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Medical-Surgical Nursing

23.4 Neurogenic Shock

Medical-Surgical Nursing23.4 Neurogenic Shock

Learning Objectives

By the end of this section, you will be able to:

  • Discuss the pathophysiology, risk factors, and clinical manifestations for neurogenic shock
  • Describe the diagnostics and laboratory values for neurogenic shock
  • Apply nursing concepts and plan associated nursing care for patients with neurogenic shock
  • Evaluate the efficacy of nursing care for patients with neurogenic shock
  • Describe the medical therapies that apply to the care of patients with neurogenic shock

The distributive type of shock that results in hypotension (low blood pressure), often with bradycardia (slowed heart rate), caused by disruption of autonomic nervous system pathways is called neurogenic shock. It most commonly occurs in patients who sustain a spinal cord injury (SCI) to the cervical vertebrae or the thoracic vertebrae above T7. It is found in 19.3 percent of patients with cervical spinal cord injury and 7 percent of patients who have thoracic spinal cord injury (Sager et al., 2023) (Figure 23.9). Other causes of neurogenic shock include complications from spinal anesthesia, severe head trauma, and the use of opioids and benzodiazepines.

Diagram of spine, labels showing cervical, thoracic, lumbar, sacrum and coccyx
Figure 23.9 Injury to thoracic 7 vertebrae or above impacts the abdominal and intercostal muscles, which are essential for the expansion of the chest in the breathing process. (credit: modification of work from Anatomy and Physiology 2e. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Pathophysiology of Neurogenic Shock

To survive and thrive, cells and body tissues need a constant supply of oxygen and nutrients. In a state of homeostasis, the sympathetic nervous system ensures the cardiovascular system functions with adequate heart rate, cardiac output, and vascular tone to provide oxygen and nutrition to cells and body tissues. In neurogenic shock, the sympathetic nervous system loses the ability to regulate the cardiovascular system, causing vasodilation and decreased perfusion to cells and, eventually, cellular and tissue hypoxia. Blood pressure is low because of vasodilation, not because of loss of circulating volume in the vascular system.

Neurogenic shock is a hemodynamic syndrome. When sympathetic nerve innervation is functioning properly, a drop in blood pressure is compensated for by an increase in heart rate. In this type of shock, however, sympathetic nerve innervation is lacking, and the body is not able to increase heart rate to compensate for low blood pressure caused by the dilation of vessels. Low blood pressure and low heart rate are hallmark findings in this type of shock. Additionally:

  • Hypotension results from the loss of sympathetic vasomotor tone to the arteries and veins.
  • Lack of sympathetic innervation to the heart results in unopposed stimulation of the vagus nerve (the main nerve of the parasympathetic nervous system), leading to bradycardia.
  • Warm skin occurs initially but changes to become cool and clammy because of massive vasodilation.

Understand that spinal shock differs significantly from neurogenic shock. It is a transient neurologic syndrome of sensorimotor dysfunction, which can occur with injury to any part of the spinal cord. The patient experiences flaccidity and loss of reflexes in the area affected by the damage to the spinal cord. Table 23.10 contrasts these conditions.

Neurogenic Shock Spinal Shock
Hemodynamic phenomena
Loss of sympathetic stimulation
Low blood pressure
Low heart rate
Flaccid muscles
Loss of reflexes
Function may return
Table 23.10 Spinal Shock vs. Neurogenic Shock

It is important to realize the cause of hypotension in patients with this type of shock is lack of vascular tone, not vascular volume. Vasomotor tone plays a major role in the maintenance of blood pressure. In neurogenic shock, significant hypotension is present—usually below 70 mmHg—because the blood vessels lack vasomotor tone, limiting their ability to expand and constrict in response to perfusion changes, therefore causing hypoperfusion to the cells and organs. The hypotension of neurogenic shock is unresponsive to fluid resuscitation because sufficient volume is present already. Treatment of hypotension is therefore focused on increasing vasomotor tone and cardiac output.

Bradycardia is present in neurogenic shock because of unopposed vagus nerve stimulation (Figure 23.10). Decreased cardiac output also occurs. Treatment of bradycardia focuses on augmenting cardiac output and cardiac rate. Most patients require treatment with vasopressors and inotropes.

Diagram showing loss of sympathetic tone in neurogenic shock leading to parasympathetic response; labels show hypothalamus, medulla, spinal cord, paravertebral ganglia, parasympathetic (vagus), heart, prevertebral ganglia, blood vessels, preganglionic sympathetic fibers, postganglionic sympathetic efferents
Figure 23.10 The image depicts the pathways of the parasympathetic nerves during neurogenic shock. Loss of sympathetic tone in neurogenic shock leads to unopposed parasympathetic response driven by the vagus nerve causing unstable blood pressure, heart rate, and temperature regulation. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Temperature regulation is altered during neurogenic shock. When sympathetic nerve stimulation is intact, the patient can maintain normal temperature by triggering their body to shiver or sweat to maintain optimal body temperature. Disruption of sympathetic stimulation results in the patient not being able to maintain normothermia. Patients in neurogenic shock may experience poikilothermia, also known as intrinsic thermoregulatory failure. The patient may go between experiences of hypothermia and hyperthermia because the body loses its ability to regulate dermal blood vessel contraction; dilation for temperature regulation is also lost due to a lack of sympathetic nerve intervention.

The massive vasodilation and decreased tissue perfusion caused by neurogenic shock affect all body systems, including the neurologic, renal, and gastrointestinal systems. Respiratory failure is also common in patients.

Clinical Manifestations

It is imperative for the nurse to assess the patient for the presence of the hallmark findings of neurogenic shock to enable the health-care team to make a rapid diagnosis and start an effective treatment. These hallmark findings include:

  • low blood pressure
    • systolic less than 90 mmHg
    • diastolic less than 60 mmHg
  • bradycardia
  • heart rate less than 60 beats per minute
  • warm skin

Other clinical manifestations of lack of vasomotor tone include absent jugular vein distention, reduced central venous pressure, altered mental status, and hypoactive bowel sounds.

Risk factors for the development of neurogenic shock include sports injuries, gunshot wounds to the spine, medications that affect the autonomic nervous system, and improper administration of anesthesia to the spinal cord.

Assessment and Diagnostics

Most patients who have neurogenic shock also have a spinal cord injury above the thoracic seven vertebrae. This creates a risk of impaired airway maintenance. The nurse should first assess that the patient has an effective airway and the ability to breathe.

The diagnosis of neurogenic shock is often a diagnosis of exclusion. When blood pressure and heart rate are low and fluids do not effectively raise blood pressure, neurogenic shock is suspected. The patient should undergo radiologic studies, including MRI, CT scan, and x-ray to assess for evidence of spinal cord injury. Routine blood work should be obtained to assess the baseline status of the patient.

Diagnostics and Laboratory Values

Patients with neurogenic shock have a variety of characteristic laboratory values, including low levels of red blood cells (RBC), hemoglobin (HGB), and hematocrit (HCT) because of the dilutional effects of volume resuscitation. Table 23.11 summarizes these findings.

Laboratory Test Laboratory Finding Cause
Red blood cells (RBC) Low Fluid resuscitation
Hemoglobin (HGB) Low Fluid resuscitation
Hematocrit (HCT) Low Fluid resuscitation
Blood urea nitrogen (BUN) High Decreased renal perfusion
Creatinine (Cr) High Decreased renal perfusion
Sodium (Na) Vary Volume resuscitation
Potassium (K) High Cell destruction
Arterial blood gas (ABG) Abnormal findings PH > 7.450 = early respiratory alkalosis
PH < 7.350 = early metabolic acidosis
Lactic acid Elevate Cell death due to anaerobic metabolism
Liver markers Elevate Hypoperfusion to liver
Table 23.11 Laboratory Values Characteristic of Neurogenic Shock

Nursing Care of the Patient with Neurogenic Shock

It is important for the nurse to identify patients at risk for the development of neurogenic shock and to act in an efficient and immediate manner. Focused assessments and timely communication with the health-care team can prevent or limit long-term or fatal complications from neurogenic shock.

Prevention of neurogenic shock is the best treatment, so education plays a pivotal role in reducing risk. Because spinal cord injury is the most common cause of neurogenic shock, health-care professionals should teach the public about how to prevent spinal cord injuries: for example, by avoiding potentially dangerous activities such as diving headfirst into a swimming pool and “heading” the ball in games such as soccer. The public should also be educated on the appropriate use of protective equipment such as seat belts and helmets.

Recognizing Cues and Analyzing Cues

The nurse can recognize cues of neurogenic shock by assessing vital signs and noting trends. Cues include low blood pressure, bradyarrhythmia, and peripheral vasodilation such as flushed warm skin that later becomes cold and clammy, and blue lips and fingertips. At-risk patients require frequent and accurate assessments to detect the onset of shock promptly and ensure treatments are most effective (Iovine et al., 2022).

  • Any patient exhibiting low blood pressure and low heart rate should be suspected of having neurogenic shock.
  • The level of the spinal cord from T7 to T12 helps control the abdominal muscles used for breathing and initiation of an effective cough. Therefore, any patient with a suspected spinal cord injury above T7 should be assessed for the presence of neurogenic shock. Injury of T7 to T12 also results in low lung volume, weak cough, and dyspnea. If the injury is above C3, the patient may need mechanical ventilation because impaired motor control of the respiratory muscles will result.

Nursing care of a patient with neurogenic shock in the emergent phase consists of following the ABCs of care:

  • A = The patient’s airway should be assessed and maintained.
  • B = The patient’s breathing status should be assessed and supplemented as needed, for example, with supplemental oxygen, endotracheal intubation, or mechanical ventilation.
  • C = The patient’s circulatory status also needs to be assessed, as significant hypotension and bradycardia are often components of neurogenic shock.

The nurse should recognize these conditions and provide appropriate treatment to stabilize the patient’s hemodynamics. Figure 23.11 shows an example of a common precautionary measure to protect against neurogenic shock.

EMS placing cervical collar on patient
Figure 23.11 EMS will likely place a cervical collar on a patient with a suspected neck injury, such as this car crash victim. (credit: Szdavid/Wikimedia Commons, CCBY 4.0)

It is important for the nurse to continually assess for volume overload when intravenous fluids are initially administered to the hypotensive patient. In addition to hemodynamic monitoring, the nurse should assess the lungs to determine the presence of adventitious breath sounds that indicate the development of pulmonary edema. It is imperative that the nurse recognize the cause of hypovolemia in patients is due to loss of blood vessel tone, not blood vessel volume.

Frequently, patients with neurogenic shock require endotracheal intubation and mechanical ventilation. The nurse should assess the patient’s response to suctioning. Insertion of a catheter into the endotracheal tube may trigger the vagus nerve, further dropping the heart rate. It is advisable to have atropine readily available for the treatment of bradycardia as needed. Some health-care providers recommend the use of pacemakers for patients with neurogenic shock who are experiencing significant bradycardia.

Hypothermia when present can be managed with a warming blanket. If the patient is hypothermic and hemodynamically unstable, slow rewarming is indicated. Studies have found that rapid rewarming may worsen the patient’s unstable hemodynamic status due to further vasodilation.

The nurse should perform frequent assessments of all body systems to assess the patient’s response to treatment. Along with a complete neurologic assessment, the nurse should assess for any change in the level of consciousness that might indicate decreased perfusion to the brain.

Prioritizing Hypotheses, Generating Solutions, and Taking Action

Caring for patients with neurogenic shock is complex and involves high attention to detail. The nurse must monitor the patient closely for signs and symptoms that indicate a decline in body systems. The nurse should assign patients experiencing neurogenic shock to a neurologic intensive care unit or spine center for close observation. Without prompt intervention, permanent, irreversible damage may result.

Meticulous skin care is essential. Patients with neurogenic shock are at high risk for developing pressure injuries because of poor perfusion to the skin and possible immobility related to spinal cord injury. Nursing care should also focus on preventing the development of aspiration pneumonia, foot drop, DVT, and other complications of immobility.

Some patients with spinal cord injury manifest changes in bowel and bladder function. Spinal cord injury may result in complete or partial loss of the patient’s ability to control or manage excretions. The nurse should assess for urinary retention and bowel obstruction or constipation and provide appropriate care. Hourly and twenty-four-hour intake and output should be accurately assessed and documented.

Neurogenic shock also places patients at risk for the development of GI stress ulcers. The nurse needs to follow through with preventive measures to decrease the chance of gastrointestinal bleeding. Stress has also been found to increase the blood glucose level of patients. Results indicate that patients who have a blood glucose of less than 180 mg/dL experience less morbidity and mortality.

Evaluation of Nursing Care for the Patient with Neurogenic Shock

Successful management of neurogenic shock begins with early diagnosis and accurate identification of the cause. Appropriate treatments to limit low blood pressure and low heart rate have been found to decrease secondary injury to the spinal cord and restore adequate oxygenation to vital tissues, thus limiting cell damage. The effectiveness of treatment can be evaluated by the presence of baseline hemodynamic status of the patient. The optimal patient outcome for neurogenic shock is the resolution of the problem with no residual deficits.

Medical Therapies and Related Care

Medical therapies for patients with neurogenic shock focus on preventing secondary injury to the spinal cord, which starts with immobilizing the spine and completing imaging studies. The patient may require surgery for spine stabilization or decompression.

Other important therapies involve enhancing sympathetic tone to the blood vessels and heart to improve cellular and body tissue perfusion. Patients with neurogenic shock often have systolic blood pressure readings of less than 70 mmHg systolic. Treatment is geared to obtain a mean arterial pressure of 85 to 90 mmHg, as this is known to ensure adequate perfusion to cells and body tissues for patients in neurogenic shock. Hemodynamic stabilization starts with the administration of fluids followed by vasopressors. Fluid therapy is useful to compensate for the vasogenic dilation that occurs because of loss of sympathetic stimulation to the blood vessels; however, it does not result in acceptable profusion to cells and body tissues. Vasopressors are frequently required to obtain baseline hemodynamics. When administering fluids, it is imperative to assess the patient for the development of fluid overload, which often manifests as heart failure or pulmonary edema.

Pharmacotherapy for loss of vascular tone in neurogenic shock often includes the following:

  • An inotropic drug (digoxin, dobutamine, milrinone) increases the force of cardiac contractions.
  • Vasopressors (phenylephrine, norepinephrine, epinephrine, and vasopressin) constrict the blood vessels to increase blood pressure. The goal is to maintain mean arterial pressure between 85 to 90 mmHg.

Pharmacologic treatment of bradycardia in neurogenic shock includes:

  • atropine, a positive chronotropic that blocks the effects of the vagus nerve on the heart
  • glycopyrrolate, a positive chronotropic that blocks the enzyme that slows heart rate
  • isoproterenol beta-1 and beta-2 adrenergic receptors, which reproduce a pure chronotropic effect
  • Methylxanthines, which provide a positive chronotropic effect for refractory bradycardia
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