Hypokalemia is a rare but important cause of rhabdomyolysis in children. Unlike typical rhabdomyolysis, hyperkalemia may be absent because the triggering factor is hypokalemia, potentially delaying diagnosis. We report a five-year-old boy with hypoplastic left heart syndrome after a Fontan procedure who developed severe hypokalemia and rhabdomyolysis following prolonged diarrhea while receiving loop diuretics. He presented with acute lower extremity weakness and inability to stand. Laboratory evaluation revealed potassium 1.9 mmol/L and creatine kinase 9,013 U/L, peaking at 32,908 U/L. Urinalysis showed myoglobinuria, and electrocardiography demonstrated ST depression and prominent U waves. Intravenous potassium replacement and diuretic adjustment resulted in rapid clinical recovery without acute kidney injury. A review of previously reported pediatric cases suggests that potassium depletion from gastrointestinal losses or renal wasting predisposes children to rhabdomyolysis. Early recognition and prompt electrolyte correction are essential.

A 31-year-old male with no prior comorbidities presented with rapid-onset quadriparesis following one week of non-bloody diarrhea. Initial evaluation revealed severe hypokalemia (1.41 mmol/L) and an electrocardiogram (ECG) demonstrating signs of cardiotoxicity (irregular rhythm, diffuse ST depression, prominent U waves, and prolonged QT interval). The patient subsequently experienced cardiac arrest due to polymorphic ventricular tachycardia (VT). VT was refractory to an initial 200 J DC shock but terminated following the rapid intravenous administration of a 40 mEq potassium chloride (KCl) bolus over 5 min. The patient achieved Return of Spontaneous Circulation (ROSC). Subsequent laboratory workup, including a low urine potassium concentration (10.20 mmol/L), confirmed the etiology was massive extra-renal (gastrointestinal) potassium loss. The patient made a full recovery, highlighting the critical role of prompt, aggressive potassium replacement in severe hypokalemic cardiotoxicity.

Accurate detection of premature atrial contractions (PACs) and premature ventricular contractions (PVCs) in single-lead electrocardiograms (ECGs) is crucial for early identification of patients at risk for atrial fibrillation, cardiomyopathy, and other adverse outcomes. In this work, we present a fully convolutional one-dimensional U-Net that reframes beat classification as a segmentation task and directly detects normal beats, PACs, and PVCs from raw ECG signals. The architecture employs a ConvNeXt V2 encoder with simple decoder blocks and does not rely on explicit R-peak detection, handcrafted features, or fixed-length input windows. The model is trained on the Icentia11k database and an in-house single-lead ECG dataset that emphasizes challenging, noisy recordings, and is validated on the CPSC2020 database. Generalization is assessed across several benchmark and clinical datasets, including MIT-BIH Arrhythmia (ADB), MIT 11, AHA, NST, SVDB, CST STRIPS, and CPSC2020. The proposed method achieves near-perfect QRS detection (sensitivity and precision up to 0.999) and competitive PVC performance, with sensitivity ranging from 0.820 (AHA) to 0.986 (MIT 11) and precision up to 0.993 (MIT 11). PAC detection is more variable, with sensitivities between 0.539 and 0.797 and precisions between 0.751 and 0.910, yet the resulting F1-score of 0.72 on SVDB exceeds that of previously published approaches. Model interpretability is addressed using Layer-wise Gradient-weighted Class Activation Mapping (LayerGradCAM), which confirms physiologically plausible attention to QRS complexes for PVCs and to P-waves for PACs. Overall, the proposed framework provides a robust, interpretable, and hardware-efficient solution for joint PAC and PVC detection in noisy, single-lead ECG recordings, suitable for integration into Holter and wearable monitoring systems.

Thyrotoxic periodic paralysis is a rare but potentially life-threatening complication of thyrotoxicosis characterised by hypokalaemia-induced flaccid paralysis due to an intracellular potassium shift rather than total body depletion. We report a male in his early 40s of Filipino origin who awoke with acute bilateral lower-limb weakness after he had consumed a large carbohydrate meal and performed strenuous exercise within the preceding 12 hours. Venous blood gas was normal; initial serum potassium was 1.7 mmol/L with phosphate 1.07 mmol/L. The ECG showed sinus tachycardia, first-degree atrioventricular block and prominent U-waves with QTc 388 ms. Urine potassium/creatinine ratio was 1.7 mmol/mmol (expected <2.0 in hypokalaemia), indicating appropriate renal conservation. A point-of-care thyroid panel did not include thyroid-stimulating hormone (TSH); the laboratory TSH was reported later as suppressed (0.001 mIU/L) with elevated FT4/FT3. There was no diuretic, insulin or β-agonist use. The patient received potassium chloride totalling 80 mEq (≤10 mEq/hour peripherally with continuous ECG monitoring) with serum potassium checks every 1-2 hour, and supplementation was stopped once K+ reached 4.0 mmol/L; propranolol 40 mg orally every 8 hours and methimazole 10 mg orally every 8 hours were started. Muscle strength normalised within 24 hours. This case underscores the diagnostic triad of hypokalaemia without an acid-base disorder, appropriate renal K+ conservation and characteristic ECG changes, and highlights pragmatic dosing/monitoring plus the need for definitive control of thyrotoxicosis to prevent recurrence.

The coexistence of atrial fibrillation (AF) and ventricular fibrillation (VF) in a structurally normal heart is a rare presentation. We describe a case of a previously healthy, 30-year-old man presenting with a family history of sudden cardiac death. The ECG during admission showed early repolarization pattern and he spontaneously developed AF, junctional rhythm and VF and dynamic QT shortening with prominent U waves during the arrhythmic storm. Genetic testing revealed novel heterozygous missense substitution p.Ile73Val in exon 2 of the CACNA1C gene.

The prognostic significance of flat T-wave findings remains unclear. This study investigated the association between flat T-wave patterns and cardiovascular events. We analyzed data from 4508 patients with cardiovascular risk who were enrolled in the multicenter, prospective Coupling Study, with available electrocardiographic (ECG) records and follow-up outcomes (mean age 69 years; 51% male). Flat T waves were defined as T waves with an amplitude <0.1 mV and a T wave-to-R wave ratio of <10% in ≥2 of leads I, II, aVL, and V4-V6. Negative ST-T findings were defined as the area below the baseline in the ST-T segment. The primary endpoint was cardiovascular events, including stroke, myocardial infarction, hospitalization for heart failure, and aortic dissection. Over a median 5.0-year follow-up, 210 cardiovascular events occurred. Compared to the control group (N = 3426), both the flat T-wave (N = 539) and negative ST-T (N = 541) groups exhibited significantly greater risk of cardiovascular events after adjustment for age, gender, smoking, comorbidities, medications, office systolic blood pressure, N-terminal pro-B-type natriuretic peptide, and troponin T (flat T: hazard ratio [HR] 1.52, 95% confidence interval [CI], 1.01-2.29; p = 0.044; negative ST-T: HR 2.23, 95% CI, 1.58-3.15; p < 0.001). Findings in patients with hypertension (N = 4135) were consistent with those in the overall cohort: the flat T group had an HR of 1.54 (95% CI, 1.03-2.33; p = 0.037), and the negative ST-T group had an HR of 2.24 (95% CI, 1.57-3.18; p < 0.001) for incidence of cardiovascular events. In conclusion, flat T-wave findings on ECG were independently associated with cardiovascular events among patients with cardiovascular risk, including those with hypertension.

Conventional Silver/Silver Chloride (Ag/AgCl) electrodes remain the clinical standard for electrophysiological monitoring but are hindered by poor skin conformity, mechanical rigidity, and signal degradation, particularly under motion or sweat. Here, two hydrogel-based alternatives are presented and benchmarked using a wireless commercial platform: a porous poly(3,4-ethylenedioxythiophene):polystyrene sulfonate scaffold infused with hydrogel (PPSCF), and an all-hydrogel, crosslinker-free electrode (PPHG) synthesizes via a scalable, one-pot process. PPHG demonstrates intrinsic stretchability, self-adhesion, and biocompatibility, forming stable, low-impedance contacts with skin. Electrochemical measurements reveal that PPHG maintains a capacitive interface with reduced resistive losses, low loss tangent, high dielectric constant, and fast relaxation dynamics, features that enable intrinsic signal smoothing and noise suppression. In a cohort of 39 participants, PPHG electrodes outperform Ag/AgCl in electrocardiography (ECG), showing reduced motion artifacts, higher signal-to-noise ratios, and clear preservation of P-, R-, and T-waves. Electroencephalography (EEG) recordings demonstrate enhanced alpha-delta separation, while electrooculography (EOG) and electromyography (EMG) signals exhibit greater amplitude and sharper features. Machine learning analysis of ECG signals reveals a 2.2-fold improvement in inter-lead classification accuracy. These findings position PPHG as a soft, adhesive, and sustainable alternative for high-fidelity, multimodal bioelectronic interfaces, with strong potential for wearables and clinical monitoring systems.

Purpose To measure the frequency of electrocardiographic (ECG) gating errors and to assess whether convolutional neural networks (CNNs) can reduce such errors. Materials and Methods ECG tracings from 120 patients who underwent cine cardiac MRI at 1.5 T and 3.0 T, along with an external dataset of ECG tracings from 47 patients, were retrospectively collected (August 2022-April 2023). The frequency of arrhythmias and ECG-gating errors was determined by manual annotation of R waves. A CNN was developed for R-wave detection using data from 79 MRI and six external patients; the remaining data were used for testing. CNN performance was compared using signal processing algorithms, including vectorcardiographic (VCG) gating and the Hamilton algorithm. Results The mean age of the 120 patients undergoing cardiac MRI was 53.7 years ± 19.8 (SD), with 72 male patients. ECG-gating errors were observed in 8.1% of patients at 1.5 T and 15.2% at 3.0 T. At 1.5 T, CNN achieved a higher F1 score (99.1%) than did VCG (98.1%; P = .048). At 3.0 T, CNN achieved a higher F1 score (99.1%) than did the Hamilton algorithm (92.4%; P = .049) and was not statistically different than VCG (95.1%; P = .68). The CNN demonstrated a lower false-positive rate (0.1%) than did the Hamilton algorithm (7.4%; P = .02) at 3.0 T and was not statistically different than VCG (4.5%; P = .28). The feasibility of retrospective image reconstruction to improve cardiac MRI quality was also demonstrated. Conclusion CNNs offer a robust method for ECG R-wave detection, particularly in the presence of MRI-induced artifacts at 3.0 T. These findings support the potential of CNNs to enhance ECG gating and improve cardiac MR image quality. Keywords: Convolutional Neural Network, ECG Gating, Deep Learning R-Wave Detection, Cardiac MRI Reconstruction Supplemental material is available for this article. © RSNA, 2025.

A 26-year-old woman with recurrent syncope was diagnosed with Andersen-Tawil syndrome (ATS) following abnormal electrocardiographic (ECG) findings. Her history of ventricular arrhythmias and prominent U waves on ECG led to genetic testing, which identified a KCNJ2 mutation. This case underscores the importance of recognizing ATS-specific ECG patterns, including broad U waves, in diagnosing arrhythmias. Following medication adjustments, her symptoms improved, highlighting the significance of tailored treatment for ATS-associated arrhythmias.

Tocilizumab, an interleukin-6 (IL-6) receptor antagonist, is widely used for inflammatory diseases such as rheumatoid arthritis and adult-onset Still's disease (AOSD). While its known side effects include hypersensitivity, neutropenia and liver dysfunction, hypokalaemia is a rare adverse effect. We report a male patient in his early 30s with AOSD who developed severe hypokalaemia (2.0 mmol/L) and acute flaccid paralysis after his third intravenous tocilizumab infusion. He had no prior neurological or electrolyte disturbances. Electrocardiography showed U waves and mild QT prolongation, while brain and spinal MRI ruled out other causes. Potassium replacement led to full recovery within 24 hours, and his treatment was switched to adalimumab. This case suggests that IL-6 inhibition may disrupt potassium homeostasis, leading to hypokalaemia. Hypokalaemia should be kept in mind in cases of sudden onset of paralysis under tocilizumab treatment.