Transcript ELECTROCARDIOGRAPH INTERPRETATION Advanced

ADVANCED EKG
INTERPRETATION
Edward Briggs DNP
12 LEAD EKG INTERPRETATION
• Objectives
• Review basic EKG components
• Discuss the process of interpreting an EKG
• Discuss Axis interpretation and clinical significance
• Discuss EKG changes indicative of:
• Ischemia (acute and resolving)
• Myocardial scar/old MI
• Hypertrophy/Strain
• Pericarditis
• Other (i.e. electrolytes and EKG changes, medication effects)
KEY POINTS
• Establish a process and follow it each time you interpret
an EKG
• Don’t skip steps
• Never trust the EKG interpretation and always confirm the
interpretation yourself
• If unsure of the interpretation consult
KEY POINTS
• Make sure it is a good tracing
• If difficult to read it have it repeated
• If old EKG is available always compare to the old EKG
• Remember to treat the clinical presentation and not the
EKG. Myocardial Infarction may not demonstrate EKG
changes initially, especially in small or multi - vessel
disease
12 Lead EKG Interpretation
• Follow the process
1.
Determine rate (normal, tachy, brady)
2.
Regularity (regular, irregular)
3.
Intervals (PR interval, QRS duration, QTc)
4.
Define underlying rhythm (sinus rhythm, atrial fib, 1st degree
block, etc.)
12 Lead EKG Interpretation
• Follow the process
5. Determine Axis (Normal, RAD, LAD, indeterminate)
6. Evaluate waveform morphology
• P wave (Peaked, notched – suggestive of atrial/pulmonary disease
process)
• QRS height (LVH), BBB, pacer spikes, widening
• T wave slurring, peaked (hyperkalemia)
12 Lead EKG Interpretation
• Follow the process
• 7. Evaluate ST segments
• Evaluate all ST’s
• Consider ST changes corresponding to region (II, III, AVF = inferior
wall, etc)
• Note the deflection and shape of any ST changes
• Depression, elevation, concave, convex
• 8. Evaluate for Q Waves
Quick Review
• The various intervals seen on the
EKG include:
• The P wave: represents atrial
depolarization
Norm
0.12 - 0.2ms
Short PR <0.12 ms
= Wolf Parkinson White
Pr > 0.2 = 1ST or 2nd Degree AVB
Quick Review
• The various intervals seen on the
EKG include:
QRS Duration
0.06 – 0.12 ms
• The P wave: represents atrial
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•
•
•
depolarization
The QRS complex: represents
ventricular depolarization
The ST segment: represents the total
ventricular repolarization time
The T wave: represents the rapid
phase of ventricular repolarization
The QT interval: represents the
entirety of ventricular systole
Norm
0.12 - 0.2ms
Short PR <0.12 ms
= Wolf Parkinson White
Pr > 0.2 = 1ST or 2nd Degree AVB
QRS >0.12 ms
=BBB or IVCD
Quick Review
• The various intervals seen on the
EKG include:
QRS Duration
0.06 – 0.12 ms
QRS >0.12 ms
=BBB or IVCD
• The P wave: represents atrial
depolarization
• The QRS complex: represents
ventricular depolarization
• The T wave: represents the rapid
phase of ventricular repolarization
• The QT interval: represents the
entirety of ventricular systole
Norm
0.12 - 0.2ms
QT Interval
Rate dependent
Normal Rate <0.44ms
Short PR <0.12 ms
= Wolf Parkinson White
Pr > 0.2 = 1ST or 2nd Degree AVB
Quick Review
• The baseline of the EKG is defined as the isoelectric or
flat line seen between the waveforms that comprise the P
wave, QRS complex, and T wave.
• When considering segment elevation or depression, each
small box represents 1 mm. You will hear ST segment
elevation or depression described by the number of
millimeters it is above or below the baseline.
Isoelectric
line
Quick Review
• The ST segment is the flat
area of baseline situated
between the QRS complex
and T wave that represents the
initial phase of ventricular
repolarization, referred to as
the plateau phase
Quick Review - Rate
• The classic 12-lead EKG represents about 6 seconds of
time. On the EKG paper, one large box is equal to 200
milliseconds or 0.2 seconds. Each large box is composed
of five smaller boxes, each equal to 40 milliseconds or
0.04 seconds. This is helpful to remember when
0.04 seconds
estimating intervals
0.2 seconds
Rate can be measured by
counting QRS occurrence in 6
seconds and multiply by ten, or
by counting number of large
boxes between QRSs, if regular
(300,150,100,75,60,50)
RATE
Quick and easy way to “guess” rate:
1. IF regular rhythm count the number of
large boxes between QRS
 If one large box between QRS
then rate = 300 BPM
 If two large boxes between QRS
then rate = 150
 If three large boxes between QRS
then rate = 75
 Etc.

If irregular rhythm count the number of
QRS complexes documented on the EKG
in the rhythm strip and multiply by 10
REGULARITY
QUICK AND EASY WAY TO DETERMINE REGULARITY IS TO MEASURE ONE
QRS COMPLEX TO THE NEXT. THEN EVALUATE IS THIS IS CONSISTENT THRO
THE EKG.
Quick Review
• The various intervals seen on the
EKG include:
QRS Duration
0.06 – 0.12 ms
• The P wave: represents atrial
•
•
•
•
depolarization
The QRS complex: represents
ventricular depolarization
The ST segment: represents the total
ventricular repolarization time
The T wave: represents the rapid
phase of ventricular repolarization
The QT interval: represents the
entirety of ventricular systole
Norm
0.12 - 0.2ms
QT Interval
Rate dependent
Normal Rate <0.44ms
RHYTHM
• Determine the underlying rhythm
• Normal Sinus Rhythm
• Sinus Arrhythmia
• Atrial Fibrillation
• Ectopic Beats
• Etc.
12 LEAD EKG
Review and discussion
12 Lead EKG
• Each of these leads records the same electrical activity,
but from a different angle.
• This is why the EKG tracing will vary from lead to lead.
• As depolarization spreads toward a positive pole, there is an
upward deflection in that lead.
• As it spreads away from a positive pole, there is a downward
deflection in that lead. Take the vantage point of each positive pole.
As electricity moves toward it, the respective EKG deflection
appears positive. As electricity moves away from it, it appears
negative
EKG CHANGES
• An analogy
• Think of the electrical flow across the myocardium as a river
• If you look at the river from different banks it looks different, but the
river hasn’t changed
• Now imagine a beaver builds a dam along that river, we see actual
change in the flow of the river
• The “dam” would be ischemia/scar that would be changing the
course of the myocardial electrical flow
12 lead EKG
• Made up of
• Bipolar leads : I, II, III
• Lead I records the electrical difference
between the left arm and the right arm
electrodes and is positive on the left and
negative on the right
• Lead II records the electrical difference
between the left leg and the right arm
electrodes and is positive at the leg and
negative at the arm
• Lead III records the electrical difference
between the left leg and the left arm
electrodes and is positive at the leg and
negative at the arm
12 lead EKG
• Unipolar Augmented Leads –
aVR, aVF, and aVL
• aVR: Augmented voltage right
arm: a combination of leads I and
II
• aVL: Augmented voltage left arm:
a combination of leads I and III
• aVF: Augmented voltage foot: a
combination of leads II and III
12 Lead EKG
• Precordial Leads: V1 V2 V3 V4 V5 V6
12 Lead EKG
• Combinations of leads represent flow of electricity as
moves over different aspects of the heart
• These 12 leads should be always considered in groups because
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•
•
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each set of leads represents a specific area of the myocardium
Leads I, aVL, V5, and V6 are the lateral leads.
Leads II, III, and aVF are the inferior leads.
Leads V1 to V4 are the anterior chest leads.
Leads V1, V2 are the anterior septal leads
12 Lead EKG
• Each myocardium region is perfused by specific coronary
arteries, therefore each cardiac region has corresponding
coronary arteries
• Anterior
• AnterioSeptal
• Inferior
• Lateral
Determine Axis
• Axis = electrically where the heart lies in the chest
Axis
• Axis refers to the general direction of electrical conduction
through the heart.
• It gives a graphical representation of the electrical position
of the heart
• Deviation from “normal” represents either malposition of
the heart itself or;
• Something is altering how the electricity flows over the
heart (ischemia, scar, blocks, etc.)
AXIS
• Axis deviations are divided into 2 categories:
• Right Axis Deviation (RAD)
• Left Axis Deviation (LAD)
• Deviations can occur from physiologic conditions such as
obesity, physical morphology (tall thin stretching out
myocardium, cavitus pectorum physically rotating the
heart)
• Deviations can occur from pathologic conditions such as
ischemia, infarct altering the electrical flow
Determining Axis
• Normal axis : 0 to -90 degrees
• RAD : + 90 to +/- 180 degrees
• LAD : 0 to -90 degrees
• Indeterminate : -90 to +/- 180
Determining Axis
• Easy Trick:
• Hold up your left thumb and right thumb
• Left thumb corresponds to lead I
• Right thumb corresponds to lead AVF
• If lead I is upright and aVF is upright axis is normal
• If lead I is upright and aVF is downward axis is left (LAD)
• If lead I is downward and aVF is upright axis is right (RAD)
• If Lead I and AVF are downward Northwest Region (No Man’s
Land)
AXIS DEVIATIONS
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LEFT AXIS DEVIATION (LAD)
Lateral wall myocardial infarction
Left ventricular hypertrophy
Left bundle branch block
Left anterior fascicular block
AXIS DEVIATIONS
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RIGHT AXIS DEVIATION (RAD)
Left posterior fascicular block
Right bundle branch block
Right ventricular hypertrophy
Obesity Tall, thin frame, cavitus pectorum
Inferior wall myocardial infarction
COPD
AXIS DEVIATIONS
NO MAN’S LAND (NORTHWEST REGION)
•emphysema/copd
•hyperkalaemia
•lead transposition
•artificial cardiac pacing
•ventricular tachycardia
Wave Form Morphology
P-Wave
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Represents Depolarization across the Atria
Normal – 1 P wave precedes each QRS
Rounded hump
Normal PR interval is < 0.20 ms
Wave Form Morphology
P-Wave
Wave Form Morphology
P-Wave
The principal cause is
pulmonary hypertension
due to:
•Chronic lung disease (cor
pulmonale)
•Tricuspid stenosis
•Congenital heart disease
(pulmonary stenosis,
Tetralogy of Fallot)
•Primary pulmonary
hypertension
Wave Form Morphology
P-Wave
P mitrale
The presence of broad,
notched (bifid) P waves
in lead II is a sign of left
atrial enlargement,
classically due to:
mitral stenosis.
Wave Form Morphology
QRS Complex
• Represents depolarization of the left and right ventricle
• Look to the QRS complexes in the precordial leads (V1-
V6)
• Evaluate R wave progress
• Evaluate height and width of the QRS complexes
Hypertrophy
• Hypertrophy is thickening of the heart muscle secondary
to some strain
• Think of increased workload (Body builders muscles
become hypertrophic in response to increase workload)
• CLUE:
• Right side think pulmonary
• Left side think systemic
Poor R Wave Progression
• Definition
• R wave height ≤ 3 mm in
V3.
• Causes
• Prior anteroseptal MI
• Left ventricular
hypertrophy
• Inaccurate lead
placement (e.g.
transposition of V1 and
V3)
• Dilated cardiomyopathy
• May be a normal variant
Wave Form Morphology
QRS Complex – Left Ventricular Hypertrophy
-QRS complex is slightly
widened (about 0.11 sec),
-Left Axis Deviation
-Tall R waves are present
in multiple leads, and
-ST-T changes (formerly
called a "strain" pattern)
are present.
-Frequent concurrent P
wave abnormalities
Left ventricular hypertrophy (LVH) refers to an
increase in the size of myocardial fibers in the
main cardiac pumping chamber. Such hypertrophy
is usually the response to a chronic volume or
pressure load.
●The two most important pressure overload states
are systemic hypertension and aortic stenosis
●The major conditions associated with left
ventricular volume overload are aortic or mitral
valve regurgitation and dilated cardiomyopathy.
Wave Form Morphology
QRS Complex – Right Ventricular Hypertrophy
Clues to the diagnosis
include:
●Right axis deviation
(>+90)
●R in V1 >6 mm
●R/S ratio in V1 >1
●Incomplete right bundle
branch block
●ST-T wave abnormalities
("strain") in inferior leads
●Right atrial
hypertrophy/overload (“P
pulmonale”)
●S>R in leads I, II, III,
particularly in children
(S1S2S3 pattern)
Right ventricular hypertrophy (RVH) is present
when there is a pathologic increase in muscle
mass of the right ventricle.
Commonly seen with pulmonary hypertension,
pulmonic stenosis, or severe lung disease and cor
pulmonale.
ABNORMAL EKG - blocks
• RIGHT BUNDLE BRANCH BLOCK
• In RBBB, activation of the right ventricle is delayed as depolarization
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•
•
•
has to spread across the septum from the left ventricle.
The left ventricle is activated normally, meaning that the early part of
the QRS complex is unchanged.
The delayed right ventricular activation produces a secondary R wave
(R’) in the right precordial leads (V1-3) and a wide, slurred S wave in
the lateral leads.
Delayed activation of the right ventricle also gives rise to secondary
repolarization abnormalities, with ST depression and T wave
inversion in the right precordial leads.
In isolated RBBB the cardiac axis is unchanged, as left ventricular
activation proceeds normally via the left bundle branch.
ABNORMAL EKG - blocks
• RIGHT BUNDLE BRANCH BLOCK
• Causes of RBBB
• Right ventricular hypertrophy / cor pulmonale
• Pulmonary embolus
• Ischemic heart disease
• Rheumatic heart disease
• Myocarditis or cardiomyopathy
• Degenerative disease of the conduction system
• Congenital heart disease (e.g. atrial septal defect)
ABNORMAL EKG - blocks
• RIGHT BUNDLE BRANCH BLOCK
• Diagnostic Criteria
• •Broad QRS > 120 ms
• •RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
• •Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
QRS >120ms
Slurred S
Wave
ABNORMAL EKG - blocks
• LEFT BUNDLE BRANCH BLOCK
• Normally the septum is activated from left to right, producing small Q
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•
•
•
waves in the lateral leads.
In LBBB, septal depolarization is reversed (becomes right to left), as
the impulse spreads first to the RV via the right bundle branch and
then to the LV via the septum.
This sequence of activation extends the QRS duration to > 120 ms
and eliminates the normal septal Q waves in the lateral leads.
The overall direction of depolarization (from right to left) produces tall
R waves in the lateral leads (I, V5-6) and deep S waves in the right
precordial leads (V1-3), and usually leads to left axis deviation.
As the ventricles are activated sequentially (right, then left) rather
than simultaneously, this produces a broad or notched (‘M’-shaped) R
wave in the lateral leads.
ABNORMAL EKG - blocks
• LEFT BUNDLE BRANCH BLOCK
• Causes
• Aortic stenosis
• Ischemic heart disease
• Hypertension
• Dilated cardiomyopathy
• Anterior MI
• Primary degenerative disease (fibrosis) of the conducting system
(Lenegre disease)
• Hyperkalemia
• Digoxin toxicity
ABNORMAL EKG - Blocks
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LEFT BUNDLE BRANCH BLOCK
Diagnostic Criteria
•QRS duration of > 120 ms
•Dominant S wave in V1
•Broad monophasic R wave in lateral leads (I, aVL, V5-V6)
•Absence of Q waves in lateral leads (I, V5-V6; small Q waves
are still allowed in aVL)
• •Prolonged R wave peak time > 60ms in left precordial leads
(V5-6)
QRS >120ms
Monophasic R waves
Dominant S
EXAMPLES
QRS >120ms
‘W’ V1
‘M’ V6
Interpretation :
Rate – 126 Regularity – Regular
Intervals
• PR – 0.16
• QRS – 160 ms
• QT – 350ms
• AXIS – Left Axis Deviation
SINUS TACH WITH LEFT
“W” in V1
“M” in V6
BBB
EXAMPLES
QRS >120ms
‘M’ V1
‘W’ V6
Interpretation :
Rate – 78 Regularity – Regular
Intervals
• PR – 0.16
• QRS – 160 ms
• QT – 340ms
• AXIS – normal
SINUS TACH WITH RIGHT
“M” in V1
“W” in V6
BBB
ABNORMAL EKG - blocks
• INTRAVENTRICULAR CONDUCTION DELAY
• Definition : Conduction of impulse is delayed as it moves through
the ventricle
• QRS duration > 100 ms in the presence of a supraventricular rhythm.
• Most commonly due to bundle branch block or left ventricular
hypertrophy.
• The most important life-threatening causes of QRS widening are
hyperkaliemia and tricyclic antidepressant poisoning.
New Onset block? Think
electrolytes and overdose!
ABNORMAL EKG - blocks
• INTRAVENTRICULAR CONDUCTION DELAY
• Types
• Left anterior fascicular block
• Left posterior fascicular block
• Left bundle branch block
• Right bundle branch block
• Bifascicular block
• Trifascicular block
ABNORMAL EKG - blocks
• INTRAVENTRICULAR CONDUCTION DELAY
• Types
• •Left anterior fascicular block
• In left anterior fascicular block (aka left
anterior hemiblock), impulses are
conducted to the left ventricle via the left
posterior fascicle, which inserts into the
infero-septal wall of the left ventricle
along its endocardial surface.
ABNORMAL EKG - blocks
• INTRAVENTRICULAR CONDUCTION DELAY
• Types
• In left posterior fascicular block
• (aka left posterior hemiblock), impulses are
conducted to the left ventricle via the left anterior
fascicle, which inserts into the upper, lateral wall of
the left ventricle along its endocardial surface.
ABNORMAL EKG - blocks
• INTRAVENTRICULAR CONDUCTION DELAY
• Types
• •Bifascicular block is the combination of RBBB with either LAFB or
LPFB.
• Trifascicular block (TFB) refers to the presence of conducting disease in
all three fascicles:
• Right bundle branch (RBB)
• Left anterior fascicle (LAF)
• Left posterior fascicle (LPF)
Electrolyte effects
Electrolyte effects
HYPERCALCEMIA
T wave
Broad tall Peaked
P wave
Flattening/absent
QRS
Widening
ST Segment
QT
HYPOCALCEMIA
narrow
Prolonged, depressed
shortened
Prolonged
U wave
Ectopy
Uncommon
J-waves
Torsades De Pointes
Electrolyte effects
HYPERKALEMIA
HYPOKALEMIA
T wave
Peaked
Negative
P wave
Flattening
QRS
Widening
ST Segment
Depression/flatten
QT
Prolonged
U wave
Present
Ectopy
Ventricular ectopy
Atrial Fib/Flutter
Vent fib
Medication Effects on ECG
The most common drugs ingested that may show QRS and/or QT
prolongation and arrhythmias (though these are not always present)
are:
•Calcium channel blockers (particularly verapamil and diltiazem)
•Beta blockers (particularly propranolol and sotalol )
•Digoxin
•Tricyclic antidepressants
•Antipsychotic drugs (particularly thioridazine)
•Anticonvulsants (particularly carbamazepine and phenytoin)
•Dextropropoxyphene
•Antimalarial drugs (chloroquine, quinine)
•Antiarrhythmic drugs
•Orphenadrine
•Lithium (cation)
ST Segment
• When examining the ST segment, be careful to look for
the presence of ST segment elevation or depression. The
ST segment should be isoelectric or flat on the baseline.
Clinical Point : Deviation of 2 mm (two small boxes) above
or below the baseline is indicative of a pathologic process.
ST SEGMENT
Critical analysis for acute ischemic events
ST Segment
• The T wave is usually concordant with the
QRS complex. Thus if the QRS complex
is positive in a certain lead than the T
wave usually is positive too in that lead.
• Accordingly the T wave is normally
upright or positive in leads I, II, AVL, AVF
and V3-V6. The T wave is negative in V1
and AVR. The T wave flips around V2, but
there is likely some genetic influence in
this as in Blacks the T wave usually flips
around V3.
• The T wave angle is the result of small
differences in the duration of the
repolarization between the endocardial
and epicardial layers of the left ventricle.
ST Segment elevation
ELEVATION OF THE ST SEGMENT OF THE ECG CAN
RESULT FROM MULTIPLE PATHOLOGIES, INCLUDING:
• LVH, LBBB, Pericarditis, Hyperkalemia, Anterior AMI.
• Acute pericarditis: ST elevation in all leads except aVR
• Pulmonary embolism: ST elevation in V1 and aVR
• Hypothermia: ST elevation in V3-V6, II, III and aVF
• Hypertrophic cardiomyopathy: V3-V5 (sometimes V6)
• High potassium (hyperkalemia): V1-V2 (V3)
• During acute neurologic events: all leads, primarily V1-V6
• Acute sympathic stress: all leads, especially V1-V6
• Brugada syndrome.**
• Cardiac aneurysm.
• Cardiac contusion
• Left ventricular hypertrophy
• Idioventricular rhythm including paced rhythm
•
** Brugada syndrome is a genetic disease that is characterised by abnormal electrocardiogram
(ECG) findings and an increased risk of sudden cardiac death.
ST Segment depression
• ST SEGMENT DEPRESSION CAN
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RESULT FROM MULTIPLE
PATHOLOGIES, INCLUDING:
Myocardial ischemia
Reciprocal ST segment depression. If
one lead shows ST segment elevation
then usually the lead 'on the other side'
shows ST segment depression. (This
is usually seen in ischemia as well.
Left ventricular hypertophy with "strain"
or depolarization abnormality
Digoxin effect
Low potassium / low magnesium
Heart rate-induced changes (post
tachycardia)
During acute neurologic events.
ST Segment depression
• Morphology of ST Depression
• ST depression can be either
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upsloping, downsloping, or
horizontal.
Horizontal or downsloping ST
depression ≥ 0.5 mm at the J-point in
≥ 2 contiguous leads indicates
myocardial ischaemia
Upsloping ST depression in the
precordial leads is highly specific for
occlusion of the LAD.
Reciprocal change has a morphology
that resembles “upside down” ST
elevation and is seen in leads
electrically opposite to the site of
infarction.
Posterior MI manifests as horizontal
ST depression in V1-3 and is
associated with upright T waves and
tall R waves.
T-Wave Inversion
• negative (or inverted) T wave> 0.5 mm
negative T wave in leads I, II, V3, V4, V5
or V6
• Possible causes of T wave changes:
• Ischemia and myocardial infarction
• Pericarditis
• Myocarditis
• Cardiac contusion
• Acute neurologic events, such as a
subarachnoid bleed.
• Mitral valve prolapse
• Digoxin effect
• Right and left ventricular hypertrophy with strain
T-Waves
• Two characteristics should be always noted with regard to
the T wave: inversion and peaked appearance .
• Inversion: May represent old infarction or resolving ischemia
• Peaked: Electrical instability (i.e. electrolyte imbalance
hyperkalemia)
Anatomy correlation
EKG leads generally correlate to different anatomical portions of the
Myocardium and the blood vessels that perfuse that region.
J point elevation
• The J point is where the QRS complex
ends and the ST segment begins. J
point elevation is a common and usually
benign finding on EKG in younger
patients.
• Early repolarization is a common finding
in young, healthy individuals. It appears
as mild ST segment elevation that can
be diffuse, however is more prominent in
the precordial leads. Early repolarization
changes are simply “J point” elevation.
Pathologic Q Waves
• Pathologic Q waves occur when the
electrical signal passes through
stunned or scarred heart muscle; as
such, they are usually markers of
previous myocardial infarctions, with
subsequent fibrosis.
• A pathologic Q wave is defined as
having a deflection amplitude of 25%
or more of the subsequent R wave, or
being > 0.04 s (40 ms) in width and > 2
mm in amplitude. However, diagnosis
requires the presence of this pattern in
more than one corresponding lead.
• Myocardial infarctions with pathological
Q waves are referred to as ST
elevation MIs.[5]
FOLLOW THE STEPS
1.
2.
3.
4.
5.
Rate
Regularity
Intervals
Rhythm
Axis

Normal

RAD

LAD

No Man’s Land
6. Waveform Morphology
 Peaked/biphasic P waves
 QRS changes
 BBB/conduction delay
 Low or High Voltage
 Pacer
 T-waves Inversions
7. ST Segment
 Elevation
 Depression
8. Q-Waves
CASE 1
• Rate:
• Rhythm:
• ST/T:
47 year old male presents with chest pain, dyspnea and diaphoresis. Sudden onset.
No prior medical history. No medications. No cardiac risk factors.
HR -122 R – 30 B/P 210/110 Pulse ox 84%
PR:
QRS:
Morphology:
Q-Waves:
Axis:
47 year old male presents with chest pain, dyspnea and diaphoresis. Sudden onset.
No prior medical history. No medications. No cardiac risk factors.
HR -122 R – 30 B/P 210/110 Pulse ox 84%
• Rate: 142
PR:
0.12
QRS: 0.06
Axis: LAD
• Rhythm:
sinus tach
Morphology: Peaked P waves/notched
• ST/T: T-wave inversion III and T-wave inversion v1-3 Q-Waves: none
This ECG is classic for PE: 1) sinus tach Hypoxia 2) right ventricular
conduction delay (R' in V1) 3) T-wave inversions in BOTH precordial leads and
in lead III. 4) S1Q3T3 (a tiny R-wave in III is equivalent to a Q-wave).
CASE 2
• Rate:
• Rhythm:
• ST/T:
64 year old male. PMH: HTN DM Lipids PSH 2 ppd x 20 yrs No cardiac hx
Sudden onset dyspnea, diaphoresis, weakness approx 1 hour ago.
PR:
QRS:
Morphology:
Q-Waves:
Axis:
CASE 2
• Rate: 100
PR:0.16
QRS:
0.06
Axis: normal
to LAD
• Rhythm:
Sinus tach
Morphology: T wave inversion diffuse
• ST/T: ST elevation II, III, AVF. ST Depression AVL. V2-5
Q-Waves: II, III, AVF
• Dx: acute inferior/lateral wall MI
CASE 3
• Rate:
• Rhythm:
• ST/T:
45 Year old male presents for preoperative clearance for hip surgery.
PMH: HTN, Dyslipidemia, Tobacco. Remote cocaine use.
PFH: adopted. PSH: None Works as a truck driver.
HR – 72 B/P 124/78 R-19 BMI -35
PR:
QRS:
Morphology:
Q-Waves:
Axis:
CASE 3
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45 Year old male presents for preoperative clearance for hip surgery.
PMH: HTN, Dyslipidemia, Tobacco. Remote cocaine use.
PFH: adopted. PSH: None Works as a truck driver.
HR – 72 B/P 124/78 R-19 BMI -35
Rate: 98
PR:0.12
QRS: 0.06 Axis: normal
Rhythm:
Sinus Morphology: T-wave inversion I, aVL
ST/T: ST elevation III, AVF, V2
Q-Waves: III, V2-V6
Dx: Anterior wall MI (Possible acute), lateral wall (old?)
CASE 4
HR: 74 Resp: 24 B/P 190/108 Pulse Ox 91%
61 year old female new to practice. Presents for first exam.
Denies any medical history but has not seen MD in a decade.
PMH: None PSH: None Meds: None PFH: Colon Ca, stroke, MI
• Rate:
• Rhythm:
• Q-Waves:
• Dx:
PR:
QRS:
Axis:
Morphology:
CASE 4
HR: 74 Resp: 24 B/P 190/108 Pulse Ox 91%
61 year old female new to practice. Presents for first exam. Denies any medical
history but has not seen MD in a decade.
PMH: None PSH: None Meds: None PFH: Colon Ca, stroke, MI
• Rate: 104
PR: 0.10 QRS:
0.06
Axis: normal
• Rhythm: Sinus Tach
Morphology: Tall QRS anterior leads, Peaked T waves
ant. T-wave inversion III, Short PR and peaked P
• Q-Waves: None
• Dx: Left ventricular hypertrophy with p pulmonale
CASE 5
•
•
•
•
•
Rate: 104
Rhythm:
Short
Q-Waves:
Dx:
68 year old male, presents with dyspnea for 1 day. Had Substernal chest pain aaprox 8
hours ago.
PMH: HTN Lipids DM PSH 60 pk yr Meds: Atenolol, silfenadil, lipitor, metformin
138/72 HR 58 R-22 Pulse Ox 94%
PR:
QRS:
Morphology
Axis:
CASE 6
•
•
•
•
•
Rate: 104
Rhythm:
Short
Q-Waves:
Dx:
94 yr old female local ALF, found unresponsive.
No medical history available, patient unresponsive
B/P 84/56 R-28 HR 75 Pulse ox 93%
PR:
QRS:
Morphology
Axis:
CASE 7
•
•
•
•
•
Rate: 104
Rhythm:
Short
Q-Waves:
Dx:
48 year old male presents for employment physical
PMH: None PSH: None Meds: None
Tobacco: None Recreational drug use : None
PR:
QRS:
Morphology
Axis:
CASE 8
•
•
•
•
•
Rate: 104
Rhythm:
Short
Q-Waves:
Dx:
64 year old male presents to office because “Doesn’t feel good”
PMH: Htn PSH: None Meds: lisinopril, silfenadil
BP 178/102 HR 54 R-20 Pulse Ox 99%
PR:
QRS:
Morphology
Axis:
CASE 9
•
•
•
•
•
Rate: 104
Rhythm:
Short
Q-Waves:
Dx:
64 yr old male presents for DMV clearance. Denies any complaints
PMH: None PSH: None Meds: None
Tobacco: remote history Drugs: none
156/95 HR 98 Resp: 24
PR:
QRS:
Morphology
Axis:
CASE 10
•
•
•
•
•
Rate: 104
Rhythm:
Short
Q-Waves:
Dx:
92 yr old female from nursing home, “confused”
PMH: HTN, CHF, Lipids, DM PSH: CABG
Meds: Metoprolol, lasix, lisinopril, spironolactone
96/48 HR: 60 Resp: 16 Pulse Ox 98%
PR:
QRS:
Morphology
Axis:
CASE 10
•
•
•
•
•
Rate: PR:
Rhythm:
Short
Q-Waves:
Dx:
74 year old male presents for routine follow up/physical exam
PMH: CAD/MI, CABG, HTN, obesity, DM
Meds: glipizide, metformin, lisinopril/hctz
BP 126/80 HR 100 R 24 Pulse ox: 100%
QRS:
Axis:
Morphology