Shock Volume

Abstract

Multiply injured patients (MIPs) in hemorrhagic shock develop oxygen debt which causes organ dysfunction and can lead to death. We developed a noninvasive patient-specific index, Shock Volume (SV), to quantify the magnitude of hypoperfusion. SV integrates the magnitude and duration that incremental shock index values are elevated above known thresholds of hypoperfusion using serial individual vital sign data. SV can be monitored in real time to assess ongoing hypoperfusion. The goal of this study was to determine how SV corresponded to transfusion requirements and organ dysfunction in a retrospective cohort of 74 MIPs. We measured SV in 6-h increments for 48 h after injury in multiply injured adults (18-65; Injury Severity Score ≥18). Patients who had accumulated 40 units of SV within 6 h of injury and 100 units of SV within 12 h of injury were at high risk for requiring massive transfusion or multiple critical administration transfusions. SV measurements were equally sensitive and specific as compared with base deficit values in predicting transfusions. SV measurements at 6 h after injury stratified patients at risk for multiple organ failure determined by Denver scores. In addition, SV values corresponded to the magnitude of organ failure determined by Sequential Organ Failure Assessment scores. SV is a patient-specific index that can be quantified in real time in critically injured patients. It is a surrogate for cumulative hypoperfusion and it predicts high-volume transfusions and organ dysfunction.

Swine hemorrhagic shock model and pathophysiological changes in a desert dry-heat environment

“…Certain conditions and various disease states can however lead to reduced DO 2 and (or) increased VO 2 , which interferes with the balance of DO 2 and VO 2 , leading to oxygen debt occurrence. This in turn leads to tissue and organ damage and may even result in organ failure or death [27]. In the present study, DO 2 , VO 2 , and O 2 ER were higher in those exposed to the dry-heat environment than in those exposed to the normal temperature environment, suggesting that dry-heat environment exposure could increase oxygen metabolism.…”

Predictive Factors for Massive Transfusion in Trauma: A Novel Clinical Score from an Italian Trauma Center and German Trauma Registry

“…The persistence of an altered hemodynamic status of a patient upon arrival in ED notwithstanding bolus infusions is more alarming than the hypotension recorded on the field. The pre-hospital shock index (SI), easily calculated from the ratio between heart rate and SBP is considered a fair predictor of MT [ 20 ], while the Shock Volume, which assesses the SI iteratively over multiple time points is more promising [ 21 ]. As demonstrated in previous studies [ 22 , 23 ], patients who receive more than 1000 mL of fluids in the pre-hospital settings and are “transient” or “no responders” will be more likely to require blood products and will have an increase in mortality.…”

Shock volume: Patient-specific cumulative hypoperfusion predicts organ dysfunction in a prospective cohort of multiply injured patients

“…In our original work, we determined that SHVL calculated with a hypoperfusion threshold of 0.9 correlated more closely with organ dysfunction compared with using 1.2 or 1.5 as the threshold value. 20 Therefore, at any time point, the magnitude of hypoperfusion was determined by subtracting 0.9 from the SI values. For SI values that were less than 0.9, the SI value for SHVL calculations was set to zero.…”

“…The accuracy of SHVL measurements is affected by temporal sampling frequency of vital signs. 20 In the first 24 hr after injury, vital signs were typically recorded every 15 minutes during the first 8 hours to 12 hours, and rarely greater than a period of 60 minutes. During the second 24 hr after injury, vital sign sampling was notably less frequent and therefore we did not calculate SHVL beyond the first 24 hr after injury.…”

“…We recently introduced a metric that measures cumulative hypoperfusion, shock volume (SHVL). 20 Shock volume is calculated by integrating serial Shock Index (SI) (heart rate/systolic blood pressure) values during any prescribed acute injury/resuscitation time frame. Specifically, the duration and magnitude that SI values are above accepted thresholds of hypoperfusion (0.9) are integrated into an index that quantifies cumulative hypoperfusion.…”