Dendrites of CA1 pyramidal cells of the hippocampus, along with those of a wide range of other cell types, support active backpropagation of axonal action potentials. Consistent with previous work, recent experiments demonstrating that properties of synaptic plasticity are different for distal synapses, suggest an important functional role of bAPs, which are known to be prone to failure in distal locations. Using conductance-based models of CA1 pyramidal cells, we show that underlying "traveling wave attractors" control action potential propagation in the apical dendrites. By computing these attractors, we dissect and quantify the effects of I(A) channels and dendritic morphology on bAP amplitudes. We find that non-uniform activation properties of I(A) can lead to backpropagation failure similar to that observed experimentally in these cells. Amplitude of forward propagation of dendritic spikes also depends strongly on the activation dynamics of I(A). I(A) channel properties also influence transients at dendritic branch points and whether or not propagation failure results. The branching pattern in the distal apical dendrites, combined with I(A) channel properties in this region, ensure propagation failure in the apical tuft for a large range of I(A) conductance densities. At the same time, these same properties ensure failure of forward propagating dendritic spikes initiated in the distal tuft in the absence of some form of cooperativity of synaptic activation.