2. Good Starting Place
• A man calls an ambulance after his 79 year
old spouse passes out while they were
walking in the park. She has no significant
medical history.
• No tobacco, alcohol, or drugs.
3.
4. • Atrial fibrillation with a rapid ventricular response.
• Right axis deviation.
• Intraventricular conduction delay.
• Right ventricular hypertrophy (RVH).
• This patient has severe mitral stenosis with pulmonary congestion,
pulmonary hypertension, and right heart failure.
• A qR in lead V1 is one of the most specific signs for right ventricular
hypertrophy. Other causes of a qR in V1 include a right bundle branch
block (RBBB) in patients with an anterior myocardial infarction or
normal patients who have a QS in V1 and subsequently develop a
RBBB. This patient has right axis deviation in addition to the qR in V1
which suggests RVH. Given atrial fibrillation and RVH one should
strongly consider mitral stenosis.
20. Leads Used
Modern ECG's utilize 12 leads which are composed
of 6 limb leads and 6 precordial leads.
• Limb leads are: I, II, III, aVR, aVL, and aVF.
– (The lower case "a" in this notation refers to
"augmented" in the sense that the person who
developed the augmented leads discovered that he had
to augment or amplify the voltage in the EKG machine
to get a tracing that would be of similar magnitude as
leads I, II, and III.)
21.
22. Precordial leads
• V1, V2, V3, V4, V5, and V6.
• These measure the amplitude of cardiac
electrical current in an anterior-posterior
aspect with regard to the heart as opposed to
the chest (limb) leads which record in the
coronal plane.
23.
24. 1. Assess the rate (atrial and ventricular) and
regularity of the underlying rhythm.
a) Assess the usual intervals and widths: PR
interval, QRS width, QT interval.
b) Interpret the rhythm itself.
2. Determine the axis.
3. Grouped lead analysis
a) Look for signs of infarct vs. ischemia in all
grouped leads
4. Look for any other abnormality
26. Step I (Rhythm strip
analysis)
Step II (Axis
determination)
Step III (Inferior lead
analysis)
Step IV (Lateral lead
analysis
Step V (Anterior
lead analysis)
Step VI (find
everything else)
27. Assessing the EKG Rhythm
Tip: the rhythm strip portion of the 12-lead ECG is a
good place to look at when trying to determine the
rhythm because the 12 leads only capture a few beats.
Lead II
Rhythm?
Atrial
fibrillation
Rhythm
strip
28. Assessing the EKG Rate
If you use the rhythm
strip portion of the
12-lead ECG the total
length of it is always
10 seconds long. So
you can count the
number of R waves in
the rhythm strip and
multiply by 6 to
determine the beats
per minute.
Rate?
14 (R waves) x 6 = 84 bpm
29. Assessing the Axis
Axis refers to the mean QRS axis (or vector) during ventricular
depolarization. As you recall when the ventricles depolarize (in a normal
heart) the direction of current flows leftward and downward because most of
the ventricular mass is in the left ventricle. We like to know the QRS axis
because an abnormal axis can suggest disease such as pulmonary
hypertension from a pulmonary embolism.
30. The QRS axis is determined by overlying a circle, in the frontal plane.
By convention, the degrees of the circle are as shown.
The normal QRS axis lies between -30o
and +90o
.
0o
30o
-30o
60o
-60o
-90o
-120o
90o
120o
150o
180o
-150o
A QRS axis that falls between -30o
and -90o
is abnormal and called left
axis deviation.
A QRS axis that falls between +90o
and +150o
is abnormal and called
right axis deviation.
A QRS axis that falls between +150o
and -90o
is abnormal and called
extreme right axis deviation.
31. Assessing the Axis
• Causes of left axis deviation
include:
– Left ventricular hypertrophy
– Inferior wall MI
– Left bundle branch block
– Left anterior fascicular block
0o
-90o
90o
180o
• Causes of right axis deviation
include:
– Right ventricular hypertrophy
– Lateral wall MI
– Right bundle branch block
– Pulmonary hypertension
32. Assessing the Axis
We can quickly determine whether the QRS axis is normal by
looking at leads I and aVF.
If the QRS complex is overall positive in leads I and aVF, the QRS axis is
normal.
In this ECG what
leads have QRS
complexes that are
negative?
equivocal?
33. Assessing the Axis
The thumb method
Always go with the positive thumb!!!!
Right Axis
Left Axis
Normal Axis
Extreme Right Axis
39. Assessing the Axis
Is the QRS axis normal in this ECG? No, there is left
axis deviation.
The QRS is
positive in I and
negative in aVF.
40.
41. • Region of myocardium dies becomes….
– Electrically silent.
• As a result of this, the rest of the electrical
forces are directed away from this area of
infarction.
• Electrode overlying this area will record a
deep negative deflection – Q-wave.
42. • Significant Q wave is one millimeter (one small square)
wide, which is .04 sec. in duration…
• … or is a Q wave 1/3 the amplitude (or more) of the QRS
complex.
• Note those leads (omit AVR) where significant Q’s are
present
* A Q wave in lead III alone is not diagnostic of
infarction, even if it is otherwise “significant” in size and
width. Qs in III are ignored unless other abnormalities are
seen b/c they usually represent…..
• Old infarcts: significant Q waves (like infarct damage)
remain for a lifetime.
43.
44.
45.
46.
47.
48. Q Wave Summary
• Causes: Septal, Infarction
• Septal: I, AVL, V5-V6, occasionally
inferior leads
Significant: Q > 1/3 QRS, or
Q > 1 box wide and NOT in
lead III
51. ST Elevation
• Signifies an acute process, ST segment returns to baseline with
time.
• ST elevation associated with significant Q waves indicates an
acute (or recent) infarct.
• ST depression (persistent) may represent “subendocardial
infarction,” which involves a small, shallow area just beneath
the endocardium lining the left ventricle. This is also a variety
of “non-Q wave infarction.
56. ST Depression Significance
• ST segment depression is considered
significant if the ST segment is at least two
boxes below baseline.
• With infarction, the location of the ischemia
is reflected in the leads in which the ST
depression occurs.
57. Flat ST Segment Depression
• Results from subendocardial infarction
58. Common Causes of ST Segment Depression
• Ischemia
• "Strain" in LVH
• Digitalis effect
• Bundle branch block
• Hypokalemia/Hypomagnesemia
• Reciprocal ST elevation
• Any combination of the above
59. • The specific cause of ST segment depression in a given tracing
may be suggested by the appearance of the ST segment and T
wave itself. For example, “strain" (for LVH) is suggested by
asymmetric ST depression in lateral leads, especially if voltage
criteria are met.
• "RV strain" is suggested if the tracing depicted in the figure is
seen in right-sided leads in a patient with RVH.
• Ischemia is suggested by symmetric T wave inversion,
especially when seen in two or more leads of a group (i.e., in
II, III, and aVF).
60. • Digoxin ("Dig effect") may produce either ST
"scooping" or a "strain"-like pattern or no change
at all.
• Can be seen in levels greater than 2.5mg/ml
62. A = Normal ST segment
B = Junctional ST segment depression (frequently a normal variant -
physiological)
C = Upward-sloping ST segment depression
D = ST segment elevation suggestive of coronary vasospasm or AMI
injury pattern
E = Flattening of the ST segment with a sharp-angled ST-T wave junction
suggesting ischemia
F = Depression of the ST segment with U wave inversion
G = Sagging ST segment depression
H = Downward-sloping ST segment depression
66. • Notching or slurring of the terminal portion of the
QRS wave
• Symmetric concordant T waves of large amplitude
• Relative temporal stability (when patients are
followed over time there will often be some variation
in the degree of ST segment elevation but generally
the change persists for years).
• Most commonly present in the precordial leads V2-5,
but often associated with pronounced ST segment
elevation in the limb leads II, III, & AvF
68. • Normally the R wave becomes progressively
taller as one moves across the precordial leads.
• A number of conditions may be associated
with "poor" R wave progression, in which
the R wave in leads V1 through V3-V4 either
does not become bigger, or only increases very
slowly in size.
69. Causes of Poor R Wave Progression
LVH
RVH
Pulmonary disease (i.e., COPD, chronic asthma)
Anterior or anteroseptal infarction
Conduction defects (i.e., LBBB, LAHB)
Cardiomyopathy
Chest wall deformity
Normal variant
Lead misplacement
73. • Only two main areas of the heart that do this:
– Inferior and lateral ones
– Septal and posterior ones.
• A set of inferior ST elevations in II, III and AVF
can produce lateral ST depressions in I, AVL, V5
and V6. You’d think that this would mean lateral
ischemia, but no – it’s a reflection, bouncing
electrically across the heart from the inferior
injury, showing up in reverse.
74.
75. • Results if ischemia
progresses
unresolved or
untreated
91. • All forms of bundle branch block involve delays or
electrical blockages within the ventricles, they are all types
of intraventricular conduction deficits (IVCD). Bundle
branch blocks may also be categorized as either partial
(incomplete) or complete, depending on which patterns of
electrical activity are detected on an EKG.
• When the criteria for BBB are partially met (e.g. < 0.12
sec), this is termed “incomplete bundle branch block”
93. • Degenerative effects of aging
• Hypertension
• Past heart attack that damaged the heart muscle
• Past viral infection
• Valvular heart disease, particularly calcific
aortic stenosis
• One of several heart or lung conditions that could have
affected the ventricles (e.g., heart failure or
chronic obstructive pulmonary disease)
• Congenital condition
• Past injury to the chest
94. • When the right bundle branch is blocked, activation of the
right ventricle begins when electrical activity “spills over”
from the left ventricle. Depolarization of the right ventricle is
delayed.
• The QRS is prolonged (over 0.10 sec) in right bundle branch
block (RBBB). This extra length of the QRS is caused by late
activation of the right ventricle, which is then seen after the
left ventricle activity. Normally, right ventricle activity is not
seen, as it is overshadowed by the larger left ventricle.
• In RBBB, a typical RsR’ wave occurs in lead V1. Also, a wide
S wave is seen in leads I, V5, and V6, along with a broad R in
lead R. When RBBB occurs in a patient with old or new septal
infarction, the initial septal R wave may not be seen in lead
V1. Instead, a wide QR complex is seen.
98. • LBBB usually indicates widespread cardiac disease. When
the left bundle is blocked, activation of the left ventricle
proceeds through the muscle tissue, resulting in a wide (>.
12 msec) QRS complex.
• In left bundle branch blockage (LBBB), the QRS usually
has the same general shape as the normal QRS, but is
much wider and may be notched or deformed. Voltage
(height of the QRS complex) may be higher.
• In LBBB, look for wide (possibly notched) R waves in I,
L, or V5-V6, or deep broad S waves in V1-V3. There is
left axis deviation. “Septal Q waves” sometimes seen in I,
L, and V5-V6 disappear in LBBB.
• T waves in LBBB are usually oriented opposite the largest
QRS deflection. That is, where large R waves are seen, T
waves will be inverted. ST segment depression may occur.
103. • The two major branches of the left bundle may be
blocked individually. When only one branch is
blocked, this is called hemiblock — either
“anterior hemiblock” or “posterior hemiblock”
depending on whether the anterior or posterior
fascicles are involved.
• Hemiblocks are commonly due to loss of blood
supply to either the anterior or posterior division
of the Left Bundle Branch.
104. • An occlusion of the Anterior Descending
Coronary Artery will produce an Anterior
Infarction, which often causes Anterior
Hemiblock.
• Left posterior hemiblock is less common
than left anterior hemiblock since the
bundle is much thicker and has a double
blood supply (left and right coronary
arteries).
105. Anterior Hemiblock Posterior Hemiblock
Left axis deviation Right axis deviation
Q waves in lead I Q waves in lead III
Wide or deep S wave
in lead III
Wide or deep S wave
in lead I
106.
107.
108. A block of both the right and the left bundle branch is a complete AV block
110. • Right atrial enlargement (RAE) is
diagnosed by the presence of a P
wave 2.5 millimeters or greater in
height. The P wave often has a sharp,
peaked appearance. This increased
voltage is caused by hypertrophy or
acute strain of right atrial tissue.
• The lead most likely to show the
right atrial enlargement is lead II.
• Causes of right atrial enlargement
include COPD, mitral stenosis,
mitral regurgitation, or pulmonary
emboli. Because RAE is so
frequently seen in chronic pulmonary
disease, the peaked P wave is often
called “P pulmonale.”
111. P pulmonale in II, III, aVF P pulmonale in V1
Classic finding in Severe Right Atrial Enlargement (RAE)
Tall Peaked and Pointed P waves in the Pulmonary leads (II, III,
aVF). If the P wave looks "uncomfortable to sit on", think RAE!!!
113. • Dilation or hypertrophy of the left
atrium may increase the
DURATION of the P wave. (Recall
that right atrial enlargement causes
an increase in the HEIGHT or
amplitude of the P wave.) The P
wave is normally less than 0.11
msec (just under three small boxes).
• The long or abnormally shaped P
wave occurs because of delay in
electrical activation of the enlarged
left atrium, as electricity moves
leftward from the SA node. A P
wave longer than 0.11 milliseconds
is diagnostic of left atrial
enlargement (LAE).
Left atrial enlargement often
occurs in mitral valve disease
(either stenosis or insufficiency).
Because of this association, a
broad notched P wave is often
called “P mitrale.” In addition LAE
often occurs with any cause of left
ventricular hypertrophy.
114. • Diagnosed by finding an m-shaped (notched) and widened P
wave ( > 0.12 second) in a "mitral" leads (I, II, aVL) and/or
a deep negative component to the P in lead V1.
• Caused by conditions that increase either pressure or
volume loading on the atria leading to enlargement and/or
hypertrophy.
– Longstanding hypertension
– Obstructive cardiomyopathy
– Aortic stenosis
– Aortic regurgitation
P mitrale in II, III, aVF P mitrale in V1
115.
116. • Atrial Enlargement Criteria
P > 2.5mm height = RAE
P > 0.11 sec or P notch > 1 box width
or P biphasic > 1 box square = LAE
117. • Right ventricular hypertrophy (RVH) increases the height of
the R wave in V1. An R wave in V1 that is greater than 7
boxes in height, or larger than the S wave, is suspicious for
RVH. Other findings are necessary to confirm the ECG
diagnosis.
– Other findings include right axis deviation, taller R waves
in the right precordial leads (V1-V3), and deeper S waves
in the left precordials (V4-V6). The T wave is inverted in
V1 (and often in V2).
• True posterior infarction may also cause a tall R wave in V1,
but the T wave is usually upright, and there is usually some
evidence of inferior infarction (ST-T changes or Qs in II, III,
and F).
• A large R wave in V1, when not accompanied by evidence of
infarction, nor by evidence of RVH (right axis, inverted T
wave in V1), may be benign “counter-clockwise rotation of the
heart.” This can be seen with abnormal chest shape.
118. RVH may occur with any process that raises the ejection work
in the right ventricle. This may be volume overload such as
atrial septal defect or tricuspid regurgitation, or may be pressure
overload such as pulmonary stenosis. Examples of pressure-
load causes of RVH include pulmonary stenosis or primary
pulmonary hypertension, pulmonary disease (COPD or
pulmonary emboli), large ventricular septal defect, or pulmonary
hypertension due to mitral valve disease.
120. • Left ventricular hypertrophy is caused by increased loads
on the left ventricle. Examples are hypertension, aortic
stenosis or regurgitation, mitral regurgitation, or subaortic
stenosis.
• Left ventricular hypertrophy (LVH) may be difficult to
diagnose with certainty from the ECG. Different scoring
criteria have been recommended. One of the simplest uses
five criteria, with the certainty of diagnosis based on the
number of criteria present. If one is present, diagnose
“possible LVH”; if two, “probable LVH”; if three are
found, “definite LVH.”
121. LVH Criteria #1:
Increased limb lead QRS voltage: R in lead I plus S in lead III greater
than 25 mm.
LVH Criteria #2:
Increased precordial QRS voltage: S in lead V1 plus R in either V5 or
V6 greater than 35 mm.
LVH Criteria #3:
Typical ST and T abnormalities: ST depression or T wave inversion
(or both) in the “lateral” leads (I, L, V4-V6)
LVH Criteria #4:
Large leftward voltage: R wave in lead AVL greater than 11 mm.
LVH Criteria #5:
Left atrial enlargement: Wide (greater than 0.11 msec) P wave. This
criterion is used IN SUPPORT of the diagnosis, not alone.
122.
123.
124. • Strain is usually associated with ventricular
hypertrophy since a ventricle that is straining
against some kind of resistance (e.g. increased
resistance from a narrowed valve or from
hypertension) will become hypertrophied in its
attempt to compensate.
• The changes seen in the EKG are called secondary
repolorization abnormalities
• Ventricular strain depresses the ST segment,
which generally humps upward in the middle of
the segment.
125. • Look for these
changes when
hypertrophy is
present to determine
if there is strain
present:
– Downsloping ST
segment
depression
– T-wave inversion
128. • RVH Criteria
R in V1 > 7 mm or > S
wave
T in V1 inverted
Right axis deviation
S waves in V5-V6
• LVH Criteria
1) R-I + S-III >25 mm
2) S-V1-2 + R-V5-6
>35 mm
3) ST-Ts in left leads
4) R-L >11 mm
5) LAE + other criteria
• Positive Criteria:
1=possible 2=probable
3=definite
129. • This is difficult, but not necessarily
impossible. Look for ST-T wave changes
or new Q waves in left-sided leads (I, aVL,
V6) with LBBB.
• New onset of LBBB is typically
representative of an MI which you must
now R/O.
• Evidence of infarction (Q waves, ST-T
changes) is easier to see with RBBB.
130. • Suspect LVH with LBBB if there is LAA
and/or very deep S waves (>30 mm) in V1,
V2 or V3.
• LVH is probably present with RBBB if the
R in aVL is >12 and/or R in V5 or V6 is
>25.
131. • ECG findings noted during the acute phase of pulmonary
embolism can include any number of the following:
– “S1Q3T3” - prominent S in lead I, Q and inverted T in
lead III
– Right bundle branch block (RBBB), complete or
incomplete, often resolving after acute phase
– Right shift of QRS axis
– shift of transition zone from V4 to V5-6
– ST elevation in VI and aVR
– generalized low-amplitude QRS
– sinus tachycardia, atrial fibrillation/flutter, or right-sided
PAC/PVC
– T wave inversion in V1-4, often a late sign.
134. pacemakers send electrical
impulses to one or more
chambers of the heart. These
signals make the heart
contract in a more regular
rhythm than the chamber
would otherwise. Pacemakers
are designed to treat cardiac
conditions that involve
bradycardia
135. A pulse generator, which
contains both the battery
and the intelligent
circuits, can be very
small, as seen here. This
device can be connected
to a lead which makes
contact with either the
atrium or the ventricular
muscle.
136. • Shown here are two leads. The
one on the top is a lead with a
"J" shape, which is used for
optimal positioning in the
atrium. It is "unipolar", and
therefore smaller, and is a
"tined" lead which makes
passive contact with the atrial
muscle.
• In contrast, the lead on the
bottom is larger because it is a
bipolar device which has more
wire within it. It has a small
screw at the end so that it can
be actively fixated to the
muscle.
137. • Here, a pulse
generator is shown
which is connected to
two leads, for dual-
chamber pacing.
144. • Sick sinus Syndrome (most common) if
symptomatic
• 3rd degree AV block
• Recurrent tachycardias
• Chronotropic incompetence (inability to
increase the heart rate to match a level of
exercise)
• Long QT syndrome
145. • Sends out electrical signals to the upper part
of the heart which are passed down the
usual intrinsic conduction system to the
lower chamber.
– Only if the A-V node and the lower portions of
the electrical system are intact.
• Recommended so that the upper chambers
can initiate a heartbeat much like the natural
heartbeat.
146. • Atrial pacing is commonly seen in patients that have
damaged atrial pacing ability, but normal ventricular
conduction.
• Notice that the pacing spikes stimulate a P wave.
148. • Seen in patients with damaged ventricular ability
• Ventricularly paced rhythms generally have a
wide (> 0.12 secs) ORS complex following the
ventricular pacing spike.
152. • A dual chamber pacer can sense and pace both
atrial and ventricular activity as programmed.
• Coordinates an electrical signal to the upper part
of the heart with a signal to the lower part of the
heart.
• When an individual requires a heartbeat similar
to a normal heartbeat, two wires are placed. One
wire detects the signal and/or stimulates the
upper chamber - atria. The other wire detects the
signal and/or stimulates the lower chamber -
ventricle.
153.
154.
155. • Ventricular inhibited
• Most commonly used type of pacemaker
• Sends out continuous, regular signals if
needed. Can turn itself off when the
individual’s heart sends out a competitive
beat.
• Fires when the pt’s own intrinsic HR falls
below a threshold level.
156. • Ventricular synchronous
• Sends out continuous, regular signals if needed. If
competitive heartbeats or electrical interference
occurs, responds up to maximum of 150 beats per
minute
• Recommended when individual will have contact
with special types of electrical machinery that can
lead to faster pacemaker activity.
• Upper pacemaker rate of 150 beats per minute
prevents unusually rapid heart rate during close
contact with machinery
157. • Characterized by pacing impulses (singly or in
groups) that are not followed by QRS
complexes and produce an irregular rhythm.
• Patient may or may not be symptomatic.
158.
159. • Commonly caused by
a damaged sensing
lead that causes the
pacemaker to
misinterpret the
patient’s native
rhythm
• Characterized by
inappropriate pacing
spikes that can occur
within ALL phases of
the cardiac cycle
160.
161. Infarct in the antereoseptal and anterior wall (Q waves in V2-V4 there is
also a probable inferior infarct (Q waves in II, III, and aVF)).
162. Ischemia across the entire anterior and lateral wall (T wave inversions in V2-V6, I
and aVL). Also note, the injury pattern in V2-3 of ST elevation, the prominent Q
waves in V2 and V3 show that some of the myocardium has also reached the
infarct stage.
