38o 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



measurable voltage must be present as long as the 

 action potential changes in time. This is always the 

 case. The name "plateau" is only an approximate 

 description of the facts : there is an immediate, but 

 slow, decline of the action potential after the spike 

 has ended. If this initial decline were homogeneous 

 all over the heart, the resulting ST segment would 

 be opposite in direction to the main QRS deflection. 

 The facts, however, show that ST starts (at the so- 

 called ST junction at the end of S, marked with J 

 by some authors) with a slowly rising phase, which 

 develops into the T wave without any sharp boundary. 

 This is the natural result of the asychrony of fiber 

 repolarization, which is present even in the very 

 earliest moments of that process. A somewhat steeper 

 rise of ST, forming the rising phase of T, cannot 

 occur before repolarization starts its steep decline. 

 The steeper this decline and the longer the plateau, 

 the more "isoelectric" is ST and the shorter and 

 higher is T. The behavior of the ST segment can be 

 quantitatively evaluated by measuring the time 

 from the ST junction until the rising phase of T 

 reaches one-half of its spike voltage. This time should 

 comprise less than 80 per cent of the interval l^etween 

 the ST junction and the top of T (47). 



No other part of the ECG is subject to so many 

 theories, interpretations, and even more misin- 

 terpretations as the ST interval. The reason is obvious. 

 If any part of the heart is damaged, and no longer 

 produces an action potential of its own, this part 

 develops an injury potential at its boundaries. This 

 potential is recorded as a superimposed monophasic 

 distortion (433, 434)- ST becomes the most important 

 indicator of such local lesions. The interpretation of 

 ST displacements is, however, extremely complicated 

 and needs careful consideration. There is, in the 

 first place, the influence of heart rate on the ST 

 segment, intimately connected with the base line 

 problem (section 10). In tachycardias, the P wave 

 starts before the U wave has ended; the PQ interval 

 is displaced by T,,, so that an apparent negative 

 displacement of ST may be merely the result of an 

 incorrect determination of the base line. ST is ele- 

 vated in bradycardias and is depressed more and 

 more as the frequency increases (464). 



The junction does not always form a sharp angle, 

 but shows, in many cases, a so-called saddle form. 

 This may l)e found in cardiac patients, but hardly 

 more frequently than in normals with slowly rising 

 ST elevations, which are often found in precordial 

 tracings from absolutely normal hearts (181, 226). 

 Positive or negative displacements of ST, whicli 



run more or less parallel to the abscissa, are abnormal 

 (with exceptions to be discussed). 



The theory of ST displacement (58, 188, 436) 

 should be discussed in detail, because of its clinical 

 importance. If an excitation wave traveling along a 

 fiber bundle reaches a region which is damaged and 

 unable to be excited, the following will happen 

 (fig. 63). If we assume the boundary between damaged 

 and intact fiber to be infinitesimally small, the mem- 

 brane potential diflference across the boundary will 

 produce a dipole of the same type as shown in figure 

 2. If the damaged fiber retains its full resting 

 membrane potential, the dipole will show a polarity 

 with the damaged area appearing positive compared 

 to the normal, excited tissue. If the damaged area 

 has no membrane potential, or a diminished one 

 whicii does not change during systole, a dipole is 

 already present at rest, the damaged area appearing 

 negative with respect to normal; but as soon as the 

 normal area becomes depolarized, this resting 

 potential difference disappears. The result is the same 

 as far as the record is concerned : during systole a 

 negativity existing at rest seems to disappear and the 

 damaged area appears to be more positive than the 

 normal. This positivity endures until the end of the 

 action potential, covering thus the whole QT seg- 

 ment. This potential is responsible for the ST dis- 

 placement. The amount of this displacement de- 

 pends on the magnitude of tlie solid angle subtended 

 by the total cross-sectional area of the damaged fibers 

 at the boundary with normal areas, as seen from the 

 electrode. One should bear in mind, however, that 

 such a boundary has no cancellation effect, such as 

 is found in the spread of excitation during the QRS 

 complex. Here, in a way similar to the generation of 

 the ventricular gradient, relatively small areas of 

 damaged fibers can lead to a comparatively large 

 ST displacement. A rough estimation shows that for 

 a displacement of o. i mv, about 400,000 fibers have 

 to be damaged or inactivated, assuming no can- 

 cellation (404). 



The polarity of an ST displacement and its re- 

 sultant vector (fig. 64) depend fully upon the electric 

 moment of the resting membrane potential and the 

 anatomical directions of the fibers producing this 

 moment and crossing the boundary between normal 

 and damaged areas. The vector therefore does not 

 change direction throughout the whole ST segment, 

 as experimental evidence shows (445). It is therefore 

 clear that similarly located injuries must produce 

 similar vector positions and ST polarities, as experi- 

 mental evidence again confirms {if>~). In dogs, for 



