David G. Benditt, MD

CASE

16.1

Patient History

These tracings were obtained in a 58-year-old female with a prior history of right middle cerebral artery stroke with subsequent seizure disorder treated with valproate. One day before this admission, the patient felt lethargic and developed sudden loss of consciousness. She was found face down on the floor and unresponsive but recovered spontaneously. There were no convulsions observed at any time. After admission to the neurology service, she underwent video EEG monitoring to evaluate for seizures.

Five-day video EEG monitoring showed the presence of continuous slowing in the right fronto-temporal-parietal region and intermittent generalized slowing, but no epileptiform discharges.

ECG monitoring showed the following evolution in heart rhythms. Baseline ECG obtained one month prior to admission when the patient was seen in clinic shows normal sinus rhythm, heart rate (HR) 65 bpm (Figure 16.1.1). On admission in a postictal state, the ECG showed sinus bradycardia with competing junctional rhythm, HR 58 bpm (Figure 16.1.2). Two hours after admission the patient developed a junctional rhythm with HR 47 bpm (Figure 16.1.3).

Figure 16.1.1 A. Baseline 12-lead ECG showing normal sinus rhythm, a heart rate (HR) of 65 bpm and normal QRS and QT intervals. B. EEG obtained at same time as Figure 16.1.1A ECG is normal.

Figure 16.1.2 A. Admission ECG: Patient has a sinus bradycardia with competing junctional rhythm, HR 58 bpm. The QRS and QT intervals remain normal. B. The EEG associated with the admission ECG reveals continuous slowing in the right fronto-temporal-parietal region (see arrows) and intermittent generalized slowing at the same time.

Figure 16.1.3 A. Approximately 2 hours after admission, the patient now shows a somewhat more dramatic bradycardia (junctional rhythm, HR 47 bpm). B. The EEG associated with the bradycardia in Figure 16.1.3A shows continuous slowing in the right fronto-temporal-parietal region and intermittent generalized slowing (arrows).

Discussion

Over the duration of in-hospital monitoring, the degree of EEG regional slowing decreased. This observation tends to support the possibility that the EEG slowing being due to recovery from a postictal state. In concert, her bradyarrhythmia tendency diminished, and ECG returned to normal.

The ECG evolution during an ictal-bradyarrhythmia episode is essentially indistinguishable from that of a vasovagal syncope or near-syncope, with sinus tachycardia being followed by progressive heart-rate slowing, which may at times progress to an asystolic pause.^1–3 Most documented pauses are of non–life-threatening duration (range, 3–20 seconds), but longer pauses have been observed.^3,4 The majority of documented ictal-induced bradyarrhythmias accompany complex partial seizures of temporal lobe origin.^1–3

References

1. Freeman R. Cardiovascular manifestations of autonomic epilepsy. Clin. Autonom. Res. 2006;16:12–17.

2. Schuele SU, Bermeo AC, Alexopoulos AC, et al. Video-electrographic and clinical features in patients with ictal asystole. Neurology. 2007;69:4341–4341.

3. Benditt DG, van Dijk G, Thijs RD. Ictal asystole: Life-threatening vagal storm or a benign seizure self-termination mechanism? Circ. Arrhythm. Electrophysiol. 2015;8(1):11–14.

4. van Dijk JG, Thijs RD, van Zwet E, et al. The semiology of tilt-induced reflex syncope in relation to EEG changes. Brain. 2014;137(pt2):576–585.

This work was supported in part by a grant from the Dr. Earl E. Bakken Family in support of heart-brain research.

Patient History

A patient was admitted to the stroke unit and placed upon rhythm monitoring. A 12-lead ECG was recorded with a monitor, showing ST-segment elevation. The patient did not report any chest pain.

Figure 16.2.1 ECG recorded by a monitoring system showing ST-segment elevation in the anterior precordial leads.

Questions

1.How do you interpret this tracing?

2.What needs to be done?

Discussion

The ST elevation was due to the high-pass filter setting (set to 0.5 Hz as shown in the bottom of Figure 16.2.1). This filter is designed to avoid baseline wander to facilitate rhythm monitoring. Non-linear high-pass filters have been shown to result in artifactual ST-segment elevation, which may mimick anteroseptal myocardial infarction.¹ The ECG was recorded again using standard filter settings (0.05–150 Hz), and was found to be normal (Figure 16.2.2).

Figure 16.2.2 New ECG recording in the patient using standard filters settings (0.05–150 Hz, shown within the red circle).

Reference

1. Burri H, Sunthorn H, Shah D. Simulation of anteroseptal myocardial infarction by electrocardiographic filters. J. Electrocardiol. 2006;39:253–258.

Patient History

A 72-year-old female with systolic heart failure being treated with beta-blockers, angiotensin-converting enzyme inhibitors, and digoxin presented with one day of confusion and an ECG (Figure 16.3.1) revealing frequent ectopy.

Figure 16.3.1

While on telemetry, she exhibited periods of additional ectopy and occasional sinus beats that failed to conduct to the ventricle (Figure 16.3.2). A prior baseline ECG was obtained for comparison (Figure 16.3.3).

Figure 16.3.2

Figure 16.3.3

Question

What is the most likely explanation for these acute abnormalities?

Discussion

This case illustrates a classic example of digoxin toxicity with manifestations of neurologic and electrophysiologic abnormalities.¹ Cardiac glycosides impart their electrophysiologic effects through reversible inhibition of the sodium-potassium ATPase exchanger, a cellular channel found in gastrointestinal, ocular, neurologic, and cardiac cells. This effect results in higher levels of intracellular sodium and activation of the sodium/calcium exchanger, thereby increasing the resting membrane potential and resulting in activation of voltage-gated calcium channels. This phenomenon induces activation of calcium channels along the sarcoplasmic reticulum and a release into the intracellular space. The higher intracellular calcium is thought to provide the increased cardiac inotropy observed with these agents. However, there is also a negative chronotropic effect of these agents, largely due to their ability to increase vagal tone.

Digitalis toxicity results in preferential discharge of the fascicles. Note the patient shows a RBBB and inferior axis compatible with origin from the left anterior fascicle.

At toxic levels, cardiac glycosides can result in delayed afterdepolarizations that can result in ventricular extrasystoles and episodes of heart block (Figure 16.3.2). Given the acute presentation of this patient, Digibind² was administered, and after several hours, resolution of her symptoms and her electrocardiographic abnormalities was observed (Figure 16.3.3).

References

1. Kanji S, MacLean RD. Cardiac glycoside toxicity: More than 200 years and counting. Crit. Care Clin. 2012;28: 527–535.

2. Chan BS, Buckley NA. Digoxin-specific antibody fragments in the treatment of digoxin toxicity. Clin. Toxicol. 2014;52:824–836.

Patient History

ECG of a 56-year-old female presenting with hypertension, atrial fibrillation, and frequent premature ventricular contractions.

Figure 16.4.1

Question

What is the ECG abnormality?

Discussion

The ECG shows left ventricular hypertrophy with strain with marked T-wave inversion across the precordial leads. Her echocardiogram and cardiac magnetic resonance imaging were normal. She was found to have a pheochromocytoma. Once the tumor was surgically removed, her ECG normalized.

Patient History

A 67-year-old male underwent mitral valve repair (degenerative mitral regurgitation).

Figure 16.5.1 Permanent atrial fibrillation. Non specific ST abnormalities.

Medications included warfarin and bisoprolol.

Six years after initial treatment, he presented with presyncope, confusion, lethargy, and severe hypothermia, suggesting severe sepsis.

Medical intensive care HR 32/min – SBP 85 mmHg possible indication for cardiac pacing?

Figure 16.5.2 Atrial fibrillation with bradycardia and Osborn wave (see arrow).

Discussion

The Osborn wave (J wave) is a deflection with a dome or hump configuration occurring at the R-ST junction (J point) on the ECG. In the historical view, different names have been used for this wave in the medical literature, such as “camel-hump sign,” “late delta wave,” “hathook junction,” “hypothermic wave,” “J point wave,” “K wave,” “H wave,” and “current of injury.” Although there is no definite consensus about terminology of this wave, “Osborn wave” and “J wave” are the most commonly used names for this wave in the current clinical and experimental cardiology. The Osborn wave can be generally observed in hypothermic patients; however, other conditions have been reported to cause Osborn waves, such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from oversedation, vasospastic angina, or idiopathic ventricular fibrillation. Our knowledge about the link between the Osborn waves and cardiac arrhythmias remains sparse and the arrhythmogenic potential of the Osborn waves is not fully understood.

Reference

1.

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