It’s a busy Friday night in resus. The red phone goes…’24 year-old male, stabbing to right groin, Blood pressure is 82/47, heart rate 52, resp rate 22, GCS 14, ETA 5 mins’. What goes through your head? Penetrating injury, and hypotensive – maybe activate the MHP? Resps are up, so maybe a missed pneumothorax? But why are they bradycardic? Bleeding patients become tachycardic right?!
Bradycardia in the trauma patient can be a perilous sign. One might observe a typical course of events in which a bleeding trauma patient progresses through the compensatory mechanisms in response to shock. It is a scary privilege to witness physiology in action. The initial response to bleeding is to increase heart rate to maintain cardiac output. This is mediated through baroreceptors in the aorta and carotid which detect a reduction in blood pressure. These receptors then fire off signals to the rostral ventrolateral medulla which increases sympathetic tone and decrease vagal tone – resulting increased inotropy and chronotropy. Vasoconstriction may occur in the peripheries to recruit volume from the capacitance vessels. Cold peripheries ensue, and it becomes increasingly difficult to find peripheral vessels for cannulation. The speed of this response is relative to the speed of bleeding. This, however, is not sustainable with ongoing haemorrhage, and eventually blood pressure will drop. If we are able to intervene then we can hope to reverse this process aka resuscitation. If we are unable to intervene we may witness the development of bradycardia. This seems counter-intuitive.
Cue the Bezold-Jarisch reflex. This is a fascinating reflex and may account for this strange phenomenon of bradycardia in the bleeding patient. Albert von Bezold originally observed what would become the eponymous reflex, and these observations were confirmed some years later by Adolf Jarisch Jnr.; Adolf Jarisch Snr. also found fame with the Jarisch-Herxheimer reaction, which those of us who treat syphilis may be familiar with. Bezold found that the injection of Veratrum alkaloids (a proposed treatment for hypertension) resulted in a triad of bradycardia, hypotension and vasodilatation. This is a cardioinhibitory reflex. Everyone ignored this for some time, until Jarisch restudied this effect 60 years later. Jarisch and co. found that this triad was mediated through myelinated (A) fibres and unmyelinated (C) fibres. The latter are more interest to this particular topic. The C-fibres have endings in the walls of the ventricles and the coronary vasculature. As haemorrhage continues the volume of blood entering the ventricle diminishes. This is detected by the C-fibres and this triggers activation of the cardioinhibitory response (the Bezold-Jarisch reflex) and causes inhibition of sympathetic tone, hence the triad of signs. The response has also been thought to be activated by increasing circulating levels of renin in response to hypovolaemia. Interestingly a similar effect is sometimes observed in patients with cardiac tamponade. This is because the C-fibres respond to both under- and over-stretch and produce the same effects. The reflex has also been proposed as contributing to:
-Post myocardial infarction bradycardia
-Hypotension during coronary reperfusion
-Exertional syncope in aortic stenosis
If you indulge in a little bit of teleology it can be fun to try and figure out why this occurs. One can imagine that this is a last ditch attempt of the body to get some blood to the myocardium. The poor heart has been giving its best, pounding away as hard as it can. At rest the heart has an oxygen extraction ratio (DO2:VO2) of around 80%, so when has to deal with bleeding it begins to struggle very quickly. This may be partly, but not exclusively (inflammation), why we see raised troponin in trauma patients (Type II MI?). As bleeding continues and volume drops, perhaps the reflex is a last ditch attempt to reduce VO2 (bradycardia) and restore perfusion (bradycardia and vasodilation of the coronary vessels). Perhaps it’s the cardiac equivalent of the Cushing reflex that we see in significant head injury.
So…if you see bradycardia in your trauma patient, please please please firstly assume that the patient is very very very sick. Once you have excluded that they are very very very sick then great, but do not be reassured by bradycardia in this context. In my experience bradycardia is more likely to be seen in penetrating injury with significant blood loss rather than blunt trauma with significant tissue injury – although the latter group may have cardiac issues from the inflammatory response. Either way, discount bradycardia at your peril and do not falsely reassure yourself with a trauma patient who does not have the ‘tachycardia you would expect’. An absence of tachycardia does not mean an absence of blood loss.
Finally, it’s always worth reflecting on how difficult it can be to assess blood loss in trauma patients. Bradycardia in the presence of other signs or symptoms should form a part of this. Let’s finish with a reminder of the ‘Hateful 8’ for exsanguinating haemorrhage.
Bezold Jarisch reflex on wikipedia https://en.wikipedia.org/wiki/Bezold%E2%80%93Jarisch_reflex
Bezold Jarisch reflex on LITFL https://litfl.com/bezold-jarisch-reflex/