A sensitive shock index for real-time patient assessment during simulated hemorrhage.

BACKGROUND: Shock index [SI = the ratio of heart rate (HR) to systolic arterial pressure (SAP)] is a metric used to diagnose patients at risk of impending hemorrhagic shock. We hypothesized that a metric called the compensatory reserve index (CRI), derived using computer modeling with continuous feature extraction from arterial waveforms, would provide an earlier indicator of cardiovascular instability than SI during progressive central hypovolemia. METHODS: There were 15 subjects (men = 8; women = 7) who underwent progressive reduction in central blood volume induced by lower body negative pressure (LBNP) until SAP < 90 mmHg. CRI was normalized on a scale of 1 (normovolemia) to 0 (circulatory volume at which instability occurs) and displayed on a colored bar. The times at which the CRI equaled 0.6 (threshold of green to amber) or 0.3 (threshold of amber to red) were compared to a clinical threshold of SI > or = 0.9. RESULTS: A SI > or = 0.9 required 22.4 +/- 6.2 min (95% CI = 19 to 25.8 min). CRI reached 0.6 (amber) at 12.5 +/- 4.9 min (95% CI = 9.8 to 15.3 min) when SI = 0.61 +/- 0.03, and became 0.3 (red) at 20.3 +/- 5.1 min (95% CI = 17.5 to 23.1 min) when SI = 0.81 +/- 1.4. CONCLUSIONS: CRI provided a significantly earlier indicator of impending hemodynamic decompensation than SI > or = 0.9 during progressive LBNP. These results support the notion that the CRI represents an improved 'shock index' as an indicator of impending hemorrhagic shock compared to standard vital signs.

Physiologic mechanisms underlying the failure of the "shock index" as a tool for accurate assessment of patient status during progressive simulated hemorrhage.

BACKGROUND: Shock index (SI), the ratio of heart rate (HR) to systolic arterial pressure (SAP), is a metric often used to diagnose patients at risk of impending cardiovascular instability and hemorrhagic shock. We hypothesized that if SI reflected impending cardiovascular instability and shock in an individual, then: (1) elevations in SI and HR would be greater in individuals with low tolerance (LT) to progressive lower-body negative-pressure (LBNP) compared with individuals with high tolerance (HT), and (2) LT would be associated with greater vagal withdrawal of the baroreflex sensitivity (BRS) compared with HT. METHODS: A total of 187 healthy subjects (HT, 125; LT, 62) underwent exposure to LBNP until a SAP of less than 80 mm Hg (instability) was achieved. HR and SAP were used to calculate SI, and BRS was determined from spontaneous fluctuations in R-R interval and diastolic arterial pressure. Maximal cardiac vagal withdrawal was calculated as the difference between BRS at baseline and BRS at 100% LBNP tolerance. RESULTS: Contrary to our hypothesis, SI at 60%, 80%, and 100% LBNP tolerance in LT (0.59 ± 0.03, 0.73 ± 0.04, and 0.97 ± 0.06, respectively) was lower (p ≤ 0.002) than SI in HT subjects at the same levels (0.66 ± 0.03, 0.84 ± 0.04, and 1.24 ± 0.06, respectively). Maximal cardiac vagal withdrawal was less (p = 0.045) in LT subjects (11.3 ± 2.2 ms/mm Hg) compared with HT subjects (14.9 ± 2.5 ms/mm Hg). The sensitivity of SI in identifying impending instability (SI, 0.9) at 80% and 100% LBNP tolerance was 13% and 63% in LT subjects and 34% and 91% in HT subjects, respectively. CONCLUSION: The low sensitivity of the SI observed in LT individuals is associated with a lower capacity to withdraw cardiac vagal activity and can lead to an undertriage of those patients most likely to develop early hemorrhagic shock.