Like many starry-eyed medical students, I was drawn to critical care because of the high stakes, its physiological underpinnings, and the apparent fact that you could take control of that physiology and make it serve your goals for the patient. On my first MICU rotation in 1997, I was so swept away by critical care that I voluntarily stayed on through the Christmas holiday and signed up for another elective MICU rotation at the end of my 4th year. On the last night of that first rotation, wistful about leaving, I sauntered through the unit a few times thinking how I would miss the smell of the MICU and the distinctive noise of the Puritan Bennett 7200s delivering their [too high] tidal volumes. By then I could even tell you whether the patient’s peak pressures were high (they often were) by the sound the 7200 made after the exhalation valve released. I was hooked, irretrievably.
I still love thinking about physiology, especially in the context of critical illness, but I find that I have grown circumspect about its manipulation as I have reflected on the developments in our field over the past 20 years. Most – if not all – of these “developments” show us that we were harming patients with a lot of the things we were doing. Underlying many now-abandoned therapies was a presumption that our understanding of physiology was sufficient that we could manipulate it to beneficial ends. This presumption hints at an underlying set of hypotheses that we have which guide our thinking in subtle but profound and pervasive ways. Several years ago we coined the term the “normalization heuristic” (we should have called it the “normalization fallacy”) to describe our tendency to view abnormal laboratory values and physiological parameters as targets for normalization. This approach is almost reflexive for many values and parameters but on closer reflection it is based on a pivotal assumption: that the targets for normalization are causally related to bad outcomes rather than just associations or even adaptations.
