Pulmonary oedema: a review

Pulmonary oedema results from derangement of a normal physiological process which is continuously producing and removing extravascular lung water according to principles stated by Starling’s equation of fluid flow across semipermeable membranes. The parameters in Starling’s equation cannot all be measured. However, experiments have suggested that increased pulmonary capillary hydrostatic pressure forces fluid extravascularly, diluting the colloid osmotic pressure of tissue fluids and increasing the hydrostatic pressure of lung tissue fluids. Once these reserves and the ability of pulmonary lymphatics to remove lung water are overcome, pulmonary oedema results. This oedema can also result from reduced colloid osmotic pressure in the pulmonary capillaries and increased capillary permeability, even at low pulmonary capillary hydrostatic pressure. Perhaps because of the reserve created by colloid osmotic pressure of tissue fluids, hydrostatic pressure of lung tissue fluids and lymphatic drainage, pulmonary oedema accumulates at a slow rate initially, and at a much more rapid rate in later stages of oedema development. The rate of oedema formation may also relate to damage to the lung created by interstitial oedema, which opens the barrier to a later stage of alveolar oedema. While lung compliance is reduced with each successive increase in oedema formation, increased shunting and hypoxaemia do not result until alveolar oedema is present, in normal lung. The diagnosis of pulmonary oedema is best made by searching for causes of oedema and by chest radiographs. The management of pulmonary oedema must begin with maintenance of oxygenation of blood. This can best be achieved by applying continuous positive pressure ventilation (CPPV). CPPV does not remove lung water (in fact it may slightly increase it), but it does improve oxygenation by ventilating alveoli that were previously filled with fluid. The improved oxygenation buys time, so that therapy directed at the cause of pulmonary oedema (Starling’s law) can be applied. Since current knowledge is inadequate we do not know how to reverse an increased capillary permeability, other than by removing its cause; or how to reduce tissue colloid osmotic pressure, or to increase the hydrostatic pressure of lung tissue fluids or the intracapillary colloid osmotic pressure or the lymphatic flow of fluid. This leaves only increasing intracapillary colloid osmotic pressure or decreasing pulmonary capillary hydrostatic pressure as the means available to reduce pulmonary oedema. In the face of a non-compliant left ventricle colloid infusions may be dangerous, as the attendant increase in blood volume may increase pulmonary capillary hydrostatic pressure and worsen pulmonary oedema. If increased capillary permeability is the cause of pulmonary oedema, colloids might leak extravascularly and draw fluid with them. Therefore the most important therapy in pulmonary oedema, regardless of cause, is to reduce pulmonary capillary hydrostatic pressure. Depending on the cause of pulmonary oedema and the associated cardiac output, pul monary capillary hydrostatic pressure may be decreased by reducing left ventricular preload, increasing myocardial contractility, reducing left ventricular after-load or some combination of these. The anaesthetic implications are that Starling reserves are large and pulmonary oedema should not occur in the normal patient. In the patient with pulmonary oedema or reduced cardio-pulmonary reserve preoperatively, every effort must be made to optimize Starling’s forces before undertaking an anaesthetic in these life threatening situations.     

Hemodynamic and oxygenation changes of combined therapy with inhaled nitric oxide and inhaled aerosolized prostacyclin

OBJECTIVE: To evaluate hemodynamic and oxygenation changes of combined therapy with inhaled nitric oxide (iNO) and inhaled aerosolized prostcyclin (IAP) during lung transplantation. DESIGN: Prospective study. SETTING: University hospital. PARTICIPANTS: Ten patients scheduled for lung transplantation. INTERVENTIONS: Ten patients, with a mean age of 38 years (range, 24 to 56 years), were scheduled for lung transplantation (2 single-lung transplantations and 8 double-lung transplantations). During first lung implantation with single-lung perfusion and ventilation, hemodynamic and oxygenation data were analyzed in 3 phases: (1) baseline, 5 minutes after pulmonary artery clamping; (2) inhaled NO phase, 15 minutes after inhaled NO administration (20 ppm) in 100% oxygen; and (3) IAP-inhaled NO phase, 15 minutes after combined administration of inhaled NO (20 ppm) and IAP (10 ng/kg/min) in 100% oxygen. MEASUREMENTS AND MAIN RESULTS: During the inhaled NO phase, reductions of mean pulmonary arterial pressure (p < 0.05) and intrapulmonary shunt (p < 0.05) were noted. After the start of prostacyclin inhalation, a further decrease in mean pulmonary arterial pressure (p < 0.05) was observed. PaO2/FIO2 increased during the IAP-inhaled NO phase (p < 0.05), whereas intrapulmonary shunt decreased (p < 0.05). CONCLUSION: This study confirms the action of inhaled NO as a selective pulmonary vasodilator during lung transplantation. Combined therapy with IAP and inhaled NO increases the effects on pulmonary arterial pressure and oxygenation compared with inhaled NO administered alone without any systemic changes.     

Pathophysiologic considerations in the diagnosis and treatment of post-traumatic pulmonary insufficiency

An understanding of normal and abnormal pulmonary fluid dynamics is essential to the clinical assessment and management of post-traumatic pulmonary insufficiency. By monitoring the pulmonary capillary wedge pressure and pulmonary artery pressure, the relative importance of increased hydrostatic pressure (fluid overload or left ventricular failure) and increased pulmonary capillary permeability (lung injury) can be assessed in the individual patient. Accurate fluid management and appropriate pulmonary support are the hallmarks of therapy.     

Case of primary pulmonary hypertension supported with non-invasive positive pressure ventilation

We report a case of primary pulmonary hypertension supported with non-invasive positive pressure ventilation (NPPV). A 20-year-old woman was diagnosed as primary pulmonary hypertension at the age of 15 and we prepared for registration of cadaver lung transplantation at the age of 20. She suffered from hemoptysis and was transferred to our ICU. We performed NPPV with continuous positive airway pressure of 4-6 cmH2O. Her systolic pulmonary artery pressure estimated with echocardiography was reduced, lung congestion on chest X ray was improved, and arterial oxygenation was improved. Considering that her condition would deteriorate only with medical therapy, we planned living donor lung transplantation. However, she died from massive hemoptysis before lung transplantation.     

Pulmonary Artery Pressure and Lung Water During Extracorporeal Circulation in Experimental Pulmonary Insufficiency

Use of the membrane oxygenator has been advocated in the management of severe respiratory insufficiency. We have compared this method to conventional therapy in an experimental model in which 23 dogs were subjected to aspiration with 0.1 N HCl and 18 were supported with a volume respirator and positive end-expiratory pressure or placed on partial bypass using a membrane oxygenator for 12 to 24 hours. Adequate oxygenation (PO₂ > 100 mm Hg) was achieved with the membrane oxygenator. The increase in lung weight during conventional therapy was significantly greater than during membrane oxygenator support.Extracorporeal support during recovery from severe pulmonary injury allows pulmonary artery pressure to be controlled and reduces the expected increase in lung water.     

Pulmonary calcification in hemodialysis patients: correlation with pulmonary artery pressure values

BACKGROUND: End-stage renal disease (ESRD) patients receiving chronic hemodialysis (HD) via an arteriovenous (A-V) access often develop unexplained pulmonary hypertension (PHT). This study evaluated the role of pulmonary calcification (PC) in this phenomenon. METHODS: The clinical manifestations, systolic pulmonary artery pressure (PAP) values measured by Doppler echocardiography and the presence and the extent of PC expressed by lung uptake of 99mTc-MDP bone scintigraphy, were studied in 49 patients with ESRD receiving chronic HD therapy via A-V access. The correlation between PC and PHT was investigated. RESULTS: There were 36 men and 13 women with a mean age of 61.7 +/- 13.2 years receiving HD therapy for 38.2 +/- 43.7 months. Twenty (40.8%) patients had PC expressed by increased lung uptake of 99mTc- MDP and 28 (57.1%) patients had PHT with a mean systolic PAP of 46 +/- 11 mm Hg. No correlation was found between PC and PHT. CONCLUSION: The data suggest that PC expressed by lung uptake of 99mTc-MDP has no role in the pathogenesis of PHT among ESRD patients undergoing HD therapy via A-V access.     

The longitudinal distribution of pulmonary vascular resistance during unilateral hypoxia

Pulmonary capillary hydrostatic pressure and the longitudinal distribution of pulmonary vascular resistance (arterial and venous components) can be determined by analysis of pressure decay curves following pulmonary artery occlusion. To validate this technique in intact animals, pulmonary artery occlusion pressure decay curves were obtained from both lungs in six anesthetized sheep during control conditions (100% O2) and during unilateral hypoxic ventilation (100% O2 versus 100% N2). Analysis of pulmonary artery occlusion pressure curves indicated the following: 1) in the hypoxic lung, unilateral hypoxia increased the precapillary portion of pulmonary vascular resistance from 72% of the total resistance to 89% of the total resistance in that lung; 2) in the nonhypoxic lung, unilateral hypoxia did not significantly affect the distribution of pulmonary vascular resistance; and 3) unilateral hypoxia produced no significant change in pulmonary capillary pressure in the hypoxic lung compared with control; however, pulmonary capillary pressure was significantly greater in the nonhypoxic lung. These results are consistent with other evidence that hypoxic pulmonary vasoconstriction acts locally and primarily affects resistance at the arteriolar level. Pulmonary artery occlusion pressure decay curve analysis appears to be a valid technique for the measurement of pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in intact anesthetized animals. These measurements pertain only to the vasculature distal to the site of pulmonary artery occlusion with the catheter, and, thus, caution must be used when applying this technique in a setting of nonhomogenous lung injury.     

Plasma thromboxane and pulmonary artery pressure in neonates treated with extracorporeal membrane oxygenation.

To examine whether neonates with persistent pulmonary hypertension are subject to a thromboxane-mediated exacerbation of their pulmonary hypertension during extracorporeal membrane oxygenator therapy (a form of partial cardiopulmonary bypass), we performed serial measurements of plasma thromboxane B2 and pulmonary artery pressure before, during, and after extracorporeal membrane oxygenation. Pulmonary artery pressure was high before extracorporeal membrane oxygenation, did not increase after the start of this therapy, but began to decrease after 48 hours of extracorporeal membrane oxygenation. During the course of extracorporeal membrane oxygenation, mean pulmonary artery pressure decreased by 50% and mean plasma thromboxane B2 levels decreased by 70%. In addition, serial plasma thromboxane B2 levels were significantly correlated with pulmonary artery pressures in individual infants with a primary diagnosis of meconium aspiration (r = 0.965 to 0.723). We speculate that the decrease in pulmonary artery pressure and plasma thromboxane B2 levels over time may reflect resolution of acute lung injury and that thromboxane B2 may play a role in regulating pulmonary artery pressure in infants with meconium aspiration.     

Comparison of conventional mechanical ventilation and synchronous independent lung ventilation (SILV) in the treatment of unilateral lung injury

Eight patients presenting with severe unilateral pulmonary injury responded poorly to conventional mechanical ventilation. Synchronous independent lung ventilation (SILV) was employed to provide support of ventilation and oxygenation without creating the ventilation/perfusion (V/Q) mismatch observed during conventional ventilation. All patients demonstrated improved oxygenation (mean increase, 80 torr) during SILV with the FIO2 unchanged from previous therapy. Invasive hemodynamic monitoring in five of eight patients showed no difference in the commonly measured cardiopulmonary parameters with the two forms of mechanical ventilation. Peak inspiratory pressure (PIP), continuous positive airway pressure (CPAP), and pressure change secondary to tidal volume delivery to the uninvolved lung were significantly less during SILV. SILV is an effective method of improving oxygenation in patients with severe unilateral pulmonary injury.     

Pneumonectomy for unilateral destroyed lung with pulmonary hypertension due to systemic blood flow through broncho-pulmonary shunts.

OBJECTIVE: Three decades ago, a few patients with pulmonary hypertension and respiratory failure associated with a unilateral destroyed lung were reported to have been treated by a pneumonectomy. In the present study, we investigated the clinical features, operative indications, and results of four cases with pulmonary hypertension that underwent a pneumonectomy for a unilateral destroyed lung. METHODS: Four patients (three males, one female) with a destroyed lung and pulmonary hypertension (mean pulmonary arterial pressure >25 mmHg) were treated by a pneumonectomy between 1999 and 2002 at our institution. Their mean age was 59 years old (range 42-68 years). The underlying lung disease, Medical Research Council (MRC) dyspnea scale, respiratory function, arterial blood gas analysis, pulmonary arterial pressure, preoperative management, operative procedure, and postoperative course for each were reviewed retrospectively. RESULTS: The underlying lung disease that caused the destroyed lung was bronchiectasis in two patients, chronic empyema with bronchopleural fistula in one, and necrotizing pneumonia in one. The average mean pulmonary artery pressure was 33 mmHg (range 25-42 mmHg), which decreased to 27 mmHg (range 19-36 mmHg) after occlusion of the pulmonary artery in the affected lung. Following the pneumonectomy, the average mean pulmonary artery pressure was decreased to 17 mmHg (range 11-25 mmHg). Chronic inflammatory symptoms and functional impairments (showed by blood gas analysis, pulmonary arterial pressure, or MRC dyspnea scale) improved post-pneumonectomy. There was no operative death, though postoperative cardiorespiratory failure occurred in one patient. All patients were discharged from the hospital. CONCLUSIONS: We concluded that a pneumonectomy procedure may be indicated for selected patients with a unilateral destroyed lung and pulmonary hypertension due to systemic blood flow though broncho-pulmonary shunts.     

An analysis of responses to levosimendan in the pulmonary vascular bed of the cat

Calcium-sensitizing drugs, such as levosimendan, are a novel class of drug therapy for heart failure. We investigated the hypothesis that levosimendan is a pulmonary vasodepressor mediated through inhibition of phosphodiesterase, adenosine triphosphate (ATP)-dependent potassium channels, or both. We investigated responses to the calcium sensitizer levosimendan in the pulmonary vascular bed of the cat under conditions of controlled pulmonary blood flow and constant left atrial pressure when lobar arterial pressure was increased to a high steady level with the thromboxane A(2) analog U-46619. Under increased-tone conditions, levosimendan caused dose-related decreases in lobar arterial pressure without altering systemic arterial and left atrial pressure. Responses to levosimendan were significantly attenuated, although not completely, after the administration of U-37883A, a vascular selective nonsulfonylurea ATP-sensitive K(+)-channel-blocking drug. Responses to levosimendan were not significantly different after the administration of the nitric oxide synthase inhibitor L-N(5)-(1-iminoethyl)-ornithine or the cyclooxygenase inhibitor sodium meclofenamate or when lung ventilation was interrupted. These data show that levosimendan has significant vasodilator activity in the pulmonary vascular bed of the cat. They also suggest that pulmonary vasodilator responses to levosimendan are partially dependent on activation of ATP-sensitive K(+) channels and independent of the synthesis of nitric oxide, activation of cyclooxygenase enzyme, or changes in bronchomotor tone in the pulmonary vascular bed of the cat. IMPLICATIONS: Calcium-sensitizing drugs, such as levosimendan, are a novel class of drug therapy for heart-failure treatment. The lung circulation affects both right- and left-sided heart failure. Levosimendan decreased lobar arterial pressure via a partial K(+)(ATP) (potassium channel sensitive to intracellular adenosine triphosphate levels)-dependent mechanism. These data suggest that, in addition to calcium-sensitizing activity, levosimendan decreases pulmonary resistance, which may also aid in the treatment of heart failure.     

Acute pulmonary thromboembolism complicating lung lobectomy; report of a case

Acute pulmonary thromboembolism is fatal if the diagnosis and treatments are delayed. Here we present a case of acute thromboembolism to the right and left pulmonary arteries after right lung lobar resection. A 52-year-old woman who admitted to our hospital with lung cancer was performed right upper lobectomy with mediastinal lymph node dissection (pT1N0M0, well differentiated adenocarcinoma). Two days after surgery, she complained sudden chest discomfort and dyspnea. The blood pressure and oxygen saturation were rapidly decreased. Because there was no lung edema or atelectasis in the chest portable roentgenogram and no ischemic change in the electrocardiogram, pulmonary thromboembolism was suspected and emergency chest computed tomography (CT) was performed. The CT showed left and right pulmonary arterial thromboembolism and immediate anti-coagulator therapy was started. Her condition was improved and chest CT, which was performed three days after the onset of the thromboembolism, showed decreased but still remained thrombus. The anti-coagulator therapy was continued and one month after the onset of the thromboembolism, thrombus was disappeared on chest CT. She is doing well 17 months after surgery. Early diagnosis and treatments are critical for the pulmonary thromboembolism.     

Atrial septal defect with borderline pulmonary vascular disease

The hemodynamic determination of operability in atrial septal defect (ASD) with severe pulmonary hypertension is problematic. Therefore, we perform an open lung biopsy prior to the corrective surgery in cases with pulmonary vascular resistance greater than 8 units ? m² and/or pulmonary arterial peak pressure greater than 70 mmHg. We present 4 cases showing occlusion of more than 70% of the small pulmonary arteries and arterioles by musculoelastosis, thromboembolism and mixed-type (musculoelastosis and plexogenic arteriopathy) which was considered borderline in terms of operability. After complete closure of the ASD and postoperative long-term oral prostacyclin (PGI₂) therapy, pulmonary artery peak pressure decreased from 110–72 (mean 84) to 105–45 (mean 74) mmHg immediately after operation and 65–40 (mean 57) mmHg after PGI2 therapy. The New York Heart Association functional status of the patients improved from class II–III to class I with oral PGI2 only. Our cases demonstrate that despite more than 70% occlusion of the small pulmonary arteries and arterioles, surgery and long-term PGI₂ therapy can reduce pulmonary artery pressure and improve the quality of life.     

Pulmonary Vascular Effects of Isoflurane Anesthesia after Left Lung Autotransplantation in Chronically Instrumented Dogs

Background: Single lung transplantation has become a viable therapy for treatment of end-stage pulmonary disease. We previously observed that left lung autotransplantation (LLA) results in a chronic increase in pulmonary vascular resistance and enhanced pulmonary vascular reactivity to sympathetic alpha adrenoreceptor activation. The effects of inhalational anesthetics on the pulmonary circulation after lung transplantation have not been investigated. In the current study, the authors tested the hypothesis that isoflurane anesthesia, known to cause systemic vasodilation, would exert a vasodilator influence on the baseline pulmonary circulation after LLA. In addition, they tested the hypothesis that isoflurane anesthesia, known to attenuate the systemic vasoconstrictor response to sympathetic alpha adrenoreceptor agonists, would reduce the magnitude of the pulmonary vasoconstrictor response to sympathetic alpha adrenoreceptor activation after LLA.

Methods: Left pulmonary vascular pressure-flow (LPQ) plots were generated in chronically instrumented dogs by measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during inflation of a hydraulic occluder implanted around the right main pulmonary artery. Left pulmonary vascular pressure-flow plots were generated in 8 dogs 2-5 weeks after LLA in the conscious and isoflurane-anesthetized states at baseline, after beta adrenoreceptor block with propranolol, and during the cumulative administration of the alpha agonist, phenylephrine. Left pulmonary vascular pressure-flow plots also were generated in eight conscious, sham-operated control dogs at baseline, after beta block, and during phenylephrine administration.

Results: Compared with conscious control dogs, LLA resulted in a leftward shift (P < 0.01) in the baseline left pulmonary vascular pressure-flow relation, indicating chronic pulmonary vasoconstriction. Despite the enhanced level of pulmonary vasomotor tone after LLA, isoflurane did not exert a vasodilator influence on the baseline left pulmonary vascular pressure-flow relation. The pulmonary vasoconstrictor response to phenylephrine was enhanced (P < 0.01) after LLA compared with the response measured in conscious control dogs. The magnitude of the pulmonary vasoconstrictor response to phenylephrine after LLA was not attenuated during isoflurane anesthesia.     

Changes in cardiorespiratory function after radical esophagectomy by bilateral thoracotomy approach in dogs

Twenty eight dogs (10-16 kg) were anesthetized with pentobarbital sodium, buprenorphine and pancuronium bromide followed by endotracheal intubation in the supine position. Twenty eight dogs were divided into two groups. Group 1 (n = 14) underwent thoracic esophagectomy with regional lymph nodes dissection under the right thoracotomy. Group 2 (n = 14) underwent the same manner of group 1. And left thoracotomy was added in the 5th intercostal space to completely dissect the left side regional lymph nodes. During surgical procedure, lactated Ringer's solution (L-R) were administered, L-R and Dextran 40 were given for postoperative fluid therapy. Cardiac output (CO), pulmonary arterial pressure (PAP), pulmonary wedge pressure (PWP), mean arterial pressure (AP), heart rate (PR), extravascular lung water (EVLW), blood gas analysis, pulmonary shunt rate (Qs/Qt), lung resistance (RL), dynamic lung compliance (CL) and colloid osmotic pressure (COP) were measured at preoperative phase and 1, 3, 6, 12 hrs after surgery. Significant differences were found in the left ventricular stroke work index (LVSWI), RL and the dosage of L-R between these dogs in groups 1 and 2. From these results, extended radical esophagotomy by bilateral thoracotomy approach for clinical cases seems to be possible under the exact indication and intensive perioperative care.     

Effects of Inhaled Nitric Oxide Following Lung Transplantation

Abstract Background: Lung transplantation offers an established therapeutic option for end‐stage lung disease. It is associated with several complications, and early allograft failure is one of the most devastating among all. Different studies are focused on an attempt to minimize these complications, especially transplant failure. We aimed to evaluate the effects of inhaled nitric oxide (iNO) treatment in patients receiving lung transplantation. Methods: Nine patients (six female, three male; mean age 42.9 ± 15.8) requiring lung transplantation for end‐stage pulmonary disease—chronic obstructive pulmonary disease (three patients), cystic fibrosis (three patients), scleroderma and systemic sclerosis (two patients), Eisenmenger's syndrome (one patient), and treated with iNO were included in this retrospective study. Hemodynamic data (mean arterial pressure, mean pulmonary arterial pressure, heart rate) and respiratory parameters were analyzed. Pretreatment data were compared with the post‐iNO treatment data at 6–8 hours and 12–14 hours. Results: The inhalation of nitric oxide was started with an initial dose of 40 parts per million (ppm) and the dose was gradually decreased until hemodynamic and pulmonary stability was achieved. Six patients underwent double‐lung transplantation and three single‐lung transplantations were performed. Cardiopulmonary bypass was used in seven patients. The iNO therapy was started before transplantation in five patients, after the procedure in four patients. Mean iNO therapy duration was 83.2 ± 74.4 hours. The administration of iNO resulted in a significant reduction in mean pulmonary arterial pressure (36.8 ± 15.8 mm Hg to 22 ± 6.8 mm Hg at 6–8 hours and 22.8 ± 7.96 mm Hg at 12–14 hours). Mean systemic arterial pressure slightly increased at 6–8 hours and significantly increased at 12–14 hours (70.2 ± 6.3 mm Hg to 90.1 ± 11.96 mm Hg). Heart rate was not significantly affected with the treatment. Arterial oxygenation improved with the treatment. All patients except one showed improvement of overall respiratory functions. The mean duration of mechanical ventilation was 12.8 ± 10.9 days. Mortality occurred in one patient due to neurologic injury. NO₂ and methemoglobin levels were closely monitored during the treatment. Methemoglobinemia did not occur and NO₂ levels remained between 0.1 and 0.4 ppm. Conclusion: Nitric oxide inhalation for the prevention and treatment of early allograft failure in lung transplant recipients is encouraging. It is superior to other vasodilators with its selectivity to the pulmonary vasculature, while having no significant side effects on systemic circulation. It appears to improve gas exchange and oxygenation properties. Further prospective randomized studies will aid to standardize inhalation nitric oxide therapy.     

A thromboxane analog increases pulmonary capillary pressure but not permeability in the perfused rabbit lung

Thromboxane has been implicated as a mediator of pulmonary hypertension and pulmonary edema in acute respiratory failure. Pulmonary edema may result from increased pulmonary capillary hydrostatic pressure or from increased pulmonary vascular permeability. We therefore studied the effects of a stable thromboxane analog, U46619, on these two parameters in the perfused rabbit lung. Pulmonary capillary pressure was measured by the double vascular occlusion method, and pulmonary vascular permeability was estimated by measurement of the pulmonary fluid filtration coefficient (Kf). U46619 infusion produced pulmonary hypertension and lung weight gain; increased both the arterial (precapillary) and venous (postcapillary) components of pulmonary vascular resistance; and increased pulmonary capillary pressure from 4.7 +/- 0.5 to 9.0 +/- 0.7 mmHg (P less than 0.01). The isogravimetric pressure (equivalent to the capillary pressure corresponding to no lung weight gain) was 4.0 +/- 0.4 mmHg before U46619 and 4.6 +/- 0.4 mmHg during U46619. Therefore, U46619 significantly increased capillary pressure above isogravimetric pressure and resulted in the development of pulmonary edema. U46619 did not affect vascular permeability as measured by Kf. We conclude that pulmonary venoconstriction resulting in increased pulmonary capillary hydrostatic pressure is the major mechanism by which thromboxane produces pulmonary edema in isolated lungs.     

Superimposed high-frequency jet ventilation induced deterioration of oxygenation during whole lung lavage in a patient with pulmonary alveolar proteinosis

A 39-year-old man suffering from pulmonary alveolar proteinosis underwent whole lung lavage of the right lung under one-lung ventilation with total intravenous anesthesia in the right lateral position. Superimposed high-frequency jet ventilation (SHFJV) was applied for approximately 10 minutes during lung lavage. The settings of HFJV were as follows: FIO2 = 1.0, rate = 150 bpm, driving pressure = 1 atm, inspiratory time = 30% of cycle. Since peak inspiratory pressure was high (29 cm H2O) during intermittent positive pressure ventilation (IPPV) due to severe bridle ventilation impairment, HFJV was performed only in the exhalation phase of IPPV. SpO2 and PaO2 at the time of unilateral lung filling declined following initiation of SHFJV, from 98% and 93 mmHg to 95% and 62 mmHg, respectively. Although pulmonary arterial pressure tended to be slightly elevated, little change in blood pressure, cardiac output and central venous pressure was observed. SpO2 was quickly restored after the end of SHFJV. The reason for deterioration of oxygenation might have been an increase in shunt due to shift of pulmonary blood flow from the ventilated lung to the nonventilated lung. These findings suggest that performance of SHFJV during lung lavage for a patient with advanced pulmonary alveolar proteinosis may cause pulmonary oxygenation capacity to deteriorate even when circulatory inhibition is minimal.     

Reduction in recalcitrant pulmonary hypertension after operation for atrial septal defect

We present the case of a patient with atrial septal defect and severe pulmonary hypertension with pulmonary artery peak pressure greater than 110 mm Hg. Open lung biopsy was done prior to the corrective operation, and pathological findings in the small pulmonary arteries included "musculoelastosis" and complete occlusion of 70% of these small arteries and arterioles. The atrial septal defect was closed, and long-term oral prostacyclin therapy was initiated. Pulmonary artery peak pressure decreased to 65 mm Hg 2 years after the operation. This case demonstrates that in a patient with 70% complete occlusion of small pulmonary arteries and arterioles resulting from "musculoelastosis," not only is surgical intervention possible but also pulmonary artery pressure decreases in the long term after operation.