The definition of shock considers a drop in the systolic arterial pressure (SAP) and/or a drop in the mean arterial pressure (MAP) associated with a low tissue perfusion state. However, this definition does not account for the diastolic arterial pressure (DAP). DAP adds valuable information to determine the mechanism of shock.
The four main classes of shock are cardiogenic, obstructive, hypovolemic, and distributive shock (of which septic shock is commonest and confers considerable mortality). In cardiogenic, obstructive and hypovolemic shock, there is a fall in the SAP associated with a drop in the pulse pressure (PP), but the DAP is sustained. In contrast, in septic shock the reduction in vascular tone causes a drop in the diastolic pressure resulting in a wide pulse pressure.
Detection of low diastolic arterial blood pressure, in the absence of aortic insufficiency, reflects systemic vasodilation and it influences the therapeutic interventions available for the patient. These include early administration of vasopressors and avoidance of unnecessary fluid therapy whilst maintaining adequate tissue perfusion. However, interpretation of diastolic blood pressure should not done without taking into consideration the normal compensatory mechanism of heart which triggers sympathetic response causing tachycardia. Similar to the shock index (HR:SAP) that reflects the severity of hemorrhagic shock, indexing the heart rate (HR) to the DAP, i.e. the Diastolic Shock Index (DSI = HR:DAP), could predict the severity of shock and the likelihood of an unfavorable outcome.
In a study of 761 patients with sepsis requiring vasopressor support (337 patients from one mixed-ICU in a university hospital in Colombia and 424 patients with septic shock from the ANDROMEDA-SHOCK trial), risk of death was compared to DSI. The study indicated a higher risk of death with increasing DSIs. It also showed that a higher risk of death is not clearly identified with either isolated low DAP or high heart rate. At similar HR or DAP values, the risk of death was increased only when DSI concomitantly increased. Therefore, DSI is a superior indicator of increased risk of death. The study suggests increasing circulatory dysfunction with progressive divergence in HR and DAP which leads to a proportional increase in the relative risk of death [1].
The authors of the study also looked at the preliminary cohort in the study and propensity matched 93 patients who had very-early start of vasopressors (within 1 hour of fluid resuscitation) with 93 delayed start vasopressor patients. Patients in the very-early start group had significantly less resuscitative fluid during the first 8 hours of resuscitation (1100 vs. 2600 mL, p < 0.001), with no significant increase in acute renal failure and/or renal replacement therapy requirements. Fluid balance at 8 and 24 hours was less in the very-early start group, and 28-day mortality was significantly lower in the very-early group compared to the delayed group (HR 0.31, CI95% 0.17–0.57, p < 0.001). Of note, the mortality benefit included patients who received vasopressors up to 6 hours [2].
A meta-analysis that included 5 studies with a total of 929 patients revealed that early initiation of norepinephrine in patients with septic shock was associated with decreased short-term mortality (hospital, 28- or 30-day mortality), faster achievement of target MAP, and less intravenous fluid volume administration [3].
Based on these studies, it seems appropriate to monitor DSI in septic patients due to its prognostic value and ability to guide early administration of vasopressors in patients with septic shock. In general, a DSI >2.2 is associated with worse outcome and has been advocated to evaluate for early start of vasopressors.
REFERENCES
1. Ospina-Tascón GA, et al. J. Diastolic shock index and clinical outcomes in patients with septic shock. Ann Intensive Care. 2020 Apr 16;10(1):41. doi: 10.1186/s13613-020-00658-8. PMID: 32296976; PMCID: PMC7160223.
2. Ospina-Tascón GA, Hernandez G, Alvarez I, et al. Effects of very early start of norepinephrine in patients with septic shock: a propensity score-based analysis. Crit Care. 2020;24(1):52. Published 2020 Feb 14. doi:10.1186/s13054a-020-2756-3
3. Li Y, Li H, Zhang D. Timing of norepinephrine initiation in patients with septic shock: a systematic review and meta-analysis. Crit Care. 2020 Aug 6;24(1):488. doi: 10.1186/s13054-020-03204-x. PMID: 32762765; PMCID: PMC7409707.
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