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In the same study, CRI was able to capture the varying risk resulting from patients with different tolerances
to total volume loss, by accurately calculating lower values at lower absolute loss volumes for patients
with lower tolerance (S. Moulton, et al. 2017).
Figure 12 - CRI in patients with different tolerances to total volume loss
Summary of Clinical Study
Background Information Regarding Use of CRI
Compensatory Reserve
Acute hemorrhage initiates a complex cascade of physiologic responses that are triggered and mediated
by cellular signals, resulting in a wide array of cardiopulmonary changes throughout the body. Some of
these changes can be measured using standard vital signs (e.g., heart rate [HR], systolic and diastolic blood
pressures, electrocardiography, respiratory rate, and pulse oximetry). Researchers and clinicians who
have studied and observed how these parameters change in the setting of acute blood loss have long
assumed that hypotension and other signs and symptoms of hemorrhagic shock mark the beginning of
circulatory compromise, rather than the beginning of decompensation. This fundamental assumption has
been based on the observation that humans are able to compensate for large volumes of blood loss with
little change in standard vital signs (S. Moulton, et al. 2013).
The unique capacity of cardiovascular
mechanisms to compensate for the intravascular volume loss an individual can tolerate before
experiencing the symptoms of cardiovascular instability and decompensation can be described as the
Compensatory Reserve.
Development of the Compensatory Reserve Index (CRI)
The Compensatory Reserve Index (CRI) was initially developed using data obtained from a well validated
laboratory method of simulating acute blood loss, the Lower Body Negative Pressure (LBNP) model
(Convertino, Grudic, et al. 2013). A large reference database composed of sensor data collected for each
