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alveolar recruitment manoeuvres after cardiac surgery

Tusman, Gerardo; Acosta, Cecilia; Longo, Silvina; Suarez-Sipmann, Fernando

European Journal of Anaesthesiology (EJA): January 2018 - Volume 35 - Issue 1 - p 62–63
doi: 10.1097/EJA.0000000000000657

From the Hospital Privado de Comunidad, Mar del Plata (GT, CA), Department of Anaesthesia, Hospital Privado de Córdoba, Córdoba, Argentina (SL), Hedenstierna Laboratory, Section of Anaesthesia and Critical Care, Department of Surgical Sciences, Uppsala University Hospital, Uppsala, Sweden (FSS) and CIBERES, Madrid, Spain (FSS)

Correspondence to Gerardo Tusman, MD, Department of Anaesthesiology, Hospital Privado de Comunidad, Mar del Plata, Argentina Tel: +54 223 4990074; fax: +54 223 4990099; e-mail:


We thank De Santo and Esquina for their interest in our recently published manuscript1 in the European Journal of Anaesthesiology. In their kind letter,2 they provide a nice description of the factors involved in the pathophysiology of lung injury and right ventricular dysfunction after cardiac surgery with cardiopulmonary bypass.3–5 In addition to general factors related to patients, surgery, anaesthesia, ventilatory management and cardiopulmonary bypass,2–5 they list a number of pathophysiological mechanisms that specifically contribute to right ventricular failure. Interestingly, among the mechanisms listed, lung collapse is not mentioned. This was precisely the goal of our study, namely to draw attention to the fact that atelectases, which are quite common as they occur in 90% of anaesthetised patients,6 must be considered an additional potential mechanism leading to right ventricular dysfunction. Even though the effect was of low magnitude, as included patients had previously uncompromised heart function, atelectasis could be a determinant factor leading to right ventricular dysfunction and failure, magnified in cases of previous right heart disease or in those submitted to increased intraoperative stress.

We fully agree that the choice of an appropriate ventilatory strategy in patients with overt right ventricular failure is critical. We would, however, extend this recommendation to all patients submitted to cardiac surgery which may be particularly important in preventing the evolution from mild dysfunction of the stunned right ventricle to overt failure. The mechanisms by which atelectasis can affect right ventricular function are well known. Lung collapse increases lung heterogeneity, decreasing the size of the functional lung contributing to alveolar overdistension even at relatively low tidal volumes. Such collapse also increases pulmonary vascular resistance by pulmonary capillary compression and hypoxic pulmonary vasoconstriction. Thus, ventilation strategies to protect the right ventricle, as we describe in our study, should also aim at restoring lung homogeneity.

De Santo and Esquina2 also discuss the limitations of our study. As they correctly state, valvular and coronary heart disease, with their corresponding surgical techniques, differently impact heart function. However, both study groups were reasonably well balanced regarding type of surgery, baseline cardiac function, surgical time, total fluid administration and doses of noradrenaline. Almost all patients (95% of total) developed some degree of mild right ventricular dysfunction associated with atelectasis, which means that this pathophysiological mechanism that was easily reversed by lung recruitment is universal irrespective of previous heart function or type of surgery.

We are grateful to De Santo and Esquina2 for their letter, because it gives us the opportunity to emphasise the ‘proof of concept’ nature of our study. We could demonstrate the presence of atelectasis (the cause), right ventricular dysfunction (the consequence) and the effect of lung recruitment (the treatment). To prove this hypothesis, we evaluated low-risk patients to avoid the bias that inotropes induce on the evaluation of cardiac contractility. In other words, we used a model that could discriminate the ‘pure’ effect of atelectasis on right ventricular performance, irrespective of whether such cardiac depression was clinically relevant.

Despite the acknowledged study limitations, we believe that we have successfully confirmed our hypothesis. It was not our intention to evaluate the effect on patients’ outcome. This could well be a next step for which a larger patient population would be needed. In the meantime, we propose lung recruitment and adequate positive end-expiratory pressure (PEEP) setting as an effective and easy way to reverse the negative consequences of lung collapse on right ventricular function.

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1. Longo S, Siri J, Acosta C, et al. Lung recruitment improves right ventricular performance after cardiopulmonary bypass: A randomised controlled trial. Eur J Anaesthesiol 2017; 34:66–74.
2. Esquinas AM, De Santo LS. Alveolar recruitment manoeuvres after cardiac surgery. Eur J Anaesthesiol 2018; 35:61–62.
3. Bignami E, Guarnieri M, Saglietti F, et al. Mechanical ventilation during cardiopulmonary bypass: a review. J Cardiothorac Vasc Anesth 2016; 30:1668–1675.
4. Haddad F, Couture P, Tousignant C, et al. The right ventricle in cardiac surgery, a perioperative perspective: II. Pathophysiology, clinical importance, and management. Anesth Analg 2009; 108:422–433.
5. Denault AY, Pearl RG, Michler RE, et al. Tezosentan and right ventricular failure in patients with pulmonary hypertension undergoing cardiac surgery: the TACTICS trial. J Cardiothorac Vasc Anesth 2013; 27:1212–1217.
6. Tenling A, Hachenberg T, Tyden H, et al. Atelectasis and gas exchange after cardiac surgery. Anesthesiology 1998; 89:371–378.
© 2018 European Society of Anaesthesiology