A pulsus bigeminus follows insufflations of ir- ritating vapors into the nostrils of tracheotomized rabbits and dogs, also from mechanical and faradic stimulations of the nasal septum. It develops independently of the vagus nerves (confirmation of Kratsch-mer and Koblanck and Roeder). This arhythmia is also elicited from faradic stimulation of the central end of the vagus in doubly vagotomized rabbits, from insufflation of benzol or ammonia into the trachea and in 1 instance it came on while uncoiling the small intestine. A bigeminal pulse has followed insufflation of benzol, xylol, chloroform, formalin, acetic acid, ammonia and oil of mustard into a nostril. It has not followed a, faradic or mechanical stimulation of the lateral wall of the nostril, the mucosa of the larynx, the tongue, the cornea, the outer surfaces of the jaws; b, opening the abdomen and thorax or inflation of the large and small intestine; c, faradic stimulation of the central end of the lingual, phrenic, depressor, cervical sympathetic, ulnar and sciatic nerves or the peripheral end of the vagus, depressor and cervical sympathetic nerves. The usual route of the naso-insufflation stimulation which evokes a bigeminal pulse is obviously over the trigeminal fibers, but under certain preceding experimental conditions the impulses probably pass over the olfactory fibers. Simultaneous apical beat, carotid pressure and superior vena cava tracings of this arhythmia reveal that the right atrium beats rhythmically while the left ventricle is in a premature systolic arhythmia. In 1 rabbit, electrocardiograms of several arhyth-mias demonstrate the premature systole to be of left-ventricular origin. Two forms or types of bigeminal pulse appear in the carotid tracings. They depend on the particular time that the premature contraction appears in the diastolic period. In rare instances the arhythmia may be a trigeminal pulse or a mixture of trigeminal, bigeminal and normal beats. In carotid pressure tracings the 1st and succeeding gigantic excursions of a bigeminal pulse are very different from the 1st and succeeding excursions following asphyxia and peripheral stimulation of the vagus. An arhythmia produced from insufflations usually comes on at the peak of a considerable rise in blood pressure, at the time of maximum slowing and strengthening of the pulse and during the arrest of respiration. It may appear when these changes are coming on, when the normal is being restored or even after the normal has been regained for some time. It sometimes occurs without pulse changes and with very little alteration of blood pressure and respiration.