Neurogenic shock is a potentially life-threatening condition and must be managed as such. Without a clear understanding of this condition inappropriate management of a trauma patient, who often suffers concomitant hemodynamic instability, could be fatal. Neurogenic shock is defined as disruption of the sympathetic nervous system with preserved parasympathetic activity. This typically occurs with patients suffering a severe SCI at the level of T6 or higher. Disruption of the sympathetic division of the autonomic nervous system affects three areas of the cardiovascular system: coronary blood flow, cardiac contractility, and heart rate. With preserved parasympathetic activity this translates clinically into bradycardia (and possibly other cardiac arrhythmias) in the setting of profound hypotension. A prudent clinician must look for these characteristics in combination, as many trauma patients are hypotensive as a result of blood loss or intravascular hypovolemia but will mount an appropriate tachycardic response.

The treatment of neurogenic shock is therefore quite difficult. Although it is theoretically possible to distinguish between hypovolemic and neurogenic shock, clinically this distinction is not so clear. In fact, acute trauma patients sustaining a high cervical SCI may suffer from both conditions. It has therefore been recommended by the Consortium for Spinal Cord Medicine to rule out other causes of shock before assuming a diagnosis of neurogenic shock. The practical treatment of these patients rests on initially restoring intravascular volume and if symptoms of neurogenic shock persist, vasopressors (such as dopamine) should be used. The goal of treatment in the first week after sustaining an SCI is to maintain a mean arterial blood pressure of 85 mm Hg.

Neurogenic shock usually refers to loss of integrated sympathetic nervous system control over the cardiovascular system. Without sympathetic innervation, the parasympathetic innervation of the heart (vagus nerve) is left without antagonism. This results in bradycardia and diminished contractility. When the sympathetic innervation of the vascular system is lost, the capacitance increases dramatically (decreased systemic vascular resistance) and relative hypovolemia is present. This loss of sympathetic tone is the most dramatic representation of the complex integrity of vascular control. Neurogenic shock occurs from trauma to the cervical spinal cord, neural conduction blockade of the spinal and sympathetic outflow (spinal and epidural anesthesia), and catastrophic head injury. Although closed head trauma does not directly result in hypotension, premortal injury with loss of sympathetic centers in the hypothalamus and brainstem results in a pattern of neurogenic shock. In situations where myocardial function is unimpaired, administration of alpha-1 agonists like phenylephrine or norepinephrine recovers vascular tone, reduces the vascular capacitance, and improves the relative hypovolemia induced by the loss of vascular tone. Fluid administration improves the relative hypovolemia without affecting the vascular tone and is also effective in neurogenic shock.

Neurologic injury during cardiac surgery most likely involves the vagus and phrenic nerves and does not encompass loss of sympathetic outflow. These nerves can be injured by stretch, cold injury from ice solution, or transection. Also, despite intact neural activity, the heart and vasculature may respond poorly if hypothermia is present or if metabolic derangements persist (hyponatremia, hypocalcemia, hypomagnesemia, hypoglycemia, acidosis). After CPB, diffuse catastrophic neurologic injury may be heralded by hyperpyrexia, seizures, and excessive sympathetic activity, only to be followed by loss of central sympathetic tone. This portends a grim prognosis.

Another unique denervation situation is present after cardiac transplantation: The heart is denervated of both sympathetic and parasympathetic systems. The autonomous pacemakers of the donor's heart will be the new natural heart rate, and contractility will also be unresponsive to nervous system activity. Nevertheless the heart will respond to endogenous circulating catecholamines and exogenous pharmacologic stimulants, of which isoproterenol is the most commonly used.