Volume 11 Supplement 3

Fourth International Symposium on Intensive Care and Emergency Medicine for Latin America

Open Access

Septic lipidic dysregulation is related to heart rate variability alteration

  • AC Nogueira1,
  • V Kawabata1,
  • P Biselli1,
  • J Barradas1,
  • M Lins1,
  • C Valeri1,
  • M Seckler1,
  • W Hoshino1,
  • L GonzagaJr1,
  • MMS Bernik1,
  • PA Lotufo1,
  • E Martins1,
  • R Curi1 and
  • FG Soriano1
Critical Care200711(Suppl 3):P18

https://doi.org/10.1186/cc5805

Published: 19 June 2007

Context

Although observational studies have demonstrated an alteration of heart rate variability (HRV) in septic patients, no single study has systematically addressed the relationship of heart damage by systemic inflammation and metabolic alterations.

Objective

To determine whether heart damage from sepsis is caused by free fatty acids (FFA) and may be detected with HRV analysis.

Design

A prospective and observational study of patients presenting with severe sepsis or septic shock.

Setting

A university hospital ICU for clinical and surgical patients.

Participants

Thirty-one patients were included with sepsis. Exclusion criteria were previous myocardial dysfunction, coronary artery disease and cancer. The data were collected and analyzed a posteriori, in two groups: survivors and nonsurvivors.

Main outcome measures

Association between troponin I elevation, FFA elevation and HRV reduction. Association between clinical evolution and HRV index, troponin, and hemodynamic parameters.

Results

The study population included 31 individuals, of whom 19 died during the follow-up of 6 days. The initial measurements of C-reactive protein and gravity APACHE score were similar in the two groups. Overall, an increase in the plasma troponin level was related to an increased mortality risk. From the first day the nonsurvivor group presented a reduced left ventricular stroke work systolic index (LVSWI), and a reduced low frequency (LF) index. The correlation coefficient for LF values and troponin was r 2 = 0.75. Patients showed FFA elevation; survivors presented 0.62 ± 0.08 mmol/l and nonsurvivors 1.05 ± 0.12 mmol/l.

Conclusion

Understanding damage to the heart from sepsis requires specific analysis of biochemical markers such as troponin I, and of hemodynamic parameters such as the LVSWI or the HRV index. Our results suggest that damage to the heart by systemic inflammation is the cause of an aberrant beat-to-beat response. FFA produce cell death (apoptosis and necrosis) through oxidative stress and induced LF alterations. FFA inducing LF alterations has been shown in the literature for healthy and diabetic patients; this is the first time it has been shown in septic patients.

Authors’ Affiliations

(1)
Emergencias Clinicas FMUSP, Hospital Universitario USP

Copyright

© BioMed Central Ltd 2007

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