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11.0 - ECG-2014-e-PUB-Lytes - (10-16.1-2014) - LOCK
11.0 - ECG-2014-e-PUB-Lytes - (10-16.1-2014) - LOCK
Initial Impression: The ECG in Figure 11.2-1 suggests acute STEMI (ST
Elevation Myocardial Infarction) — in that there is coved ST elevation with T
wave inversion and reciprocal ST depression. That said — there are 3 elements
about the history given and the ECG in Figure 11.2-1 that should be cause for
contemplation: i) There is no history of chest pain; ii) The patient has
advanced lung cancer; and iii) The shape of the ST segment elevation is a bit
“off” for acute STEMI.
KEY Clinical Point: Despite valid concern about possible acute infero-postero-
lateral STEMI (either from a proximal right coronary vs dominant left circumflex
occlusion) — the lack of chest pain and lack of any defined “onset” of symptoms
in the context of a patient with advanced cancer should prompt additional
data gathering prior to cath lab mobilization.
Initial serum troponins were negative.
The patient was taken to the cath lab. No acute lesion and no significant
coronary disease was found.
While in the cath lab — additional lab values returned showing a markedly
elevated serum Calcium value = 17 mg/dL.
Comparison ECGs were ultimately found. These were clearly abnormal. While
a similar degree of ST elevation was not seen on prior tracings — there was
definite ST segment coving with T wave inversion present on earlier tracings.
Clinical SYNTHESIS: This case is admittedly subtle and complex. It is clearly
beyond-the-core for the beginning interpreter. Nevertheless — We feel it is an
excellent teaching example for emphasizing a number of clinical points that are
of interest for providers of any level. These include the following principles:
All ST segment elevation is not necessarily the result of acute coronary
occlusion! In addition to common “other causes” of ST elevation (ie, early
repolarization variants; LVH; acute pericarditis) — chronic ST elevation may
result from either ventricular aneurysm or cardiomyopathy. This case serves
to remind that Hypercalcemia is yet another potential STEMI-mimic.
Textbooks describe QT interval shortening as the principal ECG
manifestation of hypercalcemia. That said — recognition that the QT
interval is “short” is not easy to detect because: i) Usually marked
hypercalcemia (levels >12.0 mg/dL) are needed before the QT noticeably
shortens; ii) it will often be difficult to distinguish clinically between a QT
interval that is within the “normal” range vs one that is “too short”; and iii)
ECG manifestations of hypercalcemia are superimposed on any baseline
abnormalities that may be present.
We mentioned that the shape of the ST elevation in this case was a bit “off”
for acute STEMI. By this — we mean that the coved ST segments seemingly
peak a tad earlier than is usually seen. That said — the overall QT interval in
this case is not shortened. If anything — the overall QT interval is lengthened
by preexisting T wave inversion that was seen to be present on prior
comparison tracings.
Clinical NOTE: At the bedside — our first inclination when told of an elevated
K+ level — is to validate the reading (and rule out hemolysis). We do this by
repeating the blood test.
At times — simply obtaining an ECG may be a faster way to determine IF
there is cause for concern. The absence of ECG signs shown in Figure 11.3-1
— suggests that serum K+ is probably not significantly elevated.
BOTTOM Line: IF it turned out that marked hyperkalemia was the reason for
the wide rhythms in Panel A and Panel B — then rather than Pacing/Atropine
— the treatment of choice would be Bicarb/Calcium.
History is ever important! Sometimes a stat K+ level is needed for accurate
diagnosis. Given the hemodynamically stable condition of each patient in
Figure 11.4-1 — there is time for lab confirmation of the diagnosis.
Knowing that a hemodynamically stable patient with a wide-QRS rhythm
without sinus P waves has renal failure — goes a long way toward
suggesting that what we are seeing in Figure 11.4-1 is a rhythm in a patient
with hyperkalemia (with changes in QRST morphology corresponding to that
seen in Panel D or Panel E from Figure 11.3-1). This is important since
optimal treatment of this patient depends on accurate diagnosis of the reason
for QRS widening.
Clinical NOTES: The ECG is the net result of the heart’s electrical activity.
Therefore — ECG changes from new hyperkalemia will be superimposed on
any preexisting ST-T wave abnormalities.
We’ll have to wait until hyperkalemia is corrected before knowing IF
abnormal findings (right axis; QS complexes; T wave peaking; ST depression
and T inversion) are due to ischemia as well as hyperkalemia.
In our experience — We have seen a great variety of abnormal ECG findings
disappear once hyperkalemia is corrected. For unknown reasons — marked
right axis (as seen in Figure 11.5-1) often resolves once serum K+ is again
normal.
Note in Figure 11.5-1 — that the negative peak of the inverted T waves in
leads III,aVF is sharp (pointed). Although positive peaked and pointed T
waves are much more commonly associated with hyperkalemia — T wave
peaking may occasionally be negative with this electrolyte disorder. We’ll
only know for sure after serum K+ is corrected and a repeat ECG is obtained.
BOTTOM Line: Be sure to repeat the ECG after hyperkalemia is corrected
and correlate tracings to the clinical situation (ie, chest pain with possible
ischemia vs simple hyperkalemia?).
FIGURE 11.7-1: What are the ECG Changes? Having conveyed potential
clinical caveats of depending on the ECG to assess hypokalemia — We review
in schematic Figure 11.7-1 those ECG Changes that have been associated with
low serum K+ values:
Panel A — The ST-T wave is normal. This is the baseline tracing.
Panel B — shows relative flattening of the T wave and ST segment. This is
typically the earliest change.
Panel C and Panel D — In association with ST-T wave flattening (and often
with some degree of ST depression) — a U wave develops (Section 11.9). A
"pseudo-P-pulmonale" pattern (with P wave peaking in inferior leads) may
sometimes be seen.
Panel E and Panel F — ST depression becomes more noticeable and the U
wave increases in size (red arrow in Panel E) — until ultimately the U wave
overtakes the T wave. At this point, distinguishing between the T wave and U
wave may be almost impossible (ie, there is really “Q-U" rather than “Q-T”
prolongation — as in Panel F).
Figure 11.10-1: ECG obtained from a patient with a history of alcohol abuse
and atypical chest pain. Are the ECG abnormalities seen likely to reflect
ischemia or electrolyte disturbance? (See text).
BOTTOM Line: There is no way to be certain from this single ECG whether the
abnormalities seen in Figure 11.10-1 represent ischemia — electrolyte
disturbance — or some combination of these, perhaps in association with
other factors.
Clinical correlation including lab values, serial tracings and close follow-up
of this patient’s clinical course — will be needed in order to know for certain.
Even IF serum electrolyte values initially come back low — this would not
exclude the possibility of ischemic T wave inversion superimposed on
electrolyte-induced ST-T wave abnormalities.
That said — We strongly suspect hypokalemia (and probably also
hypomagnesemia) are at least in part responsible for the ECG abnormalities
seen in Figure 11.10-1 because: i) the history of alcohol abuse predisposes
the patient to low K+/low Mg++ levels; and ii) the presence of very
prominent U waves in several leads plus marked QT prolongation are
both highly characteristic of these electrolyte disorders. Resolution of ECG
abnormalities on serial tracings as electrolyte disturbance is corrected would
confirm a cause-and-effect relationship.