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| [[Puzzle 2005_11_428 - Answer|Answer]] | | [[Puzzle 2005_11_428 - Answer|Answer]] |
| [[Image:Puzzle_2005_11_428_fig2.jpg|Figure 2|thumb]]
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| [[Image:Puzzle_2005_11_428_fig3.jpg|Figure 3|thumb]]
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| The ECG is remarkable due to the lack of P waves,
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| and the extremely broad QRS (merging directly into
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| the prominent T waves in rS complexes). A diagnosis of
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| severe hyperkalaemia should be considered immediately.
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| Laboratory work-up revealed the following relevant
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| findings: sodium 127 mmol/l, potassium 8.8 mmol/l,
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| creatinine 866 μmol/l, urea 63.4 mmol/l, and a
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| metabolic acidosis with a pH of 7.08 and serum lactate
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| 4 mmol/l. Acute renal failure was diagnosed as the
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| cause, due to a combination of forward failure, high
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| dose of furosemide, spironolactone, in addition to
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| colchicine and an nonsteriodal anti-inflammatory drug
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| (NSAID) prescribed because of the patient’s gout,
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| compounded by the metabolic acidosis. The ECG in
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| figure 1 is a classic example of the effects of hyperkalaemia:
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| resting potential is reduced, partially inactivating
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| the sodium channels, reducing the depolarising
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| current and slowing atrial, AV and ventricular
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| conduction. Flattening and finally disappearance of
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| the P wave and broadening of the QRS complex result.
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| Life-threatening ventricular tachyarrhythmias with a
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| sinusoidal appearance may ensue in severe cases. Just
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| minutes after the ECG in figure 1, the ECG in figure
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| 2 demonstrated onset of ventricular tachycardia.
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| Emergency measures were undertaken to lower the
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| serum potassium (i.e. correction of acidosis, insulin
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| and glucose iv, and calcium levulate iv). The patient
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| survived this episode; the ECG in figure 3 was taken
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| two days later at which time the serum potassium was
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| normal. He died several months later of progressive
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| heart failure.
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