Introduction: Arrhythmias are common in pulmonary arterial hypertension (PAH) causing severe symptoms and sudden death. Current treatments are often ineffective and have considerable side effects and therefore new therapies are required. Methods: Male Wistar rats (200 g) were injected with either monocrotaline (MCT) (60 mg/kg) or saline (control). They were sacrificed if they showed clinical deterioration or on day 28. In vivo echocardiography and ECG were performed under isofluorane anaesthesia. For whole heart experiments, the heart was excised and mounted on a Langendorff perfusion column at 37°C. For right atrial (RA)/atrioventricular (AV) node experiments, a tissue preparation was superfused at 37°C. Baseline ECG and atrio-His (AH) interval were recorded. Stimulation protocols were used to measure conduction velocity (CV) along the crista terminalis, AV effective refractory period (AVERP) and AV functional refractory period (AVFRP). Optical mapping was used to record the activation sequence across the right atrium. Results: Echocardiography demonstrated PAH (decrease in pulmonary artery acceleration time and increase in pulmonary artery deceleration) and right ventricular (RV) hypertrophy (increase in RV wall thickness) in the MCT rats. The whole heart experiments demonstrated an increase in AVERP and AVFRP in the MCT rats. The isolated RA/AV node preparation demonstrated a reduction in CV along the crista terminalis and a high incidence of complete heart block in the MCT rats (Table 1). The decrease in CV was supported by the optical activation sequences. Conclusions: Our data demonstrate slow atrial conduction and impaired AV node function in PAH which may serve as a basis for supraventricular arrhythmias. Reversing these changes is a potential theraputic target.