The electrical excitation of the heart is first initiated by the sinoatrial node, and then spreads along the cardiac conduction system and throughout the ventricles. The propagation of electrical activity throughout the heart can be characterised by a one-dimensional (1D) model of the cardiac tissue along its major conduction pathway. This approach offers further insight into cardiac electrical excitation conduction than the standard single cell models, but without the computational demands of a higher dimension anatomical model. In this study, we have developed a 1D computational model for the rabbit whole heart with considerations to the intrinsic electrical heterogeneity of cardiac tissue from the sinoatrial node (SAN) to the left ventricular wall. The 1D whole heart model accounts for the heterogeneous nature of cardiac tissue, incorporating well established single cell models for SAN (Zhang et al. 2000), atrial muscle (Aslanidi et al. 2008), atrio-ventricular node (AVN) (Inada et al. 2009), and Purkinje fibre (PF) and left ventricular tissue (Aslanidi et al. 2010). The cells were coupled together into a single strand using the monodomain equation. The model also considered the fast and slow conduction pathways of the AVN. The choice of gap junctional conductance values for each distinctive region of tissue in the 1D model was validated by reproducing the corresponding conduction velocities of the excitation wave and matching them to experimental data. The developed model was used to simulate the effects of ionic channel blockers, such as TTX, Nifedipine and Ivabradine (blocking INa, ICa,L, and If respectively) on a simulated ECG. Blocking INa caused the PP interval, PR interval and QRS duration to increase in a dose-dependent manner, which was accompanied by a slight increase in QT interval (< 5%). 70% block of INa caused Purkinje-ventricular junction block, subsequently abolishing the QRS complex. Blocking ICa,L by a low percentage did not alter the PP, RR and QRS intervals; however, a 70% block of ICa,L caused His-Purkinje fibre block, and higher ICa,L block caused the leading pacemaker site to shift to the atrio-ventricular node (AVN). QT interval and T wave dispersion both increased with ICa,L block. For block of If, the PP and RR intervals showed a small prolongation (~7 ms / 10% block), and the QT interval was slightly increased (~5 ms at 100% block of If), otherwise no significant changes were observed. These simulations were quantitatively comparable to experimental data obtained from Langendorff whole heart preparations with applications of TTX, Nifedipine and Ivabradine. In conclusion, a 1D whole heart model for the rabbit has been developed, providing a time-efficient way of studying cardiac excitation wave conduction and actions of anti-arrhythmic drugs.