THE RESPIRATORY CENTER. 753 



gasping respirations occur. Then the exhausted muscles cease con- 

 tracting entirely, and soon the movement of the heart also ceases. This 

 condition is designated asphyxia and it may terminate fatally in suf- 

 focation. If, however, the causative factors can be removed, the 

 asphyxia can be dissipated under favorable conditions by means of ar- 

 tificial stimulation of the respiratory muscles and of the cardiac activity, 

 so that following the state of dyspnea that of eupnea may be again 

 obtained. If the state of the blood becomes only gradually more 

 and more venous, asphyxia may result without the signs of previous 

 dyspnea, death taking place quietly and gradually. The condition here 

 is in a certain measure one of insidiousness of the irritation. 



Convulsions are associated with the dyspnea of acute onset. Extirpation of 

 the cerebral hemispheres, likewise deep narcosis by means of chloroform, renders 

 these slight or abolishes them. After removal of the optic thalami general 

 convulsions appear not to take place. 



Among the causes of dyspnea there should be mentioned: 



i. Direct limitation of the activity of the respiratory organs: Diminution in 

 the respiratory surface in consequence of inflammation, acute edema or collapse 

 of the alveoli, occlusion of the alveolar capillaries, compression or collapse of the 

 lungs in consequence of the entrance of air into the pleural cavities and stenosis 

 of the air-passages. 2. Exclusion of the normal respiratory air through stran- 

 gulation, enclosure in narrow spaces, drowning. 3. Failure of the circulation, in 

 consequence of which a sufficient amount of blood is not sent to the medulla and 

 as a result the necessary ventilation does not take place, as in connection with 

 degenerations of the heart, valvular lesions, artificially through ligature of the 

 carotid arteries, also obstruction to the escape of the venous blood from the cranial 

 cavity, finally through the injection of large quantities of air or of indifferent 

 bodies into the right heart. 4. Direct loss of blood, which may be effective 

 likewise through interference with the gaseous interchange in the medulla. In 

 this category belongs also the dyspneic gasping for air of the decapitated head, 

 particularly of young animals. 



If the rapidity with which these factors influence the respiratory activity be 

 observed it will be noted that there occurs first accelerated and deepened breathing; 

 there then follows, after the general convulsions and the associated expiratory 

 spasm, a stage of complete respiratory rest, in relaxation, asphyctic respiratory 

 pause. Finally, there occur only a few gasping inspirations before death takes 

 place. 



Generally the deficiency of oxygen and the excess of carbon dioxid tend at 

 the same time to excite the dyspnea, although in the variations of the inspired 

 air from the normal, the increase of carbon dioxid has an irritating effect earlier 

 and in more marked degree than the diminution of oxygen, i. Dyspnea from 

 deficiency of oxygen occurs on breathing in closed space of moderate size, in a 

 space the air of which is rarefied, as well as on breathing indifferent gases free 

 from oxygen. On intense ventilation of the blood with nitrogen or hydrogen, 

 the amount of carbon dioxid contained may even be diminished, and death takes 

 place, nevertheless, amid the signs of asphyxia. 2. Dyspnea from excess of 

 carbon dioxid occurs on breathing mixtures of gas rich in carbon dioxid (which 

 form also on breathing for a long time in a closed space of considerable size or 

 in an atmosphere of pure oxygen) . Gaseous mixtures rich in carbon dioxid cause 

 dyspnea even when the amount of oxygen contained is greater than that of the 

 atmosphere. Even the blood itself may be found to contain more oxygen than 

 normal. 



Elevation of temperature also may stimulate the respiratory center to increased 

 activity. This takes place even when the brain alone receives warmer blood, as 

 was observed by A. Fick and Goldstein when they imbedded the exposed carotid 

 arteries in heated tubes. In this experiment the heated blood obviously affects 

 directly the medulla and the cerebral respiratory centers. Direct lowering of the 

 temperature diminishes the irritability. When the temperature is elevated, apnea 

 cannot be induced by means of forced artificial respiration and the resulting 

 arterialization of the blood. Emetics act in the same manner. 



Kronecker and Marckwald found electrical irritation of the center also effective. 

 Irritation of the medulla oblongata separated from the brain excited respiratory 

 48 



