The susceptible region in A-V conduction / by Thomas Lewis, Paul D. White and John Meakins.
- Thomas Lewis
- Date:
- [1914?]
Licence: Public Domain Mark
Credit: The susceptible region in A-V conduction / by Thomas Lewis, Paul D. White and John Meakins. Source: Wellcome Collection.
5/14 page 291
![ARV GH eo hele BOD Ky 29] on the other, predominates. When vagal impulses affect the heart beating in response to an S-A rhythm, the usual or forward type of heart-block is alone seen. When, on the other hand, an A-V rhythm is established, vagal stimulation produces reversed block, that is to say the auricle lags and may fail to respond, while the ventricle is apparently unaffected in this respect. It seemed from these observations that the chief seat of changed conduction lies, during vagal stimulation, in the A-V node and predominately to the auricular side of the impulse source. A separate series of experiments* upon extrasystoles carried out by two of us (Lewis and White) has led us to a similar conclusion in regard to the changes of conduction which occur as accompaniments of this form of cardiac disturbance. The view that the A-V node or immediately neighbouring tissue forms a susceptible point, so far as changes of conduction are concerned, appealed to us and we have sought and found strongly confirmatory evidence in the effects of asphyxia. Our procedure has been constant in each series of experiments. We produce changes in conduction by some form of interference and test the effect of dislocating the pacemaker from S-A to A-V node upon these changes of conduction. We anticipated that should the susceptible point be the same for vagal stimulation and for asphyxia we should obtain with the latter, not the ordinary effect of forward block, but reversed block. This anticipa- tion has been fulfilled. The curves of asphyxia in cats need little description, they have. been fully illustrated by Lewis and Mathison.? The curves of simple asphyxia in the present series were similar in every respect. After one or a few minutes of asphyxia, prolongation of the P-£ interval is seen and is quickly complicated by missed ventricular responses ; eventually auricular and ventricular rhythms become completely dissociated. In producing A-V rhythm we have utilised cold applied to the sulcus terminalis and have taken repeated control curves during the course of an experiment, to ascertain the constancy of the reaction of the natural pace- maker to cooling. In these curves cooling is followed by slowing and by an abrupt change of mechanism, from the usual sequence to simultaneous beating in which the auricle slightly precedes the ventricle (Fig. 2a). If, in the cat, A-V rhythm is established and maintained, the effects of asphyxia are as follows: In the initial stages of asphyxia the auricle usually beats immediately before the ventricle and the P-f interval is conspicuously curtailed. As asphyxia proceeds, the auricular and ventricular systoles become quite synchronous, so that P is lost in & (Fig. 26, last cycle) ; after a little while P creeps out upon the far side of & and an &-P interval is developed (Fig. 3 and 1 a, b, c). This R-P interval gradually increases (Fig. 1 a, b,c, 4b, and 5) and eventually the auricle fails constantly to respond. A condition is now established for a short while in which the auricle beats at exactly half the rate of the ventricle (Fig. 1 d and 5), and this condition may be identified readily by simple inspection of the heart. Finally and * Subsequently to be reported.](https://iiif.wellcomecollection.org/image/b33430433_0005.jp2/full/800%2C/0/default.jpg)
