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. 2015 Aug 6;10(8):e0134387.
doi: 10.1371/journal.pone.0134387. eCollection 2015.

Heart Rate Variability Analysis in an Experimental Model of Hemorrhagic Shock and Resuscitation in Pigs

Edgard Salomão Jr  1 , Denise Aya Otsuki  1 , Andre Luis Correa  1 , Denise Tabacchi Fantoni  1 , Fernando dos Santos  2 , Maria Claudia Irigoyen  2 , Jose Otavio Costa Auler Jr  1
Affiliations

Heart Rate Variability Analysis in an Experimental Model of Hemorrhagic Shock and Resuscitation in Pigs

Edgard Salomão Jr et al. PLoS One. .

Abstract

Background: The analysis of heart rate variability (HRV) has been shown as a promising non-invasive technique for assessing the cardiac autonomic modulation in trauma. The aim of this study was to evaluate HRV during hemorrhagic shock and fluid resuscitation, comparing to traditional hemodynamic and metabolic parameters.

Methods: Twenty anesthetized and mechanically ventilated pigs were submitted to hemorrhagic shock (60% of estimated blood volume) and evaluated for 60 minutes without fluid replacement. Surviving animals were treated with Ringer solution and evaluated for an additional period of 180 minutes. HRV metrics (time and frequency domain) as well as hemodynamic and metabolic parameters were evaluated in survivors and non-survivors animals.

Results: Seven of the 20 animals died during hemorrhage and initial fluid resuscitation. All animals presented an increase in time-domain HRV measures during haemorrhage and fluid resuscitation restored baseline values. Although not significantly, normalized low-frequency and LF/HF ratio decreased during early stages of haemorrhage, recovering baseline values later during hemorrhagic shock, and increased after fluid resuscitation. Non-surviving animals presented significantly lower mean arterial pressure (43±7 vs 57±9 mmHg, P<0.05) and cardiac index (1.7±0.2 vs 2.6±0.5 L/min/m2, P<0.05), and higher levels of plasma lactate (7.2±2.4 vs 3.7±1.4 mmol/L, P<0.05), base excess (-6.8±3.3 vs -2.3±2.8 mmol/L, P<0.05) and potassium (5.3±0.6 vs 4.2±0.3 mmol/L, P<0.05) at 30 minutes after hemorrhagic shock compared with surviving animals.

Conclusions: The HRV increased early during hemorrhage but none of the evaluated HRV metrics was able to discriminate survivors from non-survivors during hemorrhagic shock. Moreover, metabolic and hemodynamic variables were more reliable to reflect hemorrhagic shock severity than HRV metrics.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Experimental protocol.
Baseline: before hemorrhage; Hemorrhage15: at the end of blood withdrawal; Shock30: 30 minutes after the end of blood withdrawal; Shock60: 60 minutes after the end of blood withdrawal; R0: at the end of fluid resuscitation; R60: 60 minutes after the end of resuscitation; R120: 120 minutes after the end of resuscitation; R180: 180 minutes after the end of resuscitation.
Fig 2
Fig 2. HRV time domain metrics in pigs submitted to acute hemorrhagic shock and fluid resuscitation.
S = survivor group. NS = non-survivor group; * = P<0.05 different from baseline; # = p<0.05 NS group different from the S group (t test).
Fig 3
Fig 3. Hemodynamic variables in pigs submitted to acute hemorrhagic shock and fluid resuscitation.
S = survivor group. NS = non-survivor group; * = P<0.05 different from baseline; # = p<0.05 NS group different from the S group (t test).
Fig 4
Fig 4. Metabolic variables in pigs submitted to acute hemorrhagic shock and fluid resuscitation.
S = survivor group. NS = non-survivor group; * = P<0.05 different from baseline; # = p<0.05 NS group different from the S group (t test).
See this image and copyright information in PMC

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