Proposed scheme of events leading to transmembrane ionic imbalances during myocardial ischemia. Net intracellular Na⁺ gain due to a mismatch of Na⁺ influx and efflux will cause net cellular K⁺ loss, extracellular K⁺ accumulation, and an increase in intracellular Ca²⁺ due to activation of the Na⁺/Ca²⁺ exchanger operating in the reverse mode. Cellular Ca²⁺ overload will cause triggered arrhythmias by the mechanisms illustrated in Figure 3. Lysophosphatidylcholine is a product of diacyl phospholipid catabolism generated by the enzyme phospholipase A2 during ischemia. Question marks indicate that the pathway/mechanism is hypothetical. [ATP]_i, intracellular concentration of adenosine triphosphate; Cx43, connexin-43; [H⁺]_i, intracellular proton concentration; I_K, delayed rectifier K⁺ current; I_K,ATP, ATP-sensitive potassium current; I_K1, inward rectifier K⁺ current; I_Na, fast Na⁺ current; Na/H, sodium-hydrogen exchanger; [K⁺]_o, extracellular K⁺ concentration; TTX, tetrodotoxin (a specific blocker of the fast sodium current).