ECG Quiz

ECG Quiz
Sonia Chacko, 5th Year Medicine

Figure 1a: ECG tracing of lead I

A B

ELECTROCARDIOGRAM 1.
Questions
1. Describe the rhythm seen in the electrocardiogram
(ECG) in Figure 1a and b.
2. What are the possible mechanisms responsible for
the production of this rhythm?
3. Is this indicative of a disease process? Figure 1b: ECG
Answers and discussion tracing of lead aVF
There are a few basic principles that should
be followed when interpreting any ECG: evaluate
rate, rhythm and shape. There are two distinctly dif- be more likely to fire abnormally. Things that
ferent QRS complexes present in ECG 1, waves A increase the automaticity of myocardial tissue are
and B. Each wave “A” is followed by (coupled hypothermia, hypoxemia, hypokalemia, and hyper-
with) wave “B” at a fixed R-R interval of 560ms. calcemia1.
This makes the rhythm a fixed bigeminal rhythm. A re-entrant mechanism is one in which the
The A-A rate is 33.3 beats per minute, as is the B-B normal current originating in the SA node passes
rate. When combined, the rate is 70 bpm. The through the ventricular tissue multiple times per
rhythm is irregular, with unequal A-B vs. B-A inter- impulse due to either auxilliary conduction path-
vals. However, the A-B intervals are constant, as are ways or an area of abnormally depressed conduc-
the B-A intervals, making this a regularly irregular tion, such as that created by infarction. Since the
rhythm. Finally, the two waveforms are obviously of generation of the second (or third etc.) ventricular
different morphologies, B being considerably wider impulse is dependent on the normal SA node-gener-
and taller than A, and never preceded by a P wave. ated current, the abnormal complex is linked to the
These characteristics indicate that wave B is of ven- normal complex. There is a repeated fixed interval
tricular origin. Therefore, the rhythm seen in the between the normal and abnormal complexes. Thus,
ECG strip is a regular, fixed coupling, ventricular the rhythm is regular in its irregularity. Circus
bigeminal rhythm. Additionally, all the ventricular rhythm, which can cause atrial fibrillation or atrial
QRS-T complexes in a given lead are identical flutter, is an example of a re-entrant mechanism
(monomorphic). Finally, there is a long interval arrhythmia. In such cases there may be multiple sites
between the abnormal T wave and the following of ischaemic tissue usually secondary to coronary
normal P wave. artery disease1.
There are two mechanisms that are thought If the PVCs are identical in form
to be involved in the generation of premature ven- (monomorphic), they are said to originate at one site
tricular complexes (PVCs). They are automaticity (unifocal); if they vary in form (polymorphic), they
and re-entry. All myocardial cells have the potential are said to have more than one site of re-entry (mul-
to be pacemakers for the heart. The sinoatrial (SA) tifocal). Re-entrant rhythms are usually sudden in
node normally predominates because it has the onset (paroxysmal), regular in rhythm, and respond
fastest rhythm, thereby suppressing all other pace- well to parasympathetic or DC shock stimulation1. It
makers. If the SA node were to cease firing, another has additionally been shown that re-entrant rhythms
focus, such as the AV node, would take over the role and bigeminy, being dependent on a necessary inter-
of pacemaker. Automaticity means that there is an val between SA impulses, are often suppressed by
abnormally active pacemaker site in the heart, which brady- or tachy-cardia2.
is firing and causing myocardial excitation despite a The long interval between the abnormal T
normally functioning SA node. The underlying wave and the following normal P wave is known as
problem is with impulse formation. This situation a compensatory pause. The impulse generated at the
results in irregular ectopic ventricular beats. SA node is conducted in a normal fashion through
Anything which brings resting myocardiocyte mem- the atria and is evident as a P wave. But the impulse
brane potential towards threshold will increase the is blocked at the ventricles since the ventricular
automaticity of these potential pacemakers; they will myocytes are either currently excited by the re-

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TSMJ Volume 2 2001: Clinical M edicine

Figure 2a: ECG Tracing of Lead III

Figure 2b: ECG Tracing of Lead aVF

lowing the re-entrant current, rendering them inca- seen in Chagas’ disease (Trypanosomiasis cruzi
pable of being further excited by the SA current. infection), Brugada syndrome (characteristic ECG
Since the rhythm is regular, it is possible to predict changes of idiopathic origin with high association
the position of these nonconducted P waves as being with ventricular fibrillation/sudden death)4, and
half way between the two adjacent conducted P hypercalcemia5. It has also been described in post-
waves. They are apparent as low-voltage depolariza- myocardial infarct patients and persons with no
tions in the otherwise smooth contour of the PVC known pathophysiology. The most likely diagnosis
(not apparent in this ECG tracing). in this patient is hypothermia, given the apparent
Bigeminal rhythms can be physiological shivering.
and do not require treatment unless they are sympto- Hypothalamic control of core body temper-
matic. ature, as manifested by shivering, is absolutely lost
below 29°C, and severely impaired below 34°C.
ELECTROCARDIOGRAM 2. Therefore, this ECG was taken when the patient was
Questions warmer than 29°C6.
1. What are the two main findings on this ECG? The J wave is caused by an exaggeration of
2. What is the most likely underlying diagnosis? the transmural voltage gradient between the epicar-
3. At what temperature was this tracing taken? dial and endocardial layers of the heart, which is cre-
Answers and discussion ated in such conditions7. The amplitude and duration
The two main findings on this ECG are the of the J wave is inversely related to the core body
violently unstable baseline and the presence of J temperature8. The J wave does normally disappear
waves (Osborn waves) on the QRS complexes with proper rewarming or treatment of the underly-
(arrowheads). The jagged baseline tracing is due to ing disease9 but the danger of J wave appearance is
rapid skeletal muscular contractions. The patient is the increased risk of potentially fatal ventricular
shivering. arrhythmias and sudden cardiac death7.
The J wave is an “extra deflection at the
end of the QRS complex”3. Also known as the ACKNOWLEDGEMENTS
Osborn wave, the J wave was first described in the My sincere thanks to Mr. PK Plunkett,
early 1950’s and was thought to be pathognomonic Cathal O’Donnell and the doctors and staff of St.
for hypothermia. Indeed, it is present in the ECGs of James’ A&E for their excellent teaching all year.
80% of hypothermic patients; however, it is also

REFERENCES
1 Phillips RE, Feeney MK. The Cardiac rhythms: A systematic 5 Anguera I, Valls V. Giant J waves in hypothermia. Circulation
approach to interpretation. 3rd ed. Philadelphia WB Saunders 2000;101(13):1627-1628.
Company, 1990, p362-377. 6 Guyton AC, Hall JE. Human physiology and mechanisms of
2 Kinoshita S, et al. Bradycardia- and tachycardia-dependent ter- disease. 6th ed. Philadelphia: WB Saunders Company, p581.
mination of ventricular bigeminy: Mechanism of ventricular 7 Yan G, Antzelevitch C. Cellular basis for the electrocardio-
extrasystoles with fixed coupling. Am. Heart J. 1995;129:557- graphic J wave. Circulation. 1996;93(2):372-379.
564. 8 Patel A, Getsos JP, Moussa G, Damato AN. The Osborn wave
3 Alhaddad I, Khlil M, Brown Jr EJ. Osborn waves in hypother-
of hypothermia in normothermic patients. Clinical Cardiology.
mia. Circulation 2000;101(25):e233-e234. 1994;17(5):273-276.
4 Brugada P, Brugada J. Right bundle branch block, persistent ST 9 Solomon A, Barish RA, Browne B, Tso E. The electrocardio-
segment elevation and sudden cardiac death: a distinct clinical graphic features of hypothermia. Journal of Emergency Medicine.
and electrocardiographic syndrome. A multicenter report. J. Am. 1989;7(2):169-173.
Col. Cardiol. 1992;20(6):1391-1396.

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