Abstract
Purpose
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.
Methods
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.
Results
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.
Conclusion
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.
Key Points
- Non-Haemorrhagic Vagal Response (NHVRT): Hypotensive bradycardia occurs due to parasympathetic activation from pain, visceral manipulation, or psychological distress, mimicking haemorrhagic shock.
- Triggers: Common stimuli include peripheral injuries, surgical manipulations, and emotional stress, mediated via vagal pathways.
- Distinction Challenges: Differentiating NHVRT from haemorrhagic shock remains difficult due to overlapping symptoms like low heart rate and blood pressure.
- Patterns of Injury: Injuries to autonomic-rich areas (e.g., celiac plexus, gall bladder) frequently elicit vagal responses.
- Patient Characteristics: Age, sex, and preexisting cardiovascular conditions show variable influence on NHVRT susceptibility.
- Onset and Duration: Timeframes for NHVRT development and resolution range widely, from seconds to over an hour, influenced by injury type and severity.
- Autonomic Integration: Vagal responses result from complex interactions between somatic and visceral inputs, modulated by the brainstem, amygdala, and periaqueductal gray.
- Clinical Implications: Misinterpretation of NHVRT as haemorrhagic shock can lead to unnecessary interventions, such as transfusions or thoracotomy.
- Diagnostic Gaps: Current diagnostic tools inadequately differentiate NHVRT from true hypovolaemia; research on biomarkers or advanced monitoring is needed.
- Educational Focus: Enhanced clinician awareness of NHVRT and its presentation can reduce diagnostic errors and improve patient outcomes.
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