--------------------------------
This is my 7th installment of Basic ECG Concepts. Rather than specific cases — the goal of
these Basic ECG Concepts is concise
review of some less advanced topics that comprise the fundamentals of ECG interpretation. This material is excerpted with
modification from my new introductory
book to ECG Interpretation = “A 1st Book on ECGs-2014” and/or the
expanded 1st-ECG-Book-ePub version. Your
feedback on this series is WELCOME!
--------------------------------
NOTE: To enhance relevance —
some advanced
points have been added illustrating clinical application (with this more advanced material excerpted
from our ECG-2014-ePub). In this
way — We hope this post is of interest and value to ECG interpreters of any level.
--------------------------------
LINKS to Previous Basic ECG Concepts:
--------------------------------
--------------------------------
Having presented our step-by-step Systematic
Approach
in Basic ECG Concepts #6 — We now focus attention on the important 6th Parameter of our Descriptive
Analysis = assessment of Q-R-S-T Changes. In many ways, evaluation of this
Parameter embodies the essence of clinical
ECG interpretation — in that it provides information regarding the likelihood
of acute ischemia/infarction (vs
the presence of other conditions that
produce ST-T wave changes). It may also provide insight to the presence and
severity of metabolic disorders.
- Our reason for delaying assessment of Q-R-S-T Changes until the end of the Systematic Approach (ie, until
after assessment of Rate, Rhythm,
Intervals, Axis and Chamber Enlargement — as in Figure-1) —
is that criteria for ischemia/infarction will be different IF the QRS Interval is prolonged and/or the patient has bundle branch
block. How we interpret ST-T wave changes may also be affected by the rate and
rhythm, and whether or not LVH or RVH is present.
CAVEAT: Our purpose
in using “Q-R-S-T” as a memory
aid —
is so that nothing is forgotten
during the process of systematic
assessment.
- The most commonly overlooked feature —
is the presence of a predominant R
wave in lead V1 and/or early
transition or presence of an rsr’ complex in lead V1. Routine inclusion
of “Q-R-S-T” in your assessment automatically reminds you to consciously evaluate the “R” component = normality of precordial lead
evolution.
 |
| Figure-1: The 6 Parameters in the Descriptive Analysis step of our Systematic Approach to ECG interpretation. The reason we assess Q-R-S-T Changes last (as the 6th Parameter) — is that criteria for ischemia/infarction may change if there are abnormalities in any of the preceding 5 Parameters. |
--------------------------------
Assessing
for Q-R-S-T Changes: Looking for Q Waves
In Basic ECG Concepts #1 — We defined a Q wave as the 1st downward
deflection of the QRS complex. We then refined our classification by
use of large or small-case letters — depending on whether the Q wave was wide
and at least 3 mm (= 3 little boxes)
deep. These features are illustrated in Figure-2.
- Small and narrow Q
Waves (as seen in Panel
A of Figure-2) — are often normally seen in healthy
subjects. This is particularly true when such small and narrow q waves are
present in one or more of the lateral leads (leads I,
aVL; V4,V5,V6) — especially
if the clinical scenario and the rest of the ECG appears to be benign.
- In contrast — large and wide
Q Waves (as seen in Panel B) — are much more likely to indicate that at some point there has been an
MI (Myocardial Infarction). The larger and wider
the Q waves are — and the more leads in which they
are seen — the more likely it becomes that they indicate prior
MI.
Advanced
Point: Be aware of
a 3rd possibility regarding Q waves — in which an all-negative complex is seen (Panel C). Because there is no positive deflection (ie, no R wave) — We are unable to tell if the all-negative
deflection that is seen is: i) a Q
wave; ii) an S wave; or iii) some combination of the two. As a “compromise” — this pattern is called a
QS complex (as seen in Panel C).
- Clinically — a QS pattern is most commonly seen
in one or more of the anterior leads.
Depending on other parameters (such as QRS complex width and ST-T wave
appearance) — clinical implications of a QS pattern may be similar to
clinical implications of a wide Q wave (= possible
previous infarction) — especially if QS complexes are seen in multiple
leads. On the other hand — the presence of one or more QS complexes may be a
normal finding (See discussion of Figure-5 below).
- NOTE: All bets are off (!)— IF QS complexes are seen in a
patient with QRS widening from LBBB (Left
Bundle Branch Block). In this situation — anterior QS complexes are not only
common, but an expected accompaniment
of LBBB (See Figure-3 in Basic ECG Concepts #6).
 |
| Figure-2: Types of Q waves. In Panel A — the q wave is small and narrow (clearly not more than 3 mm in depth). Q waves this small and narrow are less likely to indicate prior infarction. In contrast — the Q wave in Panel B is much wider and deeper. The wider and deeper a Q wave is — and the more leads in which they are seen — the more likely it becomes that such Q waves indicate prior MI. Finally, in Panel C — there is a QS pattern (because the QRS complex is all negative without any positive deflection). Clinically — a QS complex may or may not indicate prior infarction. |
--------------------------------
Clinical
NOTES: Even when
large and wide Q waves indicate that prior infarction has taken place (as would
be suggested by Panel B) —
the mere presence of such Q waves
does not tell us anything about the “age” of the infarct (ie, whether it occurred years ago —
or fairly recently).
- To determine IF an MI might be “acute”
(ie, beginning within the
past few hours — and possibly still ongoing) — We use a combination of: i) History (ie, Is there new-onset chest pain?
— or —
Is chest discomfort more of a longterm problem without recent onset?); ii) Assessment of ST-T
wave changes on serial ECGs (as will be discussed momentarily); iii) Blood tests, such as
cardiac troponin assays — that
within hours show progressively increasing troponin levels roughly correlating
with the amount of cardiac damage; and on occasion, iv) Use of other
tests (which may include an Echocardiogram
at the bedside looking for abnormal heart wall movement — or — cardiac catheterization to
look for an acutely occluded major coronary vessel).
- Advanced
Points = CAVEATS:
Although deep and wide Q waves often serve as a “marker” of prior infarction —
this ECG sign is not without
exceptions. Certain conditions (ie, cardiomyopathy)
may produce Q waves not due to
infarction (See ECG Blog #45). Further
complicating assessment of Q waves on ECG — is the clinical reality that infarction-related Q waves do not always persist after the
event. With time — Q waves may either
decrease in size or disappear entirely. As a result — even small q waves may at times be a “marker”
of prior infarction (ie, if a previously
large infarction-Q-wave shrunk in size but did not disappear). Awareness of
the clinical history and what the patient’s baseline ECG looked like would be needed to know if persistent
small q waves in that patient were
serving as a marker of prior infarction (assuming
lead placement issues and a shift in axis were not the reasons for change in Q
wave morphology).
--------------------------------
Q-R-S-T Changes: Assessing “R Wave Progression"
As alluded to
in our introduction to this ECG Basic Concepts #7 — Our purpose in using “Q-R-S-T” as a memory aid
— is so as not to
forget to evaluate the “R” component = “R” Wave Progression
in the precordial leads. We schematically illustrate this concept in
Figure-3 — in which the
heart’s electrical activity is depicted in the Transverse (Horizontal) Plane. The predominant direction of
this electrical activity is to the left and posteriorly
(as suggested by the red arrow in Figure-3).
This predominant direction of electrical activity accounts for the change in appearance of the QRS complex
in precordial leads V1-thru-V6 as we move across the chest:
- Initially in right-sided lead V1 — the QRS
is predominantly negative (an rS complex). This is because lead V1
sees most of the heart’s electrical activity as moving away from the
right as the much larger and thicker LV (Left
Ventricle) is depolarized.
- Note how the R Wave “progresses”
— by getting taller as one moves from
leads V1 and V2 toward left-sided
leads V5 and V6.
In general — R wave amplitude “tops out” by lead V5, and then becomes smaller
in lead V6. This is the situation in Figure-3 — although many variations
on this pattern of R wave progression are possible.
- We define the
point of “Transition” — as the place where the R wave
becomes taller than the S wave is deep (highlighted by the green arrow in Figure-3). Normally
— transition occurs between leads V2-to-V4.
It occurs between lead V3-to-V4 in Figure-3.
 |
| Figure-3: Schematic blow-up cross-section of the heart. Precordial lead placement of recording electrodes is suggested by the yellow ovals. Note our focus on the predominant direction of the heart’s electrical activity during ventricular depolarization (red arrow) — and the effect this has on progression of R wave amplitude in the precordial (chest) leads. Initially (ie, in leads V1,V2) — there is a predominant S wave (negative deflection) — because most of the heart’s electrical activity is moving away from these right-sided leads. As one moves across the chest — the R wave becomes taller until the point of transition is reached where the R wave becomes taller than the S wave is deep (green arrow). This occurs between lead V3-to-V4 in this Figure (Transition normally occurs somewhere between lead V2-to-V4). |
--------------------------------
Septal
Depolarization: The final point illustrated in schematic Figure-3 — is the
effect septal depolarization
may have on the ECG. After the Sinus-Node-conducted
impulse leaves the AV Node — the very first
part of the ventricles to be depolarized is the left side of the interventricular septum. As a result — septal
activation normally proceeds from left-to-right (small
blue arrow in
Figure-3).
- Because septal activation normally
moves toward right-sided lead V1
— there will often be a small initial r wave (positive deflection) in lead V1 as well as in lead V2 (as is
seen in these leads in Figure-3). This small initial r wave may be
lost when there is septal infarction.
- At the same time — septal activation
normally moves away from left-sided leads V5,V6. As a result — one or more lateral
leads (ie, leads I,aVL; V4,V5,V6) will often manifest a small initial q wave (negative deflection) simply as a reflection of normal septal activation.
As discussed in explanation to Figure-2 — lateral q waves are unlikely
to indicate prior infarction IF: i)
these q waves are small and narrow; and ii) the clinical scenario and the rest of the ECG appears to
be benign.
--------------------------------
TEST
YOURSELF: Where is the Point of Transition?
Look at the 3 schematic precordial lead sequences in Panels A, B
and C of Figure-4. Comment on R wave progression in each of these sequences.
- In each
case — Indicate the 2 leads between which
Transition occurs.
- What do you think is meant by the term,
“late” Transition?
 |
| Figure-4: Identify the point of Transition for the 3 precordial lead sequences shown in this Figure. What is meant by the term, “late” Transition? HINT: Transition normally occurs somewhere between lead V2-to-V4. |
--------------------------------
ANSWER to Figure-4: The R wave “progresses” in each of the 3 sequences shown in this
Figure. By this we mean that R wave amplitude is smallest in lead V1 — and then gets taller as one moves to the next
precordial leads.
- Normal Transition
occurs in Panel B. That is —
the R wave becomes taller than the S wave is deep between lead V3-to-V4.
- In Panel A
— there is “early” Transition.
By this we mean that the R wave becomes taller than the S wave is deep before the normal point of transition.
Specifically — Transition in Panel A occurs between V1-to-V2.
- In Panel C
— there is “late” Transition.
That is, the R wave becomes taller than the S wave is deep after the normal point of transition. Specifically —
Transition in Panel C occurs between
V4-to-V5.
--------------------------------
Putting
It Together: Assessing “R Wave Progression"
Insight
into the clinical utility of routinely
assessing the “R” component in the “Q-R-S-T” parameter is
forthcoming from review of Figure-5.
- Panel
A in Figure-5
— shows normal R wave
progression. Note progressive
increase in R wave amplitude across successive
precordial leads until the R wave “tops out” in lead V5. Transition is normal
in Panel A (occurs between lead
V3-to-V4). FINE Points: Although a QS complex is present in lead
V1 — this is unlikely to reflect
prior septal infarction because the QS complex is limited to lead V1 (ie, an r wave develops by lead V2 in Panel
A). The small and narrow q waves in leads
V5,V6 almost certainly represent normal
septal q waves. They are unlikely to indicate prior infarction —
because of their small size and expected lateral
location.
- In contrast — anterior infarction is suggested by the
precordial lead sequence in Panel B.
This is because a QS complex is seen not only
in leads V1,V2 — but also in lead
V3. FINE
Points:
We can more specifically qualify location of the infarct in Panel B as
being “antero-septal”
— because there is loss of the
initial r wave in leads V1,V2. Note that despite
the QS in V1-thru-V3 — transition is
still “normal” (occurs between lead
V3-to-V4). Finally — the isolated
small and narrow q wave in lead V6 of Panel B is unrelated to the
anterior infarction and almost certainly once again reflects a normal
septal q wave.
- In contrast, in Panel C — a QS
pattern is seen in both lead V1 and V2, but not in
lead V3. That is — a small-but-definite
initial positive deflection (r wave)
is seen in lead V3. The finding of a QS complex in V1,V2 but not in V3 — may or may not be a
“normal” finding. Instead, it could indicate: i) a technical lead placement error; ii) septal infarction; or iii) a normal variant. Since there may not be any
reliable way to distinguish between normal variant vs lead placement
error vs prior septal
infarction — We simply acknowledge, “QS in
V1,V2; Suggest clinical correlation” in
our interpretation. FINE Points: Statistical odds are far greater (approximately 4-to-1) that either normal variant or
lead placement error rather than septal
infarction are the reason for a QS
complex in V1,V2 but not V3 (as seen in Panel C).
 |
| Figure-5: Normal RWP (R Wave Progression) is seen in Panel A. This is in comparison with precordial lead sequences suggestive of anterior MI (Panel B) vs an indeterminate pattern showing a QS complex in leads V1,V2 but not in V3 (Panel C). |
--------------------------------
- Advanced
NOTE-1: The above comments regarding clinical implications of a QS complex in
leads V1,V2,V3 hold true only
when the QRS complex is narrow. As we have already noted — QRS widening due to LBBB commonly produces QS complexes in
anterior leads that are simply the result of the conduction defection and are not indicative of anterior infarction (See Figure-3 in Basic ECG Concepts #6).
- Advanced
NOTE-2: There are at least 3 other common reasons for PRWP (Poor R Wave Progression)
with a narrow QRS complex that are not the result of prior
infarction. These are: i) LVH; ii) LAHB; and iii) Severe pulmonary disease/COPD. Usually at least some r wave will be seen by lead V3 with these other conditions —
though not always. Bottom
Line: It is sometimes extremely difficult to know with certainty the
cause of PRWP when R waves in leads V1,V2,V3 are either very small or absent. Clinical correlation is essential.
Beyond-the-Core: It is insightful to appreciate the physiologic reason why R wave
progression is often “poor” in the presence of these other conditions.
- LVH (Left
Ventricular Hypertrophy) — produces an increase in leftward
and posterior forces. When marked — these leftward and posterior forces may
totally predominate over initial
rightward and anterior forces seen in leads V1,V2,V3. The result is reduction
in r wave amplitude in anterior leads. At times — there may even be elimination
of any r wave at all in V1,V2,V3.
- LAHB (Left
Anterior HemiBlock) — The bundle of conduction fibers
in the LAH (Left Anterior Hemifascicle)
lies slightly in front of (anterior to)
fibers in the LPH (Left Posterior
Hemifascicle). As a result — block in the LAH (as occurs with LAHB) results in an initial posterior direction for electrical activity that is first conducted
over the intact LPH. The result may once again be reduction in r wave amplitude
in the anterior leads.
- COPD (Chronic
Obstructive Pulmonary Disease) — Severe longstanding
pulmonary disease leads to an increase in right ventricular forces. In addition
— orientation of the heart’s electrical forces in 3 dimensions may be altered
by the large emphysematous chest of a patient with chronic COPD. These
physiologic changes may result in ECG signs of poor R wave progression;
persistence of relatively deep precordial S waves in lateral chest leads; and
development of an indeterminate axis
in the transverse plane. In the extreme — R waves are markedly reduced in size
(and may even be absent) in anterior
precordial leads.
--------------------------------
QRST:
Assessing
for ST-T Wave Abnormalities
We are finally up to assessment of ST-T Wave Changes.
Clearly — this is a topic unto itself that requires clinical application and much practice to attain a level of
comfort in your assessment. We limit presentation here to basic description of
the changes we look for — with our Goal being to reinforce these principles in future installments of Basic ECG Concepts.
- In Basic ECG Concepts #6 — We defined the baseline from which ST
segment deviation (either elevation or
depression) is judged. The normal ST segment is isoelectric. It lies on the baseline — and, is neither “elevated” nor “depressed” (Figure-6). Although our
preference in general is to use the PR
segment baseline — the TP baseline may be selected instead.
Particular features on a given
tracing (such as the amount of baseline
wander or the presence of PR depression) may influence our selection of
which baseline to choose — or
whether to combine use of PR and TP
segments in a given case.
- Heart rate is another factor that may influence our choice
of which baseline to use (PR, TP or both).
For example, sinus tachycardia may shorten
the PR interval, as well as reducing
duration of the TP segment. Clearly — accurate determination of the true
“baseline” for judging ST-T wave deviations will not always be as clear cut as it is in Figure-6.
 |
| Figure-6: Overview illustration of ST-T Wave Changes. ST segment deviation (either elevation or depression) — is judged with respect to the PR Segment Baseline (green arrow in Panel A). Alternatively — the TP baseline may be used. Panels B and C show several millimeters (little boxes) of ST Elevation (B) or ST Depression (C). Given how distinct boundaries between P wave, QRS complex and T wave are — it does not matter in this Figure whether one selects the PR or the TP segment as the “baseline”. Panel D shows the J-Point (defined as the point where the end of the QRS — joins the beginning of the ST segment). Note that there is at least 1mm of J-point ST elevation in Panel D. J-point notching as seen here — is very characteristic of Early Repolarization. |
--------------------------------
ST-T Wave Shape:
Descriptive analysis assessment of the ST segment and T wave entails attention
to the following:
- Is there ST elevation or depression?
IF so — How much? How far is the J-point deviated above or below the
baseline?
- What is the shape of any ST-T wave changes? (ie,
upward concavity = “smiley”-shape — or more worrisome coved = “frowny”-shape — See Figure-7 below).
- What part (location) of the heart manifests ST segment
deviations (elevation or depression)?
— or are ST-T wave
changes generalized as they might be
with the diffuse ST elevation of acute pericarditis — or the diffuse ST depression of
very severe coronary disease. (NOTE: The various Lead Groupings for localizing
ST-T wave changes was reviewed in Basic ECG Concepts #4).
About Lead aVR: For purposes of “the basics” — We do not concern ourselves with lead
aVR at this point beyond our expectation that there may normally be a Q wave and/or T wave inversion in this lead.
Instead — Focus your attention on the remaining 11 leads, looking at each lead for QRST changes.
- Optimal use of Lead aVR is an advanced
topic. For those with an interest in
this subject — Click HERE to download a PDF excerpted from our ECG-2014-ePUb that explores in detail
various ways we use of lead aVR in ECG interpretation.
--------------------------------
FIGURE-7: More
on ST-T Wave Changes
Descriptive analysis of the ST-T wave entails
recognition of several basic morphologies. We schematically illustrate these in
Figure-7 — in which we
compare the normal ST-T wave with the most common ST-T
wave changes you are likely to see. Note the following:
- Panel
A (in Figure-7) — The ST-T wave is normal. That is — there
is no ST segment elevation or depression. Note that there is a smooth
transition between the end of the ST segment and the beginning of
the T wave. In a normal ECG — the T wave
will be upright in most leads
that have a positive (predominantly
upright) QRS complex. This will become readily apparent as we look at more
ECGs.
- Panel B (in
Figure-7) — There is a flat ST-T wave. The presence of ST-T wave flattening makes it difficult to tell where the ST
segment ends and the T wave begins. This is a nonspecific change
— which simply means that the ST-T wave is not “normal”, but we
do not know the reason
why.
- Panel C — There is slight ST
depression. There are many possible causes of ST
depression. These include ischemia — “strain” from LVH (See Figure-4 in Basic ECG Concepts #5) — electrolyte imbalance — fast heart rate — and/or
noncardiac factors such as emotional stress or hyperventilation. It is because
there are so many potential causes
for ST-T wave flattening or depression — that clinical correlation
is essential for optimal ECG interpretation.
- Panel D — There is asymmetric ST-T wave depression (red arrow). When QRS amplitude is
increased in a patient with longstanding hypertension or heart disease — this
type of asymmetric ST depression is
characteristic of LV “strain” from LVH.
- Panel E — There is symmetric T wave inversion. In contrast to the asymmetric ST depression associated with
LVH (Panel D) — the more symmetric shape of T wave inversion in Panel E (green arrow) is much more suggestive of ischemia.
- Panel F and Panel
G — illustrate
different shapes for ST elevation (See below).
 |
| Figure-7: Schematic Illustration of various forms of ST elevation and depression (See text). |
--------------------------------
FIGURE-8: 4
ECG Signs of
Acute MI
The hallmark of acute coronary
artery occlusion (that is
the cause of most acute MIs)
— is development of ST elevation on ECG. While the ECG is not
a perfect indicator for determining who is or is not having an acute
MI — the ECG will often be able to tell IF acute
blockage of a major artery has occurred (based
on the pattern of ST elevation and depression in various leads). We review
the 4 ECG Signs of Acute
MI in Figure-8:
- The 1st ECG change (seen
in Panel 1 of Figure-8)
— is coved ST elevation that develops in leads overlying
the area of acute infarction. The “frowny” icon in Panel
F (from Figure-7) — helps recall the worrisome shape that often indicates acute
STEMI (ST Elevation Myocardial
Infarction) in a patient with chest pain. In contrast — the “smiley”
icon in Panel G (from
Figure-7) — helps recall the upwardly concave
shape that will often be benign.
- Q waves (seen in Panel 3 of Figure-8) — often develop in one or more leads
in a given lead area after myocardial necrosis. Q waves serve as a marker
that infarction has occurred.
- Symmetric T wave inversion (as in Panel 2) — typically indicates ischemic (but
not yet irreversibly damaged) myocardium.
- ST depression (as in Panel 4) — may be seen in leads opposite to (or away from) the area of ST elevation —
in which case this ST depression is known as “reciprocal” changes. Alternatively
— ST depression may simply indicate ischemia
(See Clinical Notes below).
 |
| Figure-8: Schematic cross-sectional view of the LV (Left Ventricle) — illustrating the 4 ECG Signs of Acute MI. The area in black depicts the site of acute myocardial damage. Panel 1 — ST elevation (occurs in leads directly over the area of acute infarction); Panel 2 — Symmetric T wave inversion (indicates ischemia); Panel 3 — Q waves (a marker of infarction that develops with time); and Panel 4 — Reciprocal ST depression (seen in leads opposite to or away from the area of ST elevation). Alternatively — ST depression may simply indicate ischemia. |
--------------------------------
Clinical
NOTES on Figure-8:
Many exceptions exist to the above
generalities for the ECG diagnosis of acute infarction. Discussion of intricacies to these exceptions — clearly extends beyond-the-scope of this blog post. That
said — the basic concepts discussed here should serve well for initial ECG
assessment of the patient with new-onset
chest pain. We highlight the following additional clinical points:
- Not all MIs develop ST
elevation and/or Q waves.
Some patients only manifest T wave inversion without ever developing Q waves. Documentation that acute MI has
occurred in such patients is forthcoming from: i) the History (ie, new-onset chest pain); and ii) positive blood tests for acute infarction (ie, elevation of serum troponin assays).
- In Theory — the ST-T wave changes in Panels 1, 2 and 4 of Figure-8
resolve
after the acute event is over such that only Q waves remain. As
emphasized in our discussion in Figure-2 above — the larger and wider that Q waves are and
the more leads in which they are seen
— the more likely it is that such Q waves indicate infarction has taken place.
- Be Aware! — A number of notorious “mimics”
of acute
infarction exist. As mentioned earlier
— there are many possible causes of ST
depression in addition to
ischemia. These include “strain” from LVH — electrolyte imbalance — fast heart
rate — and/or noncardiac factors such as emotional stress or
hyperventilation. There are also other causes of ST elevation
including early repolarization patterns and acute pericarditis. BOTTOM Line: It is not always easy to determine the
cause of ST-T wave abnormities. It is because there are so many potential
causes of ST-T wave abnormalities — that the clinical History is so important in evaluation
of each patient.
SUMMARY: The KEY to use of the ECG for assessing the patient with chest pain — is
to recognize acute STEMI (ST Elevation Myocardial
Infarction) at the earliest
opportunity. This is the group of patients who are most likely to benefit from acute reperfusion (= prompt opening
of the acutely occluded coronary vessel — either by balloon angioplasty during emergency cardiac catheterization or by ‘clot-busting’ thrombolytic medication).
- Remember the ECG Signs in Figure-8.
An acute
STEMI is suggested by the following:
i) a History of new-onset chest pain (usually within the past few hours); ii) worrisome
ST elevation (“frowny”-shape) — in 2 or more leads in a given lead
area; iii)
Reciprocal
ST depression in other lead areas; and iv) No
more than small Q waves at
the time you first see the patient (as
development of large Q waves suggests that the infarction is not as recent).
- Remember
that exceptions exist
to the above generalities.
--------------------------------
PRACTICE
TRACINGS: Assessing for Q-R-S-T Changes
Let’s apply the concepts covered thus far — with a series of Practice Tracings. Because of space constraints — interpretation of the first 5
Parameters (ie, Rate-Rhythm-Intervals-Axis-Hypertrophy)
is given. We begin with the ECG in Figure-9
— obtained from a patient with new-onset
chest pain.
- Assess the
ECG in Figure-9 for Q-R-S-T Changes.
- In view of
the history — What is your Clinical
Impression?
 |
| Figure-9: ECG obtained from a patient with new-onset chest pain. |
--------------------------------
The
first 5 Parameters: The rhythm in Figure-9 is sinus
— as determined by the upright P wave
with fixed PR interval in lead II (blue
arrow). The rate is ~75/minute. All intervals are normal. That is — the PR interval is not more than 1 large box; the QRS is not more than 1/2 large
box; and the QT is not more than 1/2 the R-R
interval. The Axis is normal (probably between +40-60 degrees). There is no chamber enlargement.
Assessment
of Q-R-S-T
Changes:
- Large Q waves are seen in each of the inferior leads (II,III,aVF) in Figure-9 — and small
q waves are seen in leads V5,V6.
- Transition is normal (the R wave
becomes taller than the S wave is deep between lead V3-to-V4).
- The most remarkable findings on this
tracing relate to the ST-T Wave Changes.
There is: i)
ST elevation
in each of the 3 inferior leads (II,III,aVF); and ii) ST depression in other leads on the tracing (I,aVL;
V2,V3,V4) with flat ST segments in leads V5,V6.
Clinical Impression: In view of the clinical history of new-onset chest pain — We would write
the following as our “Clinical
Impression” for
this ECG:
- Sinus rhythm at ~75/minute.
- Acute Inferior STEMI (since the leads showing ST elevation
are the 3 inferior leads). We would urge immediate
clinical correlation — as
this patient appears to be an excellent candidate for acute reperfusion.
Additional
NOTES on Figure-9:
All of the ECG signs of acute evolving
MI are present in this patient who
presents with new-onset chest pain:
- There is ST elevation in each of the inferior leads (Note ST
segments are clearly elevated above the PR segment baseline — as seen within
the red ovals in Figure-9). In addition — the inferior T wave in lead III looks
peaked, which suggests a “hyperacute”
change.
- There are Q waves in each of the inferior
leads.
- There is “reciprocal” ST depression in other
leads (including leads I,aVL;
V2,V3,V4) The finding of ST-T wave depression in leads away from the lead area showing ST elevation (leads II,III,aVF) — strongly supports our impression that inferior ST elevation in this tracing is acute
in this patient with new-onset chest
pain.
- Beyond-the-Basics: A number of more advanced points may be made about this tracing: i) In
addition to being a “reciprocal change”
— ST depression in leads V2-to-V4 may
also reflect acute posterior infarction; ii) The “culprit” (= acutely occluded) artery — is probably the RCA (Right Coronary Artery) —
because ST elevation in lead III is clearly more than in lead II; and iii) We also suspect acute
RV (Right Ventricular)
infarction — because instead of similar
ST depression as is seen in lead V2 — the
ST segment in right-sided lead V1 is
flat (presumably because ST elevation in right-sided lead V1 from acute RV MI has cancelled out some of the ST depression we expected to see in lead V1 from the posterior MI).
- Final
Point: Be aware
that fairly large Q waves are already present on this tracing!
This finding puts the “age” of this STEMI in some question — since it usually takes at
least a little bit of time for infarction Q waves to develop. That said — because the history is of “new-onset” chest pain and other ECG changes look acute — this patient may still benefit from acute reperfusion.
--------------------------------
TEST
YOURSELF: Is there an Acute
STEMI?
Interpret the ECG in Figure-10 — obtained from a patient with new-onset
chest pain.
- Assess the
ECG in Figure-10 for Q-R-S-T Changes.
- In view of
the history — What is your Clinical
Impression?
 |
| Figure-10: ECG obtained from a patient with new-onset chest pain. |
--------------------------------
The
first 5 Parameters: The rhythm in Figure-10 is
sinus — as again determined by the upright
P wave with fixed PR interval in lead II (green
arrow). The rate is ~60/minute. All intervals are normal. The Axis is
normal (probably between +60-85 degrees).
There is no chamber enlargement.
Assessment
of Q-R-S-T
Changes:
- No Q waves are seen.
- Transition is normal
(the R wave becomes taller than the S wave is deep between lead V2-to-V3).
- The most remarkable finding on this
tracing relates to dramatic ST elevation
that begins in lead V1 — and extends across all 6 of the chest leads. ST
elevation is coved in appearance (“frowny”-shape) — and is most marked in leads V2-thru-V4. In addition
— there is reciprocal ST depression
in the inferior leads (II,III,aVF).
Clinical Impression: In view of the clinical history of new-onset chest pain — We would write
the following as our “Clinical Impression” for this ECG:
- Sinus rhythm at ~60/minute.
- Extensive and
Acute Antero-Lateral STEMI. We would urge immediate
clinical correlation — as
this patient appears to be an excellent candidate for acute reperfusion.
Additional
NOTES on Figure-10:
This is a large infarct! ST elevation is seen in all 6 precordial leads — and
the amount of ST elevation in several
of these leads is marked. That said, the
“good news” — is that the ECG picture in Figure-10 suggests that the MI
is still in a relatively early stage of evolution because: i) ST segments are still markedly
elevated; ii) There is reciprocal ST depression in other leads; and iii) No Q waves have yet formed. We
make the following additional points:
- Further precision regarding how “old”
this infarct is — might be obtained
simply by asking the patient, “WHEN did
your chest pain begin?
- The sooner the “culprit” artery (that is acutely blocked by clot) can be reperfused (ie, opened to
restore blood flow to the heart — either by balloon angioplasty or
‘clot-busting’ thrombolytic medication) —
the better the outcome.
This is why it is so important to identify acute
STEMIs like the one shown in Figure-10 at an early point in the process.
- As discussed in Basic ECG Concepts #4 — the anatomic areas of
the heart that appear to be most involved in Figure-10 are: i) the Septum (ST elevation in leads
V1,V2); ii)
the Anterior
wall (ST elevation in leads V2-thru-V4); and iii) the Lateral wall (ST elevation in leads V4-thru-V6). We can summarize this involvement by saying the STEMI is either an
extensive anterolateral stemi or
an antero-septal-lateral stemi.
- Beyond-the-Basics: Several more advanced points may be made about this tracing: i) Reciprocal ST depression is seen in the inferior leads. That said — reciprocal ST depression is not always seen with every acute
anterior MI; ii)
The “culprit”
(= acutely occluded) artery
— is probably the LAD (Left Anterior Descending) coronary artery — because
of the anterior lead area of maximal
ST elevation; iii) We can go one step further in suspecting a proximal
LAD occlusion because of marked ST elevation in lead V1 and
reciprocal ST depression in the inferior
leads (whereas mid- or distal LAD
occlusions typically show neither of those findings); and iv)
Left-main disease is less likely in Figure-10
because there is marked ST elevation
in lead V1 but no ST elevation
in lead aVR (whereas severe left-main
disease typically manifests ST elevation in aVR with a lesser amount [if any]
of ST elevation in lead V1).
--------------------------------
TEST
YOURSELF: Acute MI vs Early Repolarization?
Interpret the ECG in Figure-11 — obtained from an asymptomatic
young adult in for a routine pre-employment exam.
- Assess the
ECG in Figure-11 for Q-R-S-T Changes.
- In view of
the history — What is your Clinical
Impression?
 |
| Figure-11: ECG obtained from an asymptomatic young adult in for a routine pre-employment exam. |
--------------------------------
The
first 5 Parameters: The rhythm in Figure-11 is
sinus — as determined by the upright
P wave with fixed PR interval in lead II (red
arrow). The rate is ~60/minute. All intervals are normal. The Axis is
normal (close to +60 degrees). Voltage
criteria for LVH would be met IF the patient was ≥35 years old.
Assessment
of Q-R-S-T
Changes:
- Small and narrow q waves are seen in leads V5,V6.
- Transition is normal
(the R wave becomes taller than the S wave is deep between lead V2-to-V3).
- The most remarkable finding on this
tracing relates to J-point concave up (ie, “smiley”-shape)
ST elevation that is present in multiple leads — including leads I, II
and V3-thru-V6. The amount of ST
elevation in these leads is considerable — attaining at least 3 mm in lead V5.
- There is no reciprocal ST depression.
Clinical Impression: In view of the clinical history (ie, that this ECG was obtained from an asymptomatic
young adult in for a routine pre-employment exam) — We would write the
following as our “Clinical Impression” for this ECG:
- Sinus rhythm at ~60/minute.
- Upward sloping ST elevation in multiple
leads that probably reflects ERP (Early Repolarization Pattern).
- Suggest clinical correlation.
Additional
NOTES on Figure-11:
The 1st clue that this ECG is likely to be benign — is the History (ie, an asymptomatic young adult in for a
routine pre-employment exam). That said —
even young adults in their 20s can on occasion develop acute MI. Therefore, the onus of proof lies on us to establish that the ST elevation seen in this
tracing does not represent an
acute stemi (rather than the other way
around). ECG signs why despite the considerable amount of ST elevation seen
in Figure-11 — these ST-T wave findings are most probably benign
include the following:
- The q waves that are seen in leads
V5,V6 are small and narrow (ie, they are
most probably normal septal q waves that are commonly seen in one or more lateral leads).
- ST elevation is “smiley” shape (which
is common and often a benign finding when it occurs in otherwise healthy young
adults).
- In addition to the upward-concavity (smiley) shape of elevated ST segments in Figure-11 — J-point notching is seen in several leads (blue
arrows in V5,V6 — and also in
leads II, aVF, V3,V4). This J-point notching (previously shown in Panel D of Figure-6 above)
— is highly characteristic
of a benign repolarization pattern.
- There is no reciprocal ST depression in Figure-11.
- Beyond-the-Basics: Knowing the History is essential for
interpreting the ECG in Figure-11. As emphasized at the end of our
discussion in Basic ECG Concepts #6 — this identical ECG might be interpreted very differently IF the
history suggested either
pericarditis or an acute coronary syndrome. It is primarily because we
are told this patient is an asymptomatic
young adult that we can confidently interpret this tracing as representing ERP.
- For
more detailed Review
of Early Repolarization
Pattern — See Sections 09.14-thru-09.24 in this pdf from ECG-2014-ePub.
--------------------------------
TEST
YOURSELF: Ischemia/Acute MI or
LV “Strain”?
Interpret the ECG in Figure-12 — obtained from a 60-year old man with longstanding hypertension.
He has been having chest pain.
- Assess the
ECG in Figure-12 for Q-R-S-T Changes.
- In view of
the history — What is your Clinical
Impression?
 |
| Figure-12: ECG obtained from a 60-year old man with a history of hypertension. He is having chest pain. |
--------------------------------
The
first 5 Parameters: The rhythm in Figure-12 is
sinus — as determined by the upright
P wave with fixed PR interval in lead II (green
arrow). The rate is ~70/minute. All intervals are normal. The Axis is
normal (close to +50 degrees).
Voltage criteria for LVH are definitely satisfied (Sum of deepest S in V1,V2 + tallest R in V5,V6 is clearly >35 mm).
Assessment
of Q-R-S-T
Changes:
- No Q waves (other than in lead aVR —
which is allowed). We believe there is a tiny-but-real initial positive deflection (r wave) in lead V1 of Figure-12. Even if an initial small r
wave was not present — an isolated
QS in lead V1 is common and not by itself abnormal.
- Transition is normal (occurs between
V2-to-V3).
- The most remarkable finding in Figure-12
is deep symmetric T wave inversion in multiple leads (ie, leads
II,III,aVF; and V3-thru-V6). The shape of these ST-T waves closely
resembles the symmetric T inversion from Panel
E in Figure-7 (especially
in leads V3,V4,V5). This should be distinguished from the asymmetric ST-T wave depression of Panel D in Figure-7, that
is more characteristic of LV “strain”. As a subtle
point — the ST-T wave in lead V6 of Figure-12 looks intermediate between the picture of Panel D vs Panel E (See blow-up insert for lead V6).
Clinical Impression: In view of the clinical history (ie, that this ECG was obtained from a 60-year
old man with hypertension and chest pain) — We would write the following as
our “Clinical Impression” for this ECG:
- Sinus rhythm at ~70/minute.
- LVH (Left
Ventricular Hypertrophy).
- Regarding ST-T Wave Changes — it
is likely that both LV “strain” and ischemia
are present in this patient with hypertension and chest pain.
- Suggest clinical correlation.
Additional
NOTES on Figure-12:
There are several important points to make about our interpretation of this
tracing.
- FIRST — We are happy IF you
simply recognized sinus rhythm — LVH
— and symmetric T wave
inversion in multiple leads
suggesting ischemia. These are the
KEY findings on this tracing.
- The ECG in Figure-12 is not suggestive of an acute STEMI.
This is because there is no ST
elevation (ie, the “ST” and “E” in STEMI
stand for ST Elevation). On the other hand — symmetric
T wave inversion (as is seen in
multiple leads in this tracing) does suggest ischemia. This may or may not be acute. That said — acute infarction may occur without ST elevation (called a “Non-STEMI” = Non-ST-Elevation
Myocardial Infarction).
- IF the clinical history of “chest pain” was suggestive of ACS
(Acute Coronary Syndrome)
— then other tests (ie, blood
troponin assays) would be needed to determine if a Non-STEMI had occurred.
- As already emphasized — the importance
of recognizing an acute STEMI at the earliest possible moment — is that this
type of infarction is almost always caused by acute occlusion of a major
coronary artery — and, outcome may be improved by acute reperfusion of the “culprit” (= acutely occluded) artery. Even IF troponins are positive (indicating that some “death” of myocardial tissue has occurred) —
acute reperfusion is unlikely to
improve outcome in patients whose symptoms are controlled and who do not have ST elevation on their
ECG. These patients without ST
elevation generally do not
need prompt cardiac catheterization.
- Beyond-the-Basics: Note in Figure-12 that in
addition to ST-T wave depression — the J-point
is also depressed below the PR segment baseline in several leads (highlighted in the lead V6 blow-up).
There is also some “coving” of the ST
segment in a number of leads (See “frowny”
figures in V3,V4). These 2 additional findings further support our
suspicion of ischemia as well as LV “strain” from LVH. Clinical correlation
will be needed to know how best to
proceed.
--------------------------------
FINAL
COMMENT: A LOT of material has been covered in this Basic
ECG Concepts #7. Routine use of a sequential Systematic Approach with special attention devoted
to assessing Q-R-S-T Changes should
yield dividends in picking almost all
key findings that you'll see on an ECG.
- As practice and review — Consider redoing your interpretation of Figures 9-thru-12 in this Blog post.
--------------------------------
—
For more information — GO TO —
- NOTE: We have made a 65-minute ECG Video on use of the Systematic Approach to ECG Interpretation — AND — Assessing for QRST Changes (www.QRSTecg.com).
- For Review on which leads may normally manifest T wave inversion and/or large isolated Q waves — Please See our ECG Blog #79 -
-
-
- NOTE: Material and Figures #1-thru-4 and 6-thru-12 have been
excerpted from our newest publication
= “A 1st Book on ECGs-2014” and/or from the expanded
1st Book ePub version
(available in kindle-kobo-nook-ibooks).
- -USE-BLOG.png)
-
- More advanced material and Figure #5 have been excerpted
from ECG-2014-Pocket Brain and/or from the expanded
ECG-2014 ePub version
(available in kindle-kobo-nook-ibooks).
- -USE-BLOG.png)
-
- Please check out Free Download of our expanded GLOSSARY of ECG-related
terms
-
-
--------------------------------------------------------------
-
%2BLABELS.png)
