The paper describes the results from a unique experimental and analytical study in a well-controlled animal model of Sudden Unexpected Death in Epilepsy (SUDEP). As the name implies, SUDEP is difficult to impossible to study in humans due to the uncertainty in the timing of death occurrence over years. It is much easier to do this with animals as they also have much shorter life span. The animal model we employed is one of two most prominent animal models of SUDEP. Our aim was to elucidate potential impairments in the functional connectivity between the brain, heart and lungs that could contribute to our better understanding of the underlying causes of SUDEP. This is the first study of its kind in SUDEP and, as far as we know, the first multivariate study between the heart, brain and lungs, part of the emerging field of organomics. In this contribution, we report for the first time results from tri-organ analysis of concurrent electroencephalographic, electrocardiographic and plethysmographic recordings in a control group (wild-type healthy mice) and a group of mice genetically predisposed to SUDEP and epileptic seizures. We were able to produce strong statistical evidence (p<0.001) that SUDEP-prone animals exhibit statistically significant inter-organ (brain, heart and lungs) abnormalities in specific functional afferent and efferent interactions. The graphic abstract is a schematic representation of the statistically significant (a) decreased and (b) increased neuro-cardio-respiratory network interactions of the KO compared to WT mice averaged over frequencies of 1-200 Hz. The thickness of arrows corresponds to the magnitude, and the (+) or (-) sign above the arrows to the signs of the difference of the ssGPDC values of KO from the ones of WT animals for each interaction. We also show the impact of epileptic seizures on the dynamics of these functional connectivities. These results suggest that the novel measures of neuro-cardio-respiratory connectivity we developed from network analysis in the frequency domain do shed light on potential pathophysiological mechanisms of SUDEP and ictogenesis, could be utilized as biomarkers of susceptibility to SUDEP and seizures, as well as in the assessment and improvement of the efficacy of current and future intervention strategies for treatment of seizures and risk to SUDEP.