Respiratory variations of the heart rate - II—The central mechanism of the respiratory arrhythmia and the inter-relations between the central and the reflex mechanisms

Abstract

It was first noticed by Traube (1865) that the respiratory cardiac arrhythmia persists after curarization and that it becomes more obvious when the curarized animal is subjected to asphyxiation. Since, in his experiments, the muscles were paralysed and with the consequence the lungs remained in a stationary position Traube concluded that the arrhythmia could not be explained otherwise than by a direct influence of the respiratory centre upon the centres regulating the heart rate. The fact that the respiratory activity continues after administration of curare and that it becomes greatly increased during asphyxia is beyond dispute. In Traube’s time this could only be conjectured, but now it can be proved by registering the electrical deflexions of the phrenic nerve or of any other inspiratory nerve. This we had occasion to verify in many experiments. The theory of Traube was for a time superseded by Hering’s theory of the reflex origin of the arrhythmia (1871). However, Frédéricq (1882), in a series of masterly experiments, advanced such indisputable proofs in favour of the central mechanism that most physiologists began to doubt even the existence of the reflex mechanism. The respiratory arrhythmia continues in an animal the chest of which is widely open so that the lungs are stationary. When the respiration stops, as a result of an over ventilation, the arrhythmia also disappears. Snyder (1915) confirmed the observations of Frédéricq and expanded them by showing that the arrhythmia can be noticed even in the absence of any visible respiratory movements, but that even under these conditions it is of a central origin and depends on the respiratory centre. He suggests that the respiratory discharges may be so insignificant that they do not lead to an effective expansion of the chest; in fact, not even to a noticeable contraction of respiratory muscles, but they, nevertheless, affect the vagus centre and cause an appreciable inhibition of it. This conclusion rests on the observation that the arrhythmia occurring in absence of any sign of respiration keeps the rhythm of the respiratory movements which had been present before and which become re-established after a period of a temporary respiratory arrest. J. F. Heymans and C. Heymans (1928, 1929) investigated this problem with the help of cross circulation. They definitely express themselves in favour of the central mechanism of the arrhythmia since it is synchronous with the respiration and not with the ventilation of the lungs and since it continued, in their experiments, after the denervation of the lungs. They also found that the changes in the heart rate are not caused by the alteration of the blood pressure which accompanies the respiratory act so that the arrhythmia could not be attributed to some vascular reflexes. Although these authors find the changes in the heart rate to be synchronous with the respiration, they do not regard them as due to an irradiation from the respiratory centre since they can be observed, as has been first stated by Snyder, in the absence of all respiratory movements. Heymans (1929) suggests that there is a common rhythm which governs the activity of the respiratory and of the vagus centres and that there is no need to suppose that the respiratory rhythm directly influences the rhythm of the vagus centre. No experimental evidence has been advanced in favour of this view. Lately Heymans, Samaan, and Bouckaert (1934) seem to have accepted the fact that the lungs also play a part in the arrhythmia. Our experiments upon the central mechanism of the respiratory arrhythmia have been carried out with the technique described in the previous paper. It is obvious that in order to study the central arrhythmia without the interfering influences arising from the pulmonary reflexes, these reflexes must be abolished. We know of three conditions in which the cardio-accelerator impulses of pulmonary origin are almost or completely stopped: during a maximal deflation of the lungs, during the “secondary slowing” occurring in protracted inflation of the lungs, and after section of the thoracic vagi just above the lungs. The last condition obviously presents greater advantages because it is inadvisable, even in the innervated heart lung preparation, to keep the lungs collapsed for a long time, and it is difficult to be sure that the secondary slowing will remain unchanged. Therefore, all our experiments were made after preliminary section of the vagi about a centimetre above the roots of the lungs.