Wenkebach simply noticed group beating with a pause which wasn't a PVC (he used a device to record radial pulse pressure waves), and he saw that the pulses got closer together as they got closer to the skipped beat. When he and a colleague recorded atrial and ventricular contractions in a dying frog heart, he saw a similar pulse phenomenon accompanied by increasing delay between atrial and ventricular contraction.
Another way to do this is by auscultation. With a short PR, the atria do not have time to completely relax, requiring relatively high ventricular pressure to shut the valves. Thus, S1 happens as the ventricles are accelerating and you get a loud S1. With a long PR, the atrial pressures are much lower and the valves shut early in systole. The ventricles have not had a chance to accelerate yet and the S1 is softer. 1st degree AV block is, in fact, one of the causes of a diminished S1, and it is possible to diagnose Wenkebach by auscultation alone because you will usually hear a progressively diminishing S1 followed by a skipped beat.
As a super-zebra note, you can get a paradoxical increase in S1 with extremely long PR intervals (above 0.36, if I recall) because the valves will actually re-open due to continuous pulmonary venous return.
I can't claim to have picked all of this up on physical exam, but the trick to good exam is "cheating" by expecting certain findings. Next time you get a patient with Wenkebach, listen to them and see if you can hear the variation in S1. If you can pick up the difference in JVPs, more power to you. I'm just happy if I see an A wave every now and then. 🙂