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Cardiovascular Complications in Spinal Cord Injury

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Cardiovascular Complications in Spinal Cord Injury Greg Nemunaitis, MD Acute Cardiovascular Complications from the NSCID 2005 Chronic Cardiovascular Complications ... – PowerPoint PPT presentation

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Title: Cardiovascular Complications in Spinal Cord Injury


1
(No Transcript)
2
Cardiovascular Complications in Spinal Cord Injury
  • Greg Nemunaitis, MD

3
  • Spinal cord injury can result in significant
    compromise of cardiovascular control
  • due to an
  • impaired autonomic nervous system
  • and
  • skeletal muscle paralysis

4
Acute Cardiovascular Complications from the
NSCID 2005
5
Chronic Cardiovascular Complications from the
NSCID 2005
6
Spinal Cord and Autonomic Nervous System Anatomy
7
Cardiovascular Anatomy
8
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.

9
Short- and long-term consequences.
  • Hypotension
  • Cardiac arrhythmias
  • Autonomic dysreflexia
  • Poikylothermia
  • Deep vein thrombosis
  • Coronary heart disease
  • Exercise response

10
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.

11
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

12
Cardiac arrhythmias
  • The ANS modulates cardiac electrophysiology and
    autonomic dysfunction can lead to ventricular
    arrhythmias.
  • Bradycardia
  • Tachycardia

13
Bradycardia
  • Unopposed Vagal Stimulation seen with SCI above T1

14
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.

15
Bradycardia due to unopposed vagal stimulation
16
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.

17
Tachycardia
  • PSVT
  • Sinuse tachycardia
  • Atrial Flutter
  • Atrial Fibrillation

18
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.

19
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..

20
Signs and Symptoms of AD
  • Headache
  • Nasal stuffyness
  • Facial flush
  • Increased spasticity
  • Elevated blood pressure
  • Seizure
  • Stroke

21
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

22
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.

23
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.

24
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
25
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.

26
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.

27
DVT Treatment
  • Anticoagulation with Lovenox, Heparin, and or
    coumadin
  • If clinically contraindicated place venacaval
    filter
  • Continue activity and compression garments

28
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.

29
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.

30
Pulmonary Embolism
31
Venacaval Filter
32
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.

33
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).

34
Response to exercise
35
Dont over eat
36
(No Transcript)
37
Eat smart
38
Fish is good
39
Get your tail off the ground
40
Not upside down
41
Fly high
42
Exercise
43
Thank you
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