REVIEW AND APPRAISAL OF PART III— BROOKS and HOFFMAN 357 



blocking the sino-auricular node ( Calm, Kilx-ri ) niii^ht be due to a lesser depression 

 of that pacemaker tissue. Continuation of a tendency to drive the heart at a rate 

 faster than it could follow might explain the result. At least the observation pro- 

 vides an example of imbalance in specific tissue effects. 



The work of Andjus, Lovelock & Smith, and that of Lewis in which cooling to 

 extremely low levels and then rewarming was accomplished shows that fibrillation 

 is not inevitable. Whether this is possible merely because of the small size of ani- 

 mals and hearts remains to be seen. 



Diastolic threshold changes in hypothermia. In the experiments reported by 

 Hegnauer, ( lollan and others, the threshold changes to stimulation go either way, 

 up or down. There are several possible ways in which this can be explained. 



(a) High thresholds. (1) In experiments in which the heart is driven at a rate 

 faster than the intrinsic frequency it is likely that the increase in threshold occurs 

 at some low temperature where the Q-T interval tends to equal the cycle length 

 (D'Amato) and thus diastolic levels of excitability are not attained. 



(2) In Hegnauer 's work (at least the earlier experiments reported in the litera- 

 ture) the measurements of "diastolic" excitability were made at a fixed point on the 

 T wave. If it is true, as some work suggests (see Brooks), that at low temperature 

 recovery of excitability lags behind repolarization in time, then a progressive in- 

 crease in thresholds will be recorded with progressive cooling. 



(b) Lozv thresholds. (1) It is interesting that in Hegnauer's work, in the ani- 

 mals which showed a decrease in thresholds and also a terminal fibrillation, the 

 decrease in threshold began to appear at around 26° C. This is also the temperature 

 at which a fairly rapid loss of resting potential and magnitude of action potential 

 appears in studies of single fibers (Weidmann, Hoffman). A good case can be con- 

 structed for both a lowering of threshold, due to loss of resting potential, and 

 failure of uniform conduction, due to loss of action potential amplitude. These 

 factors could easily lead to fibrillation. 



(2) The difference in electrodes and electrode placement may explain the differ- 

 ence in threshold of the ventricle to stimulation in the papers by Brooks and by 

 Hegnauer and Covino. This same difference in technique may also explain the 

 greater constancy obtained in experiments reported by Brooks and his associates. 

 The observation by Hegnauer that animals in which cardiac threshold drops 

 markedly on cooling are prone to fibrillate causes one to wonder if in these cases 

 injury currents or currents originating from asymmetrical cooling (Berne: cooled 

 coronary blood and fibrillation) might not have occurred and rendered the hearts 

 vulnerable to fibrillation by the mechanism discussed by Brooks. Animals with 

 more constant thresholds survived as did the animals of Gollan. A similar concept 

 is in fact expressed by Hegnauer but the ECG asymmetry reported, though not 

 thought to be due to injury, is not explained. 



The fact that the cathode and anode can both stimulate (Durrer), and that at 

 certain parts of the cycle the cathode is more effective while at other times the 

 anodal stimulation predominates (Brooks, Durrer), should be taken into account 

 When the two electrodes are on different chambers of the heart (Hegnauer), 

 multiple recordings are required to determine just what is happening. 



