Abstract 2060: A Novel Hemorrhagic Shock Model To Study Compensatory Mechanisms and Circulatory Collapse
Background: When immediate resuscitation from hemorrhagic shock (HS) is not possible, neuro-humoral homeostatic mechanisms alone account for the initial adaptive response. Traditional animal models of HS based on fixed bleeding fail to ensure circulatory collapse (CC) in most subjects and do not adjust for inter-subject compensatory variability. We describe a pressure-controlled porcine model of severe HS that reliably provokes compensatory response exhaustion, allowing for the study of the mechanisms of CC.
Methods: 34 isofluorane-anesthetized female pigs (median wt 29 kg) were bled to a mean arterial pressure (MAP) of 30 mmHg with repeat bleeds if MAP increased to 40 mmHg. CC was defined as a decrease in MAP <30 mmHg for 10 min or < 20 mmHg for 10s. Asanguineous resuscitation with Hextend was started when CC occurred. Animals sustaining MAP between 30 – 40 mmHg for 90 minutes were also resuscitated. Survival was defined as lack of CC without further intervention 2h after resuscitation. Time to CC and time in shock (min), volume bled (ml), base deficit (BD) and lactate (Lac) level (mmol/dl) were measured. Median values and interquartile ranges used to present the data.
Results: 79% of the animals reached CC and 35.3% of these did not survive. The number of bleeding episodes needed to maintain shock varied from 1 to 7. The total volume bled (ml/%) was 831 ml/43.8% (644 –1023ml / 33–55%). The total duration of shock was 93 (72–124) min, time to CC after last bleeding 40.2 (18 – 87) min. BD and Lac were 3.5 (1.8 –5.7) mmol/dl and 1.2 (1.0 –1.6) mmol/dl at baseline and −3.2 (−5.2– 0.2) mmol/dl and 4.6 (3.5– 6.8) mmol/dl at decompensation, respectively.
Conclusion: Titrating the degree of bleeding to the animal’s individual physiologic response to shock rather than arbitrary fixed hypovolemic insults provides a robust model of CC in HS and illustrates the variability of compensatory responses. The majority of animals demonstrated CC with a high mortality rate, suggesting that this experimental paradigm can lead to exhaustion of compensatory mechanisms despite varying levels of intra-subject responsiveness.