Team

In 1971 a University of Florida Philosophy Professor, while driving was hit broadside by a drunk driver. He was admitted to the surgical intensive care unit, where I was the Critical Care Fellow. I had just learned to calculate right-to-left intrapulmonary shunt fraction from Jay Block, MD, the head of Pulmonary Medicine at UF. The calculation necessitated mixed venous blood, so the Chief resident in CV Surgery and I inserted the first Swan Ganz catheter ever used at UF. Arterial and venous blood samples were collected while the patient was receiving 8 cmH2O PEEP. For comparison purposes, PEEP was raised to 12 cmH2O, the maximum allowable level, and shunt decreased significantly. Surprisingly, the arterial-venous O2 content difference decreased, indicating an increase in cardiac output. It was 3AM, I was the only physician in the unit and it occurred to me that a further increase in PEEP might be beneficial. PEEP was raised to 15 cmH2O, with the same result previously observed.
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As a consequence of both A-V O2 content and shunt decreasing, PaO2 rose dramatically, allowing inspired O2 to be decreased from 100% to 40%. A further increase in PEEP to 18 cmH2O resulted in even more improvement. The next morning, I presented the case to our Visiting Professor Henrik Bendixen, MD, who had just left the Massachusetts General Hospital to be Chair of Anesthesiology at UC San Diego. He was a co-founder of the Respiratory Intensive Care Unit at MGH and coauthored the “Bible” of respiratory Care. He was very generous in his praise for my daring at exceeding the guidelines for PEEP, which largely emanated from The MGH RICU, and suggested that I collect a series of patients and publish the results, which I did in 1973 (Anesth Analg 52:210-214, 1973). Also, in 1973 I also published the paper describing IMV. Unfortunately, I chose to introduce IMV as a weaning technique, even though I had progressed to using it as a ventilatory support mode that allowed patients to breathe spontaneously, while receiving ventilatory assistance (Chest 64:331-335, 1973). In August of 1973, following my Critical Care Fellowship, I was assigned as the Officer in Charge of the surgical ICU at Wilford Hall Medical Center, Lackland AFB, San Antonio, TX. My Commanding Officer, Colonel Joseph Dannemiller gave me free reign over the unit and I began treating patients with IMV and the level of PEEP that minimized shunting, without decreasing cardiac output. We added continuous flow to the ventilator circuit, so that CPAP, rather than PEEP, was provided. A middle-aged lady from Laredo, TX, who developed septicemia following a cholecystectomy, came to us in severe respiratory failure with a P/F ratio of 75 mmHg. We aggressively resuscitated her, treated her with IMV, spontaneous respiration and 22 mmHg (31 cmH2O) CPAP with no detriment to her cardiac output. Her case report became the first of a series of publications describing the use of IMV, spontaneous breathing and high levels of CPAP (Anesth Analg 54:31-34, 1975). Over the next two years we had opportunity to treat 54 patients with severe ARDS, whose P/F ratio averaged 80 mmHg, with a minimum of 27 cmH2O CPAP. Our 3-month survival was 80% and 13 patients returned to Wilford Hall for pulmonary function testing, which revealed minimal long-lasting lung injury, with the exception of reduced diffusion capacity (Chest 71:18-23, 1977). Following my USAF service, I returned to UF to run the first VA Hospital Surgical ICU Service in the Country. Our results with high CPAP levels and IMV led to more than a decade of controversy, contentious debate and, in some cases, general disbelief. In 1980, I left Gainesville, FL and UF for a quasi-private practice in Urbana, IL. The long Winters and an abundance of free time gave me ample opportunity for contemplation. Obviously, when expiratory airway pressure is nearly 30 cmH2O, peak airway pressure during mandatory (mechanical) breaths is necessarily higher than what would be considered injurious by today’s standards. We rarely, if ever, saw the ventilator induced lung injury (VILI) commonly spoken of, now, likely because the high levels of CPAP maintained an open-lung and avoided the repetitive collapse and tearing open caused by current ARDSNet strategy using low levels (20 cmH2O) of PEEP. In spite of success in treating patients with ARDS, (improved gas exchange, decreased time on the ventilator and 80% survival) it was that a method of ventilation that could avoid high airway pressures, would be desirable. As often is the case with sudden enlightenment, a question occurred to me one night, “if I can provide CPAP and ventilate patients with a positive pressure breath on top of the CPAP, why not simply decrease the CPAP briefly, say, for one second and allow the patient to exhale carbon dioxide?” That seemed very intuitive. Then followed the difficult tasks of a name for this new mode of ventilatory support and the methodology to provide it. I discussed these problems with Robert Kirby, MD, a former teacher and coauthor, Michal Douglas, MD, a former resident, colleague and coauthor and M. Christine Stock, MD, a Northwestern anesthesiology resident and frequent coauthor, who later became my Critical Care Fellow. All agreed the concept seemed rational. In 1985 I moved to Ohio State University to be Director of Research for the Department of Anesthesiology. With the assistance of Gerald McGinnis, Roger Dzwonczyk (both brilliant engineers) and Chris Stock, we were able to build a simple CPAP circuit, with an exhalation valve that would momentarily release the airway pressure. Thus, the name airway pressure release ventilation (APRV). A patent was applied for and granted in 1986, this in an attempt to prevent slip shod devices that failed, (as occurred with IMV on multiple occasions and publications) from allowing naysayers to claim the technique didn’t work (as also occurred, then and now, with IMV). Dr. Stock and I first tested the device on each other, before proceeding to test the device on normal and lung injured animals. Shortly thereafter, we published the favorable results of ventilating post cardiac surgical patients, comparing assist-control ventilation with APRV (Chest 94:779-781, 1988). The Editor Will Shoemaker, MD put the editorial introducing APRV (Crit Care Med 15: 459-461, 1987) just before the scientific proof of concept (Crit Care Med 15:462-466, 1987), in order that I could be the one to introduce the concept (editorials were placed in the back of the Journal in those days). Immediately, publications appeared claiming APRV was nothing more than pressure limited mechanical ventilation, or inverse ratio ventilation and unlikely to be of any value. Those critical of APRV then and now totally missed the concept of an open lung ventilation strategy that permits spontaneous breathing, impossible with both pressure controlled and Inverse I:E ratio ventilation. Ironically, over thirty years of validation in both animal models and human subjects with severe ARDS have not decreased the fervor with which APRV is resisted by some clinicians, most of whom have never used the technique and who have little understanding of the physiologic effects. As IMV was resisted as an “unproven weaning technique”, APRV now is resisted as an unproven “rescue modality.” Both are modes of ventilation, that by permitting unrestricted spontaneous ventilation, promote venous return, cardiac output, patient comfort, less sedation and almost always, no need for paralysis. Hopefully, the chronology of the events will promote some greater understanding of both IMV and APRV. John B. Downs, MD, FCCM, FCCP