HYPERJEMIA OF THE LUNG. 139 



den ness. Hence such cases are called pulmonary apoplexy (JJungen- 

 schlagfluss). The shortness of breath quickly increases to a serious ex- 

 tent ; the breathing grows hurried and scarcely to be counted. The 

 feeling of fulness and compression causes fear of death and a sensa- 

 tion of choking ; every cough fills the mouth with a copious, frothy, 

 bloody expectoration. The heart beats visibly, the radial pulse and 

 the carotids betray the tension of the arteries. The face is reddened. 

 The oedema, which follows this form of hyperaemia, soon makes itself 

 felt The vesicles, filled with serum, can admit no more air ; an acute 

 surcharge of the blood with carbonic acid changes the scene. The 

 restless patient becomes still and drowsy, the face paler, the muscles of 

 the bronchi, palsied with the other muscles, cannot rid the tubes of their 

 serous contents. Coarse, moist rdles, audible even in the trachea, 

 announce the approaching end, the threatening suffocative effusion. 



The symptoms of acute fluxion, brought on by the inhalation of irri- 

 tating gases, are modified by the coexistence of irritation of the larynx 

 and bronchial mucous membrane, and are accompanied by violent 

 coughing-fits. The hyperasmia to which tuberculosis, cancer of the 

 lung, etc., give rise, and which most generally produce pulmonary and 

 bronchial haemorrhage, are to be treated of in the next chapter. 



Collateral fluxion to the lungs forms a grand feature in the descrip- 

 tion which we shall present of pneumonia, pleuritis, and pneumothorax. 

 Here a large part of the dyspnoea depends upon the overfilling of the 

 capillaries and swelling of the vesicles, in the portions of the lung un- 

 affected by the inflammation. Without this complication, or, to speak 

 more properly, if no such condition arose when the circulation is im- 

 peded, the unaffected vesicles could better obtain their supply of air. 

 If the blood pressure be lessened by venesection, the collateral fluxion 

 is reduced, the dyspnoea often completely disappears^ although the chief 

 disease continues unabated. When patients die in the first stages of 

 pneumonia or pleuritis, or shortly after air has penetrated into the pleural 

 sac, and compressed the lung, they die of collateral hyperaemia and 

 collateral oedema. If we examine the records of post-mortem examina- 

 tions, we shall not fail to find evidence of this form of hyperaemia, 

 although it is but little appreciated in interpreting the symptoms. 



Passive hyperaemia (Blut-stauung), even when unaccompanied by 

 pulmonary oedema, creates greater dyspnoea than fluxion to the lung. 

 Patients with insulncience and contraction of the mitral, even if they 

 have no bronchial catarrh, and when the engorgement does not extend 

 from the alveolar capillaries into their anastomoses so as to produce 

 tumefaction of the mucous membrane and contraction of the tube, 

 nevertheless usually suffer from a very distressing shortness of breath, 

 aggravated by the slightest movement This is easily accounted for, 



