Flail chest가 호흡 및 순환기능에 미치는 영향에 관한 실험적연구, 특히 이때에 기관절개술의 역할에 대하여
During the past two decades, tracheostomy has been widely used in the treatment of the crushing injury of the chest, disease of the lower respiratory tract and the respiratory insufficiency following the surgery of the chest. It is generally accepted that the advantage of the tracheostomy is to maintain toilet of the airway, to reduce the respiratory dead space and to reduce the airway resistance. In the past, however, reports on experimental studies of the effect of the crushing injuries of the chest or the effect of tracheostomy performed as a treatment of flail chest were few. It is the purpose of this experiment to observe the effect of flail chest and tracheostomy on respiratory and circulatory function in animals.
Twenty mongrel dogs weighing from 12 to 17kg. were used. The animal was anesthetized using pentobarbital sodium, and the pulmonary artery and the abdominal aorta were cannulated through a cutdown in the jugular vein and femoral artery, respectively. The catheterization of the pulmonary artery was done under X-ray
fluoroscopy. A 17cm. long rubber tube, the inner diameter of which measured 1.6cm., was placed just above the epiglottis and the oro-nasal cavity was made air-tight by packing the cavity with gauze bandage and also by using a tight rubber face mask.
The animal breathed through the tube only. The epiglottis was secured anteriorly to prevent airway obstruction during the experiment. Under this condition, respiratory rate, tidal volume, minute ventilation, ventillatory equivalent, pulse rate, stroke
volume, cardiac index, mean pressure of abdominal aorta, total peripheral vascular resistance, O^^2 consumption, O^^2 saturation of the mixed venous blood, A-V O^^2 difference, mean pressure of the pulmonary artery and total pulmonary arterial resistance were observed. Then a long skin incision was made on the chest and approximately 5∼6cm. long segment of bone was removed subperiosteally from 8∼16 ribs of unilateral or bilateral chest, thus causing moderate or severe paradoxical motion of the chest wall. Under this condition the same observations were made as
in the basal state under anesthesia. After this a tracheostomy was made near the lower end of the cervical trachea, and a tuve with a cuff was introduced to the trachea. By inflating the cuff the animal was made to breathe through the tracheostomy tube only. Under this condition the same observations were repeated.
In 14 dogs, a thin rubber tube 7cm with a diameter of 0.5cm, was placed in the thoracic esophagus, and this was connected to a water manometer to observe the changes in the intrathoracic pressure indirectly.
It was observed that the flail chest caused a profound decrease in the respiratory function, manifested by a significant increase in respiratory rate, decrease in tidal volume and increase in minute ventilation and ventilatory equivalent.
When trachesotomy was done on the animal with a flail chest, the respiratory function improved remarkably. The respiration rate decreased markedly. Though the tidal volume decreased slightly the minute veintilation and ventilatory equivalent
significantly. The intraesophageal pressure, particularly the positive pressure, dropped markedly following tracheostomy was made on the animal with a flail chest.
The improved ventilatory function of the lung following tracheostomy is thought to be due to (1) the decrease in the respiratory dead space which increases the alveolar ventilation, (2) the decrease of the air-way resistance enabling the inspiratory and expiratory air to travel the respiratory tract with less effort, and (3)the decrease in the intrathoracic pressure, thus minimizing the paradoxical motion of the chest wall, which in turn relieves the harmful ventilation phenomena
of flail chest such as mediastinal flutter and cross ventilation between right and left lung. In contrast to the considerable improvement in the respiratory function after tracheostomy, the changes in the circulatory function were not marked. In the
animal with a flail chest, the pulse rate remained unchanged. The stroke volume and cardiac index decreased, and both the mean pressure of the abdominal aorta and the total peripheral vascular resistance dropped. The decrease of the stroke volume and cardiac index is thought to be the result of the surgical trauma, the blood loss, decrease in central blood volume and the change in respiratory state which affects the mechanisms of respiratory augmentation of the venous return to the thoracic vena cavae and the right heart.
When tracheostomy was made on animals with a flail chest, both the stroke volume and cardiac index decreased further, while the mean pressure of the abdominal aorta and the total peripheral vascular resistance increased. Total peripheral vascular resistance in this experiment seems to be affected by the extensive trauma of the soft tissue of the chest sustained by surgical procedure.
All these changes in circulatory function, however, were within normal range, and it was concluded that the circulatory system functioned normally despite the profound respiratory distress of the animal with flail chest and also with the improved respiratory state following tracheostomy.
Oxygen consumption did not change throughout all phases of the experiment, and this seems to be due to the fact that the metabolic requirement of the peripheral tissue did not change in the various phases of the experiment.
The O^^2 saturation of the arterial blood exceeded 100% in all instances, and the changes of O^^2 saturation of the mixed venous blood and A-V O^^2 difference were minor and were within normal values. These changes are secondary to the changes in cardiac output. This observation further proves that the circulatory system maintained the normal function in all the phases of the experiment.
The pulmonary arterial mean pressure did not change appreciably though the blood flow through the pulmonary artery decreased with the flail chest and further decreased following tracheostomy. This stable pulmonary arterial pressure was the result of the rise in the total pulmonary arterial resistance. This change in total pulmonary arterial resistance seems to be due to the expansibility of the pulmonary vascular bed, the distensibility of the pulmonary vasculatures, the changes in lung volume and change in respiratory state.