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The external respiration has been studied in 221 patients. The disorders in pulmonary gas exchange subsequent to an injury are due to decreased ventilation volumes, delayed diffusion of inhaled gases and disturbed blood circulation in the lungs. Functional disorders are often aggravated by pulmonary complications.
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The function of pulmonary respiration was studied in 28 patients with acute postinfarction aneurysms of the heart, in 20 normal individuals and in 25 patients with transmural myocardial infarction non-complicated by by cardiac aneurysm. A comparative analysis of the obtained data has shown that patients with acute postinfarction aneurysms of the heart have more severe pulmonary respiration disorders than those with transmural myocardial infarctions. The degree of these disorders grows in accordance with the degree of circulation insufficiency. The authors believe the main cause of such pulmonary respiration disorders in cardiac aneurysms to consist in a reduced contractile capacity of the heart muscle with subsequent disturbances in the intracardiac haemodynamics and the development of pulmonary hypertension. The authors recommend to take into account the degree of pulmonary respiration disorders when determining the vital and occupational prognosis, as well as the indications for a surgical management of this complication of myocardial infarction.
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During sleep, of ventilated newborns and young infants, spontaneous respiratory movements may occur, unrelated to the ventilation impulsions. The respiratory pattern is then classified as "active". On the contrary, the respiratory pattern is classified as "passive", when all respiratory movements are related to the ventilation insufflation. The factors which influence the dependence on the ventilator are studied in a group of 20 newborn and young infants. Prematurity, some biological data such as hyperoxia, hypocapnia, seem to favor this dependence. A rapid rate of ventilation (superior to 30/minute) is rarely related to an active respiration; a slow rate of ventilation seems favor this respiratory pattern. It is clear that adaptation to artificial ventilation is better during quiet sleep than during active sleep. Some physiopathological considerations are developed.
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Studies of vocal cord function were undertaken in a quadriplegic patient requiring ventilatory assistance, and in 2 normal subjects during controlled ventilation in a tank-type respirator. When the patient and the normal subjects relaxed and made no conscious effort to assist the respirator, the vocal cords were observed to close during inspiration and a large pressure gradient (12 to 19 cm H2O) developed across the cords. When the subjects made a slight inspiratory effort ("assist" mode), the cords opened widely during inspiration. There were large increases in flow and tidal volume in the "assist" mode compared with passive ventilation. Measurements of transdiaphragmatic pressure and esophageal pressure showed that these variables did not increase with the slight assist. Thus, increase in ventilation during the "assist" mode appeared to be due to alleviation of inspiratory obstruction at the level of the vocal cords. The same phenomenon was observed in the patient during phrenic nerve pacing. A pacemaker was designed to be triggered by the electromyographic impulse from an accessory muscle of respiration. In this manner, vocal cord opening could be coordinated with the mechanical assist given by the phrenic nerve pacer.
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To investigate the role of ventilation-perfusion (VA/Q) imbalance in the hypoxemia observed after head injury, 5 male subjects (17 to 26 years of age) with isolated head trauma and subsequent hypoxemia were studied. Disturbances of ventilation and perfusion were assessed using the steady-state elimination of six inert gases of different solubilities. Paired studies were conducted during mechanical ventilation with a volume-cycled ventilator and during spontaneous ventilation. Distributions recovered from studies of spontaneous ventilation show a mode of ventilation and perfusion near a VA/Q of 1.0. In addition, 41% of the cardiac output was distributed to a second population of lung units with low VA/Q (less than 0.1) and shunt. During mechanical ventilation, perfusion to these regions of low VA/Q decreased to 21% of the cardiac output, whereas shunt fraction was unchanged. This was associated with a marked broadening of the VA/Q mode near 1.0, relative to the studies during spontaneous ventilation. Mean functional residual capacity during mechanical ventilation was not different from that during spontaneous ventilation. These results suggest that head injury can lead to hypoxemia through a failure of VA/Q regulatory mechanisms.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.