Gas Exchange Function Research Articles

Trauma patients treated with extracorporeal membrane oxygenation

Aim: Severe trauma with is a cause of death either due to fatal injuries without any treatment option or due to life threatening complications in the early course. Early complications such as bleeding shock and/or severe respiratory failure following chest trauma or massive blood transfusion are a major task in the treatment of these patients. Massive blood transfusions may result in decreased cardiac output and pulmonary gas exchange, and either massive blood transfusion or pulmonary contusion may lead to acute respiratory distress syndrome (ARDS). In these cases extracorporeal membrane oxygenation (ECMO) as a lifesaving treatment may improve or take over the gas exchange function of the lung or provide additional cardio-circulatory support.

Two-year home-based nocturnal noninvasive ventilation added to rehabilitation in chronic obstructive pulmonary disease patients: A randomized controlled trial

BackgroundThe use of noninvasive intermittent positive pressure ventilation (NIPPV) in chronic obstructive pulmonary disease (COPD) patients with chronic hypercapnic respiratory failure remains controversial as long-term data are almost lacking.The aim was to compare the outcome of 2-year home-based nocturnal NIPPV in addition to rehabilitation (NIPPV + PR) with rehabilitation alone (PR) in COPD patients with chronic hypercapnic respiratory failure.MethodsSixty-six patients could be analyzed for the two-year home-based follow-up period. Differences in change between the NIPPV + PR and PR group were assessed by a linear mixed effects model with a random effect on the intercept, and adjustment for baseline values. The primary outcome was health-related quality of life (HRQoL); secondary outcomes were mood state, dyspnea, gas exchange, functional status, pulmonary function, and exacerbation frequency.ResultsAlthough the addition of NIPPV did not significantly improve the Chronic Respiratory Questionnaire compared to rehabilitation alone (mean difference in change between groups -1.3 points (95% CI: -9.7 to 7.4)), the addition of NIPPV did improve HRQoL assessed with the Maugeri Respiratory Failure questionnaire (-13.4% (-22.7 to -4.2; p = 0.005)), mood state (Hospital Anxiety and Depression scale -4.0 points (-7.8 to 0.0; p = 0.05)), dyspnea (Medical Research Council -0.4 points (-0.8 to -0.0; p = 0.05)), daytime arterial blood gases (PaCO2 -0.4 kPa (-0.8 to -0.2; p = 0.01); PaO2 0.8 kPa (0.0 to 1.5; p = 0.03)), 6-minute walking distance (77.3 m (46.4 to 108.0; p < 0.001)), Groningen Activity and Restriction scale (-3.8 points (-7.4 to -0.4; p = 0.03)), and forced expiratory volume in 1 second (115 ml (19 to 211; p = 0.019)). Exacerbation frequency was not changed.ConclusionsThe addition of NIPPV to pulmonary rehabilitation for 2 years in severe COPD patients with chronic hypercapnic respiratory failure improves HRQoL, mood, dyspnea, gas exchange, exercise tolerance and lung function decline. The benefits increase further with time.Trial registrationClinicalTrials.Gov (ID NCT00135538).

Noninvasive positive pressure ventilation in COPD

Educational aims To take up the ongoing debate on whether long-term noninvasive positive pressure ventilation (NPPV) should be applied in chronic obstructive pulmonary disease (COPD) patients with chronic hypercapnic respiratory failure. To elucidate the impact of NPPV techniques on NPPV success in COPD. To describe the technique and scientific evidence for the new concept of high-intensity NPPV. To provide practical considerations on how to commence high-intensity NPPV. To outline important unknowns regarding long-term NPPV in COPD patients. Summary Home mechanical ventilation, as provided by long-term NPPV, is a widely accepted treatment option for many patient groups with chronic hypercapnic respiratory failure, including also those with COPD, even though the rationale for long-term NPPV in COPD patients is still disputed. This is based on clinical observations that conventional NPPV using assisted ventilation and low mean inspiratory pressures of Recently, however, a promising technique of NPPV has been described, which aims at maximally improving gas exchange by the use of controlled ventilation and considerably higher inspiratory pressures, typically ranging 20–40 cmH2O. This is known as high-intensity NPPV. This approach clearly contrasts with the conventional, low-intensity approach. High-intensity NPPV has been shown to improve physiological parameters such as breathing pattern, gas exchange and lung function. In addition, it also provides clinical benefits, with improvements in dyspnoea, walking distance and specific aspects of health-related quality of life. The superiority of high- over low-intensity NPPV has been clearly established by randomised crossover trials. Increasing evidence now exists to support the contention that long-term high-intensity NPPV offers a new therapeutic option in the treatment of hypercapnic COPD. However, the questions of whether high-intensity NPPV is also capable of improving survival and how to best select candidates to undergo long-term high-intensity NPPV remain pressing. This article also provides detailed practical descriptions of how to initiate high-intensity NPPV.

Comments on Point:Counterpoint: High altitude is/is not for the birds!

TO THE EDITOR: The debate between Scott et al. (6) and Llanos et al. (4) highlights the remarkable ability of birds and mammals to adapt and survive at high altitudes and cope with reduced oxygen (O2) availability. Scott and colleagues (6) make a compelling argument that birds are far superior to mammals at adapting and thriving in hypoxic environments, both at rest and during exercise. While their argument is supported by comparisons between birds and terrestrial mammals, it ignores marine mammals. Marine mammals such as seals are routinely exposed to and tolerate long bouts of hypoxia during breath-hold diving. For example, elephant seals may dive to depths of nearly 1,600 m and occasionally remain submerged for 2 h (3). Moreover, marine mammals can be exposed to partial pressures of arterial oxygen (PaO2) as low as 12 mmHg during free dives (5), which is less than the 20 mmHg observed in the bar-headed goose (6). Interestingly, a PaO2 of 12 mmHg observed in elephant seals corresponds to arterial saturations and O2 content of only 8% and 2.7 ml O2/dl (5). Thus marine mammals such as the elephant seal demonstrate a remarkable hypoxia tolerance. The integration of several key physiological adaptations including 1) substantially greater myoglobin concentrations compared to other mammals, 2) reductions in metabolism, 3) a greater reliance on aerobic metabolism (i.e., less lactate production), 4) a host of dramatic acute cardiovascular adjustments; and 5) an increased intrinsic cerebral hypoxia tolerance allow marine mammals to thrive in hypoxic environments and enable long deep dives (1–3).

Measurement of respiratory function: an update on gas exchange

Gas exchange is the main function of the lungs. Oxygen and carbon dioxide diffuse along their partial pressure gradient across the alveolar-capillary membrane. Lungs have a large reserve for gas exchange. Alveolar ventilation and pulmonary circulation are closely matched to provide efficient gas exchange in the lungs. Hypoxaemia often results from mismatch in ventilation–perfusion. Gas exchange can be impaired in various disease states. Measurement of the diffusing capacity for carbon monoxide (DLCO) provides estimation of the gas exchange function. A low DLCO indicates an impairment of oxygen transfer across the alveolar-capillary membrane. Anaesthesia and surgery adversely affect pulmonary function, many of which adverse effects can be prevented.

Relationship between the surface area and volume of human middle ear cavity and the transmucosal gas exchange function

Relationship between the surface area and volume of human middle ear cavity and the transmucosal gas exchange function

Acute respiratory distress syndrome: A clinical review.

The acute respiratory distress syndrome (ARDS) is a complex disorder of heterogeneous etiologies characterized by a consistent, recognizable pattern of lung injury. Extensive epidemiologic studies and clinical intervention trials have been conducted to address the high mortality of this disorder and have provided significant insight into the complexity of studying new therapies for this condition. The existing clinical investigations in ARDS will be highlighted in this review. The limitations to current definitions, patient selection, and outcome assessment will be considered. While significant attention has been focused on the parenchymal injury that characterizes this disorder and the clinical support of gas exchange function, relatively limited focus has been directed to hemodynamic and pulmonary vascular dysfunction equally prominent in the disease. The limited available clinical information in this area will also be reviewed. The current standards for cardiopulmonary management of the condition will be outlined. Current gaps in our understanding of the clinical condition will be highlighted with the expectation that continued progress will contribute to a decline in disease mortality.

Invited Commentary

Invited Commentary

Fossil evidence for low gas exchange capacities for Early Cretaceous angiosperm leaves

The photosynthetic gas exchange capacities of early angiosperms remain enigmatic. Nevertheless, many hypotheses about the causes of early angiosperm success and how angiosperms influenced Mesozoic ecosystem function hinge on understanding the maximum capacity for early angiosperm metabolism. We applied structure-functional analyses of leaf veins and stomatal pore geometry to determine the hydraulic and diffusive gas exchange capacities of Early Cretaceous fossil leaves. All of the late Aptian—early Albian angiosperms measured possessed low vein density and low maximal stomatal pore area, indicating low leaf gas exchange capacities in comparison to modern ecologically dominant angiosperms. Gas exchange capacities for Early Cretaceous angiosperms were equivalent or lower than ferns and gymnosperms. Fossil leaf taxa from Aptian to Paleocene sediments previously identified as putative stem-lineages to Austrobaileyales and Chloranthales had the same gas exchange capacities and possibly leaf water relations of their living relatives. Our results provide fossil evidence for the hypothesis that high leaf gas exchange capacity is a derived feature of later angiosperm evolution. In addition, the leaf gas exchange functions of austrobaileyoid and chloranthoid fossils support the hypothesis that comparative research on the biology of living basal angiosperm lineages reveals genuine signals of Early Cretaceous angiosperm ecophysiology.

87 Aerosolized Pfc Improves Pulmonary Function and Gas Exchange in a Preterm Lamb Model

Background: The aerosolization of PFC has emerged as a feasible alternative to the instillation for the experimental treatment of Respiratory Distress Syndrome.Aim: To determine the effects of aerosolized perfluorocarbon (PFC) on pulmonary gas exchange and lung function in preterm lambs.Methods: 12 preterm lambs (80-90%GE) were used. Lambs were randomly assigned to receive aerosolized PFC (10 ml/kg/h for 2h), delivered via an inhalation catheter, coupled to a jet nebuliser, and placed at the distal end of the endotracheal tube connected to a ventilator (PFC-aerosol) or not (CONTROL), both groups were maintained during 6h on IMV. Cardiovascular parameters, arterial partial pressure of CO2 (PaCO2), pH, oxygenation index (IO), arterial-alveolar oxygen ratio (a/APO2), alveolar-arterial oxygen gradient (A-a)DO2 and pulmonary function (compliance Cdyn and tidal volumen VT) were measured each 30 min during the experiment. Mean±SD, ANOVA, p< 0.05.Results: After 90min of treatment, animals in PFC-aerosol group, significantly improved gas exchange in comparison to Control group, being the improvement persistent until the end of the experiment: PaCO2 (37±6 vs. 93±12 mmHg), pH (7.41±0.11 vs. 7.15±0.09), IO (9±3 VS. 77±44), a/APO2 (0.29±0.11 vs. 0.04±0.02), (A-a)DO2 (294±133 vs. 572±20). Moreover, the pulmonary function significantly improved after 60 min of treatment in PFC-aerosol group compared to Control group, the improvement was sustained during the experimental period: Cdyn (0.53±0.05 vs. 0.27±0.04 ml/cmH2O/kg), VT (12.5±2.4 vs. 5.2±1.8 ml/kg). During all the experimental period there were not changes on cardiovascular parameters.Conclusion: Our results show that administration of aerosolized PFC improves pulmonary function and gas exchange. FIS07/0733-GV2007111046

TRPV1 Agonist Capsaicin Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Capsaicin, a transient receptor potential vanilloid type 1 (TRPV1) agonist, was found to protect against myocardial and renal ischemia-reperfusion (IR) injury. This study was carried out to investigate the role of capsaicin in lung IR injury in vivo. Forty male New Zealand rabbits were randomized into four groups (10 per group) as follows: sham group (sham thoracotomy), IR group (occlusion of the left pulmonary hilus for 1 h followed by reperfusion for 3 h), CAP (capsaicin) group (a bolus injection of CAP 5 min before ischemia), CPZ (capsazepine) group (a bolus injection of the TRPV1 antagonist CPZ 5 min before ischemia). Blood and lung tissue samples were obtained for blood gas and biochemical analyses, wet/dry weight ratio measurements, and histologic evaluation. Protein levels and neutrophils in the bronchoalveolar lavage fluid (BALF) were also measured. Pretreatment with capsaicin improved gas exchange function, decreased lung wet/dry ratio and protein levels and neutrophil counts in BALF, decreased lung malondialdehyde levels and myeloperoxidase activities, increased superoxide dismutase activities, along with an elevation of calcitonin gene-related peptide (CGRP) level (P < 0.05 versus IR group). Capsaicin also attenuated IR-induced pathological lesions. By contrast, capsazepine exacerbated gas exchange abnormality, increased pulmonary microvascular permeability, oxidative stress, neutrophils infiltration, and also revealed a decreased CGRP level (P < 0.05 versus IR group). Results from the present study show that capsaicin confers protection against lung IR injury. These protective effects seem to be closely related to the inhibition of inflammation and oxidative stress via the activation of TRPV1 and the release of CGRP.

DROUGHT TOLERANCE IN MULBERRY (MORUS SPP.): A PHYSIOLOGICAL APPROACH WITH INSIGHTS INTO GROWTH DYNAMICS AND LEAF YIELD PRODUCTION

SUMMARYThe present study documents critical analysis of drought-induced physiological responses in mulberry (Morus spp.) with insights into growth dynamics and leaf productivity. The study was performed for two years in a two-phase experimental design combining both field (experiment no. 1) and glasshouse (experiment no. 2) observations. In field assays, we surveyed 15 mulberry genotypes under two irrigation regimes: well-watered (20 to 24 irrigations in each growing season) and water-limited (irrigated once in a fortnight in each growing season). The genotypes were assessed for variation in key leaf gas exchange characteristics: net photosynthetic rates (Pn), stomatal conductance of CO2 (gs), transpiration rates (E) and instantaneous water use efficiency (WUEi). Leaf yield/plant was considered to determine the tolerance index (TI). Drought stress severely down-regulated leaf-level physiological variables in the susceptible genotypes resulting in poor leaf yield. However, genotypes S-13 and V-1 performed better in terms of leaf gas exchange and proved their superiority over other genotypes in drought tolerance. Conversely, genotypes DD and Bogurai were highly susceptible to drought. Under glasshouse conditions, the combined leaf gas exchange/chlorophyll a fluorescence measurements further dissected out stomatal and non-stomatal restrictions to Pn. As internal/ambient CO2 ratio (Ci/Ca) decreased concurrently with gs in non-irrigated stands, it appeared that greater stomatal limitation to Pn was associated with decreased photo-assimilation and leaf yield production. Further, higher leaf temperature (TL) (&gt;35 °C) and down-regulation of maximum quantum yield of photosystem II (Fv/Fm) were apparent in the susceptible compared to the tolerant genotypes, which indicated chronic photoinhibition due to photo-inactivation of photosystem II centres in the susceptible genotypes. Drought-induced trade-offs in biomass allocation were also highlighted. Overall, our results suggest that greater rooting vigour and leaf hydration status, minimal stomatal inhibition and stabilized photochemistry might play major roles in maintaining higher Pn and associated gas exchange functions in drought-tolerant mulberry genotypes under water stress conditions. The higher leaf yield production in tolerant than susceptible genotypes can be attributed to minimal plasticity in foliar gas exchange traits and better quantitative growth characteristics under low water regimes.

Regulation of cell proliferation in the stomatal lineage by the Arabidopsis MYB FOUR LIPS via direct targeting of core cell cycle genes.

Stomata, which are epidermal pores surrounded by two guard cells, develop from a specialized stem cell lineage and function in shoot gas exchange. The Arabidopsis thaliana FOUR LIPS (FLP) and MYB88 genes encode closely related and atypical two-MYB-repeat proteins, which when mutated result in excess divisions and abnormal groups of stomata in contact. Consistent with a role in transcription, we show here that FLP and MYB88 are nuclear proteins with DNA binding preferences distinct from other known MYBs. To identify possible FLP/MYB88 transcriptional targets, we used chromatin immunoprecitation (ChIP) followed by hybridization to Arabidopsis whole genome tiling arrays. These ChIP-chip data indicate that FLP/MYB88 target the upstream regions especially of cell cycle genes, including cyclins, cyclin-dependent kinases (CDKs), and components of the prereplication complex. In particular, we show that FLP represses the expression of the mitosis-inducing factor CDKB1;1, which, along with CDKB1;2, is specifically required both for the last division in the stomatal pathway and for cell overproliferation in flp mutants. We propose that FLP and MYB88 together integrate patterning with the control of cell cycle progression and terminal differentiation through multiple and direct cell cycle targets. FLP recognizes a distinct cis-regulatory element that overlaps with that of the cell cycle activator E2F-DP in the CDKB1;1 promoter, suggesting that these MYBs may also modulate E2F-DP pathways.

The effects of normothermic heparin pulmonary infusion on the transplanted lung injury hi a porcine lobar lung auto-transplantation model

Objective To observe the effects of normothermic heparin pulmonary artery infusion on pulmonary function and ultra-structures in the swine model of left single lung auto-transplantation. Methods Eighteen healthy local pigs were used as experimental animals, received left pneumonectomy and lobar lung auto-transplantation (left lower lobe) , and divided into three groups randomly (n=6 in each group) according to different pulmonary artery perfusion protocols (control group with normothermic saline, normothermic heparin group with heparin in normal temperature, and cold EC group with 4 X. Euro-Collins). The blood samples and lung tissues were collected at baseline, 0. 5 , 1,2, and 4 h after lobar lung auto-transplantation respectively. The indices were determined as follows: PvO2, PvCO2, dynamic lung compliance (Cdyn), and myeloperoxidase(MPO) content in the transplanted lung tissues. The lung tissue wet/dry ratio (W/D) was analyzed. At 4 h after lung (or lobar lung) auto-transplantation, the pulmonary grafts were sampled for ultra-structure observation under the electronic microscopy. Results Compared to control group at the 4th h post-operation, PvO2, PvCO2, Cydn, MPO and W/D levels and ultra-structures had significant difference in normothermic heparin group and cold EC group (P<0.05), but there was no difference between normothermic heparin group and cold EC group. Conclusion Pulmonary artery perfusion with normothermic heparin or cold Euro-Collins solution can preserve the transplanted lobar lung structure, reduce the ischemia-reperfusion injury, and maintain the gas exchange function. Pulmonary artery infusion with normothermic heparin meets the requirement of lobar lung auto-transplantation. Key words: Swine; Lung auto-transplantation; Perfusion fluid; Heparin

Lung Procurement for Transplantation: New Criteria for Lung Donor Selection

In Italy, like everywhere in the world, the organ shortage for transplantation is a real problem. It is well known that lung donors (LD) are particularly difficult to procure and that management of the organ do not care during the diagnosis of cerebral death represents a difficult challenge. In this context, the salvage of the so-called “marginal donors” may increase the pool of donors, favoring organ retrieval. To increase lung procurement, the intensivist must recognize “marginal donors,” optimizing organ selection and function. The aim of our study was to review LD procured in 2008, as identified by the unrestricted criteria, of the Nord Italian Transplant program Center (NITp). Particularly, the age and habits of donors and the presence of a parenchyma contusion were not sufficient per se to exclude donation. We revisited lung ventilation and monitoring modalities during cerebral death before retrieval. In 2008, the application of enlarged criteria for LD enabled us to collect 21 LD, namely 33% of all cerebral deaths, versus 13% in 2007. Seeking to maintain good gas exchange and lung function, we implemented a safe ventilation program avoided high peak pressures, and fluid therapy properly guided by the cardiac index and extravascular lung water index monitoring. Specific actions to improve LD procurement may help cope with the organ-donor shortage. Although our series was small, our results were encouraging; they underline the necessity to continuously review donor criteria and care, allowing good donor/recipient matching.

Mastoid structural properties determined by imaging analysis of high resolution CT-scanning

Hypothesis: The structure of the mastoid air cells can be described by quantitative imaging analysis of high-resolution CT-scans, which may contribute to understand its function in normal and pathological ears. Background: Negative middle ear pressure is a common factor in middle ear diseases resulting from an imbalance between mastoid gas exchange and Eustachian tube function. While the Eustachian tube function has been the main focus of research, more recent studies indicate that the mastoid may play an active role in pressure regulation. The mastoid structure with numerous air cells reflects a large area to volume ratio (AV-ratio) adapted to efficient gas exchange. Imaging analysis applied to high resolution CT-scanning can describe quantitative measures, which may reveal important information about mastoid function and its role in healthy and diseased ears. Materials and methods: Quantitative analysis was performed on a series of unselected high resolution CT-scans (voxel size: 0.29 _ 0.29 _ 0.625 mm) from 36 ears in 24 patients. Area and volume were determined using Cavalieri’s method, i.e. by summing cross-sectional areas. The AV-ratio was computed for each scan. Results: Mean area was 69 cm2 (range: 23–134cm2), mean volume was 4 cm3 (range: 1.3–10.8 cm3), and mean AV-ratio was 16 cm-1 (range: 11.2–21.0 cm-1). The area correlated linearly to the volume by A = 17.2*V-0.2. Conclusion: The area and volume values corresponded with previous studies, and the additional AV-ratio reflected the functional properties of the mastoid in terms of capability for gas exchange. Due to a series of similarities between structure and function of the lungs and mastoid, it seems likely to propose a tree-structure of dividing mastoid cells. In respiratory research, analysis describing the dimensions of series of bronchi generations has been applied, and based on current results; our aim of future research is to establish similar details of mastoid tree-structure. Funding source: Various private Danish funds.

Normal Development of the Lung and Premature Birth

The following review focuses on the normal development of the lung from conception to birth. The defined periods of lung development-Embryonic, Pseudoglandular, Canalicular, Saccular and Alveolar-will be explored in detail in relation to gestational age. Cellular differentiation, formation of the conducting airways and respiratory zone and development of the alveoli will be reviewed. Pulmonary vascular development will also be examined within these periods to relate the formation of the blood-air barrier to the lungs for their essential function of gas exchange after birth. The development of the surfactant and cortisol systems will also be discussed as these need to be mature before the lungs are able to take on their role of respiration following birth. It is clear that premature birth interrupts normal lung development so the effect of preterm birth on lung development will be examined and the respiratory consequences of very preterm birth will be briefly explored.

Pulmonary complications of neuromuscular disease: A Respiratory mechanics perspective

Paediatric neuromuscular disease compromises both the gas exchange and pump functions of the respiratory system. This can have profound implications for both growth and development of the respiratory system, as well as morbidity and mortality. Aspiration lung disease is common, and leads to increasingly restrictive pulmonary physiology over time. Abnormal lung and chest wall mechanics, and weak respiratory muscles, can combine to cause respiratory failure. Improving the balance between the work of breathing (by decreasing the respiratory load) and the respiratory pump (by improving respiratory muscle strength and decreasing respiratory muscle fatigue) can help prevent the onset of respiratory failure. Airway clearance techniques and non-invasive ventilation are two important tools in this effort. Better ways of assessing the respiratory pump, mechanical function, control and fatigue are needed especially in children.

Transforming Growth Factor- Signaling across Ages: From Distorted Lung Development to Chronic Obstructive Pulmonary Disease

The transforming growth factor (TGF)-beta superfamily of secreted growth factors consists of more than 40 members, including the TGF-beta isoforms themselves, bone morphogenetic proteins, and activins. Most of these factors have been shown to be essential for proper organ development, a process often recapitulated in chronic diseases. Importantly, TGF-beta superfamily members are key regulators of extracellular matrix composition and alveolar epithelial cell and fibroblast function in the lung. Both during lung development and disease, TGF-betas therefore control lung homeostasis by providing the structural requirements and functional micromilieu needed for physiological epithelial cell function and proper gas exchange. Prolonged alterations of TGF-beta signaling have been shown to result in structural changes in the lung that compromise gas exchange and lung function, as seen in arrested lung development, a feature of bronchopulmonary dysplasia, lung fibrosis, and chronic obstructive pulmonary disease. All these syndromes share a loss of functional alveolar structures, which ultimately leads to a decreased life expectancy. In this review, we cover our current understanding of the impact of TGF-beta signaling on chronic lung disease. We focus on distorted TGF-beta signaling in bronchopulmonary dysplasia and chronic obstructive pulmonary disease as prototype diseases of the premature and matured lung, respectively, which are both characterized by functional and structural loss of alveolar units.

Hemodynamic monitoring in one-lung ventilation

One-lung ventilation causes adverse effects in pulmonary gas exchange and cardiocirculatory function. These adverse effects become particularly important for patients with underlying cardiopulmonary comorbidities. Alterations in pulmonary gas exchange have been investigated in several experimental and clinical trials. However, the hemodynamic consequences of one-lung ventilation are to a great extent unknown. Furthermore, no conclusive recommendations exist as to which kind of hemodynamic monitoring should be preferred in the situation of one-lung ventilation. Many issues regarding hemodynamic monitoring in one-lung ventilation remain unacknowledged. This article will review the current literature on hemodynamic monitoring in one-lung ventilation in order to derive recommendations for the application of hemodynamic monitoring in this specific peri-operative situation.