These terms imply a more or less sudden and complete interference with the process of respiration, whether by interruption to the entrance of air into the lungs or to the passage of blood through them. So far as the medulla oblongata is concerned, the effect of a block in the pulmonary circulation will be similar to that of a closure of the larynx or trachea. In either case the blood reaching the respiratory centres will be deficient in oxygen, and the result is an excessive stimulation of these centres.
The first result of a sudden and complete obstruction to the airpassages, as when a foreign body gets into the larnyx, or in drowning or other modes of suffocation, is the development of an urgent dyspnoea. All the respiratory muscles are brought into violent exercise, but the expiratory phase is more laboured than the inspiratory. These violent, muscular contractions extend to other muscles, and in About a minute they develop into general convulsions. This is followed by relaxation of the muscles and gradual diminution of the respirations and death. During the acute period there is a great rise in the arterial blood-pressure as measured by the kymograph. In the later period the blood-pressure falls to the normal or subnormal.
During the active period of suffocation small haemorrhages or ecchymoses occur. These are most common in the lungs and pleura and in the pericardium, but are also met with in certain of the softer tissues of the body, as the conjunctiva, pia mater, or retina. Those in the pleura and pericardium, as they are the most frequent and most readily observed, afford the most direct evidence post-mortem of death from asphyxia. The most obvious explanation of these haemorrhages is that, they are the result of the excessive increase of the arterial blood-pressure. This is doubtless the explanation of the haemorrhages in the conjunctiva and pia mater, but in the case of the pleura and pericardium another element enters which acts along with the increased blood-pressure and determines the greater frequency of ecchymosis within the chest. This element is the suction action of the violent inspiratory efforts producing a partial vacuum in the chest and so diminishing the support of the vessels. It may be stated here that the author is able to state from observations of his own that the haemorrhages in the chest are not limited to the pleura and pericardium, but affect the parenchyma of the lung as well. But in the lung the bleeding is chiefly in the interlobular connective tissue and not into the lung alveoli. This determines that the haemorrhage is from the bronchial artery, which supplies the connective tissue of the lung, and not from the pulmonary artery. It is the bronchial artery also which supplies the pulmonary pleura. The influence of the rise in blood-pressure is here seen. The blood in the pulmonary artery does not take part in the rise in pressure, but that in the bronchial arteries does so, as these arteries belong to the systemic system. The pleural and pulmonary ecchymoses are thus due directly to the rise in blood-pressure, but their frequency in these situations is to be referred to the local circumstances of the dyspnoea.
Cohnheim has fallen into the curious error of regarding these haemorrhages as occurring from the pulmonary arterial system and ignoring the bronchial arteries. As the pulmonary system is not affected by the rise in blood-pressure he infers that the suction of inspiration is the only cause of the haemorrhages, although admitting that the haemorrhages in the conjunctiva and pia mater are due to the rise in blood-pressure.
Where the interference with the access of air or with the pulmonary circulation is less sudden or less complete, the phenomena are much less urgent than those above noted, and are of the character rather of those of dyspnoea as already described.