The non-haemorrhagic vagal response to trauma: a review of hypotensive and bradycardic responses to injury in the absence of bleeding

Trauma has the potential to cause haemorrhage, tissue damage, pain, visceral manipulation and psychological distress. Each of these consequences of trauma can cause changes in autonomic outflow, which dictates a patient’s vital signs. Patients who are hypotensive and bradycardic due to a vagally mediated parasympathetic response to pain, psychological distress and visceral manipulation may be confused with those who exhibit bradycardia and hypotension following significant blood volume loss.

This review summarises literature that describes specific stimuli, patterns of injury and patient characteristics that are associated with a non-haemorrhagic vagal response to trauma.

Twenty-six records described predominantly parasympathetic responses to trauma (both blunt and penetrating) and surgery (“iatrogenic trauma”). Such a non-haemorrhagic vagal response occurs following a wide variety of injury patterns. Patient age and sex are poor predictors of the likelihood of a non-haemorrhagic vagal response. The development and resolution of a non-haemorrhagic vagal response occurs over a heterogenous time period. It is unclear whether speed of onset and resolution is linked to the pattern of injury or other factors causing a predominantly parasympathetic response following non-haemorrhagic trauma.

The pattern of injury, patient demographic and speed of onset / resolution associated with the non-haemorrhagic vagal response to trauma may is heterogenous. It is therefore challenging to clinically distinguish between the hypotensive bradycardia due to hypovolaemia secondary to haemorrhage, or a parasympathetic response to trauma in the absence of bleeding.