Cardiovascular Concerns in Spinal Cord Injury
Concerns in spinal cord injury (SCI) include its ability to compromise cardiovascular control, with associated short- and long-term consequences.
For example, impaired control of the autonomic nervous system (ANS), especially in individuals with high thoracic and cervical SCI, can lead to hypotension, bradycardia, and autonomic dysreflexia. [1, 2, 3] Additional associated cardiovascular concerns in SCI include deep venous thrombosis (DVT) and long-term risk for coronary heart disease (CHD)
Symptoms that patients report after acute SCI differ depending on the underlying condition. 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.
Symptoms of autonomic dysreflexia include the following  :
In patients with DVT, symptoms may include the following:
Acute-onset extremity swelling (usually asymmetrical)
Because CHD may be asymptomatic in individuals with SCI (due to decreased sensory feedback of angina), better recognition of the CHD health risks may help to reduce morbidity and mortality in these patients.
Blood, serum, and urinary studies
Hemoglobin concentration and/or hematocrit: To evaluate for hypovolemia and blood loss
White blood cell (WBC) count: To rule out either an underlying infectious etiology of hypotension or noxious stimuli for autonomic dysreflexia
Serum glucose level: Can be elevated in prediabetic states
Serum triglyceride and cholesterol levels: If risk of long-term CHD is a concern
C-reactive protein (CRP) level: Can be elevated in pro-inflammatory conditions (such as metabolic syndrome) and has a role in the development of CHD
Urinalysis: To check for urinary tract infection as a possible etiology for hypotension or noxious stimuli for autonomic dysreflexia
Imaging studies, such as spinal radiography, magnetic resonance imaging (MRI), and/or computed tomography (CT) scanning, can be used to determine the location, severity, and stability of injuries to the vertebral spine and spinal cord.
Other evaluations, to look for additional injuries or sources of hemodynamic instability, can include the following:
Chest radiography: To evaluate pulmonary contusions, effusions, pulmonary edema, mediastinal widening, indistinctness of the heart, and the aortic border
Chest/abdominal CT scanning or ultrasonography
Venous Doppler ultrasonography: To evaluate for the presence of DVT
Diagnostic peritoneal lavage
Pharmacologic stress testing with cardiac imaging
Electrocardiography and cardiac monitoring: To evaluate bradycardia, look for dysrhythmias (most commonly, supraventricular tachyarrhythmias), and assess for ST-T wave abnormalities indicative of ischemia [4, 5]
Exercise options for patients with SCI include the following:
Electrically assisted exercises for leg cycling, arm ergometry, endurance sports, circuit resistive training, and ambulation (especially in patients with paraplegia)
Resistive exercise therapy: Can improve arterial health after chronic SCI, which may reduce the risk of CHD
Body weight–supported treadmill training: May improve cardiovascular function
Hybrid–functional electrical stimulation (FES) rowing: May be more advantageous for patients with SCI than most other exercise options, owing to the increased aerobic activity it provides 
If conservative, nonpharmacologic measures are not entirely effective in treating hypotension and bradycardia, medication should be considered. If intravenous (IV) pressors are chosen, use invasive hemodynamic monitoring to guide their use.
After a patient with SCI is stabilized, goals include elimination of IV medications and treatment of hypotension with oral agents. In general, use salt tablets as the first medication, but if NaCl is inadequate, use pseudoephedrine, then fludrocortisone, and finally midodrine.  Other medications used in patients with SCI include the following:
Desmopressin (DDAVP), erythropoietin, and octreotide: Have also been studied and used in the management of orthostatic hypotension
Atropine: Drug of choice for bradycardia but rarely used in rehabilitation settings except during emergencies (phenylephrine and dopamine also can be considered)
Alpha-adrenergic agonists: Improve the patient’s hemodynamic status by increasing myocardial contractility and heart rate
Corticosteroids: Cause sodium and fluid retention, resulting in improvements in symptomatic orthostatic hypotension
Sympathomimetics: Augment coronary and cerebral blood flow
Anticholinergics: Administered to improve conduction through the atrioventricular (AV) node
Concerns in spinal cord injury (SCI) include its ability to produce clinically significant compromise of cardiovascular control, with associated short- and long-term consequences. [8, 9] Impaired control of the autonomic nervous system (ANS), especially in individuals with high thoracic and cervical SCI, can lead, for example, to hypotension, bradycardia, and autonomic dysreflexia. [2, 3] 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.
The communication between the brainstem and the ANS is important for the control of the cardiovascular system and is often compromised after SCI. [10, 11, 12] 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 vasoactive neurons and tracts in the cervical and upper thoracic spinal cord. [13, 14] 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. 
In individuals with tetraplegia or high paraplegia, both resting systolic and diastolic blood pressure remain lower than in normal subjects. [16, 17] 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 decreased muscle activity and venous pooling (in the viscera and dependent lower extremities) leads to a reduction in venous blood return, stroke volume, and blood pressure. [18, 19, 20, 21] Additionally, there may also be an up-regulation of nitric oxide (a potent vasodilator), altered baroreceptor sensitivity, or altered salt and water balance.  Tachycardia may occur as a consequence of reduced vagal activity via the carotid sinus, but it is not sufficient to compensate for the diminished sympathetic nervous system (SNS) response.
Neurogenic shock (reduced blood pressure from neurologic causes) is common in patients with acute tetraplegia or high-level paraplegia (T1-T4). Hypotension may exacerbate central nervous system injury, contributing to spinal cord hypoperfusion. Early appropriate fluid resuscitation is necessary for all patients with spinal cord injury (SCI) to maintain tissue perfusion, though care must be taken to avoid fluid overload. Uncontrolled studies that used fluids and vasopressors to achieve a mean arterial pressure of 85-90 mm Hg for a minimum of 7 days in patients with acute SCI have reported favorable outcomes. Further study is needed to define ideal mean arterial pressure (MAP) and the potential role for fluids or pharmacologic treatment. In the setting of neurogenic shock, it is essential to first ensure that intravascular volume is restored, and then vasopressors (dopamine, norepinephrine, phenylephrine) may be used to treat hypotension.
Orthostatic hypotension is defined as a drop in systolic blood pressure of greater than 20 mm Hg and/or a decrease in diastolic pressure of greater than 10 mm Hg, when changing from supine to upright positioning.  Symptoms include light-headedness, dizziness, blurry vision, or fatigue. Hypotension, especially orthostasis, usually improves within days to weeks as compensatory changes occur in the vascular wall receptor hypersensitivity, skeletal muscle tone, and renin-angiotensin-aldosterone system. 
The ANS modulates cardiac electrophysiology, and autonomic dysfunction can lead to dysrhythmias. [25, 26] 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 (eg, during suctioning), tracheal intubation, hypoxia, Valsalva maneuver, and defecation. [2, 27] Administration of oxygen and atropine (sometimes phenylephrine or dopamine) may be needed, and temporary (sometimes permanent) cardiac pacemakers have been used for refractory cases. [28, 29] This problem usually resolves over the first 2-6 weeks after an SCI.
The loss of descending supraspinal control of hyperreflexic SNS activity can lead to signs or symptoms known as autonomic dysreflexia (AD). It often occurs secondary to a 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 can lead to an increase in blood pressures.  AD is defined as an increase in blood pressure more than 20 mm Hg above baseline and may include other symptoms such as headache, flushing/sweating (above injury level), and bradycardia. Clinical manifestations vary from mild, annoying symptoms to acute, life-threatening situations accompanied by significant hypertension and risk of cerebral hemorrhage.
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 a transient hypercoagulable state with reduced fibrinolytic activity along with increased factor VIII activity.
Individuals with SCI seem to be at accelerated risk for developing metabolic syndrome (MetS), a recognized but somewhat controversial concept. Factors identified in the definitions of MetS are central obesity (not well defined), abnormal carbohydrate metabolism (fasting plasma glucose >100 mg/dL), elevated blood pressure (≥130/85 mm Hg), abnormally high triglycerides (≥150 mg/dL), and abnormally low HDL cholesterol (≤50 mg/dL in women and ≤40 mg/dL in men). MetS is recognized as being associated with the development of type 2 diabetes and cardiovascular disease.
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 proinflammatory states) in persons with SCI. [30, 31, 32] 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. 
Causes for decreased HDL-C values after SCI remain unconfirmed, although poor diet, adrenergic dysfunction, and physical deconditioning are likely explanations.  A ratio of TC to HDL-C of greater than 5.0 is considered high risk for CHD. Goals for optimal cholesterol management currently include an LDL-C level of less than 100 mg/dL, and a TC level of under 200 mg/dL. Lipid-lowering drug therapy for dyslipidemia is a clinical option, although optimal pharmacologic agents have not been identified.
The risk of CHD may become increasingly important as the life expectancy of people with SCI lengthens. Major modifiable risk factors for CHD prevention include high blood pressure, smoking, obesity, physical inactivity, and unhealthy cholesterol and/or lipid levels and can be addressed through lifestyle changes or pharmacotherapy, if necessary. Dyslipidemia, metabolic syndrome, and glucose intolerance should be evaluated and pharmacotherapy should be considered. The frequency of glucose intolerance is increased in persons with SCI, and diabetes should be treated according to standard recommendations.
A Swedish cross-sectional descriptive study, by Jörgensen et al, found a high rate of cardiovascular risk factors in the study cohort, which consisted of older adults (mean age, 63 years) with long-term spinal cord injury (mean time, 24 years). The investigators reported that 55% of patients, at assessment, had a blood pressure of 140/90 mm Hg or above, while 16% had a history of diabetes, 15% had a fasting glucose level of 7 mmol/L or above, 76% had dyslipidemia, 16% had prediagnosed dyslipidemia, 16% smoked regularly, 93% were overweight, and 60% had a waist circumference that was considered to pose a cardiometabolic risk. 
Because CHD may be asymptomatic in individuals with SCI (due to decreased sensory feedback of angina), better recognition of the CHD health risks may help to reduce morbidity and mortality. In addition, encouraging smoking cessation and ways to enhance physical activity are important components of a treatment plan.
The incidence of SCI in the United States is about 40 cases per 1 million population (approximately 11,000 persons) annually. [36, 37] 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. [15, 38] The prevalence rate of symptomatic CHD in SCI is 30-50%, in comparison to 5-10% in the general able-bodied population.
Autonomic dysreflexia is 3 times more prevalent in complete tetraplegia than with incomplete injury. Of persons with motor incomplete cervical injuries (ASIA grades C and D), 35-71% develop bradycardia, but few have hypotension or require pressors. Among patients with thoracolumbar injuries, 13-35% have bradycardia. DVT occurs in 47-90% of patients, depending on the degree of prophylaxis. [39, 40] Risk factors decline in 8-12 weeks. Proximal progression of DVT and pulmonary embolism occur in 20-50%.
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.
No sex predilection exists in cardiovascular abnormalities. Approximately 80% of people with traumatic SCI are male.
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 age 55 years. 
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 age 60 years at injury has increased to 11% of the total.
Weight gain and obesity after SCI are not uncommon.  Physical inactivity, decreased energy expenditure, and the secondary effects of muscle paralysis decrease muscle and lean body mass, increase the percentage of body fat, increase insulin resistance, and increase the risk for CHD. 
Dietary guidelines suggest that reductions be made in the patient’s intake of calories, fat (< 30% of calories), and cholesterol (< 300 mg).  However, some have noted that dietary intervention has shown limited effectiveness because of the concomitant depression of HDL-C concentrations with TC levels.
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.
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.  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.
The mortality rate 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.
The education of patients, their families, and staff members is extremely important for the recognition and management of cardiovascular complications (eg, low blood pressure, orthostasis, bradycardia, autonomic dysreflexia, DVT, CHD). Teach patients to recognize the clinical symptoms and to report them immediately.
For orthostatic hypotension, family and staff members must respond quickly by reclining the patient and elevating his/her legs.
Staff and family must understand that patients should never be left unattended after being placed in a sitting position, because their blood pressure may drop and cause syncope before they can call for help. This precaution is particularly applicable to patients with tetraplegia who may not have access to a bedside call button.
Education about the reasons for medications, abdominal binders, anti-embolism stockings (eg, TED hose), tilt and/or reclining wheelchairs, and elastic bandages (ACE wraps) is important to ensure compliance.
Education of the respiratory and nursing staff is important to prevent bradycardia resulting from increased vagal tone; this is particularly the case in patients with a tracheostomy, during endotracheal suctioning. [2, 27] If necessary, hyperventilate patients and administer atropine before suctioning.
Symptoms that patients report after acute SCI differ depending on the underlying condition. 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.  DVT symptoms may include acute-onset extremity swelling (usually asymmetrical), warmth, erythema, and pain/tenderness. Patients may have a low-grade fever.
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.
Vital signs, including blood pressure, pulse, respiratory rate, and temperature, should be monitored.  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. 
Monitor 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 determine the neurologic level and completeness of the injury and 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.  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.)  These can be useful measures of obesity, which is associated with CHD in this population.
Immediately after acute SCI, differentiate neurogenic shock from hypovolemic shock. In the absence of other injuries, patients with low blood pressure resulting from SCI do not need aggressive fluid resuscitation. In fact, patients with tetraplegia commonly develop pulmonary edema if given too much volume. The etiology of this phenomenon is not clear, but it may be related to decreased pulmonary vascular resistance and/or a lack of sympathetic innervation to the lungs. Therefore, following resuscitation with about 2 L, start pressors to maintain blood pressure after hypovolemia due to other trauma has been ruled out.
Conditions to consider in the differential diagnosis of cardiovascular disease in patients with spinal cord injury include the following:
Infection or septic shock
Cardiac injury of dysfunction
Adverse pharmacological effects or drug overdose
Determine the hemoglobin concentration and/or hematocrit to evaluate for hypovolemia and blood loss. Of note, normochromic, normocytic anemia is not uncommon after SCI. Determine the white blood cell (WBC) count to rule out either an underlying infectious etiology of hypotension or noxious stimuli for autonomic dysreflexia.
In chronic SCI, check serum glucose, which can be elevated in prediabetic states. Check serum triglyceride and cholesterol levels if the risk of long-term CHD is a concern. C-reactive protein (CRP) can be elevated in pro-inflammatory conditions (such as metabolic syndrome) and has a role in the development of CHD. [31, 32, 33]
Order urinalysis to check for urinary tract infection as a possible etiology of hypotension or noxious stimuli for autonomic dysreflexia.
If they have not previously been performed, consider using imaging studies, such as spinal radiography magnetic resonance imaging (MRI) and/or computed tomography (CT) scanning, to determine the location and severity of and stability of injuries to the vertebral spine and spinal cord.
Chest radiography may be needed to evaluate pulmonary contusions, effusions, pulmonary edema, mediastinal widening, indistinctness of the heart, and the aortic border.
Other evaluations to look for additional injuries or sources of hemodynamic instability may include chest/abdominal CT scanning or ultrasonography, diagnostic peritoneal lavage (DPL), and pelvic radiography. In addition, perform venous Doppler ultrasonography to evaluate for the presence of DVT. Consider additional testing, such as venography, CT scanning, or D-dimer, as warranted.
Electrocardiography and cardiac monitoring may be indicated to evaluate bradycardia, to look for dysrhythmias (most commonly, supraventricular tachyarrhythmias), and to assess for ST-T wave abnormalities indicative of ischemia. [4, 5]
Traditional exercise stress testing may be limited in individuals with SCI. Consider pharmacologic stress testing (by using dobutamine or dipyridamole) with cardiac imaging (echocardiography or scintigraphy) to document defects of the myocardial wall.
Intensive monitoring of the patient’s hemodynamic status is occasionally necessary and is best accomplished with the insertion of a Swan-Ganz catheter.  This procedure, in association with measurements of pulse, blood pressure, and urine output, clarifies the patient’s volume status.
After the patient’s condition is stabilized and he/she leaves the intensive care unit (ICU), perform further monitoring for orthostatic hypotension by measuring pulse and blood pressure.
The initial care of patients with SCI who suffered neurogenic shock with clinically significant hypotension includes careful monitoring of their cardiovascular and fluid status.  Use pressors to maintain systemic vascular resistance and provide cardiac inotropic support.
Increased intravascular volume and pulmonary capillary permeability may lead to neurogenic pulmonary edema, the result of massive neural discharges that increase systemic and pulmonary vascular pressures, forcing blood into the central circulation. This condition may be worsened by the overly judicious use of fluids, rather than pressors, to support blood pressure. In general, in the absence of hypovolemia from blood loss, do not administer more than 2-3 L of fluid without considering the use of a Swan-Ganz catheter to monitor the patient. 
Monitor body temperature, remembering that patients with lesions above T6 are poikilothermic and cannot regulate their body temperature.
Studies support keeping a mean arterial pressure (MAP) of at least 85 mm Hg to maintain spinal cord perfusion and to help prevent secondary ischemia.
Monitor heart rate and, if indicated, provide support with medications (eg, dopamine) that increase heart rate and blood pressure. Keep atropine and a transcutaneous pacer at the patient’s bedside for emergencies. If prolonged or excessive bradycardia occurs, insert the transvenous pacer; however, permanent pacing is rarely necessary. Bradycardia usually resolves 2-6 weeks after the SCI.
Before performing any procedure that increases vagal tone (eg, suctioning), correct hypoxia with the administration of 100% oxygen and premedicate the patient with atropine. Full lung expansion before suctioning may decrease vagal tone; therefore, provide a full breath with a ventilator or bag-valve-mask resuscitator (Ambu bag).
Cardiac arrest and hypokalemia can result from hypersensitivity of muscle-cell membranes if a patient with SCI is given succinylcholine. Use of this drug should be avoided in patients with SCI.
DVT resulting from venous stasis is common in the SCI population, especially in the acute postinjury period. It may manifest as a fever of unknown origin. Because DVT can lead to pulmonary embolism and death, aggressive preventive measures should include, but not be limited to, baseline and serial screening, Doppler ultrasonography of the lower extremities, the use of compression garments, the administration of low–molecular weight heparin, or the placement of an inferior vena cava filter (although this can have its own inherent risks, including migration).
Monitor patients with acute cervical SCI for cardiac arrhythmias, because bradycardia and tachyarrhythmias are common. As mentioned previously, hypoxia and vagal stimulation can cause bradycardia, leading to asystole. Therefore, close observation, repeat medication with atropine, and hyperventilation may be necessary when endotracheal suctioning procedures are performed.
Never leave a patient alone in a sitting position until after his/her blood pressure has stabilized, because the individual may become hypotensive and syncopic before being able to call for help.
The use of salt in the diet and the intake of fluids should be encouraged to offset symptoms of orthostasis.
Biofeedback and functional electrical stimulation relieve symptoms and may have a role in the patient’s care.
A study by Fougere et al indicated that intradetrusor injections of onabotulinumtoxinA can reduce the rate and severity of bladder-associated autonomic dysreflexia episodes in persons with high-level SCI. The study included 17 patients with chronic, traumatic SCI at the sixth thoracic level or higher. 
Cardiac rehabilitation in an individual with SCI requires the use of adaptations (eg, progressive wheelchair propulsion) to address limitations in mobility, as well as special consideration of the patient’s inability to tolerate traditional anti-anginal medications (because of low blood pressure).
Patients should be questioned about their use of sildenafil (Viagra) for erectile dysfunction, because it is contraindicated with concomitant use of nitrate medication. Aspirin and beta blockers may be recommended.
Other considerations are as follows:
Hypotension and bradycardia – As discussed previously, hypotension and bradycardia typically improve within days to weeks, and the patient can be weaned off medications
Complete cervical injury – Patients with complete cervical injuries often have a relatively low resting pulse rate and blood pressure
Conservative measures – Discontinue conservative measures only after medications have been stopped and the patient is doing well
Abdominal binder and anti-embolism stockings (eg, TED hose) – Patients frequently continue to need these for orthostasis and to control lower-extremity edema after discharge
Tilt-in-space device – Many patients need to use a wheelchair with a reclining or tilt-in-space mechanism to allow for quick achievement of a supine posture if they become dizzy or light-headed
At first, the patient with acute traumatic SCI is typically under the care of neurosurgeons. Depending on cardiovascular concerns, consult a cardiologist and/or an internist to assist in management. Physical medicine and rehabilitation (PM&R) physicians have special training in SCI medicine and should be involved in the acute phase. After the patient leaves the ICU, his or her care is typically transferred to PM&R physicians.
The goal for management of orthostatic hypotension is to alleviate the disabling symptoms, not to normalize the patient’s blood pressure. Acceptable and tolerated systolic blood pressure for individuals with cervical SCI may be 80-100 mm Hg. Early management of orthostatic hypotension begins with assessment of potential exacerbating factors, including prolonged recumbency, rapid changes in positioning, underlying infection, dehydration, and adverse drug effects. Medications that should be avoided include antihypertensives, diuretics, tricyclic antidepressants (TCAs), anticholinergics, and narcotic analgesics.
Treatment options for orthostatic hypotension include physical measures and pharmacologic intervention. Before moving a patient out of a supine position, apply an abdominal binder and thigh-high antiembolism stockings (eg, TED hose; Kendall-Futuro, Milford, Ohio) or elastic bandages (ACE wrap; Becton, Dickinson and Co, Franklin Lakes, NJ) to the lower extremities. These techniques decrease venous pooling in the lower extremities (stockings) and increase intra-abdominal pressure (binder), increasing venous return to the heart.
The patient should be instructed to move slowly and with assistance from a supine position to a relatively more upright position. Ensure that the patient is first transferred into a reclining wheelchair so that his or her head can be lowered immediately if hypotension develops. The use of elevated leg rests also may be helpful. Using a tilt table with slow increases in degrees of tilt can help the patient to acclimate to an upright position.
During the period of acclimatization, include active arm exercises to maintain blood pressure while the patient is on the tilt table. Never leave the patient alone in the upright position lest hypotension progresses to syncope and the patient is unable to get help.
In the general population, physical activity has several beneficial effects with respect to CHD, including reduction of blood pressure, reduction in the risk of atherosclerosis secondary to improved lipid profiles, and increase in insulin sensitivity.  In individuals with SCI, obvious limitations are paralysis, limited muscle mass, and sympathetic dysfunction. In addition, for these persons, everyday mobility and activities of daily living are inadequate to meet the requirements for cardiovascular fitness.  In response to a chronically reduced blood flow demand in inactive muscle tissue, there is a decrease in capillary density and diameter, leading to increased vascular resistance.
The reduction in cardiovascular fitness benefits result from the loss of sympathetic control and functional mass.  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. [48, 49] The end result contributes to exercise intolerance, eventually leading to general deconditioning.
Several exercise options to increase cardiac fitness are available and should be considered, though they need to be used 3-4 times weekly at moderate intensity for ultimate cardiac benefits.  They include the use of electrically assisted exercises for leg cycling, arm ergometry, endurance sports, circuit resistive training, and ambulation (especially in patients with paraplegia). Resistive exercise therapy can improve arterial health after chronic SCI, which may reduce the risk of CHD. Body weight–supported treadmill training may improve cardiovascular function in this population.
Another exercise option is hybrid–functional electrical stimulation (FES) rowing. FES rowing provides more benefits to individuals with SCI than arms-only rowing, including greater peak oxygen consumption as well as a typically lower peak respiratory exchange ratio and peak heart rate. This results in a 35% greater oxygen pulse. FES rowing may be more advantageous to those with SCI than most other exercise options, owing to the increased aerobic activity. 
Aerobic exercise effectively improves the lipid profiles of persons with paraplegia but provides less such improvement in patients with tetraplegia. It is recommended that exercise be at a moderate intensity level for 20-30 minutes and at least 3 times a week. The effects of training programs for individuals with SCI may plateau at 4-6 weeks.  An independently maintained exercise program is advocated to support active lifestyles, health, and quality of life.
Precautions worthy of consideration during exercise programs in patients with SCI include the avoidance of injury to and overuse of the muscles and tendons (especially those of the shoulder), the avoidance of fractures secondary to severe osteoporosis, and the avoidance of autonomic dysreflexia and thermal instability or overheating (especially in SCI above T6).
Some elite high-level SCI athletes use the practice of “boosting,” whereby they intentionally increase their blood pressure or induce hyperreflexia to improve physical performance ability. With boosting, there has been shown to be significant increases in blood pressure, noradrenaline concentration, oxygen uptake, and arterial venous oxygen difference, as well as a reduction in stroke volume.
Initially treat hypotension and bradycardia with conservative, nonpharmacologic measures. If these procedures are not entirely effective, medication should be considered. If intravenous (IV) pressors are chosen, use invasive hemodynamic monitoring to guide their use.
After the patient with SCI is stabilized, goals are to eliminate IV medications and treat hypotension with oral agents in order to allow rehabilitation to proceed. In general, use salt tablets (NaCl 1-2 g tid/qid) as the first medication. If the administration of NaCl is not adequate, use pseudoephedrine, then fludrocortisone, and finally midodrine.  Additional medications that have been studied and used in the management of orthostatic hypotension include desmopressin (DDAVP), erythropoietin, and octreotide.
For bradycardia, atropine is the drug of choice, although it is rarely used in rehabilitation settings except during emergencies. Phenylephrine and dopamine also can be considered.
Alpha-adrenergic agonists improve the patient’s hemodynamic status by increasing myocardial contractility and heart rate, increasing cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.
Corticosteroids cause sodium and fluid retention to improve symptomatic orthostatic hypotension, and sympathomimetics augment coronary and cerebral blood flow. Anticholinergics are administered to improve conduction through the atrioventricular (AV) node; this is accomplished by a reduction of vagal tone by way of muscarinic receptor blockade.
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William McKinley, MD Professor, Director of Spinal Cord Injury Medicine, Director of PMR Residency Program, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University Medical Center
William McKinley, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, Academy of Spinal Cord Injury Professionals, American Spinal Injury Association, Association of Academic Physiatrists
Disclosure: Nothing to disclose.
David J Powell, III, MD Resident Physician, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University Health System
Disclosure: Nothing to disclose.
Houman Danesh Virginia Commonwealth University School of Medicine, Medical College of Virginia
Disclosure: Nothing to disclose.
Jeffrey T Tubbs, Jr, MD Resident Physician, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University School of Medicine
Jeffrey T Tubbs, Jr, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Patrick M Foye, MD Director of Coccyx Pain Center, Professor of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School; Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital
Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans
Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.
J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR Senior Associate Dean, Interim Dean of Clinical Medicine, Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Manipulative Medicine, Lincoln Memorial University-DeBusk College of Osteopathic Medicine
J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Osteopathic Examiners, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, Gold Humanism Honor Society, International Society for Communication Science and Medicine, Michigan Osteopathic Association, Oklahoma Osteopathic Association, Tennessee Osteopathic Medical Association
Disclosure: Nothing to disclose.
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Susan V Garstang, MD, to the development and writing of the source article.
Cardiovascular Concerns in Spinal Cord Injury
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