Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: can irreversibility be anticipated?

Abstract

Background: The causes of cardiovascular collapse (CC) during hemorrhagic shock (HS) are unknown. We hypothesized that vascular tone loss characterizes CC, and that arterial pulse pressure/stroke volume index ratio or vascular tone index (VTI) would identify CC.

Methods: Fourteen Yorkshire-Durock pigs were bled to 30 mmHg mean arterial pressure and held there by repetitive bleeding until rendered unable to compensate (CC) or for 90 min (NoCC). They were then resuscitated in equal parts to shed volume and observed for 2 h. CC was defined as a MAP < 30 mmHg for 10 min or <20 mmHg for 10 s. Study variables were recorded at baseline (B0), 30, 60, 90 min after bleeding and at resuscitation (R0), 30, and 60 min afterward.

Results: Swine were bled to 32% ± 9% of total blood volume. Epinephrine (Epi) and VTI were low and did not change in NoCC after bleeding compared with CC swine, in which both increased (0.97 ± 0.22 to 2.57 ± 1.42 mcg/dL, and 173 ± 181 to 939 ± 474 mmHg/mL, respectively), despite no differences in bled volume. Lactate increase rate (LIR) increased with hemorrhage and was higher at R0 for CC, but did not vary in NoCC. VTI identified CC from NoCC and survivors from non-survivors before CC. A large increase in LIR was coincident with VTI decrement before CC occurred.

Conclusions: Vasodilatation immediately prior to CC in severe HS occurs at the same time as an increase in LIR, suggesting loss of tone as the mechanism causing CC, and energy failure as its probable cause.

Figure 1

Schematic representation of the hemorrhagic shock protocol (above). Mean arterial pressure (MAP), Total peripheral resistance (TPR) and Cardiac Output (CO) trends during the experiment for CC and NoCC animals.

Figure 2

Figure 2A. Graph representing the pressure/flow relationships using MAP/Stroke volume index (Figure 2A), and using Pulse Pressure/Stroke volume index (Figure 2B) in a CC animal during the stabilization period (yellow diamonds), hemorrhage (red circles), CC (black squares) and resuscitation (blue triangles).

Figure 2

Figure 2A. Graph representing the pressure/flow relationships using MAP/Stroke volume index (Figure 2A), and using Pulse Pressure/Stroke volume index (Figure 2B) in a CC animal during the stabilization period (yellow diamonds), hemorrhage (red circles), CC (black squares) and resuscitation (blue triangles).

Figure 3

Graph representing the relationships between VTI, Epi, MAP and TPR throughout the experiment in CC and NoCC animals.

Figure 4

Bar chart showing vasomotor tone measured by VTI in S and NS.

Figure 5

Graph representing lactate increase rate in the entire cohort (ALL), as well as in CC and NoCC groups. * = p value between CC and NoCC, p < 0.034; ^‡ = p value of LIR between all time points in the CC group, p = 0.051; ^£ = p value between time points B60-B90 and B90-R0, p = 0.046.

Figure 6

Figure 6A. Graph showing pH trend during the experiment in CC and NoCC animals. Figure 6B. Graph showing base excess (BE) trend during the experiment in CC and NoCC animals.

Figure 6

Figure 6A. Graph showing pH trend during the experiment in CC and NoCC animals. Figure 6B. Graph showing base excess (BE) trend during the experiment in CC and NoCC animals.