Interpretation of pulmonary artery wedge pressure and pullback blood gas determinations during positive end-expiratory pressure ventilation and after exclusion of the bronchial circulation in the dog

Left atrial pressure (LAP) and pulmonary artery wedge pressure (PWP) were measured at different heights during graded increases in positive end-expiratory pressure (PEEP). Six healthy anesthetized dogs were placed in lateral decubitus positions with a balloon-tipped pulmonary artery catheter inserted in each lung. PWP in the gravitationally superior lung overestimated LAP at 15 and at 20 cm H2O PEEP (p less than 0.05). PWP in the dependent lung was virtually identical to LAP at all degrees of PEEP. Wedge blood could be aspirated through the distal lumen of the pulmonary artery catheters during balloon inflation at all degrees of PEEP except for 3 attempts. PCO2 in wedge blood in both the nondependent and dependent lungs at all degrees of PEEP was consistently lower than PCO2 in arterial blood (p less than 0.05). Wedge blood was arterialized, i.e., oxygen saturation greater than 95%, in all but 4 specimens. Surgical elimination of the bronchial artery supply to the lung in 3 dogs did not affect PWP or blood gas measurements. We conclude that in this animal model: (1) the tip of a pulmonary artery catheter must be below the level of the left atrium, Zone III location, to accurately reflect LAP at high degrees of PEEP; (2) arterialization of wedge blood samples does not guarantee that PWP reflects LAP; (3) bronchial artery blood supply does not affect PWP or wedge blood gas measurements, even at high degrees of PEEP.     

Left atrial pressure can be accurately transmitted to the pulmonary artery despite zone 1 conditions

Pulmonary arterial occlusion pressure is not thought to reflect left atrial pressure (Pla) when alveolar pressure (PA) exceeds pulmonary venous pressure because alveolar capillaries collapse and the required continuous fluid column between the pulmonary artery and left atrium is interrupted. However, arterial-to-venous flow can occur when PA exceeds both the pulmonary arterial pressure (Ppa) and pulmonary venous pressure (i.e., in Zone 1 conditions), indicating the existence of a continuous patent vascular channel. Accordingly, Ppa should reflect Pla under these conditions. To investigate this connection cannulas were placed in the pulmonary arteries and left atria of eight excised rabbit lungs. Ppa and Pla were set 5 cm H2O above PA, which ranged from 0 to 25 cm H2O. Pla was then reduced in 2 to 4 cm H2O decrements while recording Ppa when arterial-to-venous flow ceased. At all PAs greater than 0 cm H2O, Pla was accurately reflected by the Ppa when both were exceeded by PA. The greater the PA, the lower the Ppa could track Pla below PA. Pla can be accurately measured by a pulmonary arterial catheter under Zone 1 conditions.     

Application of tracheal gas insufflation to acute unilateral lung injury in an experimental model

In unilateral lung injury, application of global positive end-expiratory pressure (PEEP) may cause overdistension of normal alveoli and redistribution of blood flow to diseased lung areas, thereby worsening oxygenation. We hypothesized that selective application of tracheal gas insufflation (TGI) will recruit the injured lung without causing overdistension of the normal lung. In eight anesthetized dogs, left lung saline lavage was performed until Pa(O(2))/FI(O(2)) fell below 100 mm Hg. Then, the dogs were reintubated with a Univent single lumen endotracheal tube that incorporates an internal catheter to provide TGI. After injury, increasing PEEP from 3 to 10 cm H(2)O did not change gas exchange, hemodynamics, or lung compliance. Selective TGI, while keeping end-expiratory lung volume (EELV) constant, improved Pa(O(2))/FI(O(2)) from 212 +/- 43 to 301 +/- 38 mm Hg (p < 0.01) while Pa(CO(2)) and airway pressures decreased (p < 0.01). During selective TGI, reducing tidal volume to 5.2 ml/kg while keeping EELV constant, normalized Pa(CO(2)), did not affect Pa(O(2))/FI(O(2)), and decreased end-inspiratory plateau pressure from 16.6 +/- 1.0 to 11.9 +/- 0.5 cm H(2)O (p < 0.01). In unilateral lung injury, we conclude that selective TGI (1) improves oxygenation at a lower pressure cost as compared with conventional mechanical ventilation, (2) allows reduction in tidal volume without a change in alveolar ventilation, and (3) may be a useful adjunct to limit ventilator-associated lung injury.     

The effect of Swan-Ganz catheter height on the wedge pressure-left atrial pressure relationships in edema during positive-pressure ventilation

We have studied the effect of the ventrical height of the pulmonary wedge catheter in the lung on the pulmonary wedge pressure-left atrial relationship during positive end-expiratory pressure ventilation in oleic acid-induced pulmonary edema. Pulmonary wedge catheters were placed above and below the left atrium in normal dogs and in dogs with oleic acid-induced edema. Wedge pressure and left atrial pressure were measured simultaneously during positive end-expiratory pressure ventilation (range, 0 to 30 cm H2O positive end-expiratory pressure). Pulmonary wedge catheters below the left atrium correctly recorded left atrial pressure and change in left atrial pressure at all positive end-expiratory pressures studied. Pulmonary wedge catheters above the atrium consistently recorded pressures higher than the normal left atrial pressure. They did not correctly respond to increases in left atrial pressure until it was increased to a value higher than the initial upper pulmonary wedge pressure. Pulmonary arterial catheters, when properly placed, should be reliable indicators of left atrial pressure during positive-pressure ventilation in normal and edematous lungs.     

Effect of airway pressure on pericardial pressure

The effect of applied positive airway pressure or PEEP on pericardial pressure was examined in closed-chest, anesthetized dogs with normal lungs and in animals with oleic acid-induced lung injury. Both groups were studied before and after vascular volume loading by dextran infusion. Pericardial pressure was measured using an air-filled flat balloon placed along the lateral left ventricular free wall within the pericardial space. A linear relation between right atrial pressure (RAP) and pericardial pressure (PP) was found (RAP = 3.9 + 0.78 PP, r = 0.76, p less than 0.01) that was independent of acute lung injury but was influenced by the application of PEEP. In the baseline volume condition, pericardial pressure increased linearly with an increase in PEEP to 15 cm H2O. After volume loading, pericardial pressure increased fourfold, but, surprisingly, did not change with applied PEEP. These relations were similar in the two groups despite a reduction in total respiratory system compliance in the oleic acid group. This suggests that transmission of airway pressure to the pericardial surface is independent of the presence of acute lung injury and that changes in pericardial pressure in response to PEEP reflect both the transmission of airway pressure to the pericardial surface and, presumably, PEEP-related changes in cardiac volume and ventricular compliance.     

Effects of alveolar hypoxia on lung fluid and protein transport in unanesthetized sheep.

To determine whether hypoxia directly affects pulmonary microvascular filtration of fluid or permeability to plasma proteins, we measured steady state lung lymph flow and protein transport in eight unanesthetized sheep breathing 10% O2 in N2 for 4 hours. We also studied three sheep breathing the same gas mixture for 48 hours. We surgically prepared the sheep to isolate and collect lung lymph and to measure average pulmonary arterial (Ppa) and left atrial (Pla) pressures. We placed a balloon catheter in the left atrium to elevate Pla. After recovery, the sheep breathed air through a tracheostomy for 2-4 hours, followed by 4 or 48 hours of hypoxia. In 13 4-hour studies, the average arterial PO2 fell from 97 to 38 torr; Ppa rose from 20 to 33 cm H2O; and lung lymph flow and lymph protein flow were unchanged. We also found that during 48-hour hypoxia, with a sustained elevation in Ppa and a decline in Pla, lymph flow and protein flow did not increase. In four sheep, we also raised Pla for 4 hours, followed by 4 hours of hypoxia with elevated Pla. Again, despite the added stress of elevated Pla, we found that lymph flow and lymph protein flow remained constant during hypoxia. We conclude that severe alveolar hypoxia, for 4 or 48 hours, alone or with increased pulmonary microvascular pressure, produced no change in lung fluid filtration or protein permeability, a finding supported by normal postmortem histology and extravascular lung water content.     

The effects of ventilation with positive end-expiratory pressure on the bronchial circulation

We studied the effects of ventilation with 10 cm H2O PEEP for 2 h in dogs with temporary unilateral pulmonary arterial occlusion (TUPAO) on bronchial blood flow to the occluded lung using the microsphere dispersion technique. We found that blood flow to the occluded left lung in dogs was 9.9 ml/min (0.122 ml X min-1 X g-1). Within 30 min following the addition of 10 cm H2O PEEP blood flow fell by 70-80% (to 2.3 ml/min) caused both by a 3-fold decrease in vascular conductance and a 25% fall in systemic blood pressure. The reduction in left bronchial blood flow persisted for at least 2 h. We conclude from these data that ventilation with PEEP in the presence of pulmonary artery occlusion has a severe, persistent adverse effect on bronchial blood flow. This reduction in bronchial blood flow is beyond what can be explained by the changes in airway pressure. The additional increase in bronchial vascular resistance may be caused by the increase in lung volume, by reflex bronchial vasoconstriction, or by release of mediators locally.     

Lung luminal liquid clearance in newborn lambs. Effect of pulmonary microvascular pressure elevation

Postnatal clearance of fetal lung liquid is complete within 6 h of birth in normal lambs. Most of the liquid drains directly from the lung lumen through the interstitium into the bloodstream, as pulmonary lymphatics appear to play a small role in this process (J Appl Physiol 1982; 53:992). To test the possibility that increased pulmonary microvascular pressure might slow the rate of removal of luminal liquid and redirect the liquid into lung lymphatics, we studied 25 lambs, 16 of which had a balloon catheter inflated in the left atrium to maintain lung microvascular pressure 10 torr greater than normal throughout the experiments. We measured pulmonary arterial and left atrial pressures, lung lymph flow, and concentrations of protein in lymph and plasma of 6 anesthetized, mechanically ventilated lambs, 1 to 3 wk old, for 2 to 4 h before and for 6 h after intratracheal instillation of warm, isotonic saline, 6 ml/kg body weight. Extravascular water was measured gravimetrically in lungs of 19 lambs (10 with increased and 9 with normal pulmonary microvascular pressure) killed at 1, 2, and 6 h after saline instillation. The percent liquid cleared from the lungs at 1 and 2 h after saline was significantly less in lambs with increased lung microvascular pressure than it was in lambs with normal microvascular pressure (48 versus 68% at 1 h, 60 versus 77% at 2 h, respectively). Thus, increased lung microvascular pressure slows liquid clearance from the newborn lung. Almost all liquid (greater than 92%) disappeared from the lungs of lambs in both groups by 6 h.(ABSTRACT TRUNCATED AT 250 WORDS)     

Timing of pulmonary and systemic blood flow during intermittent high intrathoracic pressure cardiopulmonary resuscitation in the dog

Simultaneous compression-ventilation Cardiopulmonary resuscitation has been shown to produce high peripheral arterial pressure and flows in comparison with conventional Cardiopulmonary resuscitation. To evaluate further the mechanisms responsible for blood flow during the large cyclical changes in intrathoracic pressure with simultaneous compression-ventilation Cardiopulmonary resuscitation this study assessed (1) the timing of blood flow from the lungs toward the aorta and periphery, and (2) the timing and mechanisms of return of blood from the periphery to the heart and lungs. After induction of ventricular fibrillation in dogs, radionuclide angiography was performed and pulmonary flow velocity measured during simultaneous compression-ventilation Cardiopulmonary resuscitation with each high (70 to 100 mm Hg) intrathoracic pressure phase lasting from 0.9 to 3.6 seconds. The abdomen was bound. Carotid flow during resuscitation was 27 ± 5 percent (mean ± standard error of the mean) of the value before cardiac arrest. With injection of technetium-99m albumin into the right atrium, the radionuclide activity cleared the right atrium only during periods of tow intrathoracic pressure between the high intrathoracic pressure periods. There was a simultaneous increase in lung activity during the periods of low pressure. Thus, blood left the right atrium and entered the lungs during these low pressure periods. Flow velocity recordings in the pulmonary artery confirmed that pulmonary flow occurred mainly during low intrathoracic pressure. There was negligible retrograde pulmonary flow during high intrathoracic pressure. This feature, together with a lack of increase in right atrial counts, suggests that the pulmonary valve was probably closed during high intrathoracic pressure. After injection of technetium-99m albumin into the distal pulmonary bed through a wedged catheter, 29.7 ± 8 percent (probability [p] < 0.005) of the activity cleared the lung during the first period of high intrathoracic pressure with no further clearance in the next period of low intrathoracic pressure (2 ± 8 percent, difference not significant). A parallel and simultaneous increase in activity in the left ventricle and aorta indicated that blood flowed from the lung, through the left ventricle, to the aorta during periods of high intrathoracic pressure. Therefore the mitral valve and aortic valves must be open during these periods.

Thus, with simultaneous compression-ventilation Cardiopulmonary resuscitation, blood flow into the lungs occurs during periods of low intrathoracic pressure and from the lungs into the left ventricle and aorta during periods of high intrathoracic pressure. The heart functions merely as a passive conduit for blood flow to and from the lungs.     

Adverse effects of large tidal volume and low PEEP in canine acid aspiration

When normal lungs are ventilated with large tidal volumes (VT) and end-inspired pressures (Pei), surfactant is depleted and pulmonary edema develops. Both effects are diminished by positive end-expiratory pressure (PEEP). We reasoned that ventilatory with large VT-low PEEP would similarly increase edema following acute lung injury. To test this hypothesis, we ventilated dogs 1 h after hydrochloric acid (HCl) induced pulmonary edema with a large VT (30 ml/kg) and low PEEP (3 cm H2O) (large VT-low PEEP) and compared their results with dogs ventilated with a smaller VT (15 ml/kg) and 12 cm H2O PEEP (small VT-high PEEP). The small VT was the smallest that maintained eucapnia in our preparation; the large VT was chosen to match Pei and end-inspired lung volume. Pulmonary capillary wedge transmural pressure (Ppwtm) was kept at 8 mm Hg in both groups. Five hours after injury, the median lung wet weight to body weight ratio (WW/BW) was 25 g/kg higher in the large VT-low PEEP group than in the small VT-high PEEP group (p less than 0.05). Venous admixture (Qva/Qt) was similarly greater in the large VT-low PEEP group (49.8 versus 23.5%) (p less than 0.05). We conclude that small VT-high PEEP is a better mode of ventilating acute lung injury than large VT-low PEEP because edema accumulation is less and venous admixture is less. These advantages did not result from differences in Pei, end-inspiratory lung volume, or preload (Ppwtm).(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood flow in pulmonary veins: III. Simultaneous measurements of their dimensions, intravascular pressure and flow

Vein flow in the large extraparenchymal pulmonary veins is pulsatile and its wave form has an inverse relationship to left atrial pressure. Extraparenchymal pulmonary veins are thin walled and collapsible. This enables them to behave as highly compliant structures. Dimensional measurements of their cross sectional area in living open chested dogs showed them to be non circular at low left atrial pressures. They rapidly assumed a circular cross section as left atrial pressure rose. Only at pressures above 1.5 kPa (11 mmHg) were the pulmonary veins circular in cross section. The aggregate volume of the large extraparenchymal pulmonary veins, when fully distended, was found to be equal to or greater than one stroke volume of the heart. The extraparenchymal pulmonary veins act as a reservoir to the left atrium so that left ventricular stroke volume can be maintained relatively unaffected by beat by beat changes in right ventricular stroke output. Their behaviour at normal mean left atrial pressures also enables them to isolate the lung capillaries from retrograde transmission of positive pressure transients from the left atrium, which could otherwise impede venous outflow of blood from the lung capillary bed.     

Effect of positive end-expiratory pressure on pulmonary vascular pressure-flow characteristics in canine endotoxin shock.

The vascular pulmonary pressure-flow (P-Q degree) relationships were studied in anesthetized dogs in order to characterize the distribution of total resistance in the pulmonary bed with respect to incremental resistance and critical closure prior to and after endotoxin insult. Incremental resistance was computed as the slope of the P-Q degree relation, whereas critical closure was referred to as the extrapolated pressure intercept at zero flow. P-Q degree coordinates were obtained by varying Q degree through graded inflation of right atrial balloon. The gradients across the arterial segment (Pa = Ppa - Pc) and across the venous segment (Pv = Pc - Pw) of the pulmonary vasculature were defined by the computation of effective capillary pressure (Pc) obtained from the analysis of the transient decay of pulmonary artery pressure (Ppa) toward wedge pressure (Pw) after arterial occlusion. Six group E dogs were infused with endotoxin at a rate of 0.25 microgram/kg min, while six additional animals served as control (group C). Endotoxin induced increases in flow resistance from 0.056 to 0.096 mm Hg/ml/min/kg due to arterial vasoconstriction and increases in critical closure from 2.3 to 8.4 mm Hg due to a venous waterfall. Before and after endotoxin insult, we assessed effects of each of three levels of static lung inflation (PEEP) on P-Q degree relationships.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of dextran solution on pulmonary plasma-lymph barrier in awake sheep

We investigated the effect of dextran solution on lung lymph flow in awake sheep with chronic lung lymph fistulas. Ten percent of dextran (molecular weight 40,000) solution or normal saline were infused at 1000 ml/h for 2 h through left atrial catheter. We measured pulmonary arterial pressure (Ppa), left atrial pressure (Pla), aortic pressure (Psa), cardiac output (CO), oncotic pressures of both plasma (IImv) and lung lymph (IIpmv), lung lymph flow rate (Qlym), and lymph-to-plasma ratio of total protein (L/P). Infusion of dextran solution caused significant increases in Ppa, Pla and CO and decrease in plasma-lung lymph oncotic pressure gradient (IImv-IIpmv), without changes in L/P. Infusion of normal saline caused significant increases in Ppa and Pla and no changes in IImv-IIpmv and CO, and slight decrease in L/P. The calculated filtration coefficients increased by 2.2 fold after dextran infusion and 1.7 fold after normal saline infusion. Moreover, an apparent increase in protein transport across microvessels as evidenced by the normal L/P despite increases in hydrostatic pressure occurred after dextran solution infusion. These results suggest that dextran solution may increase permeability of microvascular wall, as well as effective net pressure gradient across microvessels, both of which result in a large net fluid filtration from microvessels to perimicrovascular compartment.     

分侧肺通气时不同呼气末正压和潮气量对单侧肺损伤犬循环的影响

目的 观察不同步分侧肺通气和同步分侧肺通气对单侧急性肺损伤(ALI)犬循环的影响.方法 取健康杂种犬12只,建立盐酸所致单侧肺损伤动物模型,行容积控制通气,将犬按随机数字表法分为不同步分侧肺通气组(NS组)和同步分侧肺通气组(S组).参数:患侧潮气量3.5 ml/kg保持不变,呼气末正压(PEEP)选择15、20、25 cm H2O(1 cm H2O=0.098 kPa);患侧PEEP 10 cm H2O不变,潮气量用随机数字表法选择5、7.5、10 ml/kg.健侧通气参数始终不变,检测不同通气条件下两组犬血流动力学和氧动力学指标.结果 (1)患侧潮气量3.5 ml/kg不变,PEEP为15、20 cm H2O时,两组血流动力学和氧动力学参数差异无统计学意义.当患侧PEEP为25 cm H2O时,NS组心率、体循环平均压(mABP)、心输出量、氧合指数和混合静脉血氧饱和度(SvO2)分别为(98±8)次/min、(84±6)mm Hg(1 mm Hg=0.133 kPa)、(1.10±0.13)L/min、(199±14)mm Hg和(55±6)%,明显低于S组[分别为(124±9)次/min、(103±7)mm Hg、(1.52±0.28)L/min、(221±15)mm Hg和(62±4)%,t值分别为-7.852、-16.561、-15.043、-13.314和-5.653,均P＜0.01].(2)患侧PEEP 10 cm H2O不变,潮气量分别为5、7.5 ml/kg时,两组的血流动力学和氧动力学参数比较差异无统计学意义.当患侧潮气量为10 ml/kg时,NS组HR、mABP、心输出量、氧合指数和SvO2均低于S组(均P＜0.01).结论 在本实验动物模型中,患侧与健侧所用PEEP水平相差≤20 cm H2O或患侧潮气量≤7.5 ml/kg时,同步和非同步分侧肺通气均能保持循环稳定.若需要更高水平PEEP时,建议选用同步分侧肺通气.     

High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure

The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the drug lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV rats. It was markedly reduced by PEEP, which, in addition, preserved the normal ultrastructural aspect of the alveolar epithelium. This was in striking contrast to the diffuse alveolar damage usually encountered in this type of edema. To our knowledge, this constitutes the first example of a protective effect of PEEP during permeability edema.     

Volumetric capnography in patients with acute lung injury: effects of positive end-expiratory pressure.

The aim of the study was to analyse the effects of positive end-expiratory pressure (PEEP) on volumetric capnography and respiratory system mechanics in mechanically ventilated patients. Eight normal subjects (control group), nine patients with moderate acute lung injury (ALI group) and eight patients with acute respiratory distress syndrome (ARDS group) were studied. Respiratory system mechanics, alveolar ejection volume as a fraction of tidal volume (VAE/VT), phase III slopes of expired CO2 beyond VAE and Bohr's dead space (VD/VT(Bohr)) at different levels of PEEP were measured. No differences in respiratory system resistances were found between the ALI and ARDS groups. VD/VT(Bohr) and expired CO2 slope beyond VAE were higher in ALI patients (0.52+/-0.01 and 13.9+/-0.7 mmHg x L(-1), respectively) compared with control patients (0.46+/-0.01 and 7.7+/-0.4 mmHg x L(-1), p<0.01, respectively) and in ARDS patients (0.61+/-0.02 and 24.9+/-1.6 mmHg x L(-1), p<0.01, respectively) compared with ALI patients. VAE/VT differed similarly (0.6+/-0.01 in control group, 0.43+/-0.01 in ALI group and 0.31+/-0.01 in ARDS group, p<0.01). PEEP had no effect on VAE/VT, expired CO2 slope beyond VAE and VD/VT(Bohr) in any group. A significant correlation (p<0.01) was found between VAE/VT and expired CO2 slope beyond VAE and lung injury score at zero PEEP. Indices of volumetric capnography are affected by the severity of the lung injury, but are unmodified by the application of positive end-expiratory pressure.     

压力-容量曲线对急性肺损伤家兔实行个体化保护性通气的应用

目的研究以压力容量（P-V）曲线确定通气参数对急性肺损伤家兔肺的保护作用。方法新西兰家兔24只,随机分为4组（V1P1、V1P2、V2P1、V2P2）,每组4只。用油酸复制急性肺损伤模型,测定P-V曲线,以下曲点压力（Pinf）和上曲点压力（Pdef）分别选择呼气末正压（PEEP）的两水平：P1＝PinfP2＝Pinf－3cmH2O,潮气量（VT）两水平：V1＝15ml／kg,V2下调使平台压小于上曲点压力（Pplat＜Pdef）。观察肺力学、血气、血循环及肺病理改变。结果4组氧合效果基本相同,动脉血二氧化碳分压（PaCO2）和pH主要受VT影响。平均动脉压在大PEEP和（或）大VT时有所下降。呼吸系统静态顺应性（Cst）则以PEEP为Pinf时改善最明显,但大VT抵消了其作用且对肺泡有明显的损伤。小PEEP组肺泡透明膜变加重。结论以呼吸系统P-V曲线选择PEEP和VT进行个体化通气,对肺的力学特性和肺的病理性损伤有明显的保护作用,可能有利于改善急性肺损伤的预后。     

Effects of independent lung ventilation and lateral position on cytokine markers of inflammation after unilateral lung acid injury in dogs

Background and objective: The aim of this study was to compare the effects of conventional ventilation, lateral (non‐injured lung‐dependent) position, asynchronous and synchronous independent lung ventilation on inflammatory markers in an animal model of unilateral lung acid injury. Methods: Twenty‐eight dogs underwent unilateral endobronchial instillation with hydrochloric acid and randomly received (n = 7 in each group) conventional ventilation in the supine (group I) or lateral position (group II), and independent lung ventilation in asynchronous (group III) or synchronous (group IV) modes. Arterial blood gases and serum cytokine levels were assessed at baseline, and 5 min and 4 h after mechanical ventilation. At the end of the study, cytokine levels were measured in individual lung lavage fluid. In three animals per group, differential lung perfusion was detected using a dual‐head gamma camera. Results: Unilateral acid injury alone worsened oxygenation as determined by the ratio of PaO₂ to fraction of inspired oxygen (PaO₂/FiO₂) and increased serum cytokine levels. Mean oxygenation (SD) was significantly preserved in group II, 338 (26); group III, 396 (28); and group IV, 395 (22) compared with group I, 173 (18) (all P < 0.01). Serum IL‐8, left‐lung lavage IL‐8 and matrix metalloproteinase‐9 levels were significantly lower in groups II–IV (all P < 0.05). Only group I showed significantly different left and right lung lavage fluid cytokine levels. Groups III and IV showed slightly decreased left lung perfusion. Cytokine levels and oxygenation were similar in groups III and IV. Conclusions: In this model of unilateral lung acid injury, lateral position and independent lung ventilation preserved oxygenation and attenuated the inflammatory response in serum and injured lung BAL fluid.     

压力—容量曲线对急性肺损伤家兔实行个体化保护性通气？…

OBJECTIVE: To explore the lung-protective effect of ventilation with tidal volume and PEEP determined on pressure-volume curve in oleic acid rabbit models of acute lung injury. METHODS: 24 New Zealand rabbits were randomly divided into 4 groups (V1P1, V1P2, V2P1, V2P2). After inducing lung injury, the P-V curves were measured and drawn. The low and upper inflection point pressure (Pinf and Pdef respectively) were manually determined. Two levels of tidal volume (V1 = 15 ml/kg, V2 reduced for Pplat < Pdef) and two levels of PEEP (P1 = Pinf, P2 = Pinf - 3 cm H2O) were selected. The peak airway pressure (PIP), plateau pressure (Pplat), mean pressure (PAW), static compliance (Cst), heart rate, arterial blood pressure and blood-gas analysis were measured. The lung tissues were pathologically analyzed with light microscope. RESULTS: The oxygenation was not significantly different among 4 groups. The reduced VT significantly raised PaCO2 and lowered pH. Larger VT reduced arterial blood pressure. VT and PEEP synergetically raised airway pressure. Larger PEEP improved Cst, which was counteracted by larger VT. Reduced VT significantly lessened alveolar barotrauma. Larger PEEP lightened alveolar hyaline membrane formation and hemorrhage. CONCLUSION: The ventilation with VT and PEEP determined on P-V curve has significant protective effect on the acutely injured lung.     

Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs

Mitral valve closure during cardiopulmonary resuscitation may result from direct cardiac compression. An alternative hypothesis is that with a rise in intrathoracic pressure, mitral valve closure can occur but may be influenced by whether the lungs are inflated or deflated. To test this hypothesis, we placed a large-bore cannula into the thoraces of 11 dogs. Intrathoracic pressure was changed by inflating and deflating the thorax through the cannula while the airway was open, as well as by inflating and deflating the lungs with the thoracic cannula clamped. Mitral valve motion was observed with two-dimensional echocardiography from the right chest wall or esophagus in eight of the dogs. With a rise in intrathoracic pressure from thoracic inflation, all eight dogs showed closure of the mitral valve, while with thoracic deflation, all showed mitral valve opening. With lung inflation and deflation alone, however, the mitral valve remained open throughout the cycle. In seven dogs, with thoracic inflation, the peak gradient from the left ventricle to the left atrium was (mean +/- SEM) 18 +/- 4 mm Hg and the average gradient was 7 +/- 3 mm Hg, while with lung inflation alone, the average gradient was -1 +/- 1 mm Hg (p less than 0.01 vs. thoracic inflation). Thus, mitral valve closure, with concomitant retrograde pressure gradients, can be produced by intrathoracic pressure changes with accompanying lung deflation. With lung inflation alone, however, the mitral valve remains open, and there are no significant transmitral pressure gradients. We conclude that intrathoracic pressure changes can cause the mitral valve to close or to remain open, depending on how intrathoracic pressure is generated.