IO8 PATHOLOGICAL VARIATIONS IN THE HEART-BEAT. 



to greater exertion in order to propel the blood through the compressed lung, 

 the apex-beat under such circumstances is usually accentuated. Marked disten- 

 tion of the lungs (emphysema), which depresses the diaphragm, also causes down- 

 ward and inward displacement of the apex-beat. Conversely, elevation of the 

 diaphragm, as a result of contraction of the lungs or of pressure by the abdominal 

 organs, has the effect of displacing the apex-beat upward sometimes as far as 

 the third intercostal space and a little to the left. Thickening of the muscular 

 wall of the heart with dilatation of the cavities (hypertrophy and dilatation) , when 

 it affects the left ventricle, causes an increase in the length and breadth of the 

 chamber, and the accentuated apex-beat becomes palpable to the left of the 

 nipple-line, sometimes in the axillary line in the sixth, seventh, or even eighth 

 intercostal space. Hypertrophy and dilatation of the right ventricle cause an 

 increase in the width of the heart: the apex-beat is felt further to the right, 

 sometimes even to the right of the sternum, but at the same time also a certain 

 distance beyond the left nipple-line. In the rare cases of transposition of the 

 viscera, in which the heart is situated in the right half of the thorax , the apex-beat 

 is of course found in exactly the corresponding situation on the right side of the 

 thorax. Landois was the first to take an apex-beat curve from a heart of this 

 kind and found that it presented all of the normal features. When the heart-beat 

 extends to the left beyond the nipple-line or to the right beyond the parasternal 

 line, the area of cardiac impulse is enlarged transversely, a condition that always 

 indicates hypertrophy of the heart. When this transverse enlargement is unusu- 

 ally great, the apex-beat may extend over several intercostal spaces or over both 

 sides of the thorax. 



The apex-beat appears abnormally weak in association with atrophy and 

 degeneration of the heart-muscle, or when the innervation of the controlling nerves 

 is impaired. The cardiac impulse may be weakened or even completely obliterated 

 also when the heart is forced away from the chest-wall by an accumulation of fluid 

 or of gas in the pericardium, by a greatly distended left lung, or by an effusion into 

 the left pleural cavity. The same condition results either when the left ventricle 

 is imperfectly filled during contraction (in consequence of marked stenosis of the 

 mitral orifice) or when, owing to extreme narrowing of the aortic orifice, it can 

 empty itself but gradually and slowly. 



An increase of the apex-beat is observed in the presence of hypertrophy of 

 the walls of the heart, as well as in association with the most diverse irritative 

 conditions (psychic, inflammatory, febrile, toxic) affecting the heart and its con- 

 trolling nerves.' Extreme hypertrophy of the left ventricle causes a heaving apex- 

 beat, so that a portion of the chest-wall is elevated, with systolic concussion. 



In some cases the apex-beat is quite distinct or even abnormally distinct, 

 while the pulse is quite small. This phenomenon is due to insufficient emptying 

 of the ventricles (spurious contraction of the heart) . 



Systolic retraction is not infrequently observed on the anterior chest -wall 

 in the third and fourth intercostal spaces on the left side under normal conditions, 

 especially when the action of the heart is accentuated and when there is excentric 

 hypertrophy of the ventricles. As the apex is somewhat displaced with each 

 ventricular contraction and the ventricles at the same time diminish in size, the 

 yielding soft parts of the intercostal space are drawn in to fill the vacuum thus 

 formed. When the heart is adherent to the pericardium and the surrounding 

 connective tissue, movement of the heart during systole becomes impossible and 

 the apex-beat is replaced by systolic retraction of the apical area. Under such 

 circumstances the chest-wall bulges during diastole, in a measure representing a 

 kind of diastolic apex-beat. 



The changes in the apex-beat that occur in association with functional dis- 

 orders of the heart are best studied by tracing apex-beat curves, as has been done 

 by a number of clinicians since Landois first published his method in 1876. 



In the curve shown in Fig. 33, P, in reduced size and obtained from a case of 

 marked hypertrophy and dilatation of the left ventricle, the ventricular contrac- 

 tion as a rule is exceedingly large (b c) , although the time occupied in contraction 

 by the greatly increased muscular mass of the ventricular wall is not materially 

 longer than under normal conditions. The curves P and Q were obtained from 

 a man with a high grade of excentric hypertrophy of the left ventricle, resulting 

 from insufficiency of the semilunar valves of the aorta. The curve Q was taken 

 purposely at a point near the epigastrium where systolic retraction was present. 

 Although the position of the individual portions of the curve is changed, the 

 individual phases of the heart's action are nevertheless well shown. 



