Anatomy based problem

[equium]

Hey guys

I have a case study to go through and to cut a long story short, I need to find out why a paraplegic laying down, with their head up at an angle of 70 degree to the horizontal, is unable to regulate their Bp effectively after an accident. It does not mention in the case if the patient is bleeding/losing any fluids.

The patient's spinal cord was transected at the T2/T3 level, several years BEFORE this accident. 5 minutes after the accident, the patient's blood pressure was 80/55 and heart rate was 120bpm. By the time the emergency services had arrived, his Bp reached 60/40 and he had therefore become unconscious.

I'm getting myself confused because I cant figure out what the underlying issue is here. Below are my thoughts:

1. His heart rate had increased to 120bpm so sympathetic innervation to the SAN may not have been effected by the spinal transection. But on the other hand, the heart rate may have increased because of noradrenaline release by the adrenal glands. But that still requires adequate sympathetic stimulation via T12.
2. The natural frequency of SAN firing is 100bpm but a 'normal' resting Hr is approx 70bpm, reflecting parasympathetic influence. So is this increase in Hr caused by increased sympathetic stimulation (despite the spinal transection) or decreased stimulation by parasymp fibres or both?
3. For the Bp to fall so low (assuming no loss of circulating volume from bleeding for e.g.) there must be a problem with peripheral vasoconstriction. But why would having a transection at T2-T3 cause problems with vasoconstriction all over the body?
4. As the paraplegic patient is usually in a wheel chair but is now lying down with a head up at 70 degrees to the horizontal, how is that relevant to his Bp? Postural hypotension came to mind but surely that occurs when going from lying/sitting to standing, rather than sitting in a wheelchair to laying down...

Any help you can give me would be great, I'm so confused!

[equium]

Just to clarify, it isn't that he is laying down flat (at zero degrees) with his head tilted forward at 70 degrees, it is that his whole body is almost at 90 degrees to the horizontal i.e. almost standing up. Which is why I thought orthostatic hypotension may have something to do with it.

Another thing I thought of is that if the spinal cord is transected at t2-t3, somatic innervation of his legs is obviously not functional, meaning the skeletal muscle pump that counteracts venous pooling will also not function. This explains the low arterial blood pressure and increase heart rate because of a decreased pre-load.

Any other ideas would be awesome.