PURPOSE: Sepsis is a leading cause of mortality in critically ill patients. Aggressive fluid resuscitation has been shown to improve outcomes in septic shock. Sepsis causes alterations in nonlinear hemodynamic parameters such as heart rate variability. We hypothesized that aggressive resuscitation would improve heart rate variability in a murine model of sepsis.
METHODS: Radio-transmitters were implanted into the aorta of C57/BL6 mice for continuous hemodynamic monitoring (n=32). After 72 hours of recovery, baseline heart rate recordings were captured for 24 hours. Sepsis was induced by cecal ligation and puncture and continuous recordings taken for the next 48 hours or death. All mice received antibiotics (ceftriaxone and clindamycin) every 6 hours. Septic mice received one of two resuscitation regimens: LOW 0.9% NaCl 35ml/kg bolus intra-operative only (n=16) or HIGH 0.9% NaCl 35ml/kg boluses every 6 hours after surgery (n=16). Heart rate volatility (HRV) measurements (% of 5 min standard deviations < cutoff, defined as lowest 5% during baseline) were compared between groups.
RESULTS: Baseline heart rate and HRV were similar between groups. During sepsis, mean heart rate was 353 beats per minute (bpm) in the HIGH group and 397 bpm in the LOW group. Aggressive fluid resuscitation was associated with improved HRV. Normal HRV was found during 33.3% of intervals in the HIGH group and only 22.6% of intervals in the LOW group (p<0.001). Aggressive fluid resuscitation trended towards improved survival. Five animals (31.25%) in the HIGH resuscitation group and 2 animals (12.5%) in the LOW group survived to 48 hours ( p= 0.39), with a mean length of survival of 42 hours in the HIGH group and 31 hours in the LOW group (p= 0.16). Improvement in HRV was seen over time in survivors from both groups.
CONCLUSIONS: Aggressive fluid resuscitation during the first 48 hours of sepsis improved heart rate variability in a murine model. This improvement correlated with survival.
CLINICAL IMPLICATIONS: Heart rate variability may be a useful marker to assess response to fluid resuscitation during sepsis.
DISCLOSURE: The following authors have nothing to disclose: Michael Kwiatt, Joe LaChant, Sergio Zanotti, Steven Hollenberg
No Product/Research Disclosure Information