3i6 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



periodic excitation. Some studies have been con- 

 cerned with ionic changes during fibrillation (66). 

 It appears questionable that flutter and fibrillation 

 are ordinarily induced by changes in the ionic en- 

 vironment of the cells, or at least that such changes 

 are necessary precursors of these arrhythmias. 



Certain interesting aspects of fibrillation suggested 

 to Lewis that some orderly sequence of e\ents must 

 lead to this condition of complete disorder. In the 

 first place, a certain volume of tissue is necessary for 

 fibrillation to occur. The cat's atrium cannot be made 

 to fibrillate by electrical stimulation, and the cat's 

 ventricle will fibrillate only transiently and recover 

 spontaneously. The dog's atrium will generally 

 fibrillate transiently and recover spontaneously, but 

 if the dog's ventricle begins to fibrillate, heroic 

 measures are required to end the condition. The 

 critical nature of tissue volume has also been ob- 

 served in lower animals. The frog's heart usually 

 will not fibrillate, but a large turtle's ventricles may 

 be made to fibrillate by rapid electrical stimulation. 

 Cooling the heart tends to increase the incidence of 

 fibrillation, and certain ionic changes or addition of 

 hormones and chemicals to bathing solutions in- 

 increase the tendency to fibrillation. Greatly increas- 

 ing the extracellular concentration of potassium is 

 effective, as is addition of hormones which increase 

 the tendency toward occurrence of ectopic impulses. 



An important relevant point is the clinical ob- 

 servation that the Q-T interval shortens as the heart 

 rate increases. This phenomenon has been extensively 

 investigated (25, 132) by means of the intracellular 

 electrode. If a cardiac cell is stimulated near the end 

 of repolarization, the record during the next beat 

 will show a decreased duration of the action potential 

 and a slightly decreased rate of initial depolariza- 

 tion. If the stimulation is repeated before the end of 

 the shortened complex, the action potential will 

 again shorten and the rate of initial depolarization 

 will again decrease. The decreased slope of initial 

 depolarization leads to slowing of the conduction 

 velocity (12). 



In the normal myocardium, the conduction veloci- 

 ties fall between 300 mm and 800 mm per sec, about 

 Q40 mm of muscle are in the depolarized state at any 

 one time and therefore completely refractory. (This 

 distance is the length of a depolarized segment of a 

 long piece of muscle with the duration of action 

 potential and conduction velocity stated; L = VT).) 

 In ventricular muscle, which conducts at 300 mm per 

 sec, the length of the depolarized segment would be 

 about 90 mm; in Purkinje tissue, about 600 mm. 



Since normal ventricular conduction utilizes myo- 

 cardial and Purkinje tissue, the length of the de- 

 polarized segment in either the atrium or the ventricle 

 is probably greater than that of any pathway nor- 

 mally found in the human heart. If, however, the 

 action potential becomes continuously shorter at the 

 same time that the velocity becomes continuously 

 slower, the length of the depolarized segment will 

 decrease. When this decrease occurs, it is possible 

 for the wave to "catch its own tail." Once this has 

 happened, the process can be repeated. Each suc- 

 cessive completion of the circuit can result in a slower 

 conduction velocity, a decreased action potential 

 duration, and a shorter pathway for the circus wave 

 until, finally, it has a very short pathway. At this 

 time, there could be a large number of circus path- 

 ways on the myocardium, possibly undergoing con- 

 tinuous change. In support of this hypothesis it has 

 been reported that, during the early stages of fibrilla- 

 tion in the cooled heart, certain frequencies are re- 

 peated on the electrical record and that these finally 

 disappear as fibrillation continues (6). 



When Sano and co-workers studied ventricular 

 fibrillation with ultramicroelectrodes, they found 

 some synchrony of activity early in fibrillation but 

 none later (iii). There were also some changes in 

 the action potential and an irregularity in the mag- 

 nitude and configuration of the action potential during 

 fibrillation. Records obtained with both intracellular 

 and extracellular electrodes indicate that once 

 fibrillation has been established, the situation is one 

 of complete chaos. 



M\wcardial Injury; Ischemia and Infarction 



PHASE I. If a region of myocardium is partially de- 

 prived of oxygen, the first change observed electro- 

 cardiographically is an alteration of the T wave. 

 Apparently the region of ischemia cannot repolarize 

 normally. Possibly the ischemic region remains de- 

 polarized after adjacent regions have returned to the 

 resting state. An overlying electrode will therefore 

 record a negative T wave that is usually larger than 

 normal. A similar change in the T wave is seen during 

 recovery from an infarction. It should be noted that 

 the T wave is a most labile portion of the electro- 

 cardiogram and less reliable for diagnostic purposes 

 than other portions of the ventricular complex. 

 Changes similar to those resulting from ischemia 

 arise also from benign causes. If the entire heart is 

 uniformly deprived of oxygen, T wave changes may 

 appear in all leads. 



