Sepsis-induced cardiomyopathy (SIC) develops as the result of myocardial calcium (Ca2+) dysregulation. Here we reviewed all published studies that quantified the dysfunction of intracellular Ca2+ transporters and the myofilaments in animal models of SIC. Cardiomyocytes isolated from septic animals showed, invariably, a decreased twitch amplitude, which is frequently caused by a decrease in the amplitude of cellular Ca2+ transients (ΔCai) and sarcoplasmic reticulum (SR) Ca2+ load (CaSR). Underlying these deficits, the L-type Ca2+ channel is downregulated, through mechanisms that may involve adrenomedullin-mediated redox signaling. The SR Ca2+ pump is also inhibited, through oxidative modifications (sulfonylation) of one reactive thiol group (on Cys674) and/or modulation of phospholamban. Diastolic Ca2+ leak of ryanodine receptors is frequently increased. In contrast, Na+/Ca2+ exchange inhibition may play a partially compensatory role by increasing CaSR and ΔCai. The action potential is usually shortened. Myofilaments show a bidirectional regulation, with decreased Ca2+ sensitivity in milder forms of disease (due to troponin I hyperphosphorylation) and an increase (redox mediated) in more severe forms. Most deficits occurred similarly in two different disease models, induced by either intraperitoneal administration of bacterial lipopolysaccharide or cecal ligation and puncture. In conclusion, substantial cumulative evidence implicates various Ca2+ transporters and the myofilaments in SIC pathology. What is less clear, however, are the identity and interplay of the signaling pathways that are responsible for Ca2+ transporters dysfunction. With few exceptions, all studies we found used solely male animals. Identifying sex differences in Ca2+ dysregulation in SIC becomes, therefore, another priority.