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Updated: Dec 9, 2025
Description of a Swine Infant Model of Volume-Controlled Hemorrhagic Shock
Published on: November 3, 2023
Does the pediatric hemodynamic cliff exist in response to hemorrhagic shock?
Kaeli J Yamashiro1, Laura A Galganski2, J Kevin Grayson3
1Department of Surgery, University of California-Davis, Sacramento, CA; Clinical Investigation Facility, David Grant USAF Medical Center, Travis Air Force Base, Fairfield, CA.
Insights
Pediatric swine showed differential vasoconstriction during hemorrhage, shunting blood to the thoracic aorta. Mean arterial pressure dropped significantly even at 20% blood loss, challenging existing shock paradigms.
Area of Science:
- Pediatric Physiology
- Hemorrhagic Shock Research
- Vascular Response Studies
Background:
- The widely accepted view is that children maintain normal blood pressure during hemorrhagic shock until 30%-45% blood loss.
- Limited data exist on the precise timing of decompensation and compensatory vascular mechanisms in pediatric hemorrhagic shock.
- This study investigates the arterial response to hemorrhage in pediatric swine to identify when mean arterial pressure (MAP) decreases.
Purpose of the Study:
- To examine the arterial response to graded hemorrhage in pediatric swine.
- To determine the point at which mean arterial pressure (MAP) decreases from baseline during hemorrhagic shock.
- To elucidate the compensatory vascular mechanisms, specifically differential vasoconstriction, in response to hemorrhage.
Main Methods:
- Pediatric swine underwent hemorrhage in 20% increments up to 60% of their total blood volume.
- Mean arterial pressure (MAP) was monitored throughout the hemorrhage protocol.
- Angiograms of the thoracic aorta and abdominal arteries were acquired to calculate the percent change in vessel area.
Main Results:
- Differential vasoconstriction was observed starting at 20% hemorrhage, with greater constriction in abdominal arteries (e.g., celiac artery) compared to the thoracic aorta.
- At 40% hemorrhage, blood flow was shunted away from abdominal visceral branches towards the thoracic aorta.
- Mean arterial pressure (MAP) decreased significantly from baseline at 20% hemorrhage and continued to decline at 40% and 60% hemorrhage.
Conclusions:
- Hemorrhage in piglets triggers a proximal blood shunting mechanism via differential vasoconstriction.
- This compensatory response is insufficient to maintain normal mean arterial pressure (MAP) even at early stages (20%) of hemorrhage.
- The findings challenge the traditional understanding of pediatric compensatory responses to hemorrhagic shock.
Background:
The paradigm that children maintain normal blood pressure during hemorrhagic shock until 30%-45% hemorrhage is widely accepted. There are minimal data supporting when decompensation occurs and how a child's vasculature compensates up to that point. We aimed to observe the arterial response to hemorrhage and when mean arterial pressure (MAP) decreased from baseline in pediatric swine.
Methods:
Piglets were hemorrhaged in 20% increments of their total blood volume to 60%. MAP and angiograms of the thoracic aorta (TA) and abdominal arteries were obtained. Percent change in area of the vessels from baseline was calculated.
Results:
Piglets (n = 8) had a differential vasoconstriction starting at 20% hemorrhage (celiac artery 36.3% [31.4-44.6] vs TA 16.7% [10.7-19.1] p = 0.0012). At 40% hemorrhage, the differential vasoconstriction favored shunting blood away from the abdominal visceral branches to the TA (celiac artery 54.7% [36.9-60.6] vs TA 29.5% [23.9-36.2] p = 0.0056 superior mesenteric artery 46.7% [43.9-68.6] vs TA 29.5% [23.9-36.2] p = 0.0100). This was exacerbated at 60% hemorrhage. MAP decreased from baseline at 20% hemorrhage (66.4 ± 6.0 mmHg vs 41.4 ± 10.4 mmHg, p < 0.0001), and worsened at 40% and 60% hemorrhage.
Conclusion:
In piglets, a differential vasocontriction shunting blood proximally occurred in response to hemorrhage. This did not maintain normal MAP at 20%, 40% or 60% hemorrhage.
Level Of Evidence:
Level II.
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