Introduction: Cardiac arrhythmias, driven by complex electrophysiological substrates, remain a major clinical challenge. This study characterized peak-to-peak voltage amplitudes across epicardial regions (right atrium [RA], left atrium [LA], ventricle [V]) in Langendorff-perfused rabbit hearts during sinus rhythm (SR), atrial tachycardia (AT), ventricular fibrillation (VF), and SR with atrioventricular block (AVB). Methods: 6 New Zealand rabbits (3.44±0.36 kg) were used in this study. The hearts were perfused in a Langendorff system with modified Krebs-Henseleit solution (37.5-38°C, bubbled with carbogen) under constant pressure (70-80 mmHg), with contractility suppression by (-)-blebbistatin (1.7 μM). To obtain different heart rhythms, arrhythmias were induced via programmed stimulation protocols (S1-S1/S1-S2) and carbachol perfusion (1 μM). Unipolar contact epicardial electrograms were acquired using silver and silver/iridium microelectrode arrays (MEAs), processed via notch (60 Hz) and bandpass (2–250 Hz) filtering. Results: A total of 8 recordings ranging from 15 seconds were analyzed. During SR, mean peak-to-peak amplitudes were 10.91±9.21 mV (RA), 15.20 ±7.53 mV (LA), and 13.64±8.07 mV (V), with 95th percentile cutoffs for healthy tissue up to at 3.89 mV (RA), 8.25 mV (LA), and 4.54 mV (V). Arrhythmias exhibited distinct amplitude patterns: AT preserved RA voltages (7.31±3.36 mV vs. SR: 8.55±2.26 mV) but increased V signals (26.2±6.72 mV vs. 21.4±6.57 mV), while VF caused marked reductions (e.g., VF: V= 0.83±0.46 mV), reflecting electrical disorganization. Silver/iridium electrodes yielded 68% higher amplitudes than pure silver (LA: 22.89±5.78 mV vs. 13.64±8.08 mV), underscoring material-dependent signal fidelity. High variability (e.g., RA: ±9.21 mV) likely stemmed from uneven electrode-tissue contact and perfusion artifacts. Conclusions: This study characterized epicardial voltage amplitudes across multiple cardiac rhythms in a Langendorff-perfused rabbit model, revealing distinct electrophysiological patterns: preserved atrial amplitudes during AT, marked reductions during VF, and enhanced ventricular signals during AT, consistent with arrhythmia-specific electrical desynchrony.