US Army Institute of Surgical Research (1998–Present)
With federal budget cuts driving decisions under the Base Realignment and Closure (BRAC) Act, our research program at Brooks AFB was terminated in 1998. With this action, I was provided an opportunity by the US Army to relocate my laboratory to their Institute of Surgical Research (USAISR) at Fort Sam Houston (San Antonio, TX). In this capacity, I continued my studies on acute and chronic physiological responses to perhaps the most extreme life-threatening environmental factor associated with reductions in central blood volume—hemorrhage induced by trauma. As such, the focus of my research on cardiovascular control during conditions of central hypovolemia was placed on advancing the emergency medical capabilities of combat medics in the pre-hospital setting of battlefield care. A primary part of this focus was to develop new clinical tools that could allow the medic to recognize that a patient was bleeding well before there was any indication from standard clinical techniques.
One of our earliest research activities was focused on providing an effective clinical tool that would control severe hemorrhage from extremity injuries. My postdoctoral fellow, Dr. Josh Wenke, conducted the first physiological testing on humans that demonstrated a deployed US Army one-handed tourniquet was not designed with the capability to stop blood flow (bleeding) in the leg [17]. The results of these tests led to the redesign of the tourniquet and the subsequent development and deployment of the Combat Applied Tourniquet (CAT) that is currently used on the battlefield and in the streets of America, and was awarded the 2005 Army’s Greatest Invention Award. The development and fielding of the CAT has and will continue to save lives of soldiers and civilians by impacting doctrine of tourniquet use.
In 2002, the Director of the US Army Combat Casualty Care Research Program (CCCRP) assigned me to manage a newly formed science effort that focused on pre-hospital emergency care of combat trauma casualties under fire called Tactical Combat Casualty Care (TCCC) Research. Since hemorrhage is the leading cause of death on the battlefield, our research team developed a human physiology laboratory that translated the use of LBNP into a noninvasive model for the study of human hemorrhage (Fig. 5). The capability to induce pre-syncope in all our subjects allowed for the development of a large data base (>260 humans) to model the hemodynamic, respiratory, autonomic, metabolic and coagulopathic responses during the compensatory and early decompensatory phases of hemorrhagic shock in otherwise healthy, conscious surrogates of military personnel. The findings from these studies led to new insights into our knowledge and understanding of identifying and treating progressive hemorrhage prior to the onset of overt shock, and proved critical to the conceptualization of three primary advances in extreme physiology and medicine.
Fig. 5 Vic Convertino undergoing a simulation of hemorrhage in the LBNP chamber during a 2006 experiment. Dr. Caroline Rickards, NRC post-doctoral fellow, is applying intrathoracic pressure regulation therapy with an impedance threshold device
First, in collaboration with Dr. Keith Lurie who developed a device that creates resistance during inspiration, we were able to find a simple operationally feasible way of counteracting syncope and hemorrhagic shock when one deals with returning astronauts or casualties on the battlefield. We demonstrated that reducing intrathoracic pressure can be an effective noninvasive resuscitation tool for restoring central blood volume as a ‘bridge’ to more definitive care where fluids may not be readily available. This therapy can be applied by having spontaneously breathing patients inspire through resistance which results in a greater vacuum within the thorax, and subsequently enhances venous return and preload to the heart in conditions of central hypovolemia (e.g., hemorrhage). In this sense, a resuscitation effect can be provided without the challenges created by carrying and infusing fluids that can dilute clotting factors or dislodge clots with elevated blood pressure. Using LBNP as our simulated progressive hemorrhage model in humans, my post-doctoral fellow Caroline Rickards demonstrated that this intrathoracic pressure regulation (IPR) therapy is capable of delaying symptoms as well as hemodynamic decompensation by protecting cerebral blood flow in addition to maintaining cardiac output [18]. Our work has led to a documented case where use of IPR therapy proved its value as a lifesaving intervention in a combat casualty. In addition to its usefulness in treating casualties with hemorrhage, the discovery that IPR therapy reduces intracranial pressure [17] speaks to its potential value as an early noninvasive intervention in the pre-hospital setting for treatment of cerebral hypoperfusion associated with traumatic brain injury. Most significantly, this technology has been placed by the US Army Tactical Combat Medical Care for use in the treatment of hypovolemic hypotension in Battalion Aid Stations and all air and land ambulances in theater, and recognized for its value to returning astronauts by its placement in the medical kit on board the Space Shuttle and International Space Station. As one of the most gratifying experiences in my career, the impedance threshold device technology used to apply IPR therapy was inducted into the Space Foundation Hall of Fame in 2008 (Fig. 6).
Fig. 6 Vic Convertino, Keith Lurie, Don Doerr, and Ahamed Idris receiving their medals while attending the Space Technology Hall of Fame Induction ceremony at Colorado Springs, Colorado on April 10, 2008
Second, we found that approximately one in three individuals have relatively low tolerance to reduced central blood volume [19]. These ‘low tolerant’ individuals demonstrated a physiology that was characterized by attenuated responses in tachycardia, peripheral vasoconstriction, sympathetic nerve activity, cardiac vagal withdrawal, and oscillations in blood pressure and cerebral blood flow [20, 21]. The identification of specific physiological signals that distinguish those patients at highest risk for early development of shock is one of the most fundamental observations that need to be considered in any assessment of advanced decision support and care for acute emergency settings.
Third, the recognition of individual capabilities to compensate for relative blood volume deficit during progressive hemorrhage led to the conceptualization of the ‘compensatory reserve’, a new paradigm for measuring the sum total of all compensatory mechanisms (e.g., tachycardia, vasoconstriction, breathing) that together contribute to ‘protect’ against inadequate tissue perfusion during blood loss. In our effort to discover a way to measure the compensatory reserve of individuals, our research efforts were refocused to the recognition that measurements of changes in arterial waveform features represented the integration of all cardiac and peripheral compensatory responses to hemorrhage and could provide us a tool to distinguish high- from low-tolerant individuals. By establishing collaboration with robotics engineers from the University of Colorado, our results have been translated to the development of the first prototype of a beat-to-beat ‘shock’ monitor that incorporates waveform feature extraction techniques with machine learning [22]. For the first time, tracking blood loss, early prediction of decompensatory shock, and accurate assessment of resuscitative interventions in a specific patient are possible. This technology has been shown to reduce the time required by paramedics to recognize an unstable patient by >40 % [23]. The applications of this technology to people getting out of bed after surgery, the nursing home, sports medicine or many other occupational settings are infinite. This will undoubtedly revolutionize medical monitoring, diagnosis, and interventional actions for the future of emergency medicine.