"Demystifying Clinical Electrocardiography" A conceptual approach to learning & applying clinical electrocardiography. Kristy Molnar, Critical Care Consultants

1. ““DEMYSTIFYING CLINICALDEMYSTIFYING CLINICAL
ELECTROCARDIOGRAPHY”ELECTROCARDIOGRAPHY”
…… HHighlightingighlighting Myocardial Ischemia, Injury & Infarct
©Kristy Molnar, Partner, Critical Care Consultants, 2013©Kristy Molnar, Partner, Critical Care Consultants, 2013

2. PHILIPS HEALTHCARE
Patient Care & Clinical Informatics

3. Continuing Education for
Healthcare Professionals
EDUCATIONALEDUCATIONAL
SERVICESSERVICES
© Copyright, 2013
Critical Care Consultants
Kristy Molnar

4. Partner, Nursing Education Consultant
CRITICAL CARE CONSULTANTS

6. Demystifying ClinicalDemystifying Clinical
Electrocardiography …Electrocardiography …

7. Goals of ECG MonitoringGoals of ECG Monitoring
To detect and document cardiacTo detect and document cardiac
arrhythmiasarrhythmias
To detect and document ST changes andTo detect and document ST changes and
evolving ischemiaevolving ischemia
To detect prolonged QT interval syndromeTo detect prolonged QT interval syndrome
To evaluate the effectiveness of treatmentTo evaluate the effectiveness of treatment

8. We’ve come a LONG Way!We’ve come a LONG Way!

9. http://www.ecglibrary.com/ecghist.html

10. Goals of ECG MonitoringGoals of ECG Monitoring
In order to meet the goals of ECG
monitoring, it should ideally be continuous
and should reflect a minimum of 12 leads
simultaneously.
Ideally 16 leads

11. Goals of ECG MonitoringGoals of ECG Monitoring
Comprehensive arrhythmia diagnosis often
requires a MULTI-LEAD perspective,
Ischemia detection can only occur IF the
associated leads are viewed,
Transient events of diagnostic/therapeutic
importance may not persist LONG
ENOUGH to allow documentation with a
standand ECG.

12. Patient Monitoring Survey-Patient Monitoring Survey-
THEN vs NOWTHEN vs NOW
Independent survey at AACN’s Advanced
Practice Institute Conference (1998)
N=400 (Acute care Nurses and Clinical
Specialists)
69% of respondents did not have the
clinical capability
31% had the ability to monitor continuous
12-Lead ECG.

13. Continuous ECG MonitoringContinuous ECG Monitoring
Those using continuous 12-Lead ECG
monitoring indicated that their primary
reasons are for:
– assessment of cardiac condition
– changes in condition
– differentiation of abnormal or irregular
rhythms.

14. Continuous ECG MonitoringContinuous ECG Monitoring
The reasons for infrequent use included
lack of training, “not a requirement”, and
no perceived need.
66% of participants responded that there
were barriers to continuous 12-lead
monitoring … number of electrodes … lack
of training was the primary barrier

15. The IdealThe Ideal
Monitoring Situation:Monitoring Situation:
Continuous, real-time
Multi-lead perspective
Sensitive and specific
Convenient and stable electrode positions
Easy to landmark (consistent, quick and
reproducible)
Patient comfort and low interference with
clinical procedures.

16. 2004 Practice Standards …2004 Practice Standards …

17. Practice Standards,Practice Standards,
the beginningthe beginning
Source: Drew, BJ et al Circulation, 2004
October 26; 110(17):2721-46.
Full text article: www.circ.ahajournals.org
Guidelines: www.guideline.gov

18. 2009 AHA, ACC, HRS Practice Standards2009 AHA, ACC, HRS Practice Standards
Recommendations for the Standardization and Interpretation of the
Electrocardiogram – Part IV (Feb. 19, 2009)

19. Learning Needs? …Learning Needs? …
it appears so!it appears so!

20. Ongoing Investigations …Ongoing Investigations …
20132013

21. Review of ElectrocardiographicReview of Electrocardiographic
PrinciplesPrinciples
Functional Anatomy
& Physiology

22. Electrical SystemElectrical System
The heart has an intrinsic electrical
system that allows for the
origination and transmission of
an electrical impulse.
– The electrical stimulus (initiating
factor)
– Depolarization (proliferating
factor)

23. Cardiac Cell PropertiesCardiac Cell Properties
Automaticity
Excitability
Conductivity
Contractility

24. Electrical Conduction SystemElectrical Conduction System
SA Node
“Internodal Pathways”
AV Junction
Bundle of His
Bundle Branches
Purkinje Fibres

25. Sinoatrial (SA) NodeSinoatrial (SA) Node
Right atrium (superior, right orientation)
Close to the superior vena cava
Specialized piece of conduction tissue with
the property of automaticity.
60-100 bpm, fastest rate of automaticity
normally, thereby setting the pace of the
heart.

26. The SA Node -The SA Node -
Automaticity & ExcitabiltyAutomaticity & Excitabilty
 Innervated by the autonomic nervous system.
 Sympathetic stimulation can accelerate the SA
node up to a rate of 150-160/min.
 Parasympathetic stimulation can slow the heart
rate to less than 60/min.
 If the heart was separated from the body’s nervous
system, the SA node could still initiate its own
impulses.

27. ConductivityConductivity
Once an electrical stimulus is originated, it
spreads throughout the remainder of the
conduction system and the heart muscle.

28. ConductivityConductivity
When the impulse is released from the SA
node, it travels throughout the atria, causing
them to depolarize and subsequently,
contract.
The depolarization wave arrives at the AV
node, which is located on the inferior-right
side of the intra-atrial septum.

29. ConductivityConductivity
The wave is delayed there for
approximately .10 seconds before arriving
at the Bundle of His … allowing for atrial
contraction to precede ventricular
contraction (contributing to adequate
ventricular filling, an additional 20-30% of
preload).

30. AV JunctionAV Junction
Under normal conditions, the AV junctional
tissue is not the pacemaker of the heart –
since it has a lower rate of automaticity than
the SA Node.
The rate of impulse formation in the AV
junctional tissue is normally 40-60/min.

31. A-V ConductionA-V Conduction
The cardiac impulse spreads to the thin
bundle of “threads” known as the bundle of
His
The bundle of His connects the AV junction
to the bundle branches (located in the right
side of the intra-atrial septum just above the
ventricles)

32. Intraventricular ConductionIntraventricular Conduction
The conduction structures in the ventricles
consist of the conduction structures below
the bundle of His, also known as the His-
Purkinje network.
The impulse passes down the Left and
Right bundle branches in a sequential
fashion.

33. Intraventricular ConductionIntraventricular Conduction

34. Bundle Branch ConductionBundle Branch Conduction
Repolarization is faster in the Left Bundle
Branch, therefore it is ready to conduct
earlier than the Right Bundle Branch.
Conduction of the impulse is normally Left
before Right.

35. Left vs. Right Bundle BranchLeft vs. Right Bundle Branch
The Right bundle is a slender fascicle that
runs along the right side of the
intraventicular septum and supplies the
electrical impulses to the Right ventricle.
The Left bundle supplies the electrical
impulses to the Left ventricle. It runs along
the left side of the intraventricular septum
and divides almost immediately into an
anterior and posterior division (fascicle).

36. Divisions of the Left BundleDivisions of the Left Bundle
Anterior Fascicle – much longer and
thinner of the two and supplies the anterior
and superior portions of the Left Ventricle
with electrical impulses
Posterior Fascicle – shorter and thicker
and supplies the posterior and inferior
portions of the Left Ventricle with electrical
impulses.

37. Purkinje Network (Fibers)Purkinje Network (Fibers)
The bundle branches terminate in a network
of fibers that are located in both the left and
right ventricular walls.
The impulse travels into the Purkinje Fibers
and cause ventricular depolarization (and
subsequently, contraction)

38. What is anWhat is an
Electrocardiogram?Electrocardiogram?

39. Electrocardiogram (ECG)Electrocardiogram (ECG)
Depolarization and subsequent
Repolarization spreading throughout the
heart can be recorded (on paper or
electronically)
Recorded process is called the
electrocardiogram.
Changes in cellular polarity (charges)
occurring during depolarization and
repolarization produces deflections on the
recording, forming an “ECG complex”.

40. ElectrocardiogramElectrocardiogram

41. ““P,Q,R,S,T & U”P,Q,R,S,T & U”
Waves, Complexes, Intervals & Segments

43. Waves and ComplexesWaves and Complexes
Deviations from isoelectric
Positive or Negative?
May be Biphasic, Notched or “Flattened”
A complex may contain multiple waves

44. P waveP wave
Atrial depolarization
P wave = Atrial Depolarization
Upright and slightly rounded
< 2.5 mm amplitude; 2.5 small squares (.10
sec) duration; not notched or peaked
Ta wave (Repolarization) normally not seen
– coincides with QRS … opposite polarity
to P wave

45. QRS ComplexQRS Complex
Wave of depolarization reaches
the ventricular myocardium via
the Purkinje fibres
Ventricular depolarization
Represented by the “QRS”
complex

46. Morphology of QRSMorphology of QRS
Complexes – “Rules”Complexes – “Rules”
QRS may be composed of a Q wave, R
wave and an S wave, or various
combinations
Positive versus Negative deflections?
R is always positive
Q and S are always negative
Q must precede an R
S must follow an R

47. Morphology of QRSMorphology of QRS
Complexes – “Questions”Complexes – “Questions”
R wave?
Q wave or a q wave?
S wave?
QS complex or a pathological Q?
RsR1
and other configurations?

48. Examples of QRS ComplexesExamples of QRS Complexes

49. Changes in R waveChanges in R wave
or a new Q wave?or a new Q wave?
R wave changes can be clinically
significant in an acute situation (conduction
abnormality or decrease in depolarization
forces) … CAUTION – Lead Placement &
Filters
What about the development of a new Q
wave?

50. T waveT wave
Ventricular repolarization is
represented by the T wave
Normally upright and slightly
rounded
Same polarity as mean QRS
vector
Should not exceed 1/3-1/4 of the
total QRS height

51. U waveU wave
Sometimes seen after a T wave
Thought to relate to events of later
repolarization of the ventricles
Same polarity as the T wave

52. Intervals and SegmentsIntervals and Segments
Intervals contain waves
Segments are between the waves

53. PR IntervalPR Interval
From the beginning of the P
wave to the beginning of the
QRS complex.
Represents depolarization of the
atria and the spread of the
depolarization wave up to and
including the Purkinje fibres

54. His Bundle ElectrocardiogramHis Bundle Electrocardiogram

55. PR SegmentPR Segment
Represents the period of
time between the P wave
and the subsequent QRS
complex.
This should be isoelectric
? PR sagging … atrial
repolarization
abnormalities

56. QRS IntervalQRS Interval
 Should be less than .
10 sec in duration
 Duration of .10 or >
should be suspect
 R-wave should not be
slanted or slurred
 No notching of R or S

57. Intervals and Segments –Intervals and Segments –
VATVAT
 Ventricular Activation Time (VAT)
 Beginning of the QRS to the peak of the R wave
(or R1
)
 Time necessary for the depolarization wave to
travel from the endocardium to the epicardium
 Time longer for LV than RV due to relative
muscle mass
 Earlier & more sensitive indicator than a global
increase in QRS duration

58. Ventricular Activation TimeVentricular Activation Time

59. ST SegmentST Segment
From the end of the QRS complex (at
junction point) to the onset of the ascending
limb of the T wave
Should be isoelectric … look for depression
or elevation

60. ST SegmentST Segment
Sensitive indicator of myocardial ischemia or injury!!

61. QT IntervalQT Interval
The time from the beginning of the QRS
complex to the end of the T wave
Represents both ventricular depolarization
and repolarization
Prolongation increases the risk of
significant dysrhythmias
QTc an important calculation and ongoing
assessment criteria

62. QT IntervalQT Interval

64. QT/QTc Interval MonitoringQT/QTc Interval Monitoring
Who, What, When, Where, Why??

65. Importance – and challenge –Importance – and challenge –
of QT monitoringof QT monitoring
QT prolongation can indicate a risk of severe
arrhythmias, torsades de pointes, and sudden
cardiac death.

66. Significance of QTcSignificance of QTc
MonitoringMonitoring

67. Importance – and challenge –Importance – and challenge –
of QT monitoringof QT monitoring
A growing number of anti-arrhythmic, anti-
psychotic, and antibiotic medications can
cause QT prolongation
A combination of variables can put your
patient at risk.

68. Increased Risk for TorsadesIncreased Risk for Torsades
de Pointesde Pointes
QT prolonging drugs (this list is LONG)
Females
Older Patients
Bradycardia
Impaired LV function (ischemia, LV
hypertrophy)
Hypokalemia
Hypomagnesemia

69. QT and QTcQT and QTc
The QT has an inverse relationship to HR.
QT = QTc at a HR of 60 bpm only
Heart rate corrected QT interval is
abbreviated as QTc
Correction formulas, including the Bazett
and Fridericia, are population based & may
not be representative for a particular patient
Drugs may also change the relationship
between QT and HR

70. Normal QTc values?Normal QTc values?
Regardless of the 4 correction formulas
used, a QTc of < 460 ms in women and <
460 ms in men is considered normal.
Clinical Guidelines suggest that Bazett and
Fridericia formulas be included in all drug
study submissions. Philips defaults to
Bazett, but the configuration supports both.

71. CompatibilityCompatibility
Continuous QT/QTc measurement is part of
the Philips ST/Arrhythmia algorithm
Available on all IntelliVue Patient
Monitors, Information Centre and
Telemetry Systems.
3-Lead, 5-Lead, 6-Lead, EASI-derived 12-
Lead & 12-Lead systems

74. ““Normal” ECG WaveformNormal” ECG Waveform

75. Understanding MonitoringUnderstanding Monitoring
Principles and ConceptsPrinciples and Concepts
Vectors, Leads, Polarity and
Deflections …
How are they all related?

76. Recording of Electrical ForcesRecording of Electrical Forces
– The Lead Concept– The Lead Concept
A lead is an electrical system to record
electrical activity
Multiple Leads are used in cardiac
monitoring and ECG recording systems
A lead is composed on a negative and a
positive pole
Sense the direction and magnitude of
electrical forces

77. Recording of Electrical ForcesRecording of Electrical Forces
– The Lead Concept– The Lead Concept
Record surface information from different
regions (or walls) of the myocardium.
The positive pole on any respective lead is
the “sensing electrode”
It records electrical activity according to its
perspective only (narrow and limited view)

78. Recording of Electrical ForcesRecording of Electrical Forces
– The Lead Concept– The Lead Concept
Electrical forces traveling TOWARD a
positive pole, will be recorded as a
POSITIVE (upright) deflection.
Forces traveling AWAY FROM the leads
positive pole (toward it’s negative pole) will
be recorded as a NEGATIVE (downwards)
deflection.

79. The Positive Electrode’s ViewThe Positive Electrode’s View
TOWARD =
POSITIVE
DEFLECTION
AWAY =
NEGATIVE
DEFLECTION

80. Planes of the HeartPlanes of the Heart
Frontal
Horizontal
Sagittal

81. Frontal PlaneFrontal Plane
Superior
Inferior
LeftRight

82. The 6 Frontal Plane LeadsThe 6 Frontal Plane Leads
Lead I
Lead II
Lead III
aVR
aVL
aVF

83. Horizontal PlaneHorizontal Plane
LeftRight Anterior
Posterior

84. The Horizontal Plane LeadsThe Horizontal Plane Leads
 V1
 V2
 V3
 V4
 V5
 V6

85. The Horizontal Plane LeadsThe Horizontal Plane Leads
 (V7)
 (V8)
 (V9)
 V1R
 V2R
 V3R
 V4R
 V5R
 V6R

86. (Sagittal Plane)(Sagittal Plane)
RightLeft
Posterior
Anterior

87. Standard 12 LeadStandard 12 Lead
2D - Frontal and Horizontal Plane Views

88. Bipolar LeadsBipolar Leads
Each lead has two physical poles, a positive
pole and a negative pole
Lead I, II and III
(also referred to as limb leads or extremity
leads, because of their placement on the
body)
Einthoven’s Triangle

89. Einthoven’s 1st ECG MachineEinthoven’s 1st ECG Machine
1896
1912
Leads I, II and III
form the equilateral “Einthoven’s Triangle”

90. Einthoven’s TriangleEinthoven’s Triangle

91. Placement of Limb LeadsPlacement of Limb Leads

92. Formation of the Triaxial SystemFormation of the Triaxial System

93. Unipolar LeadsUnipolar Leads
Many years following Einthoven’s simple
invention, the ECG was improved by
adding the unipolar leads (Wilson, 1934)
These leads are unipolar since there is only
a designated positive electrode
The negative pole is electrically averaged
by the ECG machine and the voltage
augmented (Goldberger, 1942)

94. Unipolar LeadsUnipolar Leads
Augmented (by 50%) Voltage …
Right, Left, Foot
aVR, aVL, aVF

95. aVR, aVL, aVFaVR, aVL, aVF
Unipolar Augmented Leads – Frontal Plane

96. Frontal Plane LeadsFrontal Plane Leads
The Hexaxial SystemThe Hexaxial System

97. Horizontal Plane LeadsHorizontal Plane Leads
 The horizontal plane is traditionally viewed by six
unipolar leads … additional leads are sometimes
applied.
 Also referred to as “Precordial Leads”, “Chest
Leads” or “V Leads”
 Positive pole is determined by the physical
placement on the chest
 The negative pole is electrically averaged (from
all three extremity electrodes) and is situated
somewhere in the middle of the chest cavity.

98. Horizontal Plane LeadsHorizontal Plane Leads
The “V” or Chest LeadsThe “V” or Chest Leads

99. Anatomical Landmarking ofAnatomical Landmarking of
Chest LeadsChest Leads
V1 – 4th
ICS immediately to the right of the
sternum
V2 – 4th
ICS immediately to the left of
sternum
V3 – Directly between V2 and V4
V4 – 5th
ICS, left mid-clavicular line
V5 – 5th
ICS, left anterior axillary line
V6 – 5th
ICS, left mid-axillary line

100. Cardiac LandmarksCardiac Landmarks

101. Placement of Chest LeadsPlacement of Chest Leads
2
3
4
5

102. The Resultant 12 LeadsThe Resultant 12 Leads

103. Right-sided Chest LeadsRight-sided Chest Leads
V1R– 4th
ICS immediately to the left of the
sternum
V2R – 4th
ICS immediately to the right of
sternum
V3R – Directly between V2R and V4R
V4R – 5th
ICS, right mid-clavicular line
V5R – 5th
ICS, right anterior axillary line
V6R – 5th
ICS, right mid-axillary line
MIRROR IMAGE OF LEFT-SIDED CHEST LEADS

104. Right Ventricular LeadsRight Ventricular Leads

105. Right Ventricular InfarctRight Ventricular Infarct

106. Posterior Chest LeadsPosterior Chest Leads
V7 – 5th
ICS posterior axillary line
V8 – 5th
ICS midscapular line
V9 – 5th
ICS midspinal line
EXTENSION OF LEADS TO LATERAL-POSTERIOR

107. 12-Lead Electrocardiogram12-Lead Electrocardiogram
Lead Options for Clinical Monitoring
and Diagnostic Purposes

108. Lead Options for ClinicalLead Options for Clinical
Monitoring and DiagnosisMonitoring and Diagnosis
CONVENTIONAL: 10 Leads applied with
Standard Limb Lead placement
MODIFIED: 10 Leads applied with
Modified Limb Lead placement (Mason-
Likar, 1966 - for exercise testing)
EASITM
Lead Placement: 5 Leads (derived
12-Lead, using vectorcardiography)

109. Conventional versus ModifiedConventional versus Modified
Lead Placement for 12 LeadLead Placement for 12 Lead
CONVENTIONAL (Standard): Limb
electrode placement on the limbs (forearms
and lower legs)
MODIFIED (Mason-Likar): Limb electrode
placement on the torso (in same locations,
as used for standard continuous ECG
monitoring ... BUT!)
Modified lead placement not to be used for
Diagnostic ECG Interpretation

110. EASIEASI® 12 Lead® 12 Lead
Continuous, Real-time & Trending
12-Lead and ST Segment Monitoring

111. EASIEASI® 12 Lead® 12 Lead
Provides 12-lead data from 5 electrodes,
instead of the standard 10 electrode system.
Uses vectorcardiography, with leads placed
in a modified X,Y, Z configuration
When compared to conventional 5-Lead
ECG monitoring systems, EASI provides
more data and has been shown to be
superior at detecting myocardial ischemia
and cardiac arrhythmias.

112. EASIEASI® 12 Lead® 12 Lead
Innovative, clinically validated approach to
ECG monitoring
Derivation of 12 ECG leads using a 5-
electrode configuration
Science behind EASI is based on Dr.
Gordon Dower’s adaptation of 3-D
vectorcardiography (modified Frank vector
leads)

113. EASIEASI® 12 Lead® 12 Lead
Innovative, clinically validated approach to
ECG monitoring
Derivation of 12 ECG leads using a 5-
electrode configuration
EASI 12-Lead algorithm derives full 12-
lead ECG data to detect and document
cardiac arrhythmias and ST changes under
continuous monitoring conditions across
the care continuum.

114. EASIEASI® 12 Lead® 12 Lead

115. 3 EASI3 EASI® Vectors® Vectors
E = Lower Sternum (Brown)
A = 5th
ICS, Right MAL (Red)
S = Upper Sternum (Black)
I = 5th
ICS, Left MAL (White)
 Lead ES S (-) to E (+)
 Lead AS S (-) to A (+)
 Lead AI I (-) to A (+)

116. 3 EASI3 EASI® Vectors® Vectors

117. Clinical Advantages ofClinical Advantages of
EASIEASI® 12 Lead® 12 Lead
Convenient, stable electrode positions on
obvious anatomical landmarks enhancing
access, accuracy and reproducibility
Need for fewer electrodes increases patient
comfort and mobility
Ease of use results in time savings for care
givers

118. Clinical Advantages ofClinical Advantages of
EASIEASI® 12 Lead® 12 Lead
Innovative lead configuration achieves
superior signal-to-noise ratios
Left precordium is always free … low
interference with clinical procedures
supports consistent 12-Lead information
across the care continuum (physical exam,
CXR, echocardiography, emergency
resuscitation etc.)

119. Clinical Advantages ofClinical Advantages of
EASIEASI® 12 Lead® 12 Lead
Ability to capture dynamic changes that
may be missed using an ECG cart, since
transient events of diagnostic/therapeutic
importance may not persist long enough to
capture.
With EASI, transient events can be
documented with full 12-Lead ECG under
continuous monitoring conditions.

120. EASIEASI® 12 Lead® 12 Lead
When compared to standard 12-Lead
ECG’s, EASI derived 12-Lead is
diagnostically comparable for detection of
cardiac arrhythmias, myocardial ischemia,
and myocardial infarction (the most
common clinical applications for cardiac
monitoring)

121. How Good is EASIHow Good is EASI® 12 Lead® 12 Lead
 99% correlation between standard ECG
monitoring and EASI for Ischemia
 Excellent agreement between 2 methods for Rate,
Rhythm and Intervals
 Perfect agreement for Arrhythmia recognition
 84-99% correlation for Axis determination
 90% and above for acute and prior MI
recognition
 (Undetermined for atrial enlargement and
ventricular hypertrophy … chronic conditions)

122. Interpreting theInterpreting the
EASIEASI® 12 Lead® 12 Lead
 The derived EASI 12-lead is approached the same
way as a standard 12-lead … all principles remain
the same in terms of interpretation.
 EASI should be used as a trending tool & as a
dynamic clinical assessment tool (Monitoring)
 Baseline EASI 12-lead should be compared to any
changes, as is done with a conventional 12-lead.
 EASI 12-lead is not meant to replace a standard
12-lead in terms of diagnostic value, but used in
combination as a clinical assessment tool.

123. Technical ConsiderationsTechnical Considerations
Lead Placement & Vectors (Thoracic versus
Limb)
Millivolt and Standard
Filters

124. Back to the Application Stuff!Back to the Application Stuff!

125. Clinical Correlation:Clinical Correlation:
Arterial Blood Supply & ECGArterial Blood Supply & ECG

126. Right VentricleRight Ventricle
Right Coronary Artery (RCA)

127. Inferior Wall of Left VentricleInferior Wall of Left Ventricle
Right Coronary Artery (RCA)

128. Posterior Wall of Left VentriclePosterior Wall of Left Ventricle
Right Coronary Artery (RCA)
(Left Circumflex)

129. Anterior Wall of Left VentricleAnterior Wall of Left Ventricle
Left Anterior Descending (LAD) branch of
Left Coronary Artery
Septal Branch

130. Lateral Wall of Left VentricleLateral Wall of Left Ventricle
Circumflex branch of Left Coronary Artery

131. ApexApex
RCA or LAD or Circumflex

132. A Diagrammatic PerspectiveA Diagrammatic Perspective
It is the LEFT ventricle which contributes the forces when viewing the 12 Lead ECG

133. Cube ConceptCube Concept
Septal/Anterior
Apical
Lateral
Inferior
Endocardial
(Posterior)
Each “face” of the cube represents a different Left Ventricular wall
Right
Ventricle

134. Inferior LeadsInferior Leads
Leads II, III and aVF
Leads III, aVF, II

135. Anterior or Anteroseptal LeadsAnterior or Anteroseptal Leads
V1 through V6 (septal + anterior + apical)
V1-V2 Septal; V3-V4 Anterior or Mid-
Precordial;V5-V6 Apical
V1, V2, V3, V4 and V5, V6

136. Apical (Low Lateral) LeadsApical (Low Lateral) Leads
V5 and V6
(Lead II)

137. Lateral LeadsLateral Leads
Lead I and aVL

138. (Posterior Leads)(Posterior Leads)
Viewed as mirror-image changes in V1-V2

139. Endocardial LeadsEndocardial Leads
aVR!
(aVL on occasion)

140. Right Ventricular LeadsRight Ventricular Leads
V3R and V4R!!
(ST > Lead III than in Lead II and aVF)*

141. The “Cone” PerspectiveThe “Cone” Perspective
L. Schamroth

142. ““OtherOther Fundamentals"Fundamentals"
Polarity

143. PolarityPolarity
An impulse traveling toward a positive
electrode will be recorded as positive … an
impulse traveling away from a positive
electrode will be recorded as negative
There are, however, varying degrees of
positivity and negativity represented by
various ECG waveforms

144. PolarityPolarity
 A lead measures
electrical activity
within an electrical
field
 The field is divided
into a positive half and
a negative half
Any impulse that falls within the positive half of the electrical field will result in a positive
complex, and any that fall within the negative half will result in a negative complex.

145. Positive & Negative FieldsPositive & Negative Fields
 The more PARALLEL
the impulse is to the
lead orientation, the
TALLER the complex.
As the impulse becomes more PERPENDICULAR to the lead orientation, it becomes more
ISOELECTRIC

146. ExploringExploring thethe ElectricalElectrical
Activation of the HeartActivation of the Heart

147. Wave of DepolarizationWave of Depolarization
The anatomic position of the heart must
also be considered, since it is the actual
position of the heart that influences the net
direction of electrical activity.
It is this NET direction that is recorded on
the ECG

148. Wave of DepolarizationWave of Depolarization
 Frontal Plane view of
mean wave of
depolarization
 Left-sided leads will
record the activity
opposite to Right-
sided leads

149. Wave of DepolarizationWave of Depolarization
 Even on a single
plane, electrical
activity can be viewed
in several directions at
once.
 Imagine a “tug-of-
war” between the LV
and RV

150. Ventricular DominanceVentricular Dominance
To apply this concept to venticular
activation, recall that the right
ventricle is a thin-walled chamber
with only one conduction pathway.
The left ventricle is a thicker muscle
mass and has two branches in it’s
conduction system.

151. Net Direction or VectorNet Direction or Vector
 Even though the
electrical activity of
the heart is travelling
in many directions at
once, one general
direction predominates
and can be determined
by averaging all of the
forces.

152. Normal ComponentsNormal Components
&& VectorsVectors

153. Introducing the 12 LeadIntroducing the 12 Lead
ElectrocardiogramElectrocardiogram
“Mapping the Heart’s Spark”

155. "The Traditional 12 Leads""The Traditional 12 Leads"
FRONTAL PLANE:
I
II
III
aVR
aVL
aVF

156. Lead I (Lateral)Lead I (Lateral)
0 degrees (LCx)0 degrees (LCx)
RA- …. LA+
P upright
Q small or none
R dominant
S < R or none
ST Isoelectric (+1 to –0.5)
T upright

157. Lead II (Inferior/Left)Lead II (Inferior/Left)
+ 60 degrees (RCA)+ 60 degrees (RCA)
RA- …. LL+
P upright
Q small or none
R dominant
S < R or none
ST Isoelectric (+1 to –0.5)
T upright

158. Lead III (Inferior/Right)Lead III (Inferior/Right)
+120 (RCA)+120 (RCA)
LA- … LL+
P upright, flat, diphasic, inverted
Q small or none
R none, diphasic to dominant
S none to dominant
ST Isoelectric (+1 to –0.5)
T upright, flat, diphasis, inverted

159. Lead aVR (Endocardial)Lead aVR (Endocardial)
- 150 degrees (global)- 150 degrees (global)
RA+
P inverted
Q small, none, large
R small or none
S dominant
ST Isoelectric (+1 to –0.5)
T inverted

160. Lead aVL (Lateral)Lead aVL (Lateral)
- 30 degrees (LCx)- 30 degrees (LCx)
LL+
P upright, flat, diphasic, inverted
Q small, none, large
R small, none, dominant
S small, none, dominant
ST Isoelectric (+1 to –0.5)
T upright, flat, diphasic, inverted

161. Lead aVF (Inferior)Lead aVF (Inferior)
+90 degrees (RCA)+90 degrees (RCA)
LL+
P upright, flat, diphasic, inverted
Q small or none
R small, none, dominant
S small, none, dominant
ST Isoelectric (+1 to –0.5)
T upright

162. "The Traditional 12 Leads""The Traditional 12 Leads"
HORIZONTAL PLANE:
V1
V2
V3
V4
V5
V6

163. Lead V1 (Septal)Lead V1 (Septal)
LAD-Septal branchLAD-Septal branch
4 ICS RSB
P upright, flat, diphasic
Q none, may be QS
R < S or none
S dominant
ST 0 to +3
T upright, flat, diphasic, inverted

164. Lead V2 (Septal)Lead V2 (Septal)
LAD-Septal branchLAD-Septal branch
4 ICS LSB
P upright
Q none
R < S
S dominant
ST 0 to +3
T upright, diphasic, inverted

165. Lead V3 (Anterior)Lead V3 (Anterior)
LADLAD
Between V2 and V4
P upright
Q small or none
R ~ S
S ~ R
ST 0 to +3
T upright

166. Lead V4 (Anterior)Lead V4 (Anterior)
LADLAD
5ICS LMCL
P upright
Q small or none
R > S
S < R
ST +1 to 0.5
T upright

167. Lead V5 (Apical)Lead V5 (Apical)
VariableVariable
5ICS LAAL
P upright
Q small
R Dominant
S small (< V4)
ST +1 to 0.5
T upright

168. Lead V6 (Apical)Lead V6 (Apical)
VariableVariable
5ICS MAL
P upright
Q small
R Dominant
S none
ST +1 to 0.5
T upright

169. “Putting the Leads Together”
Frontal Plane
Horizontal Plane

170. ““AdditionalAdditional Leads"Leads"
HORIZONTAL PLANE: Right-Sided Leads
V1R
V2R
V3R
V4R
V5R
V6R

171. ““AdditionalAdditional Leads"Leads"
HORIZONTAL PLANE: Posterior Leads
V7
V8
V9

172. "Systematic Approach""Systematic Approach"
to the Electrocardiogramto the Electrocardiogram

173. A Systematic ApproachA Systematic Approach
Establish underlying rhythm (atrial &
ventricular rates, PR interval, AV
conduction)
Measure the QRS (including VAT) and QT
interval
Determine the Mean Frontal Plane Axis

174. A Systematic ApproachA Systematic Approach
Screen For:
 Conduction Delays (based on prior assessment)
– Atrioventricular and/or Intraventricular
 Presence of Ischemia, Injury & Infarction
 Endocardial or Epicardial abnormalities
 Chamber Enlargement
– Atrial and/or Ventricular
 Other
– Electrolyte Abnormalities
– Drug Effects

175. A Systematic ApproachA Systematic Approach
Interpretation and Documentation:
Primary Rhythm
Conduction Disturbances
Secondary Rhythm (e.g. junctional escape)
Other abnormalities (ST, T, QT)
Significance?
Management?

176. The Electrical AxisThe Electrical Axis

177. Axis … No Problem!Axis … No Problem!

179. The Electrical AxisThe Electrical Axis
Intensity and direction that the electrical
impulse takes during depolarization &
repolarization
The general, mean or dominant direction of
the various vectors is known as the MEAN
VECTOR, and electrocardiographically as
the MEAN QRS AXIS

180. The Electrical AxisThe Electrical Axis
The electrical axis is determined by:
Magnitude
Direction
Polarity
It’s direction is determined from the frontal
plane (“rotation” on the horizontal plane)

181. Significance of theSignificance of the
Electrical AxisElectrical Axis
“The use of the Electrical axis in the clinical
interpretation of the electrocardiogram
constitutes a most important diagnostic
procedure and elevates electrocardiographic
interpretation from the empirical to the
deductive.”
Leo Schamroth. The Electrical Axis. It’s determination and significance.

182. Application of QRS AxisApplication of QRS Axis
Differentiation of different types of MI’s
Ventricular Dominance
Ventricular Ectopy vs Aberrancy
Hemiblocks
Pacemaker Function
W-P-W Syndrome
Dextrocardia

183. (Application of P Wave Axis)(Application of P Wave Axis)
P pulmonale
P congenitale
Retrograde activation of the atrium

184. (Application of T Wave Axis)(Application of T Wave Axis)
Ventricular hypertrophy
Coronary insufficiency
Fully evolved phase of acute myocardial
infarction

185. (Application of ST Axis)(Application of ST Axis)
Infarction
Subendocardial vs. Subepicardial injury

186. Calculating the MeanCalculating the Mean
QRS AxisQRS Axis

187. Determination of the AxisDetermination of the Axis
There are several methods for estimation of
the frontal plane axis.
Ideal method would be both the most
simplistic and accurate, thus lending itself
to efficient clinical application.

188. Steps for Calculation of AxisSteps for Calculation of Axis
1. Most equiphasic or smallest complex on
frontal plane?
2. Which lead is 900
(perpendicular) to this
lead?
3. Is this lead mostly positive or negative? If
positive, go to the positive pole … if
negative, go to the negative pole
4. Axis?

191. Lead AssociationsLead Associations
For any lead, there is another lead that is
always perpendicular to it, and visa versa
Perpendicular to a bipolar lead is always an
associated unipolar lead, and visa versa
Example: look at Lead II … what lead is
perpendicular to Lead II? (Lead II also
then must divide that lead into a positive
and a negative field)

192. Quick AssociationQuick Association

193. Memory TrickMemory Trick
I … aVF
II … aVL
III … aVR

194. Determination of AxisDetermination of Axis

195. Abnormal Axis orAbnormal Axis or ReversedReversed
Arm ElectrodesArm Electrodes?!??!?

196. Determination of AxisDetermination of Axis
1
2

197. Determination of AxisDetermination of Axis
3
4

198. Determination of AxisDetermination of Axis
5
6

199. Determination of AxisDetermination of Axis
7
8

200. Determination of AxisDetermination of Axis
9
10

201. Determination of theDetermination of the
Electrical AxisElectrical Axis

202. Axis DeviationAxis Deviation

203. ECG Patterns of Ischemia,ECG Patterns of Ischemia,
InjuryInjury && InfarctInfarct
Clinical Recognition

204. Ischemia, Injury & InfarctIschemia, Injury & Infarct
Myocardial Oxygenation
– Supply
– Demand
Regional versus Global deficits

205. Ischemia, Injury & InfarctIschemia, Injury & Infarct
Myocardial ischemia is often missed in
cases of silent ischemia
ST segment monitoring, though not the
most specific or sensitive, is the only
technology that can be applied continuously
(it is also non-invasive)
Silent Ischemia is as clinically significant as
that associated with chest pain … Total!

206. Ischemia, Injury & InfarctIschemia, Injury & Infarct
One must also correlate the coronary
arterial blood supply to the various
structures to the regions on the ECG and
other clinical considerations …
Without making this correlation, clinical
significance of ECG changes is
questionable.

207. Right Coronary ArteryRight Coronary Artery
Right Atrium
Right Ventricle
Inferior wall of Left Ventricle
Posterior wall of Left Ventricle
Posterior 1/3 of Intra-Ventricular Septum
SA node in 65% of population
AV node in 90% of population
Posteroinferior Division of Left Bundle
Branch

208. Left Anterior DescendingLeft Anterior Descending
Branch of Left Coronary ArteryBranch of Left Coronary Artery
Anterior wall of Left Ventricle
Anterior 2/3 of Intra-Ventricular Septum
(Apex of the Left Ventricle)
Bundle of His
Right Bundle Branch
Both Divisions of Left Bundle Branch

209. Left Circumflex Branch of LeftLeft Circumflex Branch of Left
Coronary ArteryCoronary Artery
Left Atrium
Lateral wall of Left Ventricle
(Posterior wall of Left Ventricle)
(Posterior 1/3 of Intra-Ventricular Septum)
SA node in 45% of population
AV node in 10% of population

210. Coronary CirculationCoronary Circulation
One must remember that this is a general
description of coronary circulation, and
applies to the majority of the population.
Individual variations in the coronary
vasculature are infinite, which explains the
varying ECG manifestations that may be
seen!

211. ECG ManifestationsECG Manifestations
The surface electrocardiogram (ECG) is the
most common noninvasive diagnostic
technique utilized to determine the presence
and location of myocardial infarction.
The limitations include not having enough
leads to view all regions, being an
intermittent assessment, and non-specific
findings.

212. The ECG as a Diagnostic ToolThe ECG as a Diagnostic Tool
The ECG is but one clinical assessment tool
used in the diagnosis of Acute Myocardial
Ischemia, Injury and Infarction.
Used in combination with History, Clinical
Assessment and Biochemical Markers, it
becomes an invaluable tool.

216. ZonesZones
Infarct, Injury & IschmiaInfarct, Injury & Ischmia
Note: Degree of involvement between Endocardium and Epicardium

217. Continuous ST-SegmentContinuous ST-Segment
Monitoring:Monitoring:
Protocol for PracticeProtocol for Practice

218. Repolarization the Key!Repolarization the Key!
Repolarization requires sufficient energy in
the form of ATP …
The Ventricular repolarization process is
normally reflected by the T wave (and U
wave)
Early repolarization abnormalities will
manifest itself in the ST segment …
resulting in ST segment changes
(repolarization wave shifts leftward)

219. What is Isoelectric?What is Isoelectric?
T-P Segment is preferable

220. What is ST Deviation?What is ST Deviation?

221. ST Segment MonitoringST Segment Monitoring
Ideally, ST segment monitoring should also
be done on a continuous basis in order to
continuously monitor & evaluate patient
progress.
Continuous computerized ST segment
monitoring is available for all 12 Leads
using “EASI 12 Lead” (5 Electrodes) or via
a Modified 12 Lead (10 Electrodes) using
specific algorithms.

222. ST Segment MonitoringST Segment Monitoring
 ST Index: avF, V2 and V5 (common lead
combination for detection of acute ischemia or
injury)
 Offers 98.4% sensitivity for acute ischemic events
 Increased sensitivity (99.3%) using Leads
III/V2/V5 or III/V2/V4
 Lead III is more sensitive for RV changes than
avF!

223. ST Segment MonitoringST Segment Monitoring
If an alarm is triggered due to an ST
segment change, only a clinician, not the
monitor, can determine the seriousness of
the event.
To ensure peak performance, the staff
should be aware of the interventions and
adjustments they can implement to enhance
the ST algorithm’s performance &
accuracy!

224. CAUTION …CAUTION …
ECG Settings!ECG Settings!

225. Sometimes it Hard to TellSometimes it Hard to Tell
What’s What … They LookWhat’s What … They Look
Similar!Similar!

226. Epicardial versusEpicardial versus
Endocardial?Endocardial?
Ischemia & InjuryIschemia & Injury
PatternsPatterns

228. ST’s up or down?ST’s up or down?
ST depression … endocardial involvement
ST elevation … epicardial involvement

229. From Who’s Perspective?From Who’s Perspective?
aVR = Endocardial Lead
(sometimes aVL also)
All other Leads = Epicardial Leads

230. ST changes Transient orST changes Transient or
Persistent?Persistent?
Transient ST changes … Anginal
syndromes
Persistent ST changes … Infarction process
(Rule out Aneurysm, Pericarditis)

232. Regional or GlobalRegional or Global
ST Changes?ST Changes?
Isolated to a specific region (remember
correlation to coronary arterial supply)
Widespread ST segment and/or T wave
changes may be seen in such conditions as
Pericarditis and Coronary Insufficiency.

234. Persistent ST ElevationPersistent ST Elevation
Concave or Convex?Concave or Convex?
Pericarditis-concave … Infarction-convex
QT Short? QT Long?

235. Acute PericarditisAcute Pericarditis

236. Indicative versus ReciprocalIndicative versus Reciprocal
ST ChangesST Changes
 Remember the cube concept … opposite walls can
show the opposite changes. Remember also,
associated leads (I/aVF, II/aVL, III/aVR) will
 ST elevation in one wall will show ST depression
in the opposite wall
 If you can turn the ST “upside down” from one set
of leads and match it to the ST in the opposing
wall, it’s most likely reciprocal … rather than a
separate process associated with a different
coronary artery.

237. Reciprocal LeadsReciprocal Leads
Think “Inside the Box”Think “Inside the Box”
Apex

238. Reciprocal PatternsReciprocal Patterns
Question: If a transmural infarct is on in the inferior wall, which leads
will show a reciprocal ST depression?

240. Can ST’s look abnormal in theCan ST’s look abnormal in the
Healthy Heart?Healthy Heart?
Early repolarization can often be found as a
normal variant, especially in the young,
blacks and athletes … this can mimic
pericarditis
Can also occur in rapid heart rates
Look at baselines and trends!
Be aware of normal variants

241. Manifestations of MyocardialManifestations of Myocardial
IschemiaIschemia
Subendocardial Myocardial Ischemia (Classic
Angina):
– Transient ST segment depression in the leads
facing the area
– T wave changes

242. Physiologic vs. Pathologic S-TPhysiologic vs. Pathologic S-T
Segment DepressionSegment Depression

243. Myocardial Ischemia –Myocardial Ischemia –
Coronary InsufficiencyCoronary Insufficiency
 Pathological
junctional ST segment
depression
 Hyperacute T-wave
(tall, peaked &
symmetrical)
 U-wave inversion

244. Exercise-Induced IschemiaExercise-Induced Ischemia

245. Manifestations of MyocardialManifestations of Myocardial
IschemiaIschemia
Prinzmetal’s (Variant) Angina:
– Transient ST segment elevation in the leads
facing the area
– ST elevation (injury pattern involving full
thickness of myocardium up to and including
the epicardium)
– Convex ST shape
– (R wave often increases in amplitude in an
injury pattern)

246. Variant Angina (Prinzmetal’s)Variant Angina (Prinzmetal’s)
A. During pain B. A few minutes after pain resolved

247. Infarction with or withoutInfarction with or without
ST elevation?ST elevation?
STEMI … ST-Elevated (Acute) MI
NSTEMI …. Non-ST-Elevated (Acute) MI

248. IIdentifying thedentifying the
“Non-“Non-TransmuralTransmural” or” or
Non-ST-ElevatedNon-ST-Elevated
MMyocardial Infarctionyocardial Infarction

249. Non-ST-Elevated MINon-ST-Elevated MI
(NSTEMI)(NSTEMI)
Persistent ST depressions and/or
Persistent T wave inversion
No Q wave
Loss of R wave amplitude

250. Non-ST-Elevated MINon-ST-Elevated MI

251. NSTEMINSTEMI

252. IIdentifying thedentifying the ““TransmuralTransmural” or” or
ST-ElevatedST-Elevated
Myocardial InfarctionMyocardial Infarction

253. ST-Elevated MI (STEMI)ST-Elevated MI (STEMI)
Persistent ST elevation and/or
Hyperacute T-wave changes … progressing
to T-wave inversion
Development of a pathological Q wave (if
untreated)
Loss of R wave amplitude

254. Evolving Inferior Wall STEMIEvolving Inferior Wall STEMI

255. Why a Q wave?Why a Q wave?
The “Electrical Window” Concept

256. Why Not a Q wave?Why Not a Q wave?
Loss of R wave amplitude is just as significant!

257. Locating the Area of InfarctionLocating the Area of Infarction
ECG Manifestations and
Clinical Implications

258. I Should Be Able to do This …I Should Be Able to do This …
Right!?!Right!?!

266. ST SegmentsST Segments
ST Trending and Mapping –
Expanding our Clinical
Monitoring for ACS
Acknowledgement: Philips Medical Systems – ST MapTM

267. Continuous ST SegmentContinuous ST Segment
MonitoringMonitoring
(2009)

268. ST Segment Monitoring –ST Segment Monitoring –
Widely Underused!Widely Underused!
CLASS I:
Acute Coronary Syndromes
Chest Pain or Anginal Equivalent
Syndromes
PTCA with suboptimal Angiographic
results
Variant Angina (Coronary Vasospasm)

269. ST Segment Monitoring –ST Segment Monitoring –
Widely Underused!Widely Underused!
CLASS II:
Postacute MI
Non-urgent Percutaneous Coronary
Intervention
High Risk for Ischemia after Cardiac or
Noncardiac Surgery
High Risk for Ischemia resulting from
Congential or Acquired Conditions (eg.
Trauma, Cardiotoxic drugs, Myocarditis …)

270. ST Segment Monitoring –ST Segment Monitoring –
Technically more difficult …Technically more difficult …
CLASS III:
LBBB, or intermittent RBBB
Ventricular Paced Rhythm
Rhythms that Obscure the ST segment
(coarse atrial fibrillation or flutter)

271. Remember that ST segment deviation is not always
an indication of ischemia/infarction…
ST elevation
 Myocardial injury
 Pericarditis
 Dyskinetic ventricle
 Ventricular aneurysm
(persistent V1-V4)
 J-point elevation (normal young
patients)
ST depression
 Ischemia
 Tachycardia
 Subendocardial infarction
 Posterior wall MI (reciprocal)
 Carbon monoxide poisoning
 Antiarrythmic drugs (eg.
Lanoxin)
 Mitral valve prolapse
 Wolf-Parkison-White syndrome
 Hypokalemia

272. Who is using ST segmentWho is using ST segment
monitoring?monitoring?
Nursing survey in 2001 found…
 Only 50% units are using ST segment monitoring consistently
 Attributed to:
– staff skill level; lack of expertise for interpretation; “trickle” down effect (from
research to bedside implementation); Too many false alarms; Cost prohibitive;
Clinician appreciation of measurement
“We hypothesized that ST segment monitoring, although clearly
sensitive for detecting myocardial ischemia, may not provide
clinically useful information in a user-friendly manner”
Survey of use of ST-segment monitoring in patients with acute coronary syndromes
Patton et al, AJCC Vol 10, No1, Pg 23-34

273. ST Segment displays…ST Segment displays…
A nice overview but what
about…
 Assistance with pattern
recognition.
 The location of the ST
changes.
 The evolution of the ST
changes.
12-Lead Display screen
ST Baseline Window
ST Segment Display Screen

276. Cardiologists & ContinuousCardiologists & Continuous
ST-Segment MonitoringST-Segment Monitoring

277. “ST Map” offers a solution…
ST “Map” = ST “Multivariate Axis Plotting”

278. ““ST Map”ST Map”™™
ENHANCED CLINICAL RECOGNITION!
Assists with Pattern Recognition (more
intuitive)
Assists with Locating the area of
involvement (diagrammatic representation)
Assists with trending, showing evolutionary
changes

279. Eindhoven’s Triangle
Frontal Plane LeadsFrontal Plane Leads
Limb Leads
Augmented Limb Leads
Inferior
Superior
Left
Right

280. Horizontal Plane LeadsHorizontal Plane Leads
Precordial (Chest) Leads
Posterior
Anterior
Left
Right

281. Creating the Multivariate AxisCreating the Multivariate Axis
Plot (Map)Plot (Map)

282. Creating the Multivariate PlotCreating the Multivariate Plot

283. …the complete picture (Frontal & Horizontal)
Limb Leads Chest Leads
(Must have minimum of 3 leads active for the ST Map to be displayed
- i.e 3 chest leads for chest map, 3 limb leads for limb map)
Inferior
Apical
Septal
Lateral
Anterior

284. Clinical and ECG Correlation…Clinical and ECG Correlation…
Anterior view
Location Leads Reciprocal Artery involved
ST elevation ST depression
Inferior II, III, aVF I, aVL Right Coronary Artery
Lateral I, aVL, (V5, V6) V1, V2 Circumflex
Large Anterior V1, V2, V3, V4, I, aVL II, III, aVF Left Coronary Artery
Anterolateral I, aVL, V4, V5, V6 II, III, aVF Left Anterior Descending
Anteroseptal V1, V2, V3 None Left Anterior Descending

285. ST Map on the 12-lead DisplayST Map on the 12-lead Display

286. ST Map (Current) WindowST Map (Current) Window
To hide
baseline

287. ST Map (Trend) WindowST Map (Trend) Window
Sends the content of the ST Map
window to the configured printer.

288. ST (Current) PrintoutST (Current) Printout

289. ST (Trend) PrintoutST (Trend) Printout

290. ST Map report forST Map report for
documentation…documentation…

291. Application of ST MapApplication of ST Map

292. A Case StudyA Case Study
Clinical Application of ST Segment Trending
using “ST Map”

293. Case StudyCase Study
A 62-year-old male presents to the Emergency Room with a
two-hour history of developing chest pain while gardening.
On arrival, patient is anxious, pale and sweating. He is also nauseated and states he
feels dizzy, complaining of chest & jaw pain (pain score 4 out 5) associated
with left arm numbness.
The patient is connected to the monitor & the following vital signs are recorded:
HR 62
RR 28 (SpO297%)
BP 90/50
T 369
ST Map shows the following localization…

294. ST Map current view in acuteST Map current view in acute
phase…phase…
ST Elevation
ST Depression

295. ST Elevation
ST Depression
12 lead ECG on arrival in the12 lead ECG on arrival in the
Emergency RoomEmergency Room

296. Location of ST changes on theLocation of ST changes on the
ECG…ECG…
Location Leads Reciprocal Artery involved
ST elevation ST depression
Inferior II, III, aVF I, aVL Right Coronary Artery
Lateral I, aVL, V5, V6 V1, V2 Circumflex
Anterior V1, V2, V3, V4, I, aVL II, III, aVF Left Coronary Artery
Anterolateral I, aVL, V4, V5, V6 II, III, aVF Left Anterior Descending
Anteroseptal V1, V2, V3 None Left Anterior Descending

297. After evaluating the presenting symptoms,
strong family history, & 12 lead ECG changes
a diagnosis of acute inferior myocardial
infarction is made.
The patient is prepared for an emergency
angiography with possible angioplasty.

298. ST Map current view usingST Map current view using
reference baseline to monitor forreference baseline to monitor for
changes during angioplasty…changes during angioplasty…
Reference baseline
ST Elevation

299. Angiogram showed a 85% occlusion of proximal
right coronary artery and a coronary stent was
successfully deployed. ReoPro™ was given as
per hospital guidelines.
The patient’s condition is stable and he is
transferred to the Coronary Care Unit for close
observation.

300. Three hours post angioplasty…Three hours post angioplasty…
ST Elevation

301. Using ST Map trends forUsing ST Map trends for
continued management…continued management…

302. 12 hours post angioplasty, the patient had a brief
episode of central non-radiating chest pain at rest not
associated with any other signs and symptoms.
The trending feature on the ST Map was set for 12
second snapshots to observe closely the changes in
the ST segments.
The pain resolved spontaneously.

303. ST Map trends using 12 secondST Map trends using 12 second
snapshots to observe closely STsnapshots to observe closely ST
changes…changes…

304. This episode of chest pain resolved
spontaneously and the patient remained pain-
free.
The ST Map at 24hrs post angioplasty, showed
that the inferior ST segments, were nearly
back to normal and that the lateral changes had
resolved completely.

305. ST Map at 24 hours shows theST Map at 24 hours shows the
ST changes nearly back toST changes nearly back to
normal…normal…

306. 12 lead serial ECG confirms ST12 lead serial ECG confirms ST
Map findings…Map findings…
Residual Q wave & T wave inversion

307. The patient remained pain-free for the remainder
of his stay in the CCU. After spending time on
the telemetry floor, the patient was discharged
home 7 days post angioplasty.

308. “Using ST MapTM
for monitoring ST segment monitoring, provides
clinically useful information in a user-friendly manner”
Survey of use of ST-segment monitoring in patients with acute coronary syndromes
Patton et al, AJCC Vol 10, No1, Pg 23-34
TM
Philips Medical Systems

310. Identifying IntraventricularIdentifying Intraventricular
Conduction DefectsConduction Defects
RBBB, LBBB, LAH, LPH,
Bifascicular & Trifascicular Blocks

311. Remember the Basics!Remember the Basics!

313. Remember the Basics!Remember the Basics!
Normally Left before Right!

314. Remember the Basics!Remember the Basics!

315. Remember the Basics!Remember the Basics!

316. Right Bundle Branch BlockRight Bundle Branch Block

317. Right Bundle Branch BlockRight Bundle Branch Block
 Normal variant
 Ischemic heart disease
 Acute myocardial infarction
 Acute coronary insufficiency
 Trauma
 Acute heart failure
 Intracardiac catheter (PA catheter)
 Right heart catheterization

318. Causes of RBBBCauses of RBBB
Cardiomyopathy
Degenerative disease of the conduction
system
Acute Infective processes
Parasites
Rheumatic heart, Syphilis, Tumors,
Congenital lesions
Surgery (Tetralogy of Fallot, VSD)

319. Salient Features of RBBBSalient Features of RBBB
Wide QRS (> .10 sec)
Increased VAT (> 0.04 sec) in RV leads
rsR’ or qR in V1
T opposite polarity to QRS in RV leads
Wide S wave in left-sided leads (V6, I, II)

320. Left Bundle Branch BlockLeft Bundle Branch Block

321. Causes of LBBBCauses of LBBB
Not as common as Right Bundle Branch
Block due to two separate fascicles
(posterior fascicle has a dual blood supply
and is much thicker)
Causes are the same as for Right Bundle
Branch Block, but involving the Left
Ventricle or Surgery to the Aortic Valve.

322. Salient Features of LBBBSalient Features of LBBB
Wide QRS (> .10 sec)
Increased VAT (> 0.04 sec) in LV leads
Wide R or notched “M-shaped R” in Left-
sided leads (V5, V6, I, aVL, II)
T opposite polarity to QRS in LV leads
Wide S or QS wave in right-sided leads
(V1)

328. The Ultimate Test!The Ultimate Test!

329. To be continued …To be continued …

330. I’m 100% saturated!I’m 100% saturated!

332. Thank you!Thank you!