BackgroundProlonged hyperoxia (96hrs) leads to adverse murine cardiac responses, but clinical therapy with high O2 levels is often short‐term. Therefore, understanding susceptibility to short‐term hyperoxia exposure is clinically important. Bone morphogenetic proteins (BMP) 2 and 4 are important in cardiac development and may influence cardiac responses to hyperoxia. We investigated cardiac responses to 24hrs hyperoxia in Bmp2+/− and Bmp4+/− mice.MethodsBmp2+/−, Bmp4+/− and WT littermates were exposed to 24hrs hyperoxia (100% O2). ECG was recorded before and during exposure.ResultsNo differences in baseline HR, QTcB, QRS, ST‐I, PR‐I, P‐wave duration (P‐d) or PR‐I/P‐d were found (P >;0.05). After ~18hrs hyperoxia, significant decreases in HR and increases in PR‐I and P‐d were found in Bmp4+/− mice only. Also, there were reductions in QTcB in the WT, but not in Bmp2+/− or Bmp4+/− mice after 17hrs hyperoxia (P <0.05).DiscussionResults suggest that developmental effects of Bmp2 or Bmp4 disruption did not affect basal cardiac function or were not detectable by ECG. During hyperoxia, Bmp4+/− mice were susceptible in terms of HR and atrioventricular conduction responses, which may have important implications for patients treated with O2 who also harbor Bmp4 mutations. Conversely, QTcB in Bmp2+/− or Bmp4+/− mice was not affected by hyperoxia, unlike WT mice, suggesting a protective effect in these genotypes.