The Study Of Correlative Effect Factors On Atelectasis After General Anesthesia

ObjectiveHypoxemia is a familiar complication during and after operation. According to reports, mild to moderate hypoxemia ( arterial oxygen saturation of between 85% -90% ) occurs in about half of all patients undergoing anesthesia and e-lective surgery. In 20% of the patients the saturation is below 81% for up to 5 min. The incidence of postoperative hypoxemia may increase to 20% ~ 50%. There are many causes can lead to hypoxemia. But in current viewpoint, the primary cause of hypoxemia is pulmonary atelectasis which has developped during anaesthesia remains in the postoperative period. It not only impair gas exchange but also stimulate alveolar macrophages to produce interleukin -1 or tumor necrosis factor, and result in decreased function of surfactant. These latter effects may contribute to direct or indirect injury of the lung. So atelectasis is also a important inducement of postoperative pulmonary complications.In their classic paper (1963 ) , Bendixen et al proposed: " a concept of atelectasis " . They had observed a successive decrease in compliance of the respiratory system and a similar successive decrease in arterial oxygenation in both anesthetized humans and animal experiments. This was interpreted as formation of atelectasis. Moreover, owing to atelectasis could not be demonstrated on conventional chest Xray. Their view did not be accepted extensively. In the eighties, new observations were made using computed tomography (CT) with transverse exposures of the chest, which demonstrated that atelectasis for sure is the primary cause of hypoxemia. Atelectasis appears in almost 90% of all patients who are anesthetized. It has been estimated that in adults with healthy lungs, 20% ~25% of lung tissue in basal regions or 15% of the entire lung may be atelec-tatic. This may result in a true pulmonary shunt of approximately 5% ~ 10% of cardiac output. Good correlations have been found between gas exchange impairment and the amount of atelectasis and intrapulmonary shunt.At present, the causes of atelectasis has remained obscure. It may be caused by a variety of factors; (1) Compression atelectasis occurs when the transmural pressure distending the alveolus is reduced, (2 ) Absorption atelectasis occurs when less gas enter the alveolus than is removed by uptake by the blood, (3) Loss - of - surfactant atelectasis occurs when the surfactant tension of an alveolus increases because of reduced surfactant action, (4) Obesity, chronic obstructive pulmonary disease and so on are often associated with atelectasis formation. The primary preventing or therapying measures are: (1) maintenance or restoration of respiratory muscle tone, (2) recruitment manoeuvres, (3) minimization of pulmonary gas adsorption, and (4) end - expiratory positive pressure (PEEP) and so on. But now there are a lot of disputes about the formation, transformation of atelectasis, and the validity and security of therapying. The purpose of our study is to explore the causes, inducements and the measures of preventing or therapying by combining human and animal experiment.Methods1 Eight albina rabbits were anesthesia by 20% urethane lg/kg intravenous injection. Then the rabbits were turned supine and remained in this position throughout the remainder of the experiment. The trachea was dissected free, and a tracheostomy tube was introduced. The phrenic nerves were dissected free bilaterally and carotid artery was inserted. Then fentanyl 40 fxg/kg was given to each rabbit by intravenous injecting. The lungs were ventilated mechanically with 80% oxygen using a small animal respirator, giving a tidal volume of 20 ml. Ventilatory frequency was adjusted to produce normocapnia. Bilateral phrenic nerve were stimulated by Sen - 3201 nerve stimulator and SS - 102J stimulus isolator at 10 min after arterial blood - gas analysis and FRC were measured. The stimulating voltage and frequency were 6v and 20Hz respective-ly. Arterial blood - gas analysis and FRC were measured once again at the same time of stimulation. Airway pressure, respiratory frequency and blood pressure were recorded by RM - 6200 multichannel electrophysiolograph.2 Six healthy male volunteers were performed computed tomography (CT) at end - expiratory position at the level of the interventricular septum. Then the subjects voluntarily reduced the end - expiratory lung volume as near to residual volume as possible for 5 min, after which the subjects allowed their end - expiratory lung volume to return to functional residual capacity, CT were performed at the same level. Then the subjects taken 10 maximal forced inspirations, CT were performed once again. After that all subjects inhaled 100% oxygen for 30 min at normal lung volume and then for a further 5 min with forced maximal expirations. Following these maneuver, CT were performed also. The images were analysed by computer at workstation. A window setting of - 1000 to +100 Hounsfield units ( HU ) was selected to assess the total lung surface. A threshold of -1000 to -500 HU was applied to quantify the amount of normally ventilated lung, a second threshold of -500 to - 100 was chosen to establish the surface of poorly ventilated lung, and third threshold of - 100 to +100 HU was set to measure the surface of atelectatic lung area. The right and left lung surfaces of pulmonary atelectasis were summed and reported to the total lung surface. The amount of atelectatic tissue was expressed as a percentage of the total lung area. The subjects were monitored blood pressure , heart rate , pulse oximetry , electrocardiogram , end tidal CO2, Fractional inspired O2 concentration throughout the study.3 Twenty patients undergoing open cholecystectomy were dividied into two groups accorrding to body mass index (BMI) , nonobese group (n= 10) BMI < 25, obese group (n = 10) BMI >30. All patients were anestheticed under intravenous anesthesia, and the references of ventilatory settings were uniformed. Persistent monitored blood pressure, heart rate, pulse oximetry, electrocardiogram , end tidal CO2, fractional inspired O2 concentration, tidal volume, airway resistance, respiratory frequency, airway pressure, dynamic state compliance of the total respiratory system and of the lung during anesthesia. Arterial (?)lood -gas analysis were measured in both groups before and at 15 min after anesthesiainducation and at 24h after operation, recored pH, PaO2, PaCO2, alveolar - arterial oxygen difference (D(a_A)O2). Functional residual capacity (FRC) was measured at end - expiration using a simplified closed - circuit helium dilution method simultaneous. Forced vital capacity ( FVC ) , forced expiratory volume in Is (FEV1) , maximal midexpiratory flow curve (MMF) were also measured before and at 24h after operation.4 Twelve elderly patients whose age exceed 70 without markedly heart and lung diseases undergoing abdominal operation were anestheticed under intravenous anesthesia, Arterial blood gas and FRC were measured before anesthesia. Tidal volume was installed as 10ml/kg without PEEP after general anesthesia. Arterial blood gas and FRC were measured at 10 min after general anesthesia. Then we performed 10 cmH2O PEEP. Arterial blood gas and FRC were measured once again after 30 min. The subjects were monitored blood pressure, heart rate, pulse oximetry, central venous pressure, electrocardiogram, end tidal CO2, fractronal inspired O2 concentration, tidal volume, airway resistance, respiratory frequency and so on throughout the study.Results1 There were significant increase in both FRG and PaO2 with significant decrease of D(a-A)O2 after bilateral phrenic nerve were stimulated (P <0. 01 ). There was a significant correlation between the increase value of FRC and the decrease value of D(a-A)O2, r=0.857 (P<0.01).2 Six subjects had not poorly ventilated lung and atelectasis at normal lung volume. There was not atelectasis but poorly ventilated lung (22. 85% ± 5. 03% ) when the subjects breathed air for 5 min at minimal lung volume. The changes were entire reversed by taking 10 maximal forced inspirations. However there was markedly atelectasis (4.45% ±1. 11% ) after inhaled 100% oxygen for 30 min at normal lung volume and then for a further 5 min with forced maximal expirations. The atelectasis was reduced to 0. 86% ±0.40% by taking 10 maximal forced inspirations. There was a slightly but significant decrease in SpO2 when the subjects breathed air or oxygen at minimal lung volume. But it can be resumed by taking 10 maximal forced inspirations. There were not signifi-...