Electrolyte abnormalities may masquerade as acute neurological or cardiac emergencies in the emergency department (ED). In such atypical presentations, a timely bedside electrocardiography (ECG) often provides the earliest and most critical clue, facilitating an accurate diagnosis, guiding appropriate management, and improving patient outcomes. A 32-year-old male presented with rapidly evolving flaccid quadriparesis without sensory or autonomic involvement. A bedside ECG provided a critical clue, revealing a Mobitz type I block with ischemia-mimicking ST-T changes and prominent U waves. This prompted urgent testing, which confirmed profound hypokalemia and hypomagnesemia. Swift intravenous repletion reversed both paralysis and conduction abnormalities within 72 h. Although electrolyte abnormalities are known to produce typical ECG changes, their presentation with conduction disturbances such as Wenckebach block is rare and easily misinterpreted as ischemia or structural heart disease. Prompt recognition of these atypical ECG findings at the bedside is critical to avoid unnecessary invasive workups and to initiate lifesaving electrolyte correction.

U-wave changes during angina are often not recognized, although a change in U-wave polarity may be the only sign of myocardial ischemia. The appearance of a positive U-wave in leads V1-4 during angina suggests posterobasal ischemia and critical stenosis of the CX or RCA coronary artery. The authors present two examples.

The authors present a case where the admission ECG showed extensive deep negative U-waves in the precordial leads, in addition to the precordial negative T-waves characteristic of Wellens syndrome. After stenting of the critical stenosis of the left anterior descending coronary artery, only the U-wave inversion disappeared, while the Wellens repolarization disorder persisted. The authors discuss the different dynamics of ischemic repolarization disorders in this case. Orv Hetil. 2026; 167(22): 885-888.

Excitable cells are commonly studied via the extracellular potentials (EPs) they generate, which underlie signals in electroencephalography (EEG), electrocardiography (ECG), and multielectrode array (MEA) recordings. However, some excitable systems produce little or no detectable EPs, for reasons that remain poorly understood. Here we show mathematically that homogeneous excitable cells and tissues - with spatially uniform ion channel distributions and no external stimulation - are extracellularly silent during spatially uniform, non-propagating action potentials (i.e., in the absence of a traveling wavefront). Specifically, an isolated, autonomous cell with uniform membrane properties generates zero EP, independent of shape, kinetics, or model complexity. The result extends to coupled cells provided the tissue remains fully homogeneous. EPs emerge only from spatial inhomogeneities, propagating electrical waves, or applied currents. We demonstrate the physiological relevance of this principle in Purkinje neurons, where clustering of sodium channels enables ephaptic synchronization, while uniform cells remain asynchronous and undetectable extracellularly. We further show that connected human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and pancreatic β-cells exhibit EPs in proportion to cellular or tissue-level heterogeneity.

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.

Alzheimer's disease (AD) affects not only memory and cognition but also the body's automatic functions, such as heart rate and blood pressure. These changes reflect the early disruption of the central autonomic network, the system that links the brain and the heart to maintain physiological balance. Electroencephalography (EEG) measures the brain's electrical activity and reveals patterns of cortical slowing and desynchronization, while heart-rate variability (HRV) reflects how flexibly the heart responds to internal and external demands. This narrative review brings together evidence published between 2000 and 2025 on the combined use of EEG and HRV as a single, integrated biomarker for AD. Studies consistently show that EEG-HRV coupling, which reflects how well the brain and heart communicate, provides better accuracy in distinguishing mild cognitive impairment and early AD than either measure alone. The findings reveal a shared loss of co-ordination between neural and autonomic systems, which is a hallmark of neurovisceral decline. The review also identifies key methodological gaps, including inconsistent recording conditions and lack of standardized analytic methods, which currently limit reproducibility. To bridge this gap, a translational roadmap is proposed to outline short-, mid-, and long-term goals for clinical validation, wearable integration, and digital health applications. Together, EEG-HRV coupling represents a scalable, non-invasive, and physiologically grounded tool that could support earlier and personalized monitoring of AD, helping to connect laboratory discovery with real-world clinical care.

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.

This report describes the case of a 44-year-old woman without structural heart disease who developed ventricular fibrillation (VF) during preoperative management of multiple pancreatic neuroendocrine tumors (NETs) associated with multiple endocrine neoplasia type 1. She had an insulinoma in the uncinate process and a non-functioning NET in the pancreatic tail. Immediately after intravenous glucose administration for recurrent hypoglycemia, VF occurred. An electrocardiogram obtained immediately before VF onset showed repolarization abnormalities with marked QTc prolongation, terminal T-wave bulging, and U waves. Laboratory testing revealed concomitant mild hypokalemia. No coronary artery disease was detected. The severe repolarization abnormalities improved after resection of the insulinoma. The presumed mechanism was that mild hypokalemia and recurrent hypoglycemia, together with hypoglycemia-induced epinephrine surge and extracellular-to-intracellular potassium shift, synergistically prolonged the action potential duration and induced early afterdepolarizations, which progressed from torsades de pointes to VF. This case highlights that unstable glycemic control in insulinoma can precipitate life-threatening arrhythmias, even in the absence of structural heart disease. Particularly when surgery is delayed, maintaining serum potassium as 4.5-5.0 mmol/L and preventing recurrent hypoglycemia are crucially important. Early recognition and intervention might help reduce arrhythmic risk in such patients.

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.