It is a well-known fact that many patients suffer from angina pectoris, whose coronary arteries are perfectly sound; such cases, I believe, are entirely due to the loss of elasticity of the cardiac muscle. We know that on any effort an extra amount of blood is sent to the heart, and the heart cavities must dilate slightly to accommodate this extra quantity, and the more severe the effort the greater the extra amount sent to the heart. But a heart with markedly defective elasticity cannot dilate without pain, and the more defective the elasticity the greater the pain. Call this the “effort syndrome” if you will, but it is also one form of Angina pectoris. Of course, we must remember that in estimating the probable state of the heart in the living, we are entirely dependent for proof, not on actual evidence, but on inference and analogy..
As the heart grows old, all physical exercise must be gradual, continuous (i.e. it must not “lie fallow”) and progressive. For it must never be forgotten that the perfectness of the elasticity of the cardiac muscle gradually diminishes from the cradle to the grave from birth to death. It is most fatal to undertake some sudden, severe, physical exertion, beyond a certain (or rather an uncertain) age, especially when the muscles have been lying fallow for some time. I have known at least six men who who have done this very thing and paid the penalty with their lives. In such cases if the heart muscle does dilate, it will remain dilated.
The heart was over stretched, and at that age it remained over-stretched, because the elasticity of the heart-muscle was so imperfect. In the young heart this would not have happened, as the over-stretched muscle would quickly have regained its former size. Note, however, that in all such cases the stress should not be laid on age, as such, but upon the imperfect elasticity.
In athletics we often hear the expression “second wind.” At one moment the athlete in action has a severe pain in the side, and is hardly able to breathe. The next moment the pain is gone and he is perfectly comfortable, and can breathe with the greatest ease. This change from torture to beatitude is due to the sudden dilatation of the heart to accommodate itself to the extra quantity of blood sent to it in a given time. This can only occur where the elasticity of the muscle fibres is “perfect.” Where it is defective there is pain, and the athlete must either stop or run the risk of dying from paralysis of the heart, due to over- distention.
The pain s due to the effort to stretch an unwilling, because imperfectly elastic, muscle. So in the “old” heart, the pain is produced by over-distension, and the attempt, in the almost complete absence of elasticity, to stretch the muscle- fibres and this pain is one form of Angina pectoris, though there may be an entire absence of any visible disease of the coronary arteries or of the muscle substance. But it must not be forgotten that defective response to effort does not always show itself by pain.
It may be also shown by distress in breathing, and this indeed is often the earliest sign of heart failure, and probably more common than angina pectoris. It is not common, I think, to find both together in the same patient, save in the cases where the first attack of angina pectoris is also the last, as in the case, of the great Arnold of Rugby, and also Thomas Chalmers, the celebrated Scotch Divine. In such cases the fault usually lies with the coronary arteries, and is not due merely to the loss of elasticity of the cardiac muscle.
In the latter case I am accustomed to tell my patients that their life depends on themselves or on their own management. The possessor of such a crippled heart must “walk softly” for the rest of his days. A great deal also depends on the common sense of the doctor attending him. Medicines are useful in special cases and at special times, but to deluge such a patient with digitalis, week-in and week-out, is fatal folly and bound to end in disaster.
What is character of this elasticity, as compared, say, with that of an elastic band?.
When stretched lengthwise the muscle extends, and when liberated from the stretching force it readily regains its former length, provided it has not been over-stretched, for there is, of course, a limit to the elasticity.
Comparing the elasticity of muscle with that of an elastic band, we find a remarkable difference in the ratio between the extending power and the resulting extension. In the rubber band it is found that the extension is proportional to the weight, that is, equal increments of weight result in equal increments of length. But in muscle equal increments of weight do not produce equal increments of length; for on applying equal weights the first weight has a greater effect than the second, the second than the third, and so on, so that the curve of elasticity of muscle resembles a hyperbole, whereas the “curve” of elasticity of an elastic band is a straight line.
“Safety-Value” action of valves of the Heart.
It is a very old idea that the tricuspid valve closes less perfectly than the mitral. Thus a certain amount of blood may be driven back into the auricle and great veins under certain circumstances. The reflux thus permitted was looked upon by the older physiologists as very important, since the amount of blood returned to the heart in a given time must be constantly varying with the varying muscular efforts and movements of the body. Since contraction of the muscles and consequent pressure upon the veins is one of the chief powers that move the blood, and carry on the circulation, especially on the venous side.
Every muscular contraction, therefore, sends an increased volume of blood to the heart, and the heart must be saved, at all costs, from over- distension; for when forcibly over-distended, like all hollow muscles, it is promptly paralysed. The risk of this in the young heart is a very slight one on account of the perfect elasticity of the heart at that age; but in the case of the “old” heart where the elasticity is defective or abolished, the risk is a very real one, and one can understand the value of some sort of “safety-valve” action.
We see, therefore, that the quantity of blood delivered by the right auricle must be subject to constant variations, while that propelled from the left auricle into the left ventricle will be more or less uniform in quantity. This was one of the reasons given for the necessity of a “safety-valve” action in the case of the tricuspid; because of this, it was said, that over-distension of the left auricle and ventricle was rendered next to impossible. But as long as the elasticity of the cardiac muscle is perfect (in the physiological sense) such a safety-valve action is unnecessary. But when that elasticity is defective or lost, then it is necessary.
Is there a “safety-valve” action of the mitral? I have always believed so, but the mechanism of its production must be quite different. Listen in the left axillary region when a patient takes as really deep breath, and I think you will hear something very like a regurgitant murmur. Note also in severe and prolonged muscular effort, when the heart is labouring, and the difficulty of free breathing is very great, how great is the relief experienced when a really deep and full inspiration can be taken. This relief, in my opinion, is due to a slight regurgitation of blood, sent back through the mitral valve.
Naturally, under normal conditions, the pressure in the chest, outside the heart, is negative, owing to the elastic recoil of the lungs, and may vary from 3 mm. Hg. during normal expiration to 30 mm. during forced inspiration. This negative pressure, in effect, may be transmitted to the interior of the heart, and this allows the heart to dilate a little in a merely mechanical manner, with possible expansion of the mitral valve orifice. If there is a safety valve action of the mitral, as long as the elasticity of the muscles is perfect, it can only show itself during deep respiration and under negative pressure.
But when the elasticity of the heart muscle is well-nigh abolished, the state of affairs is quite different. Instead of the merely, possible, safety-valve action, and this only under certain circumstances, we are far more likely to get and do get a permanent incompetence of the mitral valve, to make up in a very imperfect way for the loss of cardiac elasticity. This is the best that Nature can do under the circumstances, and the only way the heart can carry on, with moderate comfort. In such cases the patients life is truly in his own hands.
THE TREATMENT OF IMPETIGO CONTAGIOSA NEONATORUM. H.G. Holder (Amer. Journ. Obstet. and Gynecol., June, 1928, p. 857) states that impetigo contagiosa of the new-born infant presents a serious problem in maternity hospitals, its ease of transmission and, at times, its high mortality causing it to be much dreaded. The treatment in 115 cases is reported, one or other of the following methods being employed: 3 per cent. tincture of iodine in 25.2 per cent. of the cases; 10 per cent. ammoniated mercury ointment in 18.2 per cent.; 1 per cent. aqueous solution of mercurochrome in 5.2 per cent., and 2 per cent. aqueous solution of gentian violet in 51.3 per cent. In each the vesicle was surrounded by the agent used, and ruptured under aseptic precautions.
