Respiratory dysfunction, particularly central apnea, accompanied by cardiac abnormalities are proposed to be the underlying causes of Sudden Unexpected Death in Epilepsy (SUDEP). Apnea in SUDEP is characterised by prologued hypercapnia with severe hypoventilation. We propose that this implies an impairment at the level of central CO2 chemoreception (CCR) drive for breathing which is coupled with cardiodysregulation. CCR can be quantified with ventilatory response to hypercapnic challenge and has not been previously studied in a chronic model of temporal lobe epilepsy, in which SUDEP may be observed. Therefore, we aim to investigate cardiorespiratory responses to acute hypercapnia in the kainic acid (KA) model. We used Wistar KA rats with severe spontaneous seizures (~5 months after KA injection, ip) and control healthy rats. Photoplethysmography method was implemented to measure interictal ventilatory frequency (fB), heart rate (HR) and oxygen saturation (PO2) before, during and after 1hr, 10%CO2 challenge. The results showed no difference in the baseline fB and HR between the groups. However, the fB and HR responses to 10%CO2 was significantly attenuated in KA rats compared to healthy rats (p<0.001, p<0.0001 respectively, 2-way ANOVA, Fisher's LSD test). In addition, PO2 in KA rats was inferior to healthy across all conditions (p<0.0001). Overall, these results indicate that in chronic KA model, severely epileptic rats display impaired cardiorespiratory response to hypercapnia. These findings model and help to understand the high-risk breathing disturbances that are observed among SUDEP cases and facilitates future studies to investigate where in the brainstem these dysfunctions originate.