Benjamin Stripe, MD
Jonathan Bui, MD
Femi Philip, MD
Ezra A. Amsterdam, MD

CASE

11.1

Patient History

A 73-year-old female was admitted to the emergency department for diabetic ketoacidosis (DKA): glucose 580 mg/dL, CO₂, 8 mEq/L, anion gap 29, potassium 7.6 mEq/L, creatinine 3.24 mg/dL (baseline 1.28). Medications included lisinopril. Multiple factors contributed to the patient’s hyperkalemia including DKA, renal insufficiency, and ACE inhibitor.

Figure 11.1.1 shows admission ECG; Figure 11.1.2 is a prior normal ECG obtained 2 weeks before admission. Figure 11.1.1 demonstrates peaked T waves in leads II, V₅, and V₆ (arrowheads), marked ST elevation in V₁ and V₂ (stars), and Q waves in V₁, V₂ (arrows). Troponin I peaked at 1.36 ng/ml (ref 0.04). The patient’s metabolic abnormalities responded to standard therapy and her ECG changes resolved, as shown in subsequent ECG (Figure 11.1.3).

Figure 11.1.1

Figure 11.1.2

Figure 11.1.3

Question

Are there any other abnormalities on the ECG?

Answer

There are several abnormalities in addition to the peaked T waves, a classic sign of hyperkalemia, including ST elevation, which has been recognized as a finding with hyperkalemia since the mid-20th century.¹ Additional abnormalities include: Absent P waves, junctional escape rhythm (ventricular rate 55/min), increased QRS duration (~110 ms) and Q waves (arrows) in leads V₁ and V₂ (q in V₃ is very diminutive). There are also tiny excursions before the QRS complexes in the inferior leads, which may be artifact or retrograde P waves originating from the junctional rhythm. Peaked T waves, flattened P waves, bradycardia, increased QRS duration, and sinus node arrest are well-established effects of hyperkalemia. ST elevation in the precordial leads with hyperkalemia was first reported over a half century ago and should be included in the differential diagnosis of acute ST elevation myocardial infarction. None of the foregoing findings were present shortly before her admission (Figure 11.1.2) or in her ECG after reversal of her metabolic abnormalities (Figure 11.1.3).

Question

Have transient Q waves been reported to occur with hyperkalemia?

Answer

Yes. Reversible Q waves have been reported previously in association with hyperkalemia and have been attributed to a ventricular conduction abnormality induced by elevated potassium.² In addition, severely deranged metabolic conditions, such as DKA, have been associated with elevated cardiac troponin.

References

1. Wang K, Asinger RW, Marriott HJ. ST-segment elevation in conditions other than acute myocardial infarction. N. Engl. J. Med. 2003;349:2128–2135.

2. Arnsdorf M. Electrocardiogram in hyperkalemia. Arch. Intern. Med. 1976;136;1161–1163.

Patient History

An 80-year-old female patient was admitted due to malaise. She had previously been implanted with a single-chamber pacemaker for atrial fibrillation and bradycardia. The blood tests revealed renal failure with hyperkalemia at 8.2 mmol/L. Her ECG recorded upon admission (Figure 11.2.1) is shown.

Figure 11.2.1 ECG recorded upon admission.

Question

What does this ECG show?

Discussion

The tracing shows ventricular tachycardia (note the very broad QRS complexes due to slowed intraventricular conduction secondary to the hyperkalemia). The ventricular rhythm is undersensed by the pacemaker, with delivery of asynchronous pacing at the programmed baseline rate of 50 bpm.

The undersensing by the pacemaker may be explained by two factors:

1. Perpendicular orientation of the pacemaker lead dipole with respect to the vector of the QRS complexes, leading to low electrogram amplitude.

2. Hyperkalemia leading to changes in the electrogram signal (with a lower slew rate). The filters of the pacemaker attenuate low-frequency components (e.g., due to repolarization), and may therefore have reduced the amplitude of the resulting electrograms.

It is unclear if there is noncapture, as all the spikes (apart possibly from the second one) fall in the ventricular myocardial refractory period.

The patient was immediately administered calcium gluconate, and the hyperkalemia was corrected, with interruption of the ventricular tachycardia and resumption of a paced rhythm.

Patient History

A 44-year-old female was resuscitated on the hematologic isolation ward, where she was hospitalised for agranulocytosis secondary to thiamazol therapy for hyperthyroidism. She was treated with claritromycine, itraconazol, propranolol among other drugs. Her serum K⁺ was 3.1 mEq/L and Ca⁺⁺ was 8.1 mEq/L.

Figure 11.3.1

Question

Do you need signal averaging to see what happens on her ECG?

Discussion

Stay updated, free articles. Join our Telegram channel

Join