A patient whose spinal cord is crushed in a car accident. A crime victim who faints from fear and extreme emotional distress. An elderly man who loses consciousness after vomiting.
What do these people have in common? They’re all at high risk for neurogenic shock.
Neurogenic shock is one of three types of distributive shock—all of them marked by insufficient intravascular volume of blood. (The other two are anaphylactic shock and septic shock). In neurogenic shock, sympathetic nervous system (SNS) depression or loss leads to uneven blood flow distribution. Vasodilation then causes cardiac preload to decrease, which ultimately results in inadequate cellular oxygenation.
What causes neurogenic shock?
The rarest form of shock, neurogenic shock is caused by SNS disruption resulting from:
• physical injury to the central nervous system, especially high thoracic spinal injury (T6 level or higher) or damage to the brainstem’s vasomotor center
• emotional trauma, in which high levels of fear, anxiety, and stress cause sudden loss of autonomic nervous system (ANS) control, leading to massive vasodilation
• vagus nerve stimulation, which may override the ANS, causing parasympathetic tone to dominate and resulting in vasodilation.
Assessing patients for neurogenic shock
Signs and symptoms of neurogenic shock fall into two categories:
• cardioinhibitory effects, such as bradyarrhythmias (possibly including asystole)
• vasodepression, which causes peripheral vascular dilatation and an overall decrease in systemic vascular resistance, resulting in hypotension through volume redistribution.
On physical assessment, you may detect bradycardia; hypotension; poikilothermy, hypothermia, or both, causing a flushed appearance; warm, dry skin (from vasodilation); and flaccid paralysis below the spinal injury level.
Other findings may include:
• absence of jugular vein distention (from vasodilation and pooling of blood in the peripheral circulation)
• reduced central venous, right arterial, and pulmonary artery wedge pressures• blood pH shifting toward the acidic range, from tissue hypoperfusion or low cardiac output and buildup of byproducts of anaerobic cellular respiration
• altered mental status, if the patient’s cerebral perfusion pressure is altered
• hypoactive or absent bowel sounds (from shunting of blood away from nonessential abdominal organs to compensate for shock symptoms).
Managing neurogenic shock
Successful management of neurogenic shock hinges on early diagnosis and treatment of acute signs and symptoms to limit the effects of hypotension and bradycardia on the rate of secondary neurologic injury. The treatment goal is to restore adequate oxygenation to vital tissues and limit cellular damage.
Because autonomic function loss leads to changes in blood pressure, heart rate, respiratory rate, and body temperature, patients should be placed where they’ll receive close observation, as in an intermediate or intensive care unit. During the acute period, vital signs and fluid intake and output must be monitored at least hourly.
Orotracheal intubation and mechanical ventilatory support may be needed, as well as aggressive blood pressure support with cautious I.V. fluids and vasoactive drugs. A central venous catheter may be placed to aid resuscitation and hemodynamic monitoring.
If the patient is hypothermic and hemodynamically unstable, slow rewarming is indicated. (Rapid rewarming may worsen an unstable hemodynamic status.) Once body temperature reaches the normal range, make every effort to maintain it in a steady, normal state.
Indications for cardiac pacing
The American Heart Association (AHA) recommends early cardiac pacing as a possible primary intervention for patients with symptomatic bradycardia. The 2002 AHA/American College of Cardiology guidelines recommend pacemaker implantation for patients with neurogenic shock. Those who’ve suffered high spinal cord injuries may have only transient symptoms and thus require only temporary pacing. However, a permanent pacemaker may be required in patients with sustained symptoms who need frequent cardiac pacing support throughout the early treatment phase; typically, it’s implanted 2 to 3 weeks after injury, if symptoms persist.
Sympathomimetic and vasopressor therapy
When bradyarrhythmias accompany hypotensive symptoms, the patient needs sympathomimetic drugs to boost sympathetic vasculature tone. Sympathomimetic drug therapy may be used alone or as an adjunct to cardiac pacing.
In hypotensive or normotensive patients, mean arterial pressure (MAP) of 85 to 90 mm Hg should be maintained to help perfuse the edematous periphery of the injured area and thus limit the amount of secondary neurologic injury. This is done through aggressive hydration and vasopressor infusions.
Data support the use of vasopressin rather than more traditional vasopressors, such as norepinephrine. Vasopressin has a less limiting effect on reactive hyperemia in organs after onset of shock symptoms, which allows essential organs to receive the oxygen they need and permits oxidation of waste products of anaerobic cellular respiration.
Besides performing frequent physical assessments, other key nursing interventions include:
• managing the patient’s airway
• monitoring urine output
• assessing for bladder distention
• implementing coughing and deep-breathing exercises
• providing skin care
• performing passive range-of-motion exercises
• implementing deep-vein thrombosis prophylaxis
• monitoring the patient’s GI status. As appropriate, start nutrition early and consider a daily bowel regimen as soon as this can be done safely.
Be sure to provide psychosocial support and education to the patient and family.
Arm yourself with knowledge
Make sure you’re familiar with the neurologic causes of hypotension and bradycardia so you’ll be prepared to care for patients with acute neurologic injuries. Be vigilant and anticipate cardiovascular complications that could threaten recovery of function after a neurologic injury.
Fortunately, the period of neurogenic shock usually is limited. If the healthcare team is alert and attentive to the patient’s needs, the prognosis for recovery is good.
Crawford MH, et al. Cardiology: The Neurogenic Heart. 2nd ed. Philadelphia: Elsevier; 2004.
Gregoratos G, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). J Cardiovasc Electrophysiol. 2002;13(11):1183-1199.
Hubert R. Strategies of medical intervention in the management of acute spinal cord injury. Spine. 2006;31(11S):S16-S21.
For a complete list of selected references, visit www.AmericanNurse Today.com.
Kenneth J. King, BSN, RN, and DaiWai M. Olson, RN, PhDc, CCRN, are staff nurses in the Neuroscience Critical Care Unit at Duke University Medical Center in Durham, N.C. Mr. Olson is also a PhD candidate at the University of North Carolina-Chapel Hill School of Nursing.