Thoracic and abdominal lymph drainage in relation to mechanical ventilation and PEEP

Frostell, Claes; Blomqvist, Hans; Hedenstierna, Göran; Halbig, I.; Pieper, R

doi:10.1111/j.1399-6576.1987.tb02592.x

Cited by 50 publications

(15 citation statements)

References 13 publications

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“…Note also the decrease in abdominal lymph flow during spontaneous breathing. Whether this reflects decreased capillary leakage remains to be shown [8].…”

Section: Lung Lymph Flowmentioning

confidence: 97%

“…Frostell et al [8] measured lung lymph flow in anesthetized dogs ventilated with or without PEEP. During mechanical ventilation with a PEEP of 10 cmH 2 O, the lymph flow from the lung was reduced almost 50% compared to that during zero end-expiratory pressure.…”

Section: Lung Lymph Flowmentioning

confidence: 99%

“…This may appear negligible, but over a 24-h period this amounts to approximately 200 ml. Moreover, in experimental canine oleic acid edema, lung lymph flow may increase 10-fold or even more so that 1-2 l may accumulate over 1 day [8].…”

Section: Lung Lymph Flowmentioning

confidence: 99%

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Lymphatics and lymph in acute lung injury

Hedenstierna

Lattuada

2008

Current Opinion in Critical Care

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“…Note also the decrease in abdominal lymph flow during spontaneous breathing. Whether this reflects decreased capillary leakage remains to be shown [8].…”

Section: Lung Lymph Flowmentioning

confidence: 97%

Section: Lung Lymph Flowmentioning

confidence: 99%

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Lymphatics and lymph in acute lung injury

Hedenstierna

Lattuada

2008

Current Opinion in Critical Care

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“…The effects of an increase in intrathoracic pressure on lymphatic flow were described a decade ago (51,52). In animal models, raising intrathoracic pressure reduced the lymphatic flow and impaired the clearance of lung edema (53)(54)(55). In our study, we found a positive correlation between the increase of esophageal pressure (i.e., the pleural pressure) and the edema formation rate after aIAP of 20 cm H 2 O (edema formation rate [ml/minute] ϭ 1.7 ϫ ⌬ esophageal pressure ϩ 7.0, r ϭ 0.83, p Ͻ 0.05, data not shown).…”

Section: Oleic Acid-injured Lungmentioning

confidence: 99%

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Quintel

Pelosi

Caironi

et al. 2004

Am J Respir Crit Care Med

166

107

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Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H 2 O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H 2 O significantly lowered the gas content, leaving the tissue content unchanged. In OAinjured lung at aIAP 0 cm H 2 O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 Ϯ 24% of the original tissue weight (455 Ϯ 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H 2 O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 Ϯ 37% (tissue weight 905 Ϯ 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OAinjured lung, the increase of IAP increases the amount of edema.Keywords: intraabdominal pressure; acute respiratory distress syndrome; pulmonary edema; lung mechanics; computed tomography scanThe importance of intraabdominal pressure (IAP) in acute lung injury and acute respiratory distress syndrome has been recently suggested (1). For a long time any change in respiratory mechanics in patients with acute lung injury/acute respiratory distress syndrome was attributed to lung mechanics, whereas chest wall mechanics was assumed to be normal. However, few studies in which chest wall elastance was actually measured have showed that it was abnormal in a substantial proportion of patients with acute lung injury/acute respiratory distress syndrome (2-4). We (5) and others (6) have described different chest wall mechanics in patients with pulmonary and extrapulmonary acute respiratory distress syndrome, mainly due to different IAP values.However, apart from respiratory mechanics, the increased intrathoracic pressure caused by chest wall impairment may have important consequences on hemodynamics (7). We investigated the effect of changing IAP during controlled mechanical ventilation in healthy and diseased lungs. Surprisingly, the increase of IAP had an unexpected impact on lung edema, likely related to its formation and clearance. We wish to report our findings and METHODS(Additional details about Methods are provided in an online supplement.)The study group consisted of seven anesthetized and paralyzed domestic pigs (41 Ϯ 4 kg) ventilated throughout the experiment in supine position, with a Vt of 12 ml/kg, respiratory rate of 12-14 breaths/minute, positive end-expiratory pressure of 5 cm H 2 O, and Fi O 2 of 1.0. The animals were fully instrumented for hemodynamic monitoring (carotid artery, right atrium, mea...

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“…The authors suggested that as the lung epithelium is progressively stretched there is an opening up of water-filled channels between the alveolar cells resulting in increased extravascular water accumulation [29]. In addition to the increased pulmonary fluid filtration, mechanical ventilation has been shown to contribute to the increased EVLWI by impeding the clearance of lung lymph in anesthetized dogs and sheep [30,31]. …”

Section: Discussionmentioning

confidence: 99%

Inhibitor of neuronal nitric oxide synthase improves gas exchange in ventilator-induced lung injury after pneumonectomy

et al. 2012

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BackgroundMechanical ventilation with high tidal volumes may cause ventilator-induced lung injury (VILI) and enhanced generation of nitric oxide (NO). We demonstrated in sheep that pneumonectomy followed by injurious ventilation promotes pulmonary edema. We wished both to test the hypothesis that neuronal NOS (nNOS), which is distributed in airway epithelial and neuronal tissues, could be involved in the pathogenesis of VILI and we also aimed at investigating the influence of an inhibitor of nNOS on the course of VILI after pneumonectomy.MethodsAnesthetized sheep underwent right pneumonectomy, mechanical ventilation with tidal volumes (VT) of 6 mL/kg and FiO2 0.5, and were subsequently randomized to a protectively ventilated group (PROTV; n = 8) keeping VT and FiO2 unchanged, respiratory rate (RR) 25 inflations/min and PEEP 4 cm H2O for the following 8 hrs; an injuriously ventilated group with VT of 12 mL/kg, zero end-expiratory pressure, and FiO2 and RR unchanged (INJV; n = 8) and a group, which additionally received the inhibitor of nNOS, 7-nitroindazole (NI) 1.0 mg/kg/h intravenously from 2 hours after the commencement of injurious ventilation (INJV + NI; n = 8). We assessed respiratory, hemodynamic and volumetric variables, including both the extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI). We measured plasma nitrite/nitrate (NOx) levels and examined lung biopsies for lung injury score (LIS).ResultsBoth the injuriously ventilated groups demonstrated a 2–3-fold rise in EVLWI and PVPI, with no significant effects of NI. In the INJV group, gas exchange deteriorated in parallel with emerging respiratory acidosis, but administration of NI antagonized the derangement of oxygenation and the respiratory acidosis significantly. NOx displayed no significant changes and NI exerted no significant effect on LIS in the INJV group.ConclusionInhibition of nNOS improved gas exchange, but did not reduce lung water extravasation following injurious ventilation after pneumonectomy in sheep.

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Thoracic and abdominal lymph drainage in relation to mechanical ventilation and PEEP

Cited by 50 publications

References 13 publications

Lymphatics and lymph in acute lung injury

Lymphatics and lymph in acute lung injury

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Inhibitor of neuronal nitric oxide synthase improves gas exchange in ventilator-induced lung injury after pneumonectomy

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