Title : Diastolic shock index as an early failure-to-normalize marker of persistent vasodilatory physiology in infection-related critical illness
Abstract:
Background: The diastolic shock index (DSI), calculated as heart rate divided by diastolic blood pressure, has emerging utility as a marker of vasodilatory shock and progression to septic shock in the emergency department. While pre-hospital shock index thresholds are recognised as high risk, the role of DSI as a dynamic marker across the ED–intensive care pathway remains unclear, particularly when physiological abnormalities persist despite early resuscitation or are blunted by rate-limiting medications.
Objectives: To characterise pre-hospital and early ED DSI in adult patients admitted directly from the ED to ITU with an infectious cause, and to assess whether persistent elevation of DSI following initial resuscitation identifies patients with ongoing physiological risk who may benefit from earlier critical care involvement.
Methods/Description: We conducted a retrospective review of adult patients (≥18 years) referred directly from the ED to ITU with an infectious cause at a single centre between 1 October 2024 and 30 September 2025 (n = 144). Pre-hospital and ED physiological data were analysed, including the highest DSI recorded pre-hospital and within the first hour of ED arrival. Additional variables included use of rate-limiting or anti-arrhythmic medications, initiation of vasopressors in the ED, and time to ITU referral from ED arrival. Fluid volumes were not analysed because of inconsistent real-time documentation in high-acuity resuscitation scenarios; ED vasopressor initiation was therefore used as a reliable marker of haemodynamic failure. Descriptive statistical analysis and distributional assessment of DSI values were performed to examine patterns of physiological response following early ED resuscitation.
Results/Outcomes: Despite a reduction in DSI following ED resuscitation, a substantial proportion of patients demonstrated persistent haemodynamic abnormality. Among 144 patients admitted to ITU, 69.4% had an ED DSI ≥ 1.5 within the first hour and 23.6% remained ≥ 2.0, indicating ongoing vasodilatory physiology despite early management. Approximately one quarter of patients were receiving rate-limiting or anti-arrhythmic medications, yet elevated DSI remained common in this subgroup, suggesting that the signal reflects physiological stress rather than tachycardia alone. Vasopressors were initiated in the ED in 11.8% of patients, representing established or rapidly evolving circulatory failure. The median time to ITU referral was 198 minutes despite early physiological warning signs frequently being present. Persistent elevation of DSI following initial resuscitation was associated with vasopressor use, ITU referral, and a physiological pattern consistent with the δ clinical phenotype characterised by refractory vasodilatory physiology.
Conclusion: Elevated DSI is frequently present at first medical contact and often persists despite early ED resuscitation in patients requiring ITU admission. DSI ≥ 1.5 should therefore be considered a failure-to-normalise marker rather than solely a screening threshold. Pre-hospital DSI identifies haemodynamic risk at first contact, while persistent ED DSI elevation may prompt earlier critical care discussion in patients with advanced infection. Persistent elevated DSI after resuscitation predicts vasopressor requirement and ICU referral, aligning with the δ clinical phenotype and supporting its use as a physiology-based tool to guide earlier escalation and more personalised haemodynamic management.
