Influence of ventilatory technique on pulmonary baroinjury in baboons with hyaline membrane disease

To assess the influence of ventilatory technique on pulmonary baroinjury in experimental hyaline membrane disease, we randomized 24 premature baboons to six treatment groups according to ventilator (PPV, positive pressure ventilator; HFO, high frequency oscillator; HFI, high frequency flow interrupter) and O2 therapy FIO2 as clinically indicated, or FIO2 1.0). PaCO2 was adjusted by varying pressure amplitude, and for PPV, also by rate (less than 60/min). HFO and HFI were set at a frequency of 10 Hz. Animals were cared for with standard NICU techniques until death or sacrifice at 11 days. One animal died at delivery and was excluded from data analysis. There were no intergroup differences in Paw, Pa/AO2, PaCO2 or oxygenation index (IO2 = [Pa/AO2]/Paw) prior to death of the first study animal at 13 h. Animals who subsequently developed airleak had higher Paw, lower Pa/AO2 and lower IO2 during this period. The degree of airleak was significantly less with HFO compared to PPV or HFI. The effect of O2 exposure did not appear different with respect to the degree of airleak or the frequency of severe tracheal injury, although survival was shortened. Severe tracheal injury was more frequent with HFI compared to PPV or HFO. BPD was found only in 100% O2 exposed animals surviving greater than 1 wk. Management of premature baboons with HFO and appropriate O2 resulted in less severe airleak, 100% survival, and no evidence of severe tracheal injury or BPD. These outcomes were not achieved with clinically similar strategies using PPV or HFI.     

Effects of carotid denervation on interactions between lung inflation and PaCO2 in modulating phrenic activity

Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration. We examined the role of carotid chemoreceptors in this response using an experimental preparation that allowed independent control of lung inflation and CO2 reflexes. Experiments were conducted in intact (n = 6) and carotid denervated (CBX; n = 12) chloralose/urethane anesthetized dogs. Integrated phrenic amplitude (Phr), f, and the inspiratory (TI) and expiratory durations (TE) were measured as a function of Paw (2-12 cm H2O) at levels of PaCO2 between 30 and 80 mm Hg. In intact dogs: (1) f decreased as Paw increased, and elevated PaCO2 decreased the slope of this relationship; (2) neither PaCO2 nor Paw affected TI; and (3) TE increased hyperbolically with Paw, and elevated PaCO2 attenuated this relationship. In CBX dogs: (1) f decreased as Paw increased, but this relationship was not affected by PaCO2; (2) TI increased as PaCO2 increased but was unaffected by Paw; and (3) TE increased as Paw increased but was unaffected by PaCO2. The results indicate that carotid chemoreceptors are necessary in the mechanism whereby hypercapnia attenuates the effects of Paw on f and TE. Furthermore, carotid denervation reveals an effect of hypercapnia on TI, an effect that is not evident in dogs with functional carotid chemoreceptors.     

Aspiration of airway dead space. A new method to enhance CO2 elimination

Alveolar ventilation and CO2 elimination during mechanical ventilation can be enhanced by reducing dead-space ventilation. Aspiration of gas from the dead space (ASPIDS) is a new principle, according to which gas rich in CO2 during late expiration is aspirated through a channel ending at the distal end of the tracheal tube. Simultaneously, fresh gas injected into the inspiratory line fills the airway down to the same site. We hypothesized that ASPIDS would allow a reduction of tidal volume (VT) and airway pressure (Paw). To test our hypothesis we studied six anaesthetized and mechanically ventilated pigs (24 +/- 4 kg). The intention was to decrease VT while keeping PaCO2 constant by using ASPIDS. VT was reduced by decreasing the minute ventilation (V E) in two steps, of 1.8 L/min (VE - 1.8) and 2.2 L/min (VE - 2.2), respectively, and by increasing respiratory rate (RR) from 20 to 46 breaths/min. At ASPIDS, peak Paw was reduced by 35% at VE - 1.8 and at VE - 2.2 (p < 0.001), and by 20% at an RR of 46 (p < 0.01). PaCO2 was maintained or reduced at ASPIDS. No intrinsic positive end-expiratory pressure developed. Arterial blood pressure and heart rate were unaffected. The results show that ASPIDS allows a reduction in VT and Paw while PaCO2 is kept constant. ASPIDS does not lead to problems associated with jet streams of gas or with gas humidification, and can be developed as a safe technique.     

Effects of hypoxemia on phrenic nerve responses to static lung inflation in anesthetized dogs

To study interactions between hypoxemia and lung stretch in modulating ventilatory activity, an experimental preparation was used that allows independent control of static airway pressure (Paw) and arterial PO2 in anesthetized dogs. Phrenic burst frequency (f) and integrated amplitude (Phr) were monitored while Paw was varied between 2 and 12 cm H2O at levels of PaO2 between 30 and 200 mm Hg. Experiments were repeated in intact (n = 8) and carotid denervated dogs (CBX; n = 7). In intact dogs, f decreased with increasing Paw through an effect on the expiratory duration (TE). Hypoxia increased f by decreasing both the inspiratory duration (TI) and TE. Hypoxia had no effect on the slope of the f vs Paw relationship, but attenuated the effect of Paw on TE. Phr was increased by hypoxia, but Paw had little effect. After CBX, f was still inhibited by Paw, but PaO2 had no consistent effect on f, TI or TE at any level of Paw. Phr was inhibited by hypoxia after CBX, but Paw had no effect. The results indicate that Paw and PaO2 exert additive effects on f in anesthetized dogs. Hypoxia attenuates the effect of Paw on TE, which alone would attenuate the slope of the f vs Paw relationship. However, the effect of hypoxia on TI enhances the slope of the f vs Paw relationship, restoring a parallel shift. These effects are abolished by carotid denervation.     

Partitioning the respiratory effects of airway citric acid and normal saline in lambs

Aspiration is common in the intubated human neonate. Thus, the ventilatory and blood gas responses to citric acid and saline instillation into different airway sites were studied in ten awake, unanesthetised lambs, breathing spontaneously via a tracheostomy tube. With a system of balloons, 1 ml of saline or citric acid was placed selectively into the midtrachea, the laryngeal area, or the lower trachea (lower tr). Changes in minute ventilation (VE), after a 30 sec baseline period, were measured 30 sec and 1 and 2 min after the challenge. Arterial blood gas changes were measured at 30 sec and 2 min. Major increases in VE were seen only when saline or citric acid was instilled into the lower tr, the citric acid responses exceeding saline ones. The arterial oxygen tension (PaO2) fell after lower tr saline, whereas the arterial CO2 tension (PaCO2) fell with midtracheal saline instillation. A rise in pH and a fall in PaCO2 accompanied citric acid given into the lower tr. An initial rise in PaO2 after citric acid into the lower tr was followed by a return to baseline despite hyperventilation. The ventilatory and blood gas changes with saline and citric acid depend on the site of airway instillation.     

Effect of thoracentesis on arterial blood gas tension

The effect of thoracentesis on arterial blood gas tension was studied in 30 patients with unilateral free pleural effusions of various causes. Arterial blood gases were measured before thoracentesis and at 20 minutes, two hours after the procedure. P(A-a)O2 was determined at the same time. The PaO2, PaCO2 and HCO3 showed significant decrease but the concurrent significant increase of the P(A-a)O2 before thoracentesis. The PaO2 showed increase and P(A-a)O2 decrease but the PaCO2 not changes after thoracentesis 20 minutes and two hours. The results suggested that pleural effusion might result in hypoxaemia and chronic compensated alkalosis.     

慢性阻塞性肺疾病患者运动高峰时肺内气体交换对运动能力的影响

目的 探讨COPD患者在运动高峰时肺内气体交换对最大运动能力的影响.方法 对42例男性稳定期COPD患者及26例健康男性进行功率递增至症状自限的踏车运动,同步实时测定摄氧量和二氧化碳产生量,在运动高峰时抽取桡动脉血,测定并计算PaO2、PaCO2、死腔容积与潮气容积比值(VD/VT)和P(A-a)O2.分别对两组资料进行正态性检验,符合正态分布的资料以x-±s表示,两组间比较采用独立样本t检验,最大摄氧量与运动高峰时的血气参数进行相关因素分析.结果 COPD组的最大摄氧量[(16±4)ml·kg-1·min-1]明显低于对照组[(19±6)ml·kg-1·min-1];PaCO2[(43±3)mm Hg,1 mm Hg=0.133 kPa]、VD/VT(0.35±0.11)和P(A-a)O2[(33±11)mm Hg]均明显高于对照组[(40±5)mm Hg、0.27±0.08和(15±7)mm Hg];最大摄氧量与VD/VT呈显著负相关(r=-0.734,P＜0.01).结论 VD/VT增加导致通气效率降低,这是引起COPD患者运动能力减低的一个重要原因.     

Improvement in pulmonary function with diuretic therapy in the hypervolemic and polycythemic patient with chronic obstructive pulmonary disease.

Central hemodynamics and gas exchange were studied in six patients with chronic obstructive pulmonary disease (mean age, 60 years). Patients were selected for the study if the volume of blood was 1 L larger than the predicted normal value, if there was no history of infection, and if no drug assumed to influence pulmonary circulation had been given during the last four weeks. Measurements were first performed in the hypervolemic state. This was followed by a venesection of 0.5 L, and the measurements were repeated 15 minutes later (immediate effects of dehydration). After two weeks to two months of intensive diuretic therapy, new measurements were performed (long-term effects of dehydration). With hypervolemia, there was pulmonary hypertension, increased pulmonary vascular resistance, and normal cardiac output. The arterial oxygen tension (PaO2) was markedly reduced. The arterial carbon dioxide tension (PaCO2) was increased in two patients, and dead-space ventilation (VD/VT) increased in all. The sole immediate effect of venesection was a small increase in heart rate and a reduction in PaCO2. The long-term effects were a maintained low blood volume (on the average, 0.7 L less than before bloodletting) and lowered hematocrit reading (8 percent less than before bloodletting), a reduced and in some patients normalized pulmonary arterial pressure, a reduced pulmonary vascular resistance, and an unchanged cardiac output. The PaO2 improved, while PaCO2 did not change; neither did VD/VT. The changes correlated partly with the diminution in blood volume and partly with the reduction in hematocrit reading.     

Safe intrahospital transport of critically ill ventilator-dependent patients

STUDY OBJECTIVE: To determine whether manual ventilation during intrahospital transport of mechanically ventilated critically ill patients results in blood gas and/or hemodynamic abnormalities. DESIGN: A single-blind prospective study evaluated arterial blood gas, blood pressure, heart rate, and arrhythmia changes during mechanical ventilation and manual transport ventilation. SETTING: University hospital ICUs and various diagnostic or treatment areas. PATIENTS: Twenty mechanically ventilated critically ill patients during intrahospital transport. INTERVENTION: Each patient received mechanical ventilation (MECH) with a volume ventilator while in the ICU and at the study/treatment area. They were manually ventilated (MAN) by a respiratory therapist during transport between areas. MEASUREMENTS AND MAIN RESULTS: The MECH settings were: VT = 0.75 +/- 0.17 L; f = 16 +/- 4; VE = 12.6 +/- 4.3 L/min; FIO2 = 0.46 +/- 0.2. Mean peak Paw = 31 +/- 12 cm H2O and mean effective Cst = 44 +/- 15 ml/cm H2O. No hemodynamic abnormalities were observed. Arterial blood gas values did not vary to any clinically significant degree, except in two patients: one patient had a reduced PaO2 and increased PaCO2 associated with an accidental O2 disconnection and clamped chest tube; another patient had an increased pH by 0.13 units with only a 9 mm Hg fall in PaCO2. CONCLUSIONS: Manual ventilation during intrahospital transport of critically ill mechanically ventilated patients is safe provided the person performing manual ventilation knows the inspired oxygen fraction and minute ventilation required before transport and is trained to approximate them during transport.     

Biologic variability in mechanical ventilation rate and tidal volume does not improve oxygenation or lung mechanics in canine oleic acid lung injury

Mechanical ventilation in patients with acute respiratory distress syndrome and acute lung injury (ALI) remains a difficult challenge because of the conflict between maintaining adequate gas exchange and furthering lung injury via overdistention. In a recent study, Lefevre and colleagues (Am. J. Respir. Crit. Care Med. 1996;154: 1567-1572) suggested that mechanical ventilation with natural biologic variability (BV) in breath-to-breath respiratory frequency (f) and VT could reduce lung injury and improve gas exchange without increases in mean airway pressure (Paw) or peak inspiratory pressure (PIP). However, significant differences in cardiac output (CO), Pa(CO(2)), pH, and delivered VT between the treatment groups in their study could have influenced these results. Because of the potential implications of these findings for patient care, we attempted to confirm these findings by Lefevre and colleagues in a canine model of oleic acid-induced lung injury. Eighteen mongrel dogs were anesthetized in the supine position, paralyzed, and mechanically ventilated with 50% O(2) at f = 15 breaths/min, and VT was adjusted to achieve an end-tidal CO(2) of 30 to 35 mm Hg. Lung injury was produced by infusion of 0.06 ml/kg oleic acid solution into the right atrium over a 30-min period. Animals were then randomized to either conventional ventilation at the baseline settings (n = 9) or to BV at the same mean VT and f (n = 9). Both groups received comparable degrees of injury, and hemodynamic and ventilatory parameters were closely matched, with no differences in mean VT, PIP, mean Paw, Pa(CO(2)), pH, CO, pulmonary artery occlusion pressure, or arterial pressure (Pa). However, no differences between the two groups were found in Pa(O(2)), shunt, or static compliance over a 4-h period. When hemodynamic and ventilatory parameters were well matched in a canine model of ALI, BV showed no advantage over conventional ventilation at constant VT and f.     

Effects of spontaneous breathing during airway pressure release ventilation on respiratory work and muscle blood flow in experimental lung injury

STUDY OBJECTIVES: To evaluate the effects of spontaneous breathing at ambient airway pressure (Paw) and during airway pressure release ventilation (APRV) on respiratory work and respiratory muscle blood flow (RMBF) in experimental lung injury. DESIGN: Prospective experimental study. SETTING: Research laboratory of a university hospital. SUBJECTS: Twelve hemodynamically stable, analgosedated, and tracheotomized domestic pigs. MEASUREMENTS: Respiratory work was estimated by the inspiratory pressure time product (PTPinsp) of esophageal pressure, and RMBF was measured with colored microspheres. Lung injury was induced with IV boli of oleic acid. The first set of measurements was performed before induction of lung injury while pigs were breathing spontaneously at ambient Paw, the second after induction of lung injury while breathing spontaneously at ambient Paw, and the third with lung injury and spontaneous breathing with APRV. RESULTS: After induction of lung injury PTPinsp increased from 138 +/- 14 to 214 +/- 32 cm H2O s/min when pigs breathed spontaneously at ambient Paw (p < 0.05) and returned to 128 +/- 27 cm H2O s/min during APRV. While systemic hemodynamics and blood flow to the psoatic and intercostal muscles did not change, diaphragmatic blood flow increased from 0.34 +/- 0.05 before to 0.54 +/- 0.08 mL/g/min after induction of lung injury and spontaneous breathing at ambient Paw (p < 0.05) and returned to 0.32 +/- 0.05 mL/g/min during APRV (p < 0.05 vs spontaneous breathing at ambient Paw [lung injury]). CONCLUSION: Respiratory work and RMBF are increased in acute lung injury when subjects breathe spontaneously at ambient Paw. Supporting spontaneous breathing with APRV decreases respiratory work and RMBF to physiologic values.     

External high frequency oscillation in cats. Experience in the normal lung and after saline lung lavage

In an effort to develop a method of assisted ventilation that would avoid endotracheal intubation, 11 anesthetized, paralyzed, nonintubated adult mongrel cats with normal lungs were externally oscillated by means of a thoracoabdominal chamber connected to a vacuum source and a high frequency oscillator. Chamber pressure was adjusted to the desired negative pressure using the vacuum source, and the animal was then oscillated above and below this pressure. The lowest PaCO2 and AaPO2 were observed at 3 Hz. Tidal volume (VT) fell (p less than 0.001) with increases in frequency, and lung volume (VL) rose with increased negative chamber pressure (p less than 0.001). In 11 additional tracheostomized cats, a stiff lung was created by repeated saline lung lavage. External high frequency oscillation (EHFO), using pressures comparable to those used for conventional mechanical ventilation (CMV), was associated with a significant increase in PaO2 (p less than 0.001), and a significant fall in AaPO2 (p less than 0.01) compared with that during CMV. Lung volume was significantly higher during EHFO (p less than 0.001) and, as in the normal lung, VT fell with increasing frequencies to 15 Hz (p less than 0.001). There were no significant frequency-dependent variations in gas exchange or VL. An increasingly negative mean chamber pressure was associated with a significant increase in PaO2 (p less than 0.05) and VL(p less than 0.005) and a significant decrease in PaCO2 (p less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanics of breathing during strenuous exercise in Thoroughbred horses

The changes induced by exercise on the mechanics of breathing, as well as the simultaneous changes occurring in arterial blood gas tensions and in respiratory gas exchange were investigated in 6 healthy thoroughbred horses, performing a treadmill exercise of increasing intensity. Respiratory airflow and tidal volume (VT) were measured with ultrasonic flowmeters. Pleural pressure changes were measured by an oesophageal balloon catheter. Gas concentration of the expired air was analysed with a mass spectrometer; the oxygen consumption (VO2) and the carbon dioxide output (VCO2) were computed breath-by-breath. Arterial blood gas values were obtained by sampling from the carotid artery. Between rest and fast gallop VT, respiratory frequency, expired minute ventilation (VE), VO2, VCO2, total pulmonary resistance (RL), mechanical work of breathing (Wrm) and PaCO2 increased significantly while PaO2 decreased significantly. The Wrm.VO2(-1) ratio in galloping horses increased exponentially with VE. This, together with the relationship between the changes in PaO2 and in PaCO2 and the increase in the ventilatory mechanics parameters, suggests that the mechanics of breathing may be one of the factors constraining further increase in ventilation in exercising healthy horses.     

小潮气量通气对创伤性ARDS的疗效分析

目的：探讨小潮气量通气对创伤性ARDS的疗效。方法：回顾性分析48例创伤性ARDS患者的病历资料,分为两组,大潮气量组23例,VT10～12ml／kg理想体重,PEEP5～10cmH2O,平台压35-50cmH2O;小潮气量组25例,VT5～8ml／kg理想体重,PEEP10～15cmH20,平台压≤35cmH2O。观察两组通气治疗前、后3dPaO2／FiO2、PaCO2、pH值及气压伤的发生情况和ICU住院期间病死率。结果：通气治疗后两组PaO2／FiO2均较通气治疗前明显升高（P〈0．05,P〈0．01）,但在第3天,小潮气量组PaO2／FiO2明显低于大潮气量组（P〈0．01）;小潮气量组出现明显高碳酸血症,但在机体可耐受范围。大潮气量组出现3例气压伤,小潮气量组无气压伤发生。小潮气量组病死率16％（4／25）低于大潮气量组26．08％（6／23）（P〉0．05）。结论：小潮气量通气可改善创伤性ARDS患者氧合状态和预后,减少呼吸机相关性肺损伤的发生。     

Airway pressure release ventilation (APRV). A human trial

After operative coronary revascularization, 14 consenting adults received conventional positive pressure ventilation (PPV). When they were hemodynamically stable, data were collected during PPV and then during airway pressure release ventilation (APRV). During APRV, airway pressure (Paw) was reduced periodically at the lowest frequency which produced normal PaCO2. As anesthesia resolved, the rate of APRV breaths was decreased until patients breathed only with CPAP. During PPV and APRV, pHa, PaO2/FIO2, and hemodynamic variables were similar. All patients were weaned from APRV without complication. Optimal ventilator design for patients with acute lung injury would provide CPAP as a primary intervention and secondarily would augment alveolar ventilation. The APRV supported oxygenation and ventilation in patients with mild acute lung injury, yet with much lower peak airway pressure than produced by PPV.     

Effects of hypercapnia on phrenic and stretch receptor responses to lung inflation

To determine if hypercapnia and reflex bronchoconstriction attenuate lung inflation effects on ventilatory activity by indirect effects on intrapulmonary stretch receptors (PSR), phrenic nerve activity and single unit PSR were monitored at controlled levels of static airway pressure (Paw) and arterial PCO2 in 15 anesthetized dogs. Paw in a vascularly isolated lung was varied between 2 and 14 cm H2O at levels of PaCO2 between 35 and 85 mm Hg. PSR activity (n = 38) in fine strands dissected from an otherwise intact vagus nerve and the integrated phrenic neurogram were recorded. The response to Paw varied from one PSR to another, but was consistent in a given unit; PaCO2 had no consistent effect on individual responses. Selected PSR (n = 15) were averaged to yield a population response to Paw; the selection criteria were: phrenic activity responded briskly to Paw and measurements were made at three levels of PaCO2. Average PSR discharge increased linearly with Paw but was unaffected by PaCO2. On the other hand, phrenic burst frequency decreased as Paw increased and hypercapnia attenuated the slope of this relationship. These results suggest that effects on the relationship between PSR activity and Paw cannot account for attenuation of the relationship between phrenic frequency and Paw in hypercapnia. The effect of PaCO2 on the phrenic frequency vs Paw relationship probably arises from integrative mechanisms in the central nervous system.     

The effects of cromolyn sodium in dogs undergoing high-frequency oscillation superimposed on conventional mechanical ventilation.

The effects on gas exchange of superimposition of high-frequency oscillation (HFO) (40 Hz) on conventional mechanical ventilation were investigated in mongrel dogs with eucapnic gas exchange on conventional mechanical ventilation (CMV). The dogs were anesthetized, paralyzed, and ventilated with CMV until stable. Oscillation was then superimposed for 15 min, followed by CMV alone for a further 30 min. During HFO superimposed on CMV (CMV-HFO), the arterial carbon dioxide tension (PaCO2) increased from 43.6 +/- 1.2 mm Hg to 47.2 +/- 1.4 mm Hg (p less than 0.02), whereas the arterial oxygen tension (PaO2) did not change at all. The change was inhibited completely by administration of intravenous cromolyn sodium (CS) (6 mg/kg/min). The mean pulmonary arterial pressure (mPAP), cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and pulmonary vascular resistance (PVR) did not change during the experiment. These results demonstrate that CMV-HFO appears to cause CO2 accumulation and eliminates the impaired O2 transfer, and that these effects are inhibited completely by CS administration.     

外源性肺泡表面活性物质联合肺泡复张手法对急性呼吸窘迫综合征的疗效

目的 观察肺泡表面活性物质(PS)、肺泡复张手法(RM)及两者联合治疗ARDS的疗效.方法 健康新西兰长耳白兔28只,反复温盐水肺泡灌洗建立ARDS动物模型,行容积控制通气,通气稳定后按随机数字表法分为对照组、PS组、RM组及PS+RM组,每组7只,分别气管内注入安慰剂、外源性PS、实施RM或PS联合RM治疗,观察动脉血气及呼吸力学指标的变化.处理后4 h处死动物,行病理组织学检查评价肺损伤程度.结果 (1)对照组、PS组、RM组和PS+RM组的PaO2分别为(74 ±15)、(234±42)、(231±17)和(253±52)mm Hg(1 mm Hg=0.133 kPa),PS、RM和PS+RIM3组均高于对照组(F=84.201,P<0.01),PS、PS+RM组氧合改善稳定,RM组PaO2随观测时间延长呈下降趋势;(2)4组的PaCO2分别为(56±11)、(46±10)、(51±8)和(46±10)mm Hg,对照组明显高于PS、PS+RM组(F=4.234,P<0.05).RM组PaCO2随时间延长呈增高趋势;(3)4组动物气道峰压分别为(33±2)、(23±1)、(24±2)和(22±1)cm H2O(1 cm H2O=0.098 kPa),静态肺顺应性(Cst)分别为(1.1±0.3)、(1.7±0.3)、(1.5±0.1)、(1.9±0.4)ml/cm H2O,PS、RM、PS+RM 3组气道峰压、Cst均较对照组显著改善(F值分别为74.911、15.863,均P<0.01).RM组Cst改善较PS+RM组差(q=2.58,P<0.05);(4)PS、RM、PS+RM 3组动物肺损伤评分分别为3.9 ±0.8、6.1±0.7和4.2±0.6,均低于对照组的13.5±0.7(F=369.6,P<0.01),RM组高于PS及PS+RM组(q值分别为6.35、5.70,均P<0.01).结论 ARDS早期补充外源性PS或实施RM均能有效改善氧合及肺脏顺应性,但RM后易出现肺泡再萎陷及呼吸机相关性肺损伤;PS联合RM治疗能防止肺泡再萎陷,并可减轻呼吸机相关性肺损伤.     

Gas transport enhancement in high-frequency oscillation

Gas transport during high-frequency oscillation (HFO) with (HFO+BT) and without bias tube (HFO-BT) was investigated in 10 anesthetized supine dogs. The oscillatory volume effectively delivered to the lungs, airway occlusion pressure and lung volume above functional residual capacity (FRC), regulated by a newly deviced pressure control system, as well as the oscillatory frequency (20 Hz) were adjusted to equal levels in HFO+BT and HFO-BT. At a fresh gas flow rate (fgf) of 3 L/min (room air), arterial CO2 partial pressures (PaCO2) decreased from 49.9 +/- 6.5 mm Hg (mean +/- SD) to 40.2 +/- 6.3 mm Hg (P less than 0.01) i.e. by 19.2 +/- 8.7%, and arterial O2 partial pressures (PaO2) increased from 71.5 +/- 13.1 mm Hg to 85.6 +/- 14.6 mm Hg (P less than 0.01) or by 20.5 +/- 12.0% in HFO-BT as compared to HFO+BT. At a fgf of 6 L/min, PaCO2 decreased less but still significantly (P less than 0.025) from 42.1 +/- 6.5 mm Hg to 37.8 +/- 6.8 mm Hg (10.4 +/- 5.6%) and PaO2 increased from 78.1 +/- 12.9 mm Hg to 84.6 +/- 16.4 mm Hg i.e. by 8.1 +/- 6.4% (P less than 0.05) in HFO-BT. The higher gas transport efficiency after removing the bias tube can be explained by two mechanisms: (1) By removing the bias tube, the volume of the bias system decreased from 54 ml in HFO+BT to 1 ml in HFO-BT and rebreathing of exhaust gas from the bias system is therefore eliminated in HFO-BT.(ABSTRACT TRUNCATED AT 250 WORDS)     

外源性肺泡表面活性物质对兔子盐酸吸入性肺损伤的治疗作用

目的 观察外源性自制猪肺表面活性物质对盐酸诱导急性肺损伤兔的治疗作用.方法 健康兔18只,随机分为3组,即健康对照组、模型组、治疗组,每组6只.模型组和治疗组兔子麻醉后,经气管导管注入pH=1.5的盐酸2 ml/kg,复制盐酸吸入性肺损伤模型,对照组经气管导管注入同等量生理盐水.治疗组在盐酸注入后4 h经气管导管给予猪肺表面活性物质120 mg/kg(浓度为80 g/L)进行干预;健康对照组及模型组在相应时间经气管导管给予同等体积的生理盐水.之后共观察6 h,并监测各预设时间点PaO2、PaCO2,处死后检测左下肺组织湿/干重比(W/D),支气管肺泡灌洗液(BALF)中总蛋白(TP)含量和自细胞(WBC)总数,并观察左上肺组织病理学改变.结果 治疗组经猪肺表面活性物质治疗后各时间点的PaO2高于模型组(P值均<0.01),但多数时间点仍低于健康对照组(P值均<0.01),各时间点的PaCO2均低于模型组(P值均<0.01),高于健康对照组(P值均<0.01).与模型组相比,治疗组左下肺W/D,BALF中TP含量和WBC明显降低(P值均<0.01),仍高于健康对照组(P值均<0.01).组织病理学观察显示:与模型组相比,治疗组兔肺损伤程度较轻,但仍然无法恢复到健康对照组的水平.结论 猪肺表面活性物质可以明显提高PaO2,降低PaCO2、左下肺W/D、BALF中TP含量和WBC数目,改善肺组织病理学结构.对家兔盐酸吸入肺损伤具有治疗作用,为临床胃液误吸性肺损伤的治疗提供了一种新方法.