Specificity of Compensatory Reserve and Tissue Oxygenation as Early Predictors of Tolerance to Progressive Reductions in Central Blood Volume

Abstract

We previously reported that measurements of muscle oxygen saturation (SmO2) and the compensatory reserve index (CRI) provided earlier indication of reduced central blood volume than standard vital signs (e.g., blood pressure, heart rate, arterial oxygen saturation). In the present study, we hypothesized that the CRI would provide greater sensitivity and specificity to detect progressive decrease in central circulating blood volume compared with SmO2. Continuous noninvasive measures of CRI (calculated from feature changes in the photoplethysmographic arterial waveforms) were collected from 55 healthy volunteer subjects before and during stepwise lower body negative pressure (LBNP) to the onset of hemodynamic decompensation. Near infrared spectroscopy was used on the forearm to obtain deep SmO2, hydrogen ion concentration ([H]), and hemoglobin volume (HbT; decreases reflect vasoconstriction). CRI decreased by 97% in a linear fashion across progressive blood volume loss, with no clinically significant alterations in vital signs. The receiver operating characteristic (ROC) area under the curve (AUC) for the CRI was 0.91, with a sensitivity of 0.87 and specificity of 0.80, when predicting decompensation at progressive levels of LBNP. In comparison, SmO2, [H], and HbT had significantly lower ROC AUC, sensitivity and specificity values for detecting the same outcome. Consistent with our hypothesis, CRI detected central hypovolemia with significantly greater specificity than measures of tissue metabolism. Single measurement of CRI may enable more accurate triage, while CRI monitoring may allow for earlier detection of casualty deterioration.

Evidence for misleading decision support in characterizing differences in tolerance to reduced central blood volume using measurements of tissue oxygenation

“…Since vessel constriction alters the volume of blood in the NIRS sensorʼs optical path, changes in HbT reflect the magnitude of change in vasoconstriction . Previous investigations conducted in humans undergoing LBNP‐induced reductions in central blood volume have demonstrated reduced forearm muscle blood flow as a result of sympathetically‐mediated arteriolar vasoconstriction that mimic reductions in forearm HbT . Consistent with our previous observations, the greater HbT reduction in HT compared to LT participants in the present study suggests that “good” compensators are characterized by a greater compensatory capacity for arteriolar vasoconstriction than “poor” compensators despite having a lower StO 2 .…”

“…The CRM represents a relative capacity for compensation and is based on measurements of changes in multiple features of each arterial waveform obtained from a photoplethysmogram (PPG) . Measurement of the compensatory reserve has proven to be a more sensitive and specific indicator of physiological state than other physiological indicators of reduced central blood volume per se . That is, 100%, 60%, 30%, and 0% compensatory reserve represent the equivalent physiological state across individuals independent of the degree of central hypovolemia.…”

“…Data obtained from progressive reduction in central blood volume of both humans and non‐human primates have demonstrated that approximately one in every three individuals can be classified as “poor” compensators who display relatively LT to experimentally‐induced central hypovolemia. An individualʼs tolerance to central hypovolemia is characterized by the depletion of oneʼs compensatory reserve, or the sum total of all compensatory mechanisms that contribute to the capacity to maintain tissue perfusion as a result of a blood volume deficit . In this regard, tolerance time to decompensation (i.e., presyncope) can be defined as a CRM of 0%.…”

Physiological comparison of hemorrhagic shock and V˙O2max: A conceptual framework for defining the limitation of oxygen delivery

“…Application of such advanced computer processing algorithms has demonstrated that measures of arterial waveform features reflect the integration of all compensatory mechanisms recruited to sustain adequate DO 2 during conditions of progressive hypovolemia with greater specificity and sensitivity compared to standard vital signs and metabolic markers. [66][67][68][69][70] Specifically, changing features of the ejection wave reflect the sum of all compensatory mechanisms that control myocardial function, while reflected wave features reflect the sum of all mechanisms associated with compensation for compromised cellular energy requirements. 63 From the initial onset of hemorrhage or exercise (illustrated in Figure 3, broken lines), recruitment of the entirety of all compensatory mechanisms (e.g.…”

The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

“…When the negative pressure is released, central blood volume returns quickly to normal baseline levels ( Figure 1(c)). The completion of several hundred LBNP experiments and development of a database have revealed the classification of individuals into two general categories: two-thirds of the population display high tolerance (HT) in their ability to compensate for reduced central blood volume while the remaining one-third have a low tolerance (LT) to reduced central blood volume 5,6 . As such, we use the criteria of those subjects who compensate beyond a À60 mmHg LBNP level as HT and those who reach presyncope at LBNP À60 mmHg as LT (Figure 1(b)).…”