Cardiovascular Complications in Spinal Cord Injury

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

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.

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), SCD�s 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. Don�t over eat

43. Thank you