Neurogenic Shock


Hi all,

I'm currently in the process of writing a paper for my advanced pharmacology class. I have to explain the pathophysiology of a patient from a case study who has sustained a spinal cord injury and is going into neurogenic shock.

The patient has sustained a compression fracture at C5. He has decreased chest expansion, diminished breath sounds at the bases, increased abdominal exclusion with breathing, and a respiration rate of 28 and shallow.

I'm having a problem explaining why he is expericing mild tachypnea. I know that neurogenic shock stops the SNS from working - leading to vasodilation and bradycardia, but isn't the SNS also responsible for increasing respirations?

If the SNS increases RR but is impaired, shouldn't this patient be hypo ventilating?

I've been looking at journal articles and websites and they're all saying that patient with neurogenic shock would have tachypnea but they don't explain 'why'.

Can anyone help me out to explain the why?


Has 2 years experience.

Hi ill give my thoughts on the situation There is a saying that goes "C5 keeps the diaphragm alive", so if he has damaged his phrenic nerve at C5 he would have had his respiratory drive shut off. Apparently that has not happened...yet but if he has massive vasodilation and is hypoperfusive he will become hypercapnic due low BP and an inability to push waste (CO2) out of the tissues. This will lead to acidosis and there is a center in the midbrain/medual that responds to increased CO2 by increasing respirations to blow off the acid.

Someone please correct me if im wrong!

Best of luck

C3-5 controls diaphragm muscles. When the lungs are having difficulty receiving air (in this case, due to lack of strength of diaphragm) the body will need to compensate to receive more oxygen- therefore, his body will make him breath faster (Respiration of 28) to get that oxygen his body needs.

In other words, the guy above me is correct :)