Transcript File - Respiratory Therapy Files

12- Lead
Process for Interpreting a 12-lead
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Look at your patient
Determine rhythm: NSR, Afib, etc.
Determine wall specific ST, T wave changes
Identify R wave progression as normal or not
Determine axis of “depolarization”: normal vs right axis deviation vs left axis
deviations.
• Look for bundle branch blocks
– RT vs LT
– Fascicular
• Look for hypertrophies
– Atrial
– Ventricular
• Other stuff
– pericarditis
– Etc.
Cardiac Anatomy
Superior
vena cava
Pulmonary
veins
Sinoatrial (SA)A node
Atrial muscle
Atrioventricular (AV) node
Left atrium
Mitral valve
Internodal
conducting
tissue
Tricuspid valve
Ventricluar
muscle
Inferior
vena cava
Purkinje
fibers
Descending aorta
The Normal EKG
0.12-0.2 s
approx. 0.44 s
approx. 0.44 s
0.12-0.2 s
QT
PR
SA
node
Atria
AV
node
R
Atrial muscle
depolarization
T
P
Q
Purkinje
Ventricle
S
Ventricular muscle
depolarization
Ventricular
muscle
repolarization
Limitations
• Sometimes 1 lead can provide clear, accurate
interpretation
• Sometimes, more than one lead is needed for
accurate interpretation
• In the case of an MI, multiple leads are definitely
needed
• Sometimes, 12-leads do not provide adequate
information for definitive diagnosis
12-Lead vs. Strip
• More leads to look at several parts of the heart
• Format: 3 row by 4 column = 12 views
• 12-lead provides only a 2.5 second view of each
lead
– Adequate to identify ischemia, injury or infarction
pattern
– Catches at least one representative complex
– Cannot be used to successful assess rate and rhythm
• So a continuous strip is added at the bottom of the print out
Time & Voltage
• Duration
• Amplitude
• Configuration
Time: Horizontal
• Time is usually expressed in SECONDS for
typical rhythm interpretation.
• IE: Narrow QRS complex < 0.12 sec
• However, the 12-lead expresses time in
milliseconds
• The smaller the unit of measurement, the more
accurate the measurement
• Remember your metric system conversions
.12 sec = 120 ms, moving the decimal 3 spaces
Voltage: Vertical
• Same measurement expression as used for
typical interpretation
• 1 small box = 1 millimeter (mm)
• 1 large box = 5 mm
Voltage: Vertical
• Standard calibration:
– 1 millivolt (mV) = 10 mm deflection
= 10 small boxes
= 2 large boxes
• If calibration is increased or decreased, so is
the deflected wave
Lead Placement
Lead placement (usually)
• White RA-right arm
• BlackLA-left arm
• Green RL-right leg
• RedLL-left leg
• BrownC-chest
Bipolar Limb Leads
• Lead 1
Left Arm View
• Lead 2
Left Leg View
• Lead 3
Right Leg View
Unipolar Limb Leads
• aVR
Right Shoulder
• aVL
Left Shoulder
• aVF
Foot View
Frontal Planar View
Lead Placement: Chest leads
(brown)
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V1 - 4th Ics, Rsb
V2 - 4th Ics, Lsb
V3 - Between V2-4
V4 - 5th Ics, MCL
V5 - Between V4-6
V6 - 5th Ics, MAL
Lead Placement
Horizontal View
View Obtained From Each Lead
is Determined by:
1. Left ventricular dominance
• Indirect measurement
• Measures net of positive and negative
currents
• So it is a measurement of the “tug of war”
between the right and left ventricle
• Which one will win?
View Obtained From Each Lead
is Determined by:
Left ventricular dominance continued:
• The QRS complex is a result of the LV
electrical activity that is left over after
canceling out all of the electrical activity
of the RV
• Only about 20% of LV electrical activity
is measured
View Obtained From Each Lead
is Determined by:
2. Position of the positive electrode
• Position determines which portion of the
LV is viewed.
• Certain leads view the same portion but
at a different angles or from a different
perspective because each lead has a
different position for its negative electrode
Vectors
• Each electrode reads
AVERAGE current
• Each electrode reads
Unique perspective
• Summation Vector =
sum of all vectors
• Magnitude of Vector
= Relative Mass
Hexaxial Reference
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Lead I = 0
Lead II = +60
Lead III = + 120
aVR = -150
aVL = -30
aVF = + 90
Memorize
Lead
View
I, aVL, V5, V6
Lateral
II, III, aVF
Inferior
V1, V2
Septal
V3, V4
Anterior
QRS COMPLEX
• Represents time required for
depolarization of the ventricles
• Measured from the beginning of the QRS
complex to the point where the last wave
of the complex begins to flatten
• J-point: the junction between the QRS
complex and the ST segment
QRS COMPLEX
• Normal:
– Predominately positive in lead II
– .10-.12 seconds or less in duration (note error in
book, it says 10 seconds)
– How many milliseconds is this?
– 2-15 mm in amplitude depending on the lead
– Composed of 3 deflections which may or may not
always be present
• Q wave: negative
• R wave: positive
• S wave: negative
QRS COMPLEX
• The width is reflective of the amount time
required for an electrical impulse to travel
through the ventricles and depolarize the
myocardium
• If the impulse in not able to follow the natural
path of conduction, it is diverted, and thus takes
longer to produce depolarization.
– QRS > 0.10 to 0.12 sec
– How many milliseconds is this?
QRS COMPLEX
• Variations of the QRS complex:
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Q and R wave with no S wave
R wave with no Q nor S wave
QS complex: entire complex is negative
More than one R or S wave: the second R or S
is term R prime (R’) and S prime (S’)
• To be labeled separately, the wave must cross the
baseline. If it does not, it is called a notch
Components of the QRS
Complex
QRS COMPLEX
• Capital letters indicate a wave 5 mm in
amplitude or more
• Lower case letters indicate a wave less than
5 mm in amplitude
Sequence of Depolarization
• 1-atria depolarize
• 2-septum depolarizes
• 3-Summation vector
Ventricular
Depolarizaton
• 4-Summation vector
Ventricular
Repolarization
Depolarization Waveforms
• Wave of Depolarization TOWARD electrode
---------Positive Deflection--------
Depolarization Waveforms
• Wave of depolarization ACROSS the electrode
----------Biphasic or Isoelectric-----------
Depolarization Waveforms
• Wave of depolarization AWAY from electrode
---------NEGATIVE deflection----------
R Wave Progression
• The morphology of the QRS complex
changes when progressing from V1 view to
V6 view
• Initially, it is mostly negative with a very
small positive r wave (rS complex)
• It begins to progress more positively at the
transition zone (V3-V4)
Poor R wave progression
ST SEGMENT
• Represents the end of ventricular
depolarization and the beginning of its
repolarization
• Begins with the end of the QRS complex
and ends with the onset of the T wave
• Remember that the J-point represents the
end of the QRS complex
J point
ST segment Elevation: ST segment deviation
is measured 0.04 seconds after the J-point from the baseline
ST SEGMENT
• Normal:
– Isoelectric
• Abnormal:
– Elevation or depression by 1 mm in amplitude above
or below the isoelectric line (measured 2 small boxes
or 0.08 sec after the J-point)
• Elevation: MI, vasospasm (Prinzmetal’s angina),
percarditis, ventricular aneurysm, or normal in some young
males due to early ventricular repolarization
• Depression: Ischemia, ventricular hypertrophy, LBBB or
RBBB, hypokalemia, and certain drugs (digoxin)
Process of Infarction
Process of Infarction
• A process that results in myocardial tissue
death
• It is important to understand this process as
a continuum.
• Early recognition of this process may
decrease morbidity
• “Myocardially infarcting”
Process of
Infarction
• Infarction occurs when
sufficient blood flow to a
portion of the myocardium
is lacking.
– Coronary artery occlusion
by clot
– Severe vasospasm
– Extreme narrowing or
occlusion of artery due to
atherosclerosis
Process of Infarction
• Most common cause is
blood clot formation that
occludes coronary blood
flow
• Myocardial cells will
immediately experience
ischemia  injury
• If clot does not dissolve,
persistent ischemia will
lead to infarction.
Process of Infarction
• Ischemia
– Temporary oxygen deficiency at
cellular level
– Usually due to an increase in
oxygen demand of myocardial
tissue supplied by a narrowed
artery
– The narrow artery inhibits
adequate blood flow to support
metabolic needs
– Demand is higher than supply
– Pain usually subsides when O2
demand is at the level of supply
provided by the narrowed artery
Nonhomogeneous Epicardial
Strain Measurements of
Anterior LV During Acute
Myocardial Ischemia
Process of Infarction
• Injury
– Supply is less than demand but not necessarily
due to increased O2 demands
– Usually a result of diminishing blood flow
– Myocardial cells are still alive but will die if
hypoxia persists
– Injury may be significant enough to produce
pumping dysfunction and electrical
instability
Process of Infarction
• Infarction:
– IschemiaInjuryInfarction
– If occlusion is not resolved all cells
that are injured will infarct
– Irreversible
ECG Changes
• Learn the clues that indicate
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Ischemia
Injury
Infarction
Location
Extent
Duration
ECG Changes
• Infarction recognition
– Determined by change in shape of which wave
forms?
• QRS, ST, T wave
– Each change occurs in relation to certain events
during the infarction
– Changes often occur in a predictable pattern
• Seen in the leads looking at the infarcting site
ECG Changes
• 1st change:
– Usually the development of
a Tall T wave
– T wave may also become
more symmetric
• Remember the normal
shape of the T wave
– T wave may become
pointed
– Hyperacute phase of the
infarction: 1st few minutes
Case 1
• A 54-year-old African American female who works out regularly, with
no history of hypertension, diabetes mellitus, high cholesterol,
smoking or significant family history of CAD presented with one
episode of chest pain.
• The discomfort was of post-prandial onset and felt like tightness and
was of intermittent nature.
• She did not have any accompanying nausea or diaphoresis.
• Patient states that it felt like upper GI discomfort but she was pain free
on arrival to the emergency department.
• Her heart rate was 71/min and blood pressure on arrival was
131/70mmHg. She was breathing at the rate of 18/min and appeared in
no distress.
• Physical examination revealed a normal JVP, normal S1 and S2 and no
S3 or S4.
• Lungs were clear to auscultation.
• Her electrocardiogram showed sinus rhythm, possible left atrial
abnormality and tall T wave in lead V2.
ECG Changes
• 2nd change:
– Signs of myocardial injury
– ST segment elevation is
the primary predictor
– May occur within the first
hour or first few hours
– Acute phase of infarction
– May also see inversion of
T wave
Case 1
• Her admission cardiac markers were slightly
elevated: CPK 159U/L, CK MB 2 ng/ml, and
Troponin I 0.3ng/ml.
• Patient experienced repeat episodes of post
prandial chest discomfort over the next 24hrs with
some evidence of ST-T changes in the precordial
leads while CPK continued to trend down.
ST Segment Elevation
• Important to remember:
– ST segment elevation is a result of changes
that affect ventricular repolarization or
depolarization
– ST segment elevation is not caused by ONLY
myocardial infarction
– Therefore diagnosing ST elevation as an AMI
all of the time would lead to misdiagnosis
ST Elevation
• Common causes:
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Increased ICP
Electrolyte imbalance
Meds
Hypothermia
LBBB
Ventricular rhythms
LVH
Pericarditis
Early repolarizations
ECG Changes
• 3rd change:
– Evidence of tissue
death
– Pathologic Q wave
• More than 40 ms wide
• Or new Q wave
– Usually seen within the
first few hours to first
several hours
– Still in acute phase
Case 1
• Exercise stress test with
myocardial perfusion imaging
revealed a partially reversible
defect of the
anteroseptal/anteroapical wall.
• She underwent cardiac
catheterization, 48hrs after
admission.
• Cardiac catheterization
revealed an 80-90% long
stenosis of the proximal LAD.
Case 1
• The lesion was wired
without difficulty and
predilated with a
2.5x25mm PTCA
balloon and then a
3mmX30mm OTW
stent was deployed.
• Post stent deployment
angiographic image is
shown.
ECG Changes
• Lastly
– T wave regains its normal contour
– ST segment returns to baseline (isoelectric
line)
– If Q wave developed, it will remain as
evidence that an infarction occurred
– Once baseline is achieved, time of infarct
cannot be determined.
ECG Changes
• Indicative changes:
– ST elevation
– Provides the strongest evidence for early recognition
of “myocardially infarcting” process
• Complimentary changes:
– T wave inversion
• Not specific to MI
• May occur with ischemia alone
• Definitive changes
– Pathologic Q wave formation
– May not occur for a few hours
ECG Changes
• Indicative changes only occur in leads
looking at the wall of the heart that is
experiencing the
ischemiainjuryinfarction
• Contiguous leads:
– Leads looking at the same wall of the heart
– If ST elevation occurs in at least two
contiguous leads, suspect MI
ECG Changes
• When ST segment elevation is observed in
two or more leads that are NOT
contiguous, MI is NOT suspected
• Infarct recognition = Infarct localization
• It is necessary to memorize which leads
look at which portion of the myocardium
Artery Recognition
• Once you have localized the infarction, you
can identify the artery that is occluded.
• This helps to prepare for future clinical
situations
– Right coronary artery occlusion calls for
different treatment than left coronary
occlusion
Artery Recognition
A heart model illustrating the
coronary artery tree.
• The RT and LT
coronary arteries
branch off of the
proximal aorta
– They have different
origins
– From the origin, the
branching distribution
differs significantly
from right to left.
A three-dimensional coronary artery image obtained using MRI.
LAD: left anterior descending coronary artery
LCX: left circumflex coronary artery
RCA: right coronary artery RV: right ventricle
Artery Recognition
• After leaving the aorta, the
LCA quickly divides into
two main branches that
continue to branch into a
network of vasculature
– LAD
– Circumflex
• Supplies the septal,
anterior, lateral, and
posterior walls
Angiogram of the left coronary artery in the anterior-posterior projection. There is
a large filling defect consistent with thrombus (large arrow) involving the left
main coronary artery, proximal left anterior descending artery, and proximal left
circumflex artery. The distal left anterior descending artery is occluded by
thrombus (small arrow).
Artery Recognition
• RCA
– Proximal branches
supply the RV
– Extends to inferior
and posterior wall of
LV
Artery Recognition
• It is most important to determine whether the
occlusion is in the right or the left.
• Differentiating between LAD and circumflex is
not feasible because of the large variation of
their distribution among individuals
• Differentiating between RT and LT produces two
very different clinical categories
• Unless you see changes in II, III, and AVF,
assume LCA occlusion
Extent of Infarction
• How many leads are showing indicative
changes?
– The more leads the larger the infarction
– The myocardially infarcting process is
occurring at a greater extent
Extent of Infarction
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Four LCA locations:
Aportion of anterior wall: V3 and V4
Bseptum: V1 and V2
Ccircumflex lateral: I, AVL, V5 V6
Dproximal, large portion of LV: most or
all of the left leads will be affected
– I, AVL, V1-V6
Extent of Infarction
• Three RCA locations: Remember that the
ECG does not show a significant amount of the
tissue supplied by the RCA
• Adistal, inferior: II, III, AVF
• Blarger amount of tissue, larger infarction:
no leads look at the posterior wall, so you will
only see indicative changes in II, III, AVF
• Cproximal, produces infarction in both
ventricles with changes usually only seen in II,
III, and AVF
RV Infarction
• RVIs complicate inferior
wall infarctions
– 40-45% of inferior wall
infarctions involve RVI
• Indicates biventricular
involvementhuge
infarction
• Getting a right-sided ECG
allows one to “see” the RV
• RV involvement will be
seen in V4R, V5R, & V6R
Acute inferior (diaphragmatic ) MI with
coexisting right ventricular infarction. Note STsegment elevation in leads V4R (and V1). The
ECG was taken 4 h after the onset of chest pain.
RV Infarction
• V4R is most specific and sensitive
– So if no time to do all right-sided leads, just switch V4 to its
equivalent place on the right
• Whenever there are ST changes in II, II, and AVF,
obtain V4R
• Clinical signs of RVI: understand cardiopulmonary blood
flow
– Hypotensiondecrease in blood volume going into the lungs and
LV
– Jugular venous distension (JVD)blood backing up from RV
– Absence of pulmonary edema (crackles)decreased pumping
function of RV
Posterior Wall Infarctions
• The standard 12-lead does not look at the
Posterior wall
• What gives suspicion of posterior MI?
• We must look at leads looking opposite to the site
of interest to identify reciprocal changes
• V1, V2, & V3 look at the posterior wall
backwards showing the following in the presence
of posterior myocardially infarcting process
– ST depression
– Large (tall) R wave
Causes of ST Depression
• Reciprocal changes
• Digitalis effect
• Ischemia
– Stress, indicating ischemic heart dz
– Zone of ischemia surrounding injured and
infarcting tissue
– Distant ischemia due to increase WL on tissue
taking up the slack for injured/infarcting tissue
Exceptions
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Indicative changes may occur in a different order
Q waves may never occur
Q waves may disappear after the infarct
Persistent ST elevation after infarction
ECG may appear normal
Variance in vascular anatomy
Patient positioning
Apical infarcts and inferolateral infarcts are
difficult to localize
What do you think?
What do you think?
What do you think?
What do you think?
What do you think?
What do you think?
What do you think?
Intraventricular blocks
Significance of BBB
• New onset may be very indicative of an
acute MI
• If it occurs with an MI, mortality rate
significantly increases
• There is also an increased probability of
cardiogenic shock
• Why?
Significance of BBB
• A new BBB is indicative of an extensive
MI resulting in a large amount of
functional tissue loss
– May result in severe hypotension
• Unless an ECG is available for comparison,
always assume that a BBB is new
• Septal and anteroseptal infarctions are
most likely to cause BBB
Significance of BBB
• New BBB also clues in to the possibility of
risk for AV block
– BBB is an infranodal block that can progress to
a complete blockreduced cardiac
ratecompromised cardiac output
– Standby pacing is indicated when BBB
complicates an AMI
Review of Conduction System
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Sinus Node
AV Node
Bundle of His
Right Bundle Branch
Left Bundle Branch
Left Common Branch Main Stem
– Left Anterior fascicle
– Left Posterior Fascicle
• Purkinje Fibers
Primary & Alternate Blood Supply
Conduction System
Primary Blood
Supply
Alternate Blood
Supply
AV Node
AV Nodal Artery
None
Bundle of His
Proximal
Distal
Right Bundle Branch
Proximal
Distal
Left Bundle Branch
Main Stem
Left Anterior Fascicle
Left Posterior Fascicle
AV Nodal Artery
LAD
None
AV Nodal Artery
LAD
LAD
AV Nodal Artery
None
LAD
LAD
LAD & PDA
AV Nodal Artery
None
None
Cause of BB Blocks
• Ischemic Heart Disease
• Idiopathic Degeneration of the conduction
system
• Cardiomyopathy
• Severe Left Ventricular Hypertrophy
• AMI
– specific for involvement of each component of
the conduction system
Miscellaneous Causes
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Acute HF, Pulmonary
Embolism
Aortic valve disease
cardiac tumors
syphilitic, rheumatic and congenital heart disease
Potassium Overdose
Trauma including:
– cardiac catheterization
– Angiograpghy
– Surgery
Treatment
• Specific treatment is usually not indicated for a
BBB if it is present alone and not the result of an
acute myocardial infarction
• TCP may be indicated if:
– new RBBB or LBBB or alternating block occurs as
the result of an AMI
– BBB is complicated by a Fascicular Block in the
setting of am AMI
– BBB progresses to a Complete Heart Block
Identification of BBB
• Forget about the notch!
– Unreliable
• Wide QRS (>120 ms) complex with atrial
activity is reliable with a couple exceptions
– This is because it is a supraventricular
rhythm that is conducted aberrantly
• Always measure the width  don’t guess
Identification of BBB
• When measuring for BBB, select the widest QRS
complex with a discernible beginning and end
• Criteria for BBB can be found in any lead
– QRS>120 ms
– P wave must be present
• When differentiating between RBBB and LBBB,
lead criteria is important
• Lead V1 is best for differentiation
RBBB
• Impulse travels through the AV node to the LBB
but not the RBB
• LBB impulses depolarize the septum in a RT-toLT fashiontoward V1producing initial
small R wave
• When the LV is completely depolarized it moves
away from V1 downward deflection
• The RV is finally depolarizes toward V1 2nd
R wave of greater amplitude
• RSR’ in V1, in the presence of QRS>120 ms
preceded by a p wave indicates a RBBB
Characteristics of RBBB
• QRS - .12 seconds or greater
• QRS axis - Normal or deviated to the Right
– if LAD is present, then LAF block is also present
• QRS Pattern
– Q waves - present and normal
– R waves - Classic Rabbit Ears in V1 - V2
• Triphasic Pattern
• ST segment - depression usually noted
• T waves - inversion may be noted
Classic Appearance of RBBB
MCL1
RBBB Pattern
3
1
1
3
2
2
Left Bundle Branch Block
• Common Acute Causes
– Anteroseptal AMI
– Acute HF
– Pericarditis and/or myocarditis
• Always indicates a diseased heart
LBBB
• Impulse travels from the AV node through the
RBB but not the LBBB
• The septum is depolarized by the RBB (the
septum is part of the LV) thus initial net
depolarization is away from V1
• The depolarization continues to move away
from V1 at the rest of the LV is
depolarizedQRS complex continues as a
negative deflection
• LBBB is indicated if there is a QS pattern in V1
and the QRS of >120 ms is preceded by a P
wave
Characteristics of LBBB
• QRS - .12 seconds or greater
• QRS Axis - usually normal but can be LAD
• QRS Pattern
– Q waves – absent
– R waves - usually small in V1 and V2
– S waves - Deep Wide in V1 and V2
• ST Segment - elevation noted in V1 - V3
• T waves - elevation noted in V1 - V3
Common Appearance
MCL1
LBBB Pattern
MCL1
1
An Easier Way
• Not all BBB will present so nicely
• Focus on the terminal force (final portion of the
QRS)
• With a BBB, the ventricles are not depolarized
simultaneously but sequentially
• The last ventricle to be depolarized is the one
with the block.
– Its depolarization will make up the later portion of
the QRS
Bundle Branch Block
RBBB
Right Ventricle
MCL1
Left Ventricle
Normal
Right Ventricle
Left Ventricle
LBBB
RT vs. LT
Exceptions
• Presence of P waves:
– Junctional rhythms typically do not produce P
waves but are supraventricular rhythms that
may be seen with a BBB
– WPW are wide and are stimulated by
supraventricular activity (incidence is 0.1%)
– Hyperkalemia can produce wide QRS
complexes
Exceptions
• Differentiating between LBBB and RBBB
– Nonspecific intraventricular conduction
delay (NSIVCD)
– Do not display the typical V1 morphologies
– May not be due to complete BBB but may be
incomplete BBB
Quick Axis Determination
• Normal Axis
– Lead I & Lead II upright
• Left Axis Deviation
– Lead I upright - Lead II negative deflection
• Right Axis Deviation
– Lead I negative deflection
– Lead II upright
• Extreme Right
– Both I & II negative deflection
Left Anterior Hemiblock
• QRS complex usually less than .10 seconds
• QRS Axis
– typically deviated to the Left
• Must rule out other causes of LAD
– Left ventricular Hypertrophy
– Inferior myocardial infarction
– Emphysema
– Usually insignificant unless associated with a
RBBB
Left Posterior Hemiblock
• Normal duration of QRS
• Typically deviated to the Right Axis
– must rule out other causes of RAD
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•
•
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Right Ventricular Hypertrophy
Pulmonary Embolism
Anterolateral infarction
Emphysema
• Most commonly Associated with RBBB
– can progress to CHB easily
LBBB
What do you think?
Left Anterior Fascicular Block
(aka Left Anterior Hemiblock)--much more common than
LPFB
• QRS complex usually less than .10 seconds
• QRS Axis
– typically deviated to the Left
• Must rule out other causes of LAD
– Left ventricular Hypertrophy
– Inferior myocardial infarction
– Emphysema
– Usually insignificant unless associated with a RBBB
• Marked LAD (QRS often > -45 degrees) without other apparent cause
• QRS may be slightly widened but rarely > 0.12 sec
• qR in I and aVL
• rS in II, III, and aVF
• Suspect in any patient with RBBB + LAD
What do you think?
What do you think?
Left Posterior Fascicular Block (aka
Left Posterior Hemiblock)--much less common than LAFB
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•
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•
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•
•
Normal duration of QRS
Typically deviated to the Right Axis
– must rule out other causes of RAD
• Right Ventricular Hypertrophy
• Pulmonary Embolism
• Anterolateral infarction
Most commonly Associated with RBBB
– can progress to CHB easily
QRS more rightward than previously but often within normal range,
– i.e. frank RAD is often absent and the diagnosis can often be made only by comparing before
& after ECG's.
– Note that some authorities require more stringent criteria for LPFB, e.g. marked RAD (>
120') w/o other known cause of RAD
QRS may be slightly widened to 0.12 sec
rS in I and aVL
qR in II, III, and aVF
What do you think?
Divisional (fascicular) block - left anterior fascicular block (LAFB) and left
posterior fascicular block (LAPB)
•
•
LAFB : severe left axis deviation ( -45 - -90 degree)
LAPB : severe right axis deviation (+90 - +120 degree)
What do you think?
What do you think?
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:
Alternating bundle branch block
alternating right and left bundle branch block
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Other Stuff
Wolf-Parkinson’s White Syndrome
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Early Repolarization
Early Repolarization
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Normal Variant: Early Repolarization-KH
Frank G.Yanowitz, M.D.
Early repolarization, a misnomer, describes a pattern of localized or diffuse ST segment
elevation. This is especially seen in leads with prominent R waves. In this example leads
I, II, V5 and V6 illustrate the early repolarization pattern. ST segments usually have a
"concave upwards" pattern and take off after a small S-wave is inscribed.
Pericarditis
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Diffuse inflammation of the pericardium and
adjoining epicardial surface of the heart
ST elevation here is not due to injured myocardium
Common post-MI and post cardiac surgery
ST segment elevation may be found in any lead
– The is because it is related to diffuse inflammation
rather than localized inflammation
– Not grouped in contiguous leads
Notching of the J point may occur
– This is indicative of noninfarct causes of ST
elevation
May produce PR segment depression
We often compare the isoelectric line to the PR interval
– If we are doing this, the ST segment may appear
elevated
– Use both the TP and PR to establish the isoelectric
line to minimize this problem
Clinical presentation
– CP
• Sharp, “knife-like”
• Not heavy, pressure
• Affected by movement, respiration, and
position
• May radiate to the base of the neck or
between shoulder blades
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Syndrome:
1. "Current of Injury" pattern: thought to be due to pressure and superficial
inflammation of the pericardium
2. PR segment changes: PR segment depression (82% of patients)
Differentiation from MI: ST segment elevation is typically less pronounced
(equal to or less than0.05mV) and the ventricular surface area is greater
(more leads involved)
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A ST/T ratio in V6 of 0.25 will allow good separation of the two entities.
ST segment elevation is typically less pronounced (equal to or less than
0.05mV) and the ventricular surface area is greater (more leads involved)
ST/T ratio
• Measure the height of the
elevated ST segment - from
the level of PR segment to the J
point where the ST segment
starts.
• Measure the height of the T
wave - from the level of the PR
segment to the top of the T
wave.
• Calculate the ratio of the height
of the ST segment: height of the
T wave (ST/T ratio):– ST/T ratio < 0.25 = BER
– ST/T ratio > 0.25 =
Pericarditis
Differentiating early repolarization
from pericarditis by ECG
The ratio of the ST-segment elevation to the T-wave amplitude in lead V6 is
useful in differentiating early repolarization (left) from pericarditis (right).
The four stages
of
electrocardiographic
changes in
acute
pericarditis
Ventricular Enlargement
Left Ventricular Hypertrophy--all criteria less valid in pts < 35yo; also less valid in the
presence of Bundle Branch Blocks which may exaggerate QRS voltages
Most specific criteria:
R in aVL > 11mm (or > 16mm with LAD)
R in I + S in III > 25mm
R in aVL + S in V3 > 28mm in men or > 20mm in women (Circ. 3:565, 1987)
Less specific criteria:
R in II or III > 25mm
R in V6 > 27mm
R in V5 or V6 + S in V1 or V2 > 35mm (Am. Heart J. 37:161, 1949; Circ. 81:815,
1990)
V6 > V5
Loss of R in V1 and V2
R in I > 15mm (or > 18mm with LAD)
Right Ventricular Hypertrophy
R > S in V1; sometimes RSR' in V1
Deep S wave in V4-6
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Atrial Enlargement
Left Atrial Abnormality (e.g. hypertrophy or dilatation)
suggested by:
p > 2.5mm wide in any lead ("p mitrale")
M-shaped p in any lead (humps at least 1mm apart)
Negative deflection of terminal portion of p in V1 (at least
1mm x 1mm)--this is the most specific criterion
Right Atrial Abnormality (e.g. hypertrophy or dilatation)
suggested by:
p > 2.5mm tall in II, III, or aVF ("p pulmonale")
Biphasic P in V1 with initial portion greater in amplitude
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hyperkalemia.
narrow and peak T waves (tenting)
AV conduction disturbance (PR
prolongation or disappeared P wave) and
wide QRS
cardiac arrest with a slow sinusoidal wave
('sine-wave pattern')
asystole
renal failure
hyperkalemia
hypocalcemia "tent on the desert'
hypokalemia
prominent U wave, prolonged ventricular
repolarization (QT interval)
hypercalcemia
prolonged QT interval
hypocalcemia
shortened QT interval
Digitalis effect
• digitalis ECG 'PR
prolongation, scooping
(sagging)' of ST-T
complex, short QT
interval
• digitalis intoxication
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