## 1 Introduction  
Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice, with a prevalence of 0.5% to 2% in the general public [1]. AF can be treated with antiarrhythmic drug therapy, direct cardioversion, and catheter ablation. Catheter ablation with pulmonary vein isolation is considered the most effective treatment of paroxysmal AF (spontaneously terminating AF lasting less than 7 days), persistent AF (lasting more than 7 days), as well as long-standing persistent AF (lasting longer than 1 year) [2]. Pulsed field ablation (PFA), based on irreversible electroporation, is a promising new intervention for the treatment of atrial fibrillation (AF), which isolates electric triggers in pulmonary veins from entering the left atrium and, thus, stops the arrhythmic beating of the heart [3, 4, 5, 6]. As PFA is being rapidly introduced into clinical practice, there is growing interest for its use in ventricular tissue as well [7, 8, 9, 10, 11, 12, 13]. Electroporation occurs when cells are exposed to short, high-voltage electric pulses [14], which leads to a transient increase in cell membrane permeability and may result in cell death. In PFA, pulses of up to several 1000 Volts and various durations (ns-ms) [15] are delivered via electrodes on a catheter intracadially, causing cell death via non-thermal mechanisms [16]. So far, preclinical and clinical studies showed that PFA represents an effective, efficient, safe, and fast method for the treatment of AF with reduced risk of injuries to the surrounding tissues [17, 18]. PFA avoids complications inherent to thermal methods (damage of the esophagus, phrenic nerve paralysis, pulmonary vein stenosis, embolic stroke) [19, 20]. Although the main goal of PFA is irreversible electroporation, it is unavoidable that, in vivo, we also achieve reversible effects [21]. Reversible electroporation occurs (unintentionally) in cells that are located further away from the electrodes/catheter than cells where PFA is performed or (intentionally) during field mapping, as recently suggested [22]. Several unanswered questions remain on how PFA affects cardiac tissue at the cellular level, especially in the areas where reversible electroporation occurs, such as how electroporation affects the contractility of cardiac cells, their pacing, and ion balances, normally regulated by different ion pumps [23; 24; 25; 26]. The most important ion pumps for the maintenance of cardiac contractility are sarco/endoplasmic reticulum Ca\({}^{2+}\)-ATPase (SERCA), plasma membrane Ca\({}^{2+}\)-ATPase (PMCA), and Na\({}^{+}\),K\({}^{+}\)-ATPase (NKA) proteins. SERCA and PMCA pumps work in combination with the sarcolemmal Na\({}^{+}\)/Ca\({}^{2+}\) exchanger and mitochondrial Ca\({}^{2+}\) unimport to transport Ca\({}^{2+}\) out of the cytosol (Figure 1A). While SERCA and PMCA only transport 2 Ca\({}^{2+}\) out of the cytosol, NKA transports 2 K\({}^{+}\) into the cell and, at the same time, transports 3 Na\({}^{+}\) out of the cell. Through this, NKA maintains a negative transmembrane voltage of cardiomyocytes, so they can be subjected to excitation contraction coupling repeatedly. In addition, by maintaining transmembrane voltage, NKA influences cell calcium and contractility by providing the driving force for Ca\({}^{2+}\) extrusion via the Na\({}^{+}\)/Ca\({}^{2+}\) exchanger. SERCA, NKA, and PMCA all need ATP to perform their pumping functions. It is reported that 60-70% of generated ATP in the heart is used to fuel contractions, while the remaining 30-40% is mostly used for ion pumps, especially for SERCA [27; 28; 29]. Electroporation increases cell plasma membrane permeability, which disrupts the ionic balance (Figure 1B). This creates a demand for ionic pumps to increase their pumping activity to reestablish ionic homeostasis, but, at the same time, ATP is lost through the leaky membrane, which creates an energy shortage in the cells [30; 31; 32].