Extravascular Lung Water and Pulmonary Vascular Permeability After Minimally Invasive Cardiac Surgery

Acute respiratory distress syndrome (ARDS) occur with an incidence of 12% after cardiac surgery with the use of cardiopulmonary bypass (CBP). Using one-lung ventilation (OLV) in addition, as it is common practice in minimally invasive cardiac surgery (MICS), one can hypothesize that the risk for ARDS increases.

The objective of this prospective, observational study is to measure extravascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) as parameters of lung edema through alteration in the pulmonary permeability by comparing three groups of surgery patients: I) patients with CPB, II) patients with OLV and III) patients with both CPB and OLV.

MICS allows coronary artery bypass grafting and cardiac valve surgery through small incisions, does not appear to be inferior to conventional surgery, but likely reduces postoperative pain, accelerates postoperative recovery and improves the cosmetic result. However, based on the available data, respiratory failure after MICS occurs at the same rate as after conventional cardiac surgery. In addition, unilateral re-expansion pulmonary edema, rarely seen after conventional cardiac surgery, has been described after MICS with CPB and OLV.

The pathophysiology of ARDS is characterized by massive inflammation that leads to a diffuse damage of both the alveolar epithelium and pulmonary vascular endothelium. Although the etiology of ARDS is multifactorial, the uniform result is an acute, nonhydrostatic, high-permeability lung injury with interstitial and alveolar protein-rich edema, epithelial damage and rapid onset of pulmonary fibrosis. This leads to the vast reduction of the pulmonary gas exchange and to hypoxemia.

Extravascular lung water (EVLW) comprises all fluids of the extravascular compartment of the lung, ie, intracellular water, lymphatic fluid, surfactant and extravasated plasma. Increased EVLW may be caused by an increased hydrostatic intravascular pressure, as it occurs in cardiogenic pulmonary edema, and/or by an increase of lung endothelial and epithelial permeability, as in ARDS. The EVLWI estimates the EVLW by using the transpulmonary thermodilution technique.The pulmonary vascular permeability index (PVPI) is the ratio between the EVLWI and the pulmonary blood volume, which is also measured by the transpulmonary thermodilution technique. The PVPI is thought to reflect the permeability of the alveolar-capillary barrier.

The combination of CPB and OLV permitted the development of MICS. CPB is an extracorporeal circulation, where a heart-lung machine takes over temporarily the pump function of the heart and the oxygenation and ventilation function of the lungs, thereby, allowing various heart and vascular surgical procedures. During CPB, blood from the right side of the heart is drained into the heart-lung machine and returned into the arterial system. This leads to a hypoperfusion of the lung, while blood flow is maintained only through the bronchial artery. OLV allows the surgeon to access the thorax cavity for the operation, while contralateral lung is ventilated.

It was originally thought that the lung is relatively resistant to ischemia due to its dual circulation. However, re-perfusion of the lung after CPB and/or OLV can trigger a fatal cascade, summarized as lung ischemia reperfusion injury (LIRI). LIRI involves intracellular injury and pertinent inflammatory responses, which result in apoptosis of the endothelium, alveolar capillary interstitial edema, hyaline membranization, and infiltration by neutrophils and macrophages. In addition, during CPB, the contact of blood components with the artificial surface of the bypass circuit contribute to the postoperative systemic inflammatory response syndrome (SIRS). Through these mechanisms, lung compliance and resistance as well as pulmonary permeability are affected, which contributes to the development of ARDS. During OLV, a combination of LIRI as well as surgical trauma and lung hyperinflation may lead to the release of inflammatory mediators which can alter endovascular permeability. Additionally, after thoracic surgery the pulmonary vascular permeability increases and re-expansion of the collapsed lungs may result in the so called re-expansion pulmonary edema.

To the best of the investigators knowledge, no study primarily aimed at examining the relationship between MICS and lung injury, although it is of high clinical interest whether the combination of CPB and OLV during MICS leads to increased EVLW and pulmonary permeability and ARDS.