The Fick Principle and the Steady State
Authors: ALFRED P. FISHMAN
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

In 1952, an unheralded paper in the Journal of Clinical Investigation marked a turning point in my career (Fishman, A. P., J. McClement, A. Himmelstein and A. Cournand, Effects of acute anoxia on the circulation and respiration in patients with chronic pulmonary disease studied during the “steady state”. J. Clin. Invest. 1952;31:770–781). The paper had a forked message: one branch showed that in patients with chronic obstructive pulmonary disease (COPD), as in normal individuals, acute hypoxia elicits an increase in pulmonary arterial pressure and blood flow (cardiac output); this increase in pressure and flow could be clinically meaningful in patients with COPD in whom bouts of acute hypoxia are likely to occur spontaneously during exercise, sleep, or upper respiratory infection; the other limb showed that to obtain accurate measurements of cardiac output during acute hypoxia, precautions have to be taken to ensure a steady state of the respiration and circulation. I arrived at the Bellevue Hospital on foot. A homeless person showed me the way to get in. Following instructions, I climbed the steps to the first floor, reached the landing a little breathless from exertion, somewhat flushed with anticipation and moderately tachycardic from both. Before opening the fire door, I paused to catch my breath. My mind raced. Although I was officially there as an “Established Investigator of the American Heart Association,” in reality I was not yet established. I had been awarded the five-year Established Investigatorship based largely on success in introducing the Kolff artificial kidney into the United States and in demonstrating its effectiveness in treating acute renal failure; this experience with acute renal failure subsequently pointed the way for using renal dialysis in treating chronic renal failure (Fishman, A. P., et al. Am. J. Med. 1949;7:15). In reality, my credentials were those of a research fellow. The period in the Cournand-Richards Cardiopulmonary Laboratory at Bellevue Hospital was primarily intended to provide proper mentoring for a career in clinical investigation. It also afforded the opportunity to learn the technique of right heart catheterization. I pulled open the fire door. It opened onto a dimly lit corridor, poorly illuminated by light let in through unwashed windows. Opposite the windows, a series of closed doors, beyond which (I was to learn later) were the individual laboratories and offices. The doors were windowless, unmarked, and invited no entry. But far down the empty corridor, I could see a beam of light. Possibly an open door. I headed for it and soon found myself in the doorway of an office—Cournand’s office. I recognized him immediately from the physiology meetings. He sat beneath the window, hunched over a large wooden desk, totally immersed in writing. I panicked. I was unexpected, unannounced and intruding. I had to back out. I began to step back. Too late. He had sensed my presence. “Who are you? What do you want? What are you doing here?” Then, without pause, he answered his own questions. “You are in the wrong place. You probably belong uptown with Stan Bradley” (uptown, at the Columbia-Presbyterian Medical Center). I desperately wanted to get away. But, a restraining hand from behind held me in place. Ruth Fabian, his longtime administrative assistant (and future wife) spoke over my shoulder. “He belongs here. You and Dr. Richards accepted him months ago. I have room for him in my office.” The crisis was over. She had saved the day. Cournand had nothing more to say. He swiveled back to his work. We were dismissed. During the next few weeks, I wandered from room to room, introducing myself, observing tests, and witnessing procedures. There was much new for me to see: cardiac catheterization, bronchospirometry, pulmonary function tests, and exercise tests; all executed by practiced teams with full compliments. But I was not enrolled in any project or assigned a mentor. I was destined to observe and, occasionally, to lend a helping hand. Between procedures, I took refuge in the analytic laboratory, presided over by Mrs. Lester, a gentle supervisor with many years of experience and loyalty to Cournand. There, between samples of blood and gas, the skilled technicians took time to show me how to use the Haldane and Van Slyke apparatuses. When they were busy, I turned to the old data books and practiced the calculations. The data books were destined to be the turning point in my Cournand-Richards experience. In one of the books, I came across the data which were the basis for a recent publication from the Laboratory on the effects of acute hypoxia on the pulmonary circulation in normal subjects (Motley, H. L., A. Cournand, et al . Am. J. Physiol. 1947;150:315). The report indicated that acute hypoxia elicited pulmonary vasoconstriction as reflected in an increase in pulmonary arterial pressure accompanied by a decrease in cardiac output. Although, the increase in pulmonary arterial pressures was no surprise, the decrease in cardiac output was unexpected. In the study by Motley and colleagues, cardiac output was determined by the general Fick equation, usually written: