6. Let’s take a moment to review the steps you should follow
every time you read an ECG.
Try to get into the habit of following the steps in the same
order each time:
1. Check the standardization and quality of the ECG (The
usual calibration is 25 mm/sec and 10mm/mV)
2. Calculate the heart rate
3. Analyze the rhythm (Is it sinus; sinus plus ectopic beats; or
some entirely non-sinus mechanism such as atrial fibrillation,
ventricular tachycardia or a junctional escape rhythm?)
4. Check the PR interval
5. Check the P wave size
6. Check the QRS width
7. Check the QT interval
8. Check the mean QRS electrical axis
9. Check the QRS voltage
10. Check the R wave progression in the chest leads
11. Look for abnormal Q waves
12. Look for ST segment abnormalities
13. Look for T wave abnormalities
14. Look for prominent U waves
7. Case #26:
21-year-old female with a
history of "seizure" disorder.
She is on no medications and
her electrolytes are normal.
8.
9. Dx: Congenital long QT syndrome. The ECG
demonstrates a prolonged QT interval of 0.6
seconds. Note the broad T waves with notching
(or possibly U waves) in the precordial leads.
This characteristic may identify patients with
long QT syndrome at increased risk for torsade
de pointes and syncope and sudden death.
Patients at high risk of recurrent syncope or
sudden death are usually considered for
implantable cardioverter defibrillator therapy
along with beta-blockade. A number of different
"channelopathies" have been identified in the
pathogenesis of congenital long QT syndrome.
(Ref: Kass RS, Moss AJ. Long QT syndrome: J
Clin Invest 2003;112:810-5.)
11. Limb lead reversal.
The left and right arm leads are reversed. The clue is
inversion of the P wave and QRS complex in lead I.
Whenever you see a negative P wave and QRS complex
in lead I the likely diagnosis is limb lead reversal.
Dextrocardia is another possibility, but in dextrocardia
there is loss of R wave progression in the left chest
leads which is not seen in this tracing. Another clue is
the dissimilarity of the morphology of the QRS
complexes in lead I and V6. (The variability in heart rate
here is due to respiratory sinus arrhythmia, a
physiologic finding that is most apparent in younger
healthy subjects.)
12. Case #28: 85-year-old male without symptoms
on no significant cardiac medications. What is
the diagnosis and does it necessitate a
pacemaker?
13. Sinus rhythm with 2:1 AV heart block.
The ECG shows a bradyarrhythmia with non-conducted sinus P
waves alternating with normally conducted P waves. It is not
possible to reliably identify the point of block (nodal vs.
infranodal) from this single ECG with 2:1 conduction. There is
no evidence of acute inferior ischemia, either. The site of
block could be proximal (in the AV node) or more distal, in the
His-Purkinje system. In general, with 2:1 block, involvement of
the AV node is favored by a narrow QRS complex and a
prolonged PR interval, or by the presence of intermittent AV
Wenckebach. Block (nfranodal) in the His-Purkinje system
would be favored by a concomitant bundle branch block and/or
with a PR interval of 160 ms or less. A possibly useful bedside
diagnostic test for chronic 2:1 block (in the absence of active
ischemia) would be to increase the sinus rate (mild exercise).
A resumption of 1:1 conduction favors AV node block while
worsening of block strongly favors infranodal disease.
Pacemaker placement is indicated for symptomatic 2:1 block
without reversible cause (e.g., drug effect) and generally for
asymptomatic 2:1 block due to infranodal disease. Intracardiac
His bundle electrogram would definitively identify the site of
block. This patient had intermittent 3:2 AV Wenckebach at
other times, and then resumed 1:1 conduction on subsequent
ECGs, consistent with AV node disease..
15. AV nodal reentrant tachycardia (AVNRT).
This tracing demonstrates a REGULAR narrow complex
tachycardia at a rate of 150. The differential diagnosis of this
supraventricular tachycardia includes: sinus tachycardia,
AVNRT, automatic atrial tachycardia, atrio-ventricular
reentrant tachycardia (AVRT), involving retrograde conduction
over a "concealed" bypass tract, or atrial flutter with 2:1 block.
If P waves can be located it can be helpful in determining the
mechanism of the tachycardia. In this tracing P waves can be
located at the end of the QRS in lead II and aVF, producing a
"pseudo S" wave. Absence of P waves or a "pseudo S" pattern
in II, III, or aVF, or a "pseudo R prime" pattern in V1 is
characteristic of AVNRT due to near simultaneous activation of
the atrium and the ventricle from the AV node. If the diagnosis
is still in doubt, adenosine may be useful in slowing
conduction in the AV node. Reentrant rhythms (AVNRT or
AVRT) may "break" abruptly, converting to sinus; the
ventricular response of other atrial tachcyardia or atrial flutter
will slow often revealing underlying atrial activity. (Note: the
final wide complex waveform is either an artifact or a
ventricular premature beat.)
16. Case #30:
The patient is an elderly man who presented to the
emergency ward with dizziness and new renal failure
17. Dx: Hyperkalemia (7.6 mEq/L) secondary to renal failure.
The ECG demonstrates findings consistent with severe
hyperkalemia -- most importantly marked widening of the QRS
complex. The QRS complex here shows a left bundle branch block
(LBBB) morphology with left axis deviation. However, the QRS
duration (about 240 ms) is much wider than seen with an
"uncomplicated" LBBB or just with left anterior fascicular block due
to intrinsic conduction disease. There is also peaking of the T
waves with prolongation of the PR interval and flattening of the P
waves. If the hyperkalemia is left untreated, the ECG will progress
to a sinusoidal pattern and eventually asystole with subsequent
hemodynamic collapse and death.
19. Sinus rhythm with AV Wenckebach with 4:3
conduction in the setting of an acute inferior
wall infarction. The ECG demonstrates Q
waves and ST elevation in leads 2, 3, and aVF.
There are also reciprocal ST segment
depressions in leads 1, aVL and V2-3. The
rhythm is Wenckebach showing progressive
prolongation of the PR intervals, shortening of
the R-R intervals and block of every fourth P
wave. The presence of "group" beating is
easily recognized and characteristic of
Wenckebach and is often associated with high
vagal tone or nodal ischemia in the setting of
an inferior wall myocardial infraction (MI). The
block is at the level of the AV node.
20. Wait! Not so fast!
What is the anti-phospholipid
antibody syndrome?
21. Antiphospholipid syndrome (APS) is a disorder characterized by
recurrent venous or arterial thrombosis and/or fetal losses
associated with typical laboratory abnormalities. These include
persistently elevated levels of antibodies directed against membrane
anionic phospholipids (ie, anticardiolipin [aCL] antibody,
antiphosphatidylserine) or their associated plasma proteins,
predominantly beta-2 glycoprotein I (apolipoprotein H), or evidence
of a circulating anticoagulant.Multiple terms exist for APS.
Unfortunately, some synonyms can be confusing. Lupus
anticoagulant (LA) syndrome, for example, is misleading because
patients may not necessarily have systemic lupus erythematosus
(SLE) and LA is associated with thrombotic rather than hemorrhagic
complications. In an attempt to avoid further confusion, APS is the
currently preferred term for the clinical syndrome (as described
below).APS can occur in patients without evidence of any definable
associated disease (primary APS). It may also occur in association
with SLE or another rheumatic or autoimmune disorder (secondary
APS). Although antiphospholipid (aPL) antibodies are clinically
linked to APS, whether they are involved in the pathogenesis or are
an epiphenomenon is unclear. (aPL antibodies are known to occur in
up to 5% of healthy individuals.)
23. 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.
24. Given atrial fibrillation and RVH one should strongly
consider mitral stenosis. Additional note on
differentiating right ventricular hypertrophy (RVH) from
lateral MI: In some cases of severe (RVH) with marked
right axis deviation, leads I and aVL may show rS or
even QS waves, simulating lateral MI. In this case, lead
V1 notably shows a narrow qR complex (not just a tall R
wave) strongly suggestive of RVH, rather than
posterior-lateral MI. Also, the lateral precordial leads
here show rS type complexes, not QR waves. Physical
examination, echocardiogram and other imaging
modalities also provide important information about
RVH vs. lateral MI in cases where the ECG is
ambiguous.
41. The ECG reveals an acute anteroseptal
myocardial infarction (MI) in the setting
of a (preexisting) right bundle branch
block (RBBB). This is a dramatic
example of the fact that ischemia and
infarction can still be diagnosed, even in
the setting of conduction abnormalities.
The anterior precordial leads reveal a
qR pattern (analagous to an RSR' with
the R replaced by a pathologic Q),
marked ST elevation, and upright T
waves. This pattern is essentially
pathognomonic for an acute infarction.
42. Three points are worth making with regard to a
RBBB:
1) Secondary T wave inversions are typically
seen in the right precordial leads (only in those
leads with a terminal R'). Upright T waves in
such leads might indicate ischemia, etc. T
wave inversions in leads with no terminal R'
might also be ischemic.
2) ST elevations are not normally seen in
RBBB.
3) Right precordial Q waves may be seen in
RBBB without an infarct (especially in the
setting of acute right ventricular overload), but
if the Q waves extend past V2 or if they are
slurred or wide, they suggest pathology.
Bottom Line: Bundle branch block, especially
RBBB does not render the ECG
uninterpretable!!
43. First Aside:
How can we diagnose an acute
infarction in the presence of a
bundle branch block?
(this is level 4 stuff, but now you
are ready for it)
44. Recognition of a myocardial infarction in the
presence of RBBB is feasible, since the former
deforms the initial part of QRS, and the latter alters
only the late part of the QRS. Thus, Q waves in
inferior leads suggest an inferior myocardial
infarction, while Q waves in precordial and lateral
leads are due to myocardial infarctions in these two
territories. PMI is cited as the single exception, since
it is thought to affect the terminal part of the QRS
complex and thus it is masked by RBBB. Normally
the posterior/basal myocardial region is the last to be
depolarized, and consequently the PMI is expected to
deform the late part of QRS, rather than to generate
early QRS abnormalities.
45. RBBB With Primary ST-T Wave Abnormalities
RBBB is recognized by 1) rR' in V1; 2) QRS duration >0.12s; 3) terminal QRS
forces oriented rightwards and anterior. In RBBB the ST-T waves should be
oriented opposite to the terminal QRS forces. In this example there are "primary
ST-T wave abnormalities" in leads I, II, aVL, V5, V6. In these leads the ST-T
orientation is in the same direction as the terminal QRS forces.
48. Pathologic Q waves are seen in leads II, III, aVF (inferior MI)
and in leads V1-3 (anteroseptal MI). RBBB is recognized by
the wide QRS (>0.12s) and the anterior/rightwards
orientation of terminal QRS forces. When an anteroseptal MI
complicates RBBB (or visa versa) the rSR' complex in V1
(typical of RBBB) becomes a qR complex.
50. Deep Q waves in II, III, aVF plus tall R waves in V1-2 are evidence for
this infero-posterior MI. The wide QRS (>0.12s) and RR' complex in V1
are evidence for RBBB. Any time RBBB has an initial R in V1 equal to
or greater than the R', true posterior MI must be considered. Q waves in
V5-6 suggest an apical lateral wall extension of this large MI.
51. Infero-posterior MI with RBBB
This is an unusual RBBB because the initial R wave is taller than the R'
wave in lead V1. This is the clue for true posterior MI. The tall initial R
wave in V1 is a "pathologic R" wave analagous to the "pathologic Q"
wave of an anterior MI.
54. As for LBBB and acute
myocardial infarctions on
EKG...
55. Three electrocardiographic criteria were found to
have independent value in the diagnosis of acute
infarction in the presence of left bundle-branch
block:
ST-segment elevation equal to or greater than 1 mm
in the presence of a positive QRS complex;
ST-segment depression equal to or greater than 1 mm
in lead V1, V2, or V3;
and ST-segment elevation equal to or greater than 5
mm in the presence of a negative QRS complex.
57. Flow Chart for the Prediction of Acute Myocardial Infarction in the Presence of Left Bundle-
Branch Block, with the Use of All Possible Combinations of the Three Independent
Electrocardiographic Criteria
59. Electrocardiogram Meeting All Three Independent Criteria for the Diagnosis of Acute Myocardial
Infarction in a Patient from the GUSTO Trial with left bundle-Branch Block.The electrocardiogram
shows ST-segment elevation of at least 1 mm that is concordant with the QRS complex (lead II),
ST-segment depression of at least 1 mm in leads V2 and V3, and ST-segment elevation of at least
5 mm that is discordant with the QRS complex (leads III and aVF)
(You are now in possession of the worst EKG
tracing in medical history)
60. Acute myocardial infarction in the presence of left bundle branch block
Features suggesting acute MI•ST changes in the same direction as the
QRS (as shown here)•ST elevation more than you'd expect from LBBB
alone (e.g. > 5 mm in leads V1 - 3)•Q waves in two consecutive lateral
leads (indicating anteroseptal MI)
62. Atypical LBBB with Primary T Wave Abnormalities
Primary T wave abnormalities in LBBB refer to T waves in the same
direction as the major deflection of the QRS. These are seen in leads I, III,
aVL, V2-4. Most likely diagnosis is myocardial infarction.
