eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Cardiovascular Concerns in Spinal Cord Injury

Author: William McKinley, MD, Director of Spinal Cord Injury Medicine, Professor and Residency Program Director, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University Medical Center
Coauthor(s): Susan V Garstang, MD, Assistant Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey; Attending Medical Staff, Director of Spinal Cord Injury Program, Department of Physical Medicine and Rehabilitation, University Hospital; Houman Danesh, Virginia Commonwealth University School of Medicine (Medical College of Virginia)
Contributor Information and Disclosures

Updated: Feb 15, 2008

Introduction

Background

Spinal cord injury (SCI) can result in clinically significant compromise of cardiovascular control with associated short- and long-term consequences.^1,2 Impaired control of the autonomic nervous system (ANS), especially in individuals with high thoracic and cervical SCI, can result in various problems, such as hypotension, bradycardia, and autonomic dysreflexia.^3,4 Additional associated cardiovascular concerns in SCI, such as deep venous thrombosis (DVT) and long-term risk for coronary heart disease (CHD), also are briefly discussed in this article.

See the following related topics in Medscape:
Resource Center Spinal Disorders

Pathophysiology

The communication between the brainstem and the ANS is important for the control of the cardiovascular system and is often compromised after SCI.^5,6,7 Sympathetic nervous system (SNS) neurons (which originate in the intermediolateral cell column at T1-L2 neurologic levels) control vasoconstriction and heart contractility. SNS innervation of the heart comes from T1-4 levels. Therefore, upper thoracic and cervical SCI, especially complete injuries, leave individuals without the ability to control all or most of their SNS function.

Immediately after SCI occurs, blood pressure rises acutely. This phenomenon is caused by the release of norepinephrine from the adrenal glands and by a pressor response from mechanical disruption of vaso-active neurons and tracts in the cervical and upper thoracic spinal cord.^8,9 This brief response is followed by a period of decreased SNS activity because of interruption of the descending sympathetic tracts. A lack of supraspinal input develops, causing cutaneous vasodilatation, a lack of sympathetic vasoconstrictor activity, and an absence of sympathetic input to the heart. In clinical terms, the patient with SCI is susceptible to hypothermia, hypotension, and bradycardia because of a lack of sympathetic input and unopposed vagal tone.¹⁰

Hypotension

In individuals with tetraplegia or high paraplegia, decreased compensatory vasoconstriction (secondary to changes in sympathetic activity and especially occurring in the large vascular beds in the skeletal muscle and splanchnic regions), in association with venous pooling in the lower extremities and decreased muscle activity, reduces venous blood return, stroke volume, and blood pressure.^11,12,13,14 Additionally, there may also be an upregulation of nitric oxide (a potent vasodilator).¹⁵

Orthostatic hypotension is defined as a drop in systolic blood pressure of >20mm Hg and/or a decrease in diastolic pressure of >10mm Hg, when changing from supine to upright positioning.¹⁶ Hypotension, especially orthostasis, usually improves within days to weeks as compensatory changes occur in the vascular beds, skeletal muscle, and rennin-angiotensin-aldosterone system.¹⁷

Cardiac arrhythmias

The ANS modulates cardiac electrophysiology, and autonomic dysfunction can lead to ventricular arrhythmias. Parasympathetic input to the heart (from the vagus nerve, cranial nerve [CN] X) remains intact and can result in bradycardia, especially in cervical SCI. Reflex bradycardia and, less frequently, cardiac arrest have been noted in acute SCI. Bradycardia is often precipitated by tracheal stimulation (for example, during suctioning) and hypoxia.^3,18 Atropine may be needed, and temporary (sometimes permanent) cardiac pacemakers have been used.^19,20 This problem usually resolves over the first 2-6 weeks after an SCI.

Autonomic dysreflexia

Loss of supraspinal control of hyperreflexic SNS activity is usually secondary to noxious stimuli below the level of injury (in individuals with SCI at T6 levels or above, that is, above the major SNS splanchnic outflow). This loss can lead to autonomic dysreflexia and dangerously high blood pressures.⁴

Deep venous thrombosis

As a result of ANS control and decreased local blood flow, circulation in the lower extremities is reduced after SCI to about 50-67% of normal. Factors predisposing individuals with acute SCI to DVT include venous stasis secondary to muscle paralysis and transient hypercoagulable state with reduced fibrinolytic activity along with increased factor VIII activity.

Long-term risk of CHD

CHD is more common and is seen at earlier ages in individuals with SCI than it is in persons without SCI; this is likely associated with the higher incidence of metabolic syndrome (obesity, dyslipidemia, hypertension, insulin resistance, increased prothrombotic and pro-inflammatory states) in the former group.^21,22,23  Abnormal lipid profiles, such as an elevation of total cholesterol (TC) and of low-density lipoprotein cholesterol (LDL-C), as well as a decrease in high-density lipoprotein cholesterol (HDL-C) levels, are not uncommon with chronic SCI and increase the risk for cardiovascular disease.²⁴

Causes for decreased HDL-C values after SCI remain unconfirmed, although poor diet, adrenergic dysfunction, and physical deconditioning are likely explanations.²⁵ A ratio of TC to HDL-C of >5.0 is considered high risk for CHD. Goals for optimal cholesterol management currently include an LDL-C level of <100 mg/dL, and a TC level of <200 mg/dL. Lipid-lowering drug therapy for dyslipidemia is a clinical option, although optimal pharmacologic agents have not been identified.

Exercise and physical fitness to prevent CHD

In the general population, physical activity has several beneficial effects with respect to CHD, including reduction of blood pressure, reduced risk of atherosclerosis secondary to improved lipid profiles, and increased insulin sensitivity.²⁶ In individuals with SCI, obvious limitations are paralysis, limited muscle mass, and adrenergic dysfunction. In addition, for these persons, everyday mobility and activities of daily living are inadequate to meet the requirements for cardiovascular fitness.²¹

The reduction in cardiovascular fitness benefits result from the loss of sympathetic control and functional mass.²⁷ Lesions above T1-4 can compromise increases in heart rate during exercise, as well as cardiac output and stroke volume. In individuals with SCI above the sympathetic output areas, increases in heart rate are usually caused by the withdrawal of vagal inhibition. When these patients exercise, their heart rate and oxygen uptake increases, but the changes do not reach the levels of their uninjured counterparts.^28,29

See also the following related topics in eMedicine:
Autonomic Dysreflexia in Spinal Cord Injury
Prevention of Thromboembolism in Spinal Cord Injury

See also the following related topics in Medscape:
Resource Center Cardiometabolic Risk Factor Management
Resource Center Heart Failure
Resource Center Hypertension
Resource Center Obesity

Frequency

United States

The incidence of SCI in the United States is about 40 cases per 1 million population (approximately 11,000 persons) annually.^30,31 Of the affected individuals, 53% have tetraplegia (ie, injuries to 1 of the 8 cervical segments of the spinal cord), and 42% have paraplegia (ie, lesions in the thoracic, lumbar, or sacral regions of the spinal cord).

Studies of cardiovascular abnormalities after SCI show that as many as 100% of patients with motor complete cervical injuries (American Spinal Injury Association [ASIA] grades A and B) develop bradycardia, 68% are hypotensive, 35% require pressors, and 16% have primary cardiac arrest.^10,32 Of persons with motor incomplete cervical injuries (ASIA grades C and D), 35-71% develop bradycardia, but few have hypotension or require pressors. Patients in this group rarely have primary cardiac arrest. Among patients with thoracolumbar injuries, 13-35% have bradycardia.

DVT occurs in 47-90% of patients, depending on the degree of prophylaxis. Risk factors decline in 8-12 weeks. Proximal progression of DVT and pulmonary embolism occur in 20-50%.

Regarding CHD in SCI, the incidence of physical inactivity, obesity, hyperlipidemia, insulin resistance, and diabetes are greater in individuals with SCI than in the general population.²¹ Because of this difference, the risk of CHD is thought to increase after SCI. This risk may be increasingly important as the life expectancy of people with SCI lengthens. CHD accounts for approximately 20% of deaths in the SCI population. Major modifiable risk factors for CHD prevention include high blood pressure, smoking, obesity, physical inactivity, and unhealthy cholesterol and/or lipid levels.

Mortality/Morbidity

Complications of loss of sympathetic control include hypotension requiring pressors, pulmonary edema because of volume overload from aggressive resuscitative efforts, bradycardia requiring atropine or transvenous pacing, primary cardiac arrest, and supraventricular tachyarrhythmias.

Direct myocardial injury can occur after SCI, as evidenced by electrical, enzymatic, and histologic changes in the heart. This phenomenon may be attributable to the surge of sympathetic mediators that are released from the adrenal glands and sympathetic nerve terminals immediately after injury.

The mortality rate that is associated with pulmonary edema is as high as 35%; this rate emphasizes the importance of DVT prophylaxis.

CHD accounts for approximately 20% of deaths in persons with SCI and is one of the leading causes of mortality in chronic SCI.

Race

Cardiovascular abnormalities after SCI depend only on the level and completeness of injury with no evidence of differences between ethnic or racial groups. In general, the current racial distribution of people with SCI is 62% white, 22% African American, 13% Hispanic, and 3% other racial or ethnic groups.

Sex

No sex predilection exists in cardiovascular abnormalities. Approximately 80% of people with traumatic SCI are male.

Age

• Current data do not support an age-related effect on the incidence of cardiovascular problems after SCI, with the exception of an increase in primary cardiac problems in patients older than 55 years.³³
• SCI affects primarily young adults; since 2000, the average age at injury has been 37.6 years. However, among individuals with SCI, the portion made up of patients who were older than 60 years at injury has increased to 11% of the total.
• The life expectancy of individuals with SCI continues to increase, but it remains lower than that of people without SCI.

Clinical

History

Symptoms that patients report after acute SCI differ depending on the underlying condition. They include the following:

• Hypotension and bradycardia - Patients may report dizziness or even loss of consciousness, as well as nausea, lightheadedness, and visual disturbances, as a manifestation of low blood pressure and slowed pulse. Orthostatic hypotension is a sudden decrease in blood pressure when the patient rises to a relatively upright or upright position.
• Autonomic dysreflexia - Symptoms include headache, sweating, piloerection, facial flushing, blurred vision, and nasal congestion.⁴
• DVT - Symptoms may include, in an extremity, swelling (usually asymmetrical), warmth, and tenderness. Patients may have a low-grade fever.
• Cardiovascular disease - Impulses for cardiac anginal pain ascend by means of the T1-5 segments. Therefore, individuals with high thoracic and cervical SCI may not perceive angina or acute myocardial infarction.

Physical

• Vital signs, including blood pressure, pulse, respiratory rate, and temperature, should be monitored.³⁴
  • In patients with cervical injuries, resting systolic blood pressure is commonly 80-100 mm Hg. Decreases of 20-30 mm Hg in systolic blood pressure when the patient changes from a supine to an upright position may be associated with orthostatic hypotension.
  • Likewise, increases of 20-30 mm Hg or more in systolic blood pressure can be consistent with autonomic dysreflexia.⁴
• Discern the patient's level of consciousness, because hypotension can lead to somnolence. Observe the patient for pallor, flushing, sweating, skin temperature, or piloerection (signs of SNS dysfunction).
• Comprehensive motor and sensory examination can reveal the neurologic level and completeness of the injury. This examination may assist with assessing the risk for SNS dysfunction. Reflex testing, especially below the level of injury, can be done to determine whether spinal shock is still present.
• Examine for peripheral edema and warmth or tenderness of the extremities. Unilateral extremity swelling may suggest DVT. Bilateral swelling may be consistent with fluid overload.
• Acute SCI results in neurogenic shock, which consists of the triad of hypotension, bradycardia, and hypothermia.³⁵ It is important to differentiate neurogenic shock from hypovolemic shock, because their treatments differ. In neurogenic shock, urine output is preserved, the skin is typically warm, and tachycardia is absent. Invasive evaluation typically reveals decreased cardiac output and decreased pulmonary and systemic vascular resistance.
• In chronic SCI, monitor ideal body weights and waist circumference. (Also consider measurement of the body mass index.)³⁶  These can be useful measures of obesity, which is associated with CHD in this population.

See also the following related topic in eMedicine:
Functional Outcomes per Level of Spinal Cord Injury

Causes

See Pathophysiology.

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