Cardiovascular Complications in Spinal Cord Injury

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Cardiovascular Complications in Spinal Cord Injury

• Greg Nemunaitis, MD

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• Spinal cord injury can result in significant
  compromise of cardiovascular control
• due to an
• impaired autonomic nervous system
• and
• skeletal muscle paralysis

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Acute Cardiovascular Complications from the
NSCID 2005
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Chronic Cardiovascular Complications from the
NSCID 2005
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Spinal Cord and Autonomic Nervous System Anatomy
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Cardiovascular Anatomy
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Evolution of the control of the cardiovascular
system

• Course of Events
• Immediately after SCI occurs, blood pressure
  rises due to release of norepinephrine from the
  adrenal glands and by a pressor response from
  mechanical disruption of vasoactive neurons and
  tracts in the spinal cord.
• This is followed by a period of spinal shock
  (decreased cortical spinal and sympathetic
  activity and unopposed vagal tone).
• Over time reflexes and spasticity return due to
  compensatory changes occur in the vascular beds,
  skeletal muscle, and rennin-angiotensin
  aldosterone system.

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Short- and long-term consequences.

• Hypotension
• Cardiac arrhythmias
• Autonomic dysreflexia
• Poikylothermia
• Deep vein thrombosis
• Coronary heart disease
• Exercise response

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Hypotension

• Decreased compensatory vasoconstriction
• Venous pooling (skeletal muscle and splanchnic
  regions),
• venous pooling in the extravascular tissues lower
  extremities (leg swelling)
• reduced venous blood return resulting in reduced
  stroke volume, and blood pressure.
• Hypotension, and especially orthostasis, usually
  improves within days to weeks as compensatory
  changes occur in the vascular beds, skeletal
  muscle, and rennin-angiotensin aldosterone
  system.

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Hypotension Management

• Leg elevation, Abd Binder, Ace wraps, Ted Hose,
  Tilt in space W/C, Tilt table, Easy stand
• Salt tablets.
• Pseudoephedrine (Actifed and Pseudofed)
• Fludrocortisone (Florinef)
• Midodrine (ProAmitine)
• Desmopressin (DDAVP)
• Erythropoietin
• Octreotide

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Cardiac arrhythmias

• The ANS modulates cardiac electrophysiology and
  autonomic dysfunction can lead to ventricular
  arrhythmias.
• Bradycardia
• Tachycardia

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Bradycardia

• Unopposed Vagal Stimulation seen with SCI above T1

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Bradycardia

• 100 of patients with motor complete cervical
  injuries develop bradycardia,
• 68 are hypotensive,
• 35 require pressors
• 16 have primary cardiac arrest.
• 35-71 develop bradycardia with motor incomplete
  cervical injuries and few have hypotension or
  require pressors. Patients in this group rarely
  have primary cardiac arrest.
• 13-35 have bradycardia with thoracolumbar
  injuries.
• This problem usually resolves over the first 2-6
  weeks after SCI.

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Bradycardia due to unopposed vagal stimulation
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Bradycardia

• It is often precipitated by tracheal or rectal
  stimulation (eg, during suctioning or bowel
  program) and hypoxia.
• Atropine may be needed, and temporary (sometimes
  permanent) cardiac pacemakers have been used.
• This problem usually resolves over the first 2-6
  weeks after SCI.

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Tachycardia

• PSVT
• Sinuse tachycardia

• Atrial Flutter
• Atrial Fibrillation

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Autonomic dysreflexia

• Due to loss of supraspinal control of
  hyperreflexic Sympathetic Nervous System
  activity, caused by noxious stimuli below the
  level of injury in individuals with SCI. This can
  lead to dangerously high blood pressures that can
  result in cerebral hemorrhage.

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Autonomic Dysreflexia

• Autonomic dysreflexia (AD) is the imbalance of
  excessive reflex sympathetic discharge occurring
  in patients with spinal cord injury (SCI) above
  the splanchnic sympathetic outflow (T5-T6) due to
  nociceptive input..

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Signs and Symptoms of AD

• Headache
• Nasal stuffyness
• Facial flush
• Increased spasticity
• Elevated blood pressure
• Seizure
• Stroke

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Treatment of AD

• Sit up
• Check the Blood Pressure
• Apply Nitropaste
• Seek out the cause
• 90 of the time it is related to the bladder so
  replace the foley
• Bowel, skin, fracture, DVT, Infection, ingrown
  toe nail, leg bag strap

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Poikylothermia

• Poikylothermia Patients with lesions above T6
  are poikilothermic and cannot regulate their body
  temperature.
• The lack of vasoconstrictors and ability shift
  blood flow to warm or cool the body
• The inability to sweat below the level of the
  lesion.

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Treatment of Poikylothermia

• Avoid excessive warm or cool environments
• Dress appropriately
• Add or remove blankets
• Wear a hat if it is cool
• Water spray bottle if it is warm
• Intravenous fluids should be warmed.

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Deep vein thrombosis (DVT)

• Overall incidence without prophylaxis is
  estimated to be 40 based on meta-analysis of DVT
  in patients with acute SCI.

Blood Flow
Powell M, Kirshblum S, O'Connor KC. Arch Phys Med
Rehabil. 1999 Sep80(9)1044-6
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DVT Pathophysiology

• Predisposing risk factors for the development of
  DVT following SCI can be classified with the
  Virchow triad
• Venous stasis results from loss of pumping
  function provided by contracting muscles.
• Hypercoagulability can occur as a result of
  stimulation of thrombogenic factors following
  injury, with resultant increase in platelet
  aggregation and adhesion (reduced fibrinolytic
  activity along with higher levels of von
  Willebrand factor antigen and Factor VIII-related
  antigen and resulting in hyperactive platelet
  aggregation
• Intimal injury may result directly from the
  release of vasoactive amines with trauma or
  surgery, or indirectly from external pressure on
  the paralyzed leg.

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Deep Venous Thrombosis

• Swelling
• Fever of unknown origin
• Increased spasticity and AD
• Clinically apparent DVT occurs in approximately
  15 to 50.
• DVT can lead to pulmonary embolism (5-10) and
  death.

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DVT Treatment

• Anticoagulation with Lovenox, Heparin, and or
  coumadin
• If clinically contraindicated place venacaval
  filter
• Continue activity and compression garments

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DVT/PE Prevention Guidelines

• All patients will be on Lovenox or Heparin to
  prevent blood clot
• Non-complicated spinal cord injury (no
  co-morbidity) will have 8 weeks of treatment
• Complicated spinal cord injury (having at least
  one co-morbidity) will have 12 weeks of treatment
• Standard of care to prevent DVT Anticoagulation
  Therapy at therapeutic doses (Lovenox 30mg SQ BID
  or Heparin 5000 units SQ BID/TID), SCDs while in
  bed, and Tedhose and/or Ace Wraps when out of bed.

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Pearls

• DVT occurs in 40-90 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.
• Historicaly clinical factors believed to be
  associated with DVT include motor complete
  injuries, paraplegia, and male gender.
• In a recent study by Powell et al, there was no
  statistical difference in incidence of DVT
  between motor complete versus motor incomplete
  injuries, tetraplegic versus paraplegic, or
  traumatic versus nontraumatic causes.
• Thus, all SCI patients are at risk of developing
  a DVT.

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Pulmonary Embolism
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Venacaval Filter
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Coronary Heart Disease

• Coronary Heart Disease is thought to increase
  after SCI due to
• physical inactivity
• obesity
• hyperlipidemia
• insulin resistance
• diabetes
• CHD accounts for approximately 20 of deaths in
  the SCI population.
• Modifiable risk factors for CHD prevention
  include high blood pressure, smoking, obesity,
  physical inactivity, and cholesterol and/or lipid
  control.
• This risk may be increasingly important as the
  life expectancy of people with SCI lengthens.

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Response to exercise

• Lesions above T1-4 can compromise increases in
  heart rate and stroke volume.
• CO HR x SV
• Stroke volume is determined by
• 1. Preload (return of venous blood),
• 2. Afterload (resistance to ventricular
  ejection).
• 3. Contractility (power of the cardiac muscle
  influenced by the sympathetic nervous system).

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Response to exercise
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Dont over eat
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Eat smart
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Fish is good
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Get your tail off the ground
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Not upside down
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Fly high
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Exercise
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Thank you