Lung-Centered Open Heart Surgery: A Call for a Paradigm Change

" The time has come, " in the famous words of Lewis Carroll, " to talk of many things, " and we would like to talk about many things that lead to severe pulmonary dysfunction after cardiac surgery. The term is broad indeed and is usually taken to represent a wide gamut ranging from well-compensated abnormalities of respiratory mechanics to symptomatic hypoxemia secondary to ventilation/perfu-sion mismatching to more significant prolonged ventilator dependency to dreaded " respiratory cripple. " Overwhelming financial and societal costs aside, prolonged ventilator dependency carries the staggering in-house mortality in excess of 40% (1). The incidence and severity was reported to vary widely between centers, partially because of disparate definitions, but significantly because of poorly defined " hospital quality " characteristics (2, 3). We agree with those who look for the causes outside the various demographic characteristics, but rather focus on performance, perioperative surgical and anesthetic techniques, experience and expertise of surgical perioperative care team (4, 5). Let us concentrate on what we actually do in the operating room and see what can be improved. Let us follow, in broad strokes, what happens to the lungs in the course of a traditional intraopera-tive care of a patient presenting for an open heart surgery. To start, the lungs are ventilated with FiO2 = 1.0, large tidal volumes, and zero end-expiratory pressure until the extracorporeal circulation is established. At that moment the mechanical ventilation is completely suspended, with resultant profound iatrogenic atelectasis. Concurrently, as venous return is diverted into cardiopulmonary bypass (CPB) circuit, pulmonary arterial flow ceases, rendering lungs dependent on bronchial arterial flow. The latter, normally approximately 10% of the nutrient flow, is highly variable during the bypass period as it is determined by systemic pressures and flows. Thus, ischemic and atelectatic organ, subjected to oxygen toxicity and ventilator-induced injury during pre-bypass period, is now exposed to CPB-induced systemic inflammatory response (SIRS), greatly potentiated by sequestra-tion of activated polymorphonuclear leukocytes in pulmonary capillaries. After completion of CPB, the lungs are again subjected to repeated stretch trauma of " bag squeezing " recruitment maneuvers, and face additional injury due to reperfusion, potentiated by reactive oxygen species in hyperoxic (FiO2 = 1.0) milieu. Additionally, the right ventricular performance may be impaired in the early post-bypass period due to cardioplegia-induced edema and swelling, regional tissue electrolyte, metabolic and temperature heterogeneity, and ischemia–reperfusion injury (silent ischemia is common and is frequently undetected …