eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury
Cardiovascular Concerns in Spinal Cord Injury: Treatment & Medication
Updated: Feb 15, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Rehabilitation Program
Physical Therapy
The goal for management of orthostatic hypotension is to alleviate the disabling symptoms, not to normalize the patient's blood pressures. 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 anti-embolism 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/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 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.
Medical Issues/Complications
The initial care of patients with SCI who suffered neurogenic shock with clinically significant hypotension includes careful monitoring of their cardiovascular and fluid status.35 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.37
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).
Consultations
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.
Other Treatment
- Salt and fluid intake - 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 - Biofeedback and functional electrical stimulation relieve symptoms and may have a role in the patient's care.
- Exercise and physical fitness to prevent CHD
- In the general population, physical activity has several benefits in terms of CHD, including the reduction of blood pressure, an increase in insulin sensitivity, and a reduction in the risk of atherosclerosis secondary to improved lipid profiles. In an individual with SCI, obvious limitations are paralysis, limited muscle mass, adrenergic dysfunction, and the fact that the patient's everyday mobility and activities of daily living are inadequate to meet the requirements for cardiovascular fitness. The magnitude of physiologic response is diminished in high thoracic and cervical SCI and often prevents heart rate increases above 120 bpm.
- Several exercise options to increase cardiac fitness are available and should be considered.29 They include the use of electrically assisted exercises for leg cycling, arm ergometry, standing, 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.
- Aerobic exercise effectively improves the lipid profiles of persons with paraplegia but provides less such improvement in patients with tetraplegia. The effects of training programs for individuals with SCI may plateau at 4-6 weeks.38 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).
- Cardiac rehabilitation
- 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 pressures).
- 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.
Medication
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.39 Specific guidelines are discussed in the medication tables. Additional medications (not discussed here) 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 (DOC), though it is rarely used in rehabilitation settings except during emergencies.
Alpha-adrenergic agonists
These agents 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.
Midodrine (ProAmatine)
Typically used after other drugs fail.
Adult
2.5-10 mg PO tid while patient is awake and upright at intervals of at least 3 h; allow >3 h between last dose and hs
Pediatric
Not established
Potentiation of alpha agonists, sodium-retaining steroids; antagonization of alpha antagonists, bradyarrhythmias, cardiac glycoside, beta blockers; CNS drugs may cause bradycardia; drugs excreted renally may affect blood levels
Documented hypersensitivity, severe heart disease, acute renal disease, urinary retention, pheochromocytoma, thyrotoxicosis, supine hypertension
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor blood pressure; urinary retention; visual problems treated with fludrocortisone acetate; renal and hepatic dysfunction; pregnancy and breastfeeding
Corticosteroids
These drugs cause sodium and fluid retention to improve symptomatic orthostatic hypotension.
Fludrocortisone acetate (Florinef)
Typically used for hypotension not responsive to NaCl and pseudo-ephedrine; works well in combination with them.
Adult
0.05-0.2 mg PO qd; typical initial dose 0.1 mg qam
Pediatric
Not established
Antagonizes effects of anticholinergics; rifampin, hydantoins, and barbiturates decrease effects; decreases salicylate levels
Documented hypersensitivity, hypertension, and systemic fungal infection
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hypothyroidism, volume-overload states (eg, congestive heart failure [CHF]), renal insufficiency, osteoporosis, ocular herpes simplex, emotional instability and psychotic tendencies, nonspecific ulcerative colitis, diverticulitis, fresh intestinal anastomoses, peptic ulcer, and myasthenia gravis; monitor serum potassium levels, a blood pressure, and weight gain.
Sympathomimetics
These drugs augment coronary and cerebral blood flow.
Pseudoephedrine (Actifed, Sudafed)
Sympathomimetic drug. Stimulates release of epinephrine stores, producing alpha- and beta-adrenergic effects. First-line agent if physical measures and NaCl are not effective.
Adult
30-60 mg PO q4-6h; not to exceed 240 mg in 24 h; avoid at night; may cause anxiety and insomnia
Pediatric
<2 years: Not recommended
2-6 years: 15 mg PO q4-6h; not to exceed 60 mg/d
6-12 years: 30 mg PO q4-6h
>12 years: Administer as in adults
Propranolol, monoamine oxidase inhibitors (MAOIs), and sympathomimetic agents may increase toxicity; methyldopa and reserpine may reduce effects
Documented hypersensitivity; severe anemia, postural hypertension or hypotension, angle-closure glaucoma, head trauma, or cerebral hemorrhage
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiovascular disease, diabetes mellitus, prostatic hypertrophy, and increased intra-ocular pressure
Ephedrine (Ephedrine sulfate)
Sympathomimetic drug. Stimulates release of epinephrine stores, producing alpha- and beta-adrenergic effects.
Adult
25-50 mg PO q4-6h; not to exceed 200 mg in 24h; avoid at night; can cause anxiety and insomnia
Pediatric
3 mg/kg/d PO in 4-6 divided doses
Theophylline, atropine, or MAOIs may increase toxicity; alpha and beta blockers decrease vasopressor effects; cardiac glycosides and general anesthetics increase cardiac stimulation
Documented hypersensitivity; angle-closure glaucoma, and cardiac arrhythmias
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in elderly and patients with diabetes mellitus, hyperthyroidism, hypertension, cardiovascular disease, prostatic hypertrophy, or cerebrovascular insufficiency
Anticholinergics
These medications 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.
Atropine sulfate (Isopto, Atropair)
DOC for intermittent acute bradycardia. Increases heart rate with vagolytic effects, increasing cardiac output.
Adult
0.5-1 mg IV; may repeat to maximum 2 mg total
Pediatric
0.01 mg/kg IV; may repeat q4-6h; maximum 0.4 mg total or 0.3 mg/m2
Co-administration with other anticholinergics has additive effects; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; tricyclic antidepressants with anticholinergic activity may increase effects
Documented hypersensitivity; acute narrow-angle glaucoma, obstructive uropathy, obstructive GI disease, ileus, tachycardia, myocardial ischemia, asthma, and myasthenia gravis
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Avoid in Down syndrome and/or in children with brain damage to prevent hyperreactive response; avoid in CHD, tachycardia, CHF, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization
More on Cardiovascular Concerns in Spinal Cord Injury |
| Overview: Cardiovascular Concerns in Spinal Cord Injury |
| Differential Diagnoses & Workup: Cardiovascular Concerns in Spinal Cord Injury |
 Treatment & Medication: Cardiovascular Concerns in Spinal Cord Injury |
| Follow-up: Cardiovascular Concerns in Spinal Cord Injury |
| References |
| « Previous Page | Next Page » |
References
Eidelberg EE. Cardiovascular response to experimental spinal cord compression. J Neurosurg. Mar 1973;38(3):326-31. [Medline].
Meinecke FW, Rosenkranz KA, Kurek CM. Regulation of the cardiovascular system in patients with fresh injuries to the spinal cord--preliminary report. Paraplegia. Nov 1971;9(3):109-12. [Medline].
Piepmeier JM, Lehmann KB, Lane JG. Cardiovascular instability following acute cervical spinal cord trauma. Cent Nerv Syst Trauma. 1985;2(3):153-60. [Medline].
Laird AS, Finch AM, Waite PM, et al. Peripheral changes above and below injury level lead to prolonged vascular responses following high spinal cord injury. Am J Physiol Heart Circ Physiol. Nov 30 2007;[Medline].
Evans DE, Kobrine AI, Rizzoli HV. Cardiac arrhythmias accompanying acute compression of the spinal cord. J Neurosurg. Jan 1980;52(1):52-9. [Medline].
Gondim FA, Lopes AC, Oliveira GR. Cardiovascular control after spinal cord injury. Curr Vasc Pharmacol. Jan 2004;2(1):71-9. [Medline].
Greenhoot JH, Shiel FO, Mauck HP Jr. Experimental spinal cord injury. Electrocardiographic abnormalities and fuchsinophilic myocardial degeneration. Arch Neurol. Jun 1972;26(6):524-9. [Medline].
Teasell RW, Arnold JM, Krassioukov A, et al. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil. Apr 2000;81(4):506-16. [Medline].
Young W, DeCrescito V, Tomasula JJ, et al. The role of the sympathetic nervous system in pressor responses induced by spinal injury. J Neurosurg. Apr 1980;52(4):473-81. [Medline].
Lehmann KG, Lane JG, Piepmeier JM, et al. Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course and severity. J Am Coll Cardiol. Jul 1987;10(1):46-52. [Medline].
Frisbie JH. Microvascular instability in tetraplegic patients: preliminary observations. Spinal Cord. May 2004;42(5):290-3. [Medline].
Mathias CJ, Christensen NJ, Frankel HL, et al. Cardiovascular control in recently injured tetraplegics in spinal shock. Q J Med. Apr 1979;48(190):273-87. [Medline].
Mathias CJ, Frankel HL. Clinical manifestations of malfunctioning sympathetic mechanisms in tetraplegia. J Auton Nerv Syst. Mar-Apr 1983;7(3-4):303-12. [Medline].
McLeod JG, Tuck RR. Disorders of the autonomic nervous system: Part 1. Pathophysiology and clinical features. Ann Neurol. May 1987;21(5):419-30. [Medline].
Wecht JM, Weir JP, Krothe AH, et al. Normalization of supine blood pressure after nitric oxide synthase inhibition in persons with tetraplegia. J Spinal Cord Med. 2007;30(1):5-9. [Medline]. [Full Text].
Claydon VE, Steeves JD, Krassioukov A. Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology. Spinal Cord. Jun 2006;44(6):341-51. [Medline].
De Groot PC, Van Kuppevelt DH, Pons C, et al. Time course of arterial vascular adaptations to inactivity and paralyses in humans. Med Sci Sports Exerc. Dec 2003;35(12):1977-85.
Mathias CJ. Bradycardia and cardiac arrest during tracheal suction--mechanisms in tetraplegic patients. Eur J Intensive Care Med. 1976;2(4):147-56. [Medline].
Ruiz-Arango AF, Robinson VJ, Sharma GK. Characteristics of patients with cervical spinal injury requiring permanent pacemaker implantation. Cardiol Rev. Jul-Aug 2006;14(4):e8-e11.
Winslow EB, Lesch M, Talano JV, et al. Spinal cord injuries associated with cardiopulmonary complications. Spine. Oct 1986;11(8):809-12. [Medline].
Myers J, Lee M, Kiratli J. Cardiovascular disease in spinal cord injury: an overview of prevalence, risk, evaluation, and management. Am J Phys Med Rehabil. Feb 2007;86(2):142-52. [Medline].
Manns PJ, McCubbin JA, Williams DP. Fitness, inflammation, and the metabolic syndrome in men with paraplegia. Arch Phys Med Rehabil. Jun 2005;86(6):1176-81. [Medline].
Maruyama Y, Mizuguchi M, Yaginuma T, et al. Serum leptin, abdominal obesity and the metabolic syndrome in individuals with chronic spinal cord injury. Spinal Cord. Jan 22 2008;[Medline].
Liang H, Mojtahedi MC, Chen D, et al. Elevated C-reactive protein associated with decreased high-density lipoprotein cholesterol in men with spinal cord injury. Arch Phys Med Rehabil. Jan 2008;89(1):36-41. [Medline].
Szlachcic Y, Adkins RH, Adal T, et al. The effect of dietary intervention on lipid profiles in individuals with spinal cord injury. J Spinal Cord Med. 2001;24(1):26-9. [Medline].
Nash MS, Jacobs PL, Mendez AJ, et al. Circuit resistance training improves the atherogenic lipid profiles of persons with chronic paraplegia. J Spinal Cord Med. 2001;24(1):2-9. [Medline].
Dela F, Mohr T, Jensen CM, et al. Cardiovascular control during exercise: insights from spinal cord-injured humans. Circulation. Apr 29 2003;107(16):2127-33. [Medline]. [Full Text].
Ditor DS, Macdonald MJ, Kamath MV, et al. The effects of body-weight supported treadmill training on cardiovascular regulation in individuals with motor-complete SCI. Spinal Cord. Nov 2005;43(11):664-73. [Medline].
Thijssen DH, Ellenkamp R, Smits P, et al. Rapid vascular adaptations to training and detraining in persons with spinal cord injury. Arch Phys Med Rehabil. Apr 2006;87(4):474-81. [Medline].
Spinal Cord Injury Information Network. Spinal Cord Injury. Facts and Figures at a Glance. 2006;[Full Text].
McKinley W, Santos K, Meade M, et al. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30(3):215-24. [Medline]. [Full Text].
Wirth B, van Hedel HJ, Kometer B, et al. Changes in activity after a complete spinal cord injury as measured by the Spinal Cord Independence Measure II (SCIM II). Neurorehabil Neural Repair. Aug 30 2007;[Medline].
Szlachcic Y, Carrothers L, Adkins R, et al. Clinical significance of abnormal electrocardiographic findings in individuals aging with spinal injury and abnormal lipid profiles. J Spinal Cord Med. 2007;30(5):473-6. [Medline].
Jacobs P, Beekhuizen K. Appraisal of Physiological Fitness in Persons with Spinal Cord Injury. Top Spinal Cord Injur Rehabil. 2005;10(4):32-50.
Tuli S, Tuli J, Coleman WP, et al. Hemodynamic parameters and timing of surgical decompression in acute cervical spinal cord injury. J Spinal Cord Med. 2007;30(5):482-90. [Medline].
Spungen AM, Adkins RH, Stewart CA, et al. Factors influencing body composition in persons with spinal cord injury: a cross-sectional study. J Appl Physiol. Dec 2003;95(6):2398-407. [Medline]. [Full Text].
Vale FL, Burns J, Jackson AB, et al. Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management. J Neurosurg. Aug 1997;87(2):239-46. [Medline].
Bizzarini E, Saccavini M, Lipanje F, et al. Exercise prescription in subjects with spinal cord injuries. Arch Phys Med Rehabil. Jun 2005;86(6):1170-5. [Medline].
Barber DB, Rogers SJ, Fredrickson MD, et al. Midodrine hydrochloride and the treatment of orthostatic hypotension in tetraplegia: two cases and a review of the literature. Spinal Cord. Feb 2000;38(2):109-11. [Medline].
Further Reading
Keywords
cardiovascular concerns in spinal cord injury, neurogenic shock, orthostatic hypotension, spinal cord injury, SCI, autonomic nervous system, ANS, autonomic dysreflexia, deep vein thrombosis, DVT, coronary heart disease, CHD, bradycardia
