Which position is used to decrease atelectasis and improve refractory hypoxemia

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Introduction

Refractory hypoxemia is an extremely complex condition with a high morbidity-mortality rate. This clinical situation represents an advanced process encompassed within the so-called acute respiratory distress syndrome [ARDS], defined by the American-European Conference of 19941 with the purpose of reaching consensus on a series of homogeneous criteria. Acute respiratory failure [ARF] is defined on the basis of clinical, radiological and blood gas parameters. Acute lung injury [ALI] in turn is defined as a PaO2/FiO2 ratio of under 300mmHg, and in ARDS it is taken to represent a ratio of under 200mmHg. Recently, in the year 2011, experts gathered in Berlin and redefined the classification [the “Berlin definition”],2 improving stratification and mortality prediction of the syndrome, but without clarifying other factors, such as the role of positive end-expiratory pressure [PEEP], or the physiopathology or etiology of the process. The term ALI has disappeared from this classification and the condition is now classified according to the PaO2/FiO2 ratio for an established PEEP as mild, moderate or severe ARDS [PaO2/FiO2 200–300 with PEEP5; PaO2/FiO2200 with PEEP5, and PaO2/FiO2100 with PEEP10, respectively].

Mechanical ventilation [MV] intrinsically implies lung aggression as described in a number of studies, such as those published by Amato et al.3 and Brochard et al.,4 where the use of lung protecting ventilatory maneuvers has been advised. Based on these data, the study made by the ARDS Network5 in the year 2000 was able to demonstrate a decrease in mortality among patients with ALI/ARDS subjected to lung protecting ventilation. This strategy aimed to reduce ventilator-induced lung injury [VILI], and was based on the avoidance of alveolar overdistension [volutrauma] and cyclic opening and closing of the alveolar units [atelectrauma]. Later studies corroborated this strategy, even in patients without lung injury criteria. This was the case of the work published by Determann et al.,6 who demonstrated an increase in the cases of ALI among patients ventilated with a tidal volume [TV] of 10ml/kg ideal body weight [ml/kg IBW] versus 6ml/kg IBW, to the point of having to interrupt the study prematurely. The study published by Needham et al.7 in 2012 analyzed survival after two years among patients with ALI subjected to ventilation with lung protecting measures. These authors recorded a mortality rate of 64% in the first two years. Compliance with the lung protecting measures in 50% of the cases implied a decrease in absolute mortality risk from two years of 4%, versus 8% when compliance was 100%. In contrast, the relative mortality risk increased 18% for every 1ml/kg IBW rise in TV.

Under these premises, any case of acute respiratory failure which under lung protecting measures persistently maintains PaO2/FiO230cmH2O can be classified as refractory hypoxemia.8 Once the diagnosis has been established, evaluation is required of different therapeutic measures that act upon different aspects of lung physiopathology. The objective of this review is to describe the therapies designed to treat hypoxia and improve survival.

Ventilatory options

Mechanical ventilation is the cornerstone of treatment and comprises different ventilatory modes and/or maneuvers that aim to improve the effective gas exchange surface: PEEP level, recruitment maneuvers, pressure regulated ventilation modalities, inverse inspiration-expiration ratio, airway pressure release ventilation [APRV], and high-frequency oscillation ventilation [HFOV].

Positive end-expiratory pressure and recruitment maneuvers

Lung disease is characterized by heterogeneous distribution between healthy alveolar units and units with different degrees of alveolar collapse, which globally reduce the surface available for gas exchange. The application of pressure to the respiratory system can decollapse the damaged alveoli. The main difficulty, however, is to reach a sufficient level of pressure to recruit [decollapse] the diseased alveolar units while simultaneously avoiding cyclic opening and closing [atelectrauma], overdistension of the healthy alveoli, and adverse hemodynamic effects [alteration of the ventilation–perfusion ratio and of cardiac output].

There are two main maneuvers for securing the greatest possible surface for gas exchange, distinguished by their intensity and duration of application. Positive end-expiratory pressure [PEEP] applies continuous pressure during ventilation, with slow and progressive recruitment, while recruitment maneuvers [RMs] involve high pressures maintained for short periods of time, with recruitment of as many collapsed alveoli as possible.

In recent years, the debate regarding PEEP has focused on the application of moderate PEEP versus high PEEP. The results show an improvement of PaO2/FiO2, with no influence upon survival. The ALVEOLI study9 compared low volume-controlled ventilation in two PEEP regimens, with the observation of improved oxygenation and respiratory mechanics in the high PEEP group. However, there were no differences in mortality, days without mechanical ventilation or in the development of barotrauma–though this possibly could be explained by the existence of a certain imbalance between the groups. In this same line, Meade et al.10 compared volume-controlled ventilation [moderate PEEP] versus pressure-controlled ventilation [PEEP high], and observed improvements in refractory hypoxemia and death due to hypoxemia in the high PEEP group, though without differences in either global mortality or the incidence of barotrauma. The study published by Mercat et al.11 in turn compared low volume-controlled ventilation in a standard group and in a group with PEEP elevation to a plateau pressure of 28–30cmH2O. Not only were no benefits observed, but adverse effects were even recorded in the high PEEP group with mild respiratory failure.

Gordo-Vidal et al. reviewed the effect of different PEEP levels in four studies of high methodological quality among the 12 studies regarded as relevant.12 The authors selected the studies of Amato et al.,13 Ranieri et al.,14 Brower et al.9 and Villar et al.,15 and concluded that PEEP level did not affect either mortality or the incidence of barotrauma. The same analysis, without considering the ALVEOLI study published by Brower et al.,9 yielded significant reductions in mortality and barotrauma [RR=0.6; 95%CI 0.4–0.8, and RR=0.2; 95%CI 0.1–0.7, respectively]. The difference was based on the fact that in these three studies PEEP was adjusted according to identification of the lower inflexion point of the ascending arm of the pressure/volume loop.

In sum, on the basis of the described studies, it can be concluded that the use of high PEEP to increase oxygenation affords better results. However, PEEP elevations that do not result in an increase in alveolar surface imply increases in transpulmonary pressure, which in turn is related to VILI.16 PEEP monitoring according to P-V loops or the “stress index” is advised in order to avoid deleterious hemodynamic or pulmonary effects.

Recruitment maneuvers expand the effective gas exchange surface through an intense and transient increase in transpulmonary pressure, resulting in the recruitment of collapsed alveoli. Studies such as that published by Oczenski et al.17 report temporary improvements in blood gas parameters. Pressures of 50cmH2O were generated during 30s, with the improvement of oxygenation for 30min. The same results were obtained by Meade et al.,18 with adverse effects, such as hypotension or barotrauma. On the other hand, the PEEP required after RM can be adjusted by identifying the inflexion point of the ascending arm of the pressure–volume curve, as in the study of Amato et al.,13 or by desaturation in the context of progressive PEEP reduction, as in the study published by Girgis et al.19 The review carried out by Fan et al.20, involving 40 studies in patients with ALI, confirmed the temporary improvement of patient oxygenation, with fewer adverse effects than in other articles. The authors concluded that the procedure should not be regarded as a routine measure but as an individualized option in patients in the context of life-threatening situations.

Recruitment maneuvering is the subject of debate, offering transient effects, and with no established optimum methodology, timing or frequency of application. We hope that the OLA multicenter study will offer clarifying results in the near future.

Ventilatory techniquesPressure-controlled ventilation

Pressure-controlled ventilation [PCV] is a ventilatory option in cases of refractory hypoxemia, since it can improve hypoxemia without adding further risks–though it does not modify patient survival. Esteban et al.21 randomized 79 patients two treatment arms, volume-controlled ventilation and pressure-controlled ventilation, and found no differences in blood gas parameters, ventilatory mechanics or in the number of organ failures.

Since this ventilation mode is applicable not only in refractory hypoxemia, the reader is advised to consult the corresponding topic in the series.

Inverse inspiration-expiration ratio

Mechanisms have been evaluated that increase mean lung pressure. Prolongation of the inspiratory phase until exceeding the expiration time, inverting the ratio, may be one such mechanism. Although feasible under any ventilation mode, it traditionally has been used in pressure-controlled ventilation, resulting in a decrease in peak pressures and improving ventilation and oxygenation, etc.22

However, over time, no clear benefits of this technique have been reported with respect to conventional ventilation modes. An increased frequency of asynchronization is observed, requiring increased sedation or even relaxation. The method increases the risk of air trapping, with the possibility of hemodynamic deterioration. Mercat et al.23 compared volume-controlled ventilation [VCV], traditional pressure-controlled ventilation, and pressure-controlled inverse-ratio ventilation [PC-IRV]. The ventilation [PaCO2: VCV 45±5mmHg, PCV 43±5mmHg, PC-IRV 39±4mmHg; p

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