA

AV

V
SIDENOTE First Degree AV Block
 Second Degree AV Block
Type 1 Type 2
 Lesion above the Bundle of  Lesion in the Bundle branch
His PR may prolong prior to fixed PR interval; drop beat.
drop beat.
 Ventricular rhythm reg/irreg
SIDENOTE

 Ventricular rhythm reg/irreg does not respond well to

responds to pharmacologic tx. drugs.
 Rarely requires pacing  Requires electronic pacing.
SIDENOTE Third Degree AV Block
SIDENOTE REVIEW

0 1 2 3 4 5 6
SIDENOTE REVIEW

0 1 2 3 4 5 6 7
PHARMACOLOGY
 Transcutaneous Pacing
 A rapid, minimally invasive method of emergency cardiac pacing
that may temporarily substitute for transvenous pacing.
 Electrodes are applied to the skin of the anterior and posterior
chest walls, and pacing is initiated with a portable pulse generator.
SIDENOTE
SIDENOTE Defibrillator
SIDENOTE
Tachy- ALGORITHMS
NARROW COMPLEX
SIDENOTE Vagal Maneuvers
WIDE COMPLEX
‘QRS’ complex
 Represents VENTRICULAR DEPOLARIZATION
▪ Q wave - 1st negative deflection
▪ R wave - 1st positive deflection
▪ S wave - negative deflection following the R wave
 One or even two of the three waveforms may not always be
present
 Duration: 0.06 - 0.10sec (N/IVCD 0.11sec)
 Relevance:
▪ Ventricular hypertrophy
▪ Bundle branch blocks
SIDENOTE
SIDENOTE
 Left Ventricular Hypertrophy
LIMB LEADS Most commonly used
 R wave in lead I + S wave in lead III > voltage criteria:
2.5mV  S in V1 + R in V6 > 3.5mV
 R wave in aVL > 1.1mV  S in V2 + R in V6 > 4.3mV
SIDENOTE

 R wave in aVF > 2.0mV  S in V1 > 2.4mV

 S wave in aVR > 1.4mV  S in V6 > 2.8mV
PRECORDIAL LEADS  R in aVL > 1.3mV + S in V3 >
2.0mV for females and > 2.8mV
 R wave in V5 or V6 > 2.6mV for males (CORNELL
 R wave in V6 + S wave in V1 > 3.5mV CRITERIA)
 Largest precordial leads > 4.5mV
 Left Ventricular Hypertrophy

S in V1
SIDENOTE

+
R in V5
> 35 mm
 Right Ventricular Hypertrophy
 R in V1 > 0.7mV  R/S ratio in V1 (or V3R) > 1
 S in V1 < 0.2mV  qR pattern in V1 (or V3R)
 S in V5 or V6 > 0.7mV Supporting criteria include the
following:
 Sum of R in V1 and S in V5 or V6 >
SIDENOTE

1.05mV  Onset of intrinsicoid deflection in

V1 later than 0.04 seconds
 R in V5 or V6 < 0.5mV
 Negative T wave in V1 in the
 R/S ratio in V5 or V6 < 1
presence of R > 0.5mV
 R in aVR > 0.5mV
 Right axis deviation > 110
 R/S ratio in V5 divided by R/S ratio in degrees
V1 < 0.4
BUNDLE BRANCH BLOCK
 Normally, the electrical impulse travels down both the right
and left branches at the same speed. Thus, both ventricles SA
contract at the same time.
 Occasionally there's a block in one of the branches, so
impulses must travel to the affected side by a detour that
slows them down. That means one ventricle contracts a
fraction of a second slower than the other. AV

V
 Right Bundle Branch Block
R, S, R-prime
 2 R-waves R and R prime WITH an intervening
S-wave in leads V1,V6 and lead 1.
 The s wave is deep in lead 1 and V1 .
SIDENOTE
SIDENOTE Right Bundle Branch Block
SIDENOTE Right Bundle Branch Block
 Left Bundle Branch Block
R, R-prime
 Seen in Leads 1 , V1 and V6 as 2 R-waves.
 R and R prime without an intervening S-wave.
 The wave between the R-waves is scooped.
SIDENOTE
SIDENOTE Left Bundle Branch Block
SIDENOTE Left Bundle Branch Block
 Sgarbossa criteria
 For detecting an AMI in the
setting of a LBBB
 Derived from the Gusto-1 trial
 Not perfect in screening for AMI.
 Holds true for LBBB pattern seen
SIDENOTE

in pacemaker patients.
SIDENOTE 2017 ECC STEMI UPDATES
 Electrical Alternans
 Consecutive, normally-conducted QRS
complexes alternate in height.
 Produced by the heart swinging backwards and
forwards within a large fluid-filled pericardium.
SIDENOTE
SIDENOTE
‘ST’ segment
 Represents EARLY VENTRICULAR
REPOLARIZATION
 Begins with the end of QRS complex J point
and ends with the onset of T wave
 Is usually not depressed more than
0.1mm in any lead
 isoelectric
SIDENOTE
SIDENOTE
Contiguous leads

S septal V1, V2

A anterior V3, V4

L lateral V5, V6 , I, aVL (high lateral)

I inferior II, III, aVF

CONTIGUOUS LEADS
SIDENOTE Culprit Lesions
BLOOD SUPPLY
Point-of-Care Ultrasound

(PLAX) (PSAX) (A4C)

Parasternal Long Axis Parasternal Short Axis Apical 4 Chamber
SIDENOTE POCUS on AMI
SIDENOTE POCUS on LOCALIZATION
SIDENOTE Parasternal Long Axis
SIDENOTE Parasternal Short Axis
SIDENOTE Apical 4 Chamber
SIDENOTE
SIDENOTE
 Inferior wall (LCX)
STE II, III, aVF, V6
STD V1-3
SIDENOTE
 Inferior wall (RCA)
STE III > II
STD I, aVL
SIDENOTE
 Inferior wall (RCA)
STE II, III, aVF, V1
SIDENOTE
 Anterior wall (Proximal LAD)
STE V1-3
W/ STD II,III,aVF
SIDENOTE
 Anterior wall (Distal LAD)
STE V1-3
NO STD II,III,aVF
SIDENOTE
 Posterior wall
 L circumflex or RCA occlusion
 Often assoc. with acute inferior or lateral wall MI
 ST depression V1-V3
 Upright, tall T and tall, wide R in V1-V3
SIDENOTE
 15 LEAD ECG : Highlights
 The degree of ST-segment elevation in the posterior leads is often
less pronounced than the ST-segment elevation seen in the
standard 12 leads in patients with STEMI.
 This diminution in posterior lead ST-segment elevation results from
both the relatively greater distance of these leads from the posterior
SIDENOTE

surface of the heart and the presence of air and soft tissue between
the epicardium and the electrocardiographic electrodes.
 It has been suggested that the threshold criterion for
intervention be lowered from the standard 1 mm of ST-segment
elevation to 0.5 mm when evaluating the posterior leads for STEMI.
 STEMI Equivalents
 Wellen’s Syndrome
 DeWinter ST/T wave complex
 Isolated ST elevation in lead AVR
 Isolated Inferior Wall ST Depression for LAD
SIDENOTE

 Isolated posterior wall MI

 Isolated AVL ST depression for inferior wall MI
 Hyperacute T waves (HATWs)
 Upright T waves in V1
 LBBB w/ Sgarbossa criteria
 Paced rhythm w/ Sgarbossa criteria
 Wellen’s syndrome
BIPHASIC T WAVES (TYPE A)

 Wellens’ syndrome is highly specific for

a critical stenosis of the left anterior
SIDENOTE

descending artery (LAD).

DEEPLY INVERTED T WAVES (TYPE B)
 There are two patterns of T-wave abnormality
in Wellens’ syndrome:
▪ Type A = Biphasic, with initial positivity
& terminal negativity (25% of cases)
▪ Type B = Deeply and symmetrically
inverted (75% of cases)
 DeWinters ST/T wave complex
 DeWinters ST/T wave complex is highly specific for a
complete proximal left anterior descending artery (LAD)
occlusion.
 Characteristics:
▪ 1mm ST-depression at the J-point, with up-sloping ST-
SIDENOTE

segments continuing into tall T-waves in the precordial

leads.
▪ Minimal (<0.5mm) ST- elevation in aVR
▪ without any ST-elevation in V1-V6
SIDENOTE DeWinters ST/T wave complex
SIDENOTE DeWinters ST/T wave complex
 Isolated ST elevation in lead AVR
 Diffuse ST depression combined with STE in AVR may be
indicative of “subendocardial ischemia” from significant left
main coronary (LMCA) stenosis, left main equivalent
disease (LMEQ, significant disease of the left anterior
descending and left circumflex), or three-vessel
disease(TVD).
SIDENOTE

 Characteristics:
▪ ST elevation in aVR ≥ 1mm
▪ ST elevation in aVR ≥ V1
▪ ST depression typically seen in lateral
SIDENOTE Isolated ST elevation in lead AVR
SIDENOTE Isolated ST elevation in lead AVR
 Isolated Inferior Wall ST Depression
 Isolated ST segment depression in the inferior wall leads
during ACS is usually an early sign of anterior wall AMI, in
which the LAD or one of its branches is the culprit artery.
SIDENOTE
 Isolated AVL ST depression
 An Isolated AVL ST segment depression is highly sensitive
marker for considerations of inferior wall MI presenting with
hyperacute T-waves.
 Characteristics:
▪ Reciprocal ST-depression (STD) in lead aVL is seen in
SIDENOTE

inferior STEMI, - as a STEMI equivalent.

▪ STD may be apparent in the absence of clear-cut ST-
elevation.
▪ Reciprocal depression in aVL
SIDENOTE Isolated AVL ST depression
 Hyperacute T-waves (HATWs)
 After QT prolongation, hyperacute T waves are the earliest-
described electrocardiographic sign of acute ischemia,
preceding ST-segment elevation.
 Hyperacute T waves are broad-based and symmetrical,
usually with increased amplitude and often associated with a
depressed ST take off.
SIDENOTE

 Characteristics: HATWs vs HyperKalemia

Hyperkalemia: narrow-based,
▪ > 5mm in the limb
symmetric, and peaked (sharp);
▪ > 10mm precordial leads
may have a widened QRS
▪ may be symmetric or asymmetric
▪ reciprocal changes in opposing leads as well as
increased R wave amplitude (if prior ECG is available).
SIDENOTE Hyperacute T-waves (HATWs)
SIDENOTE Hyperacute T-waves (HATWs)
 Upright T wave lead V1
 It might be worthwhile to routinely evaluate the polarity of
the T wave in lead V1 in patients with suspected CAD, since
it appears to have additional risk stratification potential.
SIDENOTE
SIDENOTE HIGH RISK NSTEMI
‘T’ wave
 VENTRICULAR REPOLARIZATION
 NV: <0.12 sec
<5-6 mm in limb leads
<10mm in precordial leads
 upright except aVR
 Relevance:
▪ Hypo-/hyperkalemia
▪ Ischemia
SIDENOTE Hypo-/Hyperkalemia
SIDENOTE Hyperkalemia
SIDENOTE Hyperkalemia
SIDENOTE
SIDENOTE Hyperkalemia
SIDENOTE Hypokalemia
SIDENOTE Hypokalemia
SIDENOTE Hypokalemia
‘QT’ interval
 Represents TOTAL VENTRICULAR ACTIVITY
 measured from the beginning of the QRS
complex to the end of the T wave
 NV: 0.35-0.44 sec
 Duration varies according to age, gender
and heart rate
 As the HR decreases, QTi increases.
 Relevance:
▪ Hypo-/hypercalcemia&magnesemia
▪ Digitalis toxicity
▪ Hypothermia
 Corrected ‘QT’ interval
 Bazett’s formula: QTC = QT / √ RR
 Fredericia’s formula: QTC = QT / RR 1/3
 Framingham formula: QTC = QT + 0.154 (1 – RR)
 Hodges formula: QTC = QT + 1.75 (heart rate – 60)
SIDENOTE
SIDENOTE Hypo-/Hyper Ca/Mg

HYPO- HYPER-
 Digitalis Toxicty
 Digoxin toxicity causes a shortened QT interval with a
scooping of the ST segment.
SIDENOTE
 J ‘Osborne’ wave
 The Osborn wave (J wave) is a positive deflection at the J point
(negative in aVR and V1).
 It is usually most prominent in the precordial leads.
SIDENOTE
ECG Patterns
Section IV
 Sinus Arrhythmia
 Variation in the sinus node discharge rate is common.
 Difference between the longest and shortest intervals exceeds 0.12 sec
 Usually present as phasic (respiratory variation) variety and less commonly
a nonphasic variety.
SIDENOTE

▪ Phasic variety, the sinus node rate accelerates during inspiration and
decelerates during expiration because of changes in vagal tone
occurring with respiration (BAINBRIDGE REFLEX)
 No treatment required.
Paced Rhythm
 Early Repolarization Syndrome
 Benign variant of normal ventricular repolarization
 Prominent, notch-like J wave on the QRS down-slope,
followed by upsloping ST-segment elevation
SIDENOTE
SIDENOTE Brugada Syndrome
Fatal Rhythms
Section V
Adult Cardiac Arrest
 ORGANIZED RHYTHM w/ a NARROW QRS.
Consider PEA or ROSC.
There is
ORGANIZED
RHYTHM. ORGANIZED RHYTHM w/ a WIDE QRS.
If the rate is < 100, consider PEA or ROSC.
If the rate is > 100, consider VTACH.
Is there an
ORGANIZED NO
RHYTHM? ORGANIZED VENTRICULAR FIBRILLATION
RHYTHM.

NO RHYTHM. ASYSTOLE PROTOCOL

SIDENOTE Ventricular Fibrillation
SIDENOTE Ventricular Tachycardia
SIDENOTE Ventricular Tachycardia
SIDENOTE Asystole
 Pulseless Electrical Activity
 Absence of detectable pulse and the presence of some
type of electrical activity
 Electro-mechanical Dissociation (EMD), Pseudo-EMD,
idioventricular rhythms, ventricular escape rhythms and
bradyasystolic rhythms
SIDENOTE
 Pulseless Electrical Activity
 In general, a systolic blood pressure (SBP)
of 60 mm Hg is required for the carotid pulse to
be palpable, 70 mm Hg for the femoral pulse,
and 80 mm Hg for the radial pulse.
SIDENOTE

Tintinalli, J. E., Stapczynski, J. S., Cline, D. M., Ma, O. J., Cydulka, R. K., & Meckler, G. D. (Eds.). (2016). Tintinalli's Emergency Medicine: A Comprehensive Study Guide (8th Edition ed.). McGraw-Hill.
SIDENOTE Pulseless Electrical Activity

Tintinalli, J. E., Stapczynski, J. S., Cline, D. M., Ma, O. J., Cydulka, R. K., & Meckler, G. D. (Eds.). (2010). Tintinalli's Emergency Medicine: A Comprehensive Study Guide (7th Edition ed.). McGraw-Hill.
 Approach to Pseudo-PEA (2010)
 Presence of ventricular
contractility visualized on
cardiac ultrasound in a patient
without palpable pulses.
 There is some observable,
SIDENOTE

although minimal, cardiac

output and have a higher
survival rate, in part because
there are often identifiable and
treatable causes of their arrest.
SIDENOTE AHA on Pseudo-PEA (2015)
 Auscultation on rhythm check
Asystole -
NON-
SHOCKABLE When
P. E. A. -/+
SIDENOTE

will you
vTach -/+ shock?!
SHOCKABLE

vFib -/+
Analyzing the strip
Section VI
R Regularity / Rhythm / Rate

A Axis

H Hypertrophy

I Ischemia / Infarct

M Miscellaneous
STEP 1:
Does the ‘QRS’ complex present with
GROSS REGULARITY?
YES
NO / NOT ALWAYS
▪ Consider ectopic beats

R A H I M
1 How to check for regularity
SIDENOTE
2 How to check for regularity
SIDENOTE
STEP 2:
What is the RHYTHM?
SINUS
JUNCTIONAL
VENTRICULAR

R A H I M
 STEP 2
STEP 1 QRS COMPLEX
NARROW WIDE

UPRIGHT SINUS
P WAVE

BUNDLE
SIDENOTE

BRANCH BLOCK
INVERTED
NODAL /
JUNCTIONAL
ABSENT VENTRICULAR
Labeling the ECG
ECTOPIC BEATS
 Escape Beat
▪ A beat comes after a long pause or arrest.
 Premature Beat
▪ A beat that comes earlier than expected.
SIDENOTE Premature Atrial Complex
SIDENOTE Premature Junctional Complex
 Variations in PVCs
Uniform / Multiform:
 PVCs similar to each other in polarity and configuration
SIDENOTE
 Variations in PVCs
Paired or Couplet:
 2 PVCs in succession with uniform appearance
SIDENOTE
 Variations in PVCs
Bigeminy:
 every other beat is a PVC
SIDENOTE

1 2 1 2 1 2
 Variations in PVCs
Trigeminy:
 every 3rd beat is a PVC
SIDENOTE

1 2 3 1 2 3 1 2 3
 Variations in PVCs
Quadrigeminy:
 every 4th beat is a PVC
SIDENOTE

1 2 3 4 1 2 3 4
SIDENOTE REVIEW
STEP 3:
What is the RATE?
Regular rhythm
 1500 / Small boxes
 300 / Big boxes 1 2 3 4 5 6

 Sequence method

Irregular rhythm
 Six-second method 1 sec 1 sec 1 sec 1 sec 1 sec 1 sec

(QRS complexes in 6
seconds) x 10

R A H I M
STEP 4:
What is the AXIS?
1. Quadrant or Eyeball method
▪ uses the leads I and aVF

2. Hexaxial method
▪ uses 6 limb leads (I, II, III, aVL, aVF, aVR)

3. Einthoven’s Triangle Hypothesis

▪ uses the 3 bipolar limb leads (I, II, III)

R A H I M
Computation for Frontal Axis
 Deduct negative deflections from positive deflections in QRS
complexes to derive the values for leads I and aVF
 If lead I is a negative integer, subtract the computed axis from
180 to get the axis.
 Note that the value for aVF in the denominator is the absolute
value, while the numerator takes the sign (positive or
negative) into consideration. This is why a predominantly
negative deflection in aVF will make the axis negative.

90 aVF
Axis = | I | + | aVF |
1 Quadrant or Eyeballing Method
STEP 5:
Chamber enlargement?
1. Atrial Enlargement
2. Ventricular hypertrophy

R A H I M
1 Atrial Enlargement
 Remember the rule of 3’s
SIDENOTE
2 Right Ventricular Hypertrophy
 Sum of R in V1 and S in V5 or V6 > 1.05mV
 R in V1 > 0.7mV
 R/S ratio in V1 (or V3R) > 1
 R/S ratio in V5 or V6 < 1
SIDENOTE

 Right axis deviation > 110 degrees

2 Left Ventricular Hypertrophy
 R wave in aVL > 1.1mV
 S in V1 + R in V6 > 3.5mV
 CORNELL CRITERIA: R in aVL > 1.3mV + S in V3
▪ > 2.0mV for females
SIDENOTE

▪ > 2.8mV for males

STEP 6:
Ischemia? Infarct?
Remember S.A.L.I.?

R A H I M
STEP 7:
Miscellaneous
 AV block
 Bundle branch block
 Ectopic beats
▪ Premature beats
▪ Escape beats
 others

R A H I M
Questions?
CRITICAL CARE CARDIAC
ELECTROPHYSIOLOGY
Department of Emergency Medicine
EAST AVENUE MEDICAL CENTER