Misleading electrocardiographic results in patient with hyperkalaemia and diabetic ketoacidosis
BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7376.1346 (Published 07 December 2002) Cite this as: BMJ 2002;325:1346All rapid responses
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this is an interesting and thought provoking case history. apart from
pseudo-infarction pattern, the ecg changes could be due to coronary spasm
induced by very severe metabolic derangement. could it be not prinzmetal
"angina"? of course pain is not necessary at all in diabetic patients. one
sees more silent mi's in diabetics than in any other condition.
i disagree
that thrombolysis has to be determined by chest pain always.the clinical
situation was already conducive to development of mi.
however, your conclusion that metabolic correction should precede
thrombolysis has certain drawbacks. the time taken to do this could very
well exceed the golden therapeutic window for thrombolysis.
a possible solution to your "thrombolyse or not" dilemma would have been
the performance of bed-side transthoracic echocardiography. the presence
of akinesia in territory of LAD would have clinched diagnosis of
mi.finally, an earlier mi, say a couple of days old ,as suggested by
another colleague would have been detected by trop t also.
Competing interests:
None declared
Competing interests: No competing interests
Dear Editor,
I have a brief comment on the informative ‘Lesson of the week’ by
Moulik and colleagues, describing an association between hyperkalaemia and
an ECG pattern suggesting acute myocardial infarction in a patient with
diabetic ketoacidosis (DKA). One of the mechanisms of hyperkalaemia in
DKA stated at the beginning of the Discussion is not strictly correct.
It
is inorganic acids, and not organic acids (including lactic acid), that
cause hyperkalaemia as a result of potassium ions leaving cells in
‘exchange’ for hydrogen ion entry (and their intracellular buffering). In
DKA, the key mechanism is lack of insulin, which is probably the most
important short-term regulator of plasma potassium concentration (through
stimulation of the cell ‘sodium’ pump – Na,K-ATPase) and defence against
acute hyperkalaemia resulting from our daily intake of potassium (~80
mmol): The extracellular pool of potassium is around 65 mmol and could
almost double after a single steak meal (~50 mmol), which is too rapid a
change for compensatory renal excretion.
In DKA, an additional mechanism
is the osmotic shrinkage of cells as a result of the high plasma glucose
concentration (and plasma osmolality), which steepens the intracellular to
extracellular potassium concentration gradient and thereby causes an
increase in potassium ion loss from cells. Of course, these observations
do not materially alter the management of DKA, but only serve to emphasise
the importance of inulin administration, glucose control and re-salination
over the use (though not excluding it in severe metabolic acidosis) of
bicarbonate, bearing in mind that such patients have usually become
potassium depleted as a consequence of earlier increased renal losses, and
therefore risk developing significant hypokalaemia during recovery.
Competing interests:
None declared
Competing interests: No competing interests
In the case reported by Moulik et al it was prudent not to give
fibrinolytic therapy regardless of the metabolic state as there is no
clear history of the timing of the onset of myocardial infarction had one
actually occurred. It is clear that the benefits of fibrinolytic therapy
fade with passage of time from the onset of the event. Referral for
emergent angiography would have been more appropriate.
Competing interests:
None declared
Competing interests: No competing interests
Drs Moulik, Nethaji and Khaleeli are to be congratulated for
presenting a critically ill patient with an intriguing ECG. I am left
wondering (with retrospective 20/20 vision), however, why thrombolysis was
considered.
First, we are told that the 42 year old diabetic man did not have
chest pain or chest pain "equivalent", a usual absolute requirement for
thrombolysis.
Secondly, no precise information is supplied as to the timing of his
presentation to the Emergency Department in relation to the onset of his
symptoms. If a 'silent' MI had been the precipitant of his illness, could
it not have conceivably occurred 3 days prior? Thrombolysis of the
patient at this stage would expose him to all of the risks of therapy with
very little opportunity for benefit. The authors state that 28% of deaths
from DKA are accounted for by AMI and CCF, but make no comment on how many
of these patients meet eligibility requirements for thrombolysis. I
suspect the figure would be substantially lower.
Additionally, having examined the ECG, the ST Segment elevation is
not confined to one vascular territory - being seen in both inferior and
anterior leads, again making an acute MI less likely. Would it not be
usual in the setting of anterior myocardial infarction to see 'reciprocal'
ST segment depression inferiorly?
In summary, I am concerned that thrombolysis was given serious
consideration in this patient based on the facts that chest pain was
absent, the symptoms were of several days duration, and the ECG is not
typical of anterior myocardial infarction.
Thus, any decision to treat this man with thrombolytic therapy would
have fallen outside the boundaries of knowledge available from clinical
trials.
My complements to the authors on stimulating thought on an
interesting topic.
Competing interests:
None declared
Competing interests: No competing interests
"Misleading electrocardiographic results"... are we all looking at the same ECG?
Regarding the paper by Moulik et al, and replies from Bailey and
Vasenwala, I am somewhat concerned about the interpretation of the
electrocardiogram at presentation.
Assuming the leads were placed correctly, the significant positive
deflection in lead V1 taken in conjunction with 'reciprocal' negative
changes in leads I, aVL and V6 (and with supportive change in lead III)
might be more suggestive of right ventricular myocardial infarction
(RVMI), perhaps occurring in the territory of a dominant right coronary
artery (RCA).
Given the positive deflection in V1, I am curious to know whether a
right precordial ECG was recorded at the time, and indeed whether coronary
angiography was subsequently performed. Although true RVMI only accounts
for 3% of all infarcts, it would be most unfortunate indeed if it
transpired that this patient had a sub-critical stenosis of a dominant RCA
which had coincidentally 'misbehaved and resolved', during a bout of
unrelated hyperkalaemia.
Competing interests:
None declared
Competing interests: No competing interests