Abstract
In a case of syphilis, chronic interstitial nephritis, dilatation and hypertrophy of the heart, auricular fibrillation, arteriosclerosis, periodic breathing, Cheyne-Stokes type, in which because the auricule was fibrillating, digitalis had been given for the purpose of showing the ventricular rate. Counts of the pulse showed the ventricle to be contracting at a rate approximating 100 during apnea and slowing to about half this rate as soon as hyperpnea began. That is, the heart rate was highest while there was no lung ventilation (apnea) and the heart beat less frequently during the period the lung ventilation was greatest (hyperpnea).
As the digitalis was continued the man complained of increasing distress, most severe during his hyperpnea. The ventricle rate did not become slower and evidently the patient was much more uncomfortable. The thought occurred that releasing the heart from vagus control might give relief, therefore, atropine gr. 1/30 was given by hypodermic injection. Record taken 27 minutes later shows the ventricle beating irregularly at the rate of 150 per minute but uninfluenced by breathing. The patient became comfortable and the cyanosis was less.
Discussion.-As the slowing of the ventricular rate followed the first inspiration after apnea and was maintained until the last part of the hyperpnea stage, it was considered to be due to the inhibition of the vagus which was stimulated by the reflexes from the lung generated by the respiratory efforts of hyperpnea. The average hyperpnea periods were of 37 sec. duration. The reflex from the lung became much less effective as a stimulant to the vagus during the descending phase of the hyperpnea; for, the ventricular rate became accelerated several inspirations before apnea began.
This loss of vagus effect upon the heart rate was due, probably, to the fact that reflex stimuli from the lung tissue when it is contracting are not so strong as when the pulmonary tissue is being distended, but not to true vagus escape of the heart.
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