This issue of eMedRef provides information to clinicians on the pathophysiology, diagnosis, and therapeutics of exercise induced collapse caused by neurocardiogenic syncope

Chang, Tony

University of Missouri: MOspace

Neurocardiogenic Syncope Page 1 of 3    1.29.09 Exercise Induced Collapse:  Neurocardiogenic Syncope Background 1. Vasovagal syncope-most common 2. Must rule out congenital heart defects  Pathophysiology 1. Mechanism-sudden reflex vasodilation/bradycardia  o May be caused by:   Stimulation of mechanoreceptors  Elevated catecholamine  Dehydration o Maximum exercise = high cardiac output   Due to increased venous return and high heart rate o Sudden stop decreases venous return o Heart continues forceful contraction with low end diastolic volume   Stimulate vasovagal reflex in medulla to increase vagal tone  Increased vagal tone leads to bradycardia/vasodilation   Hypotension/syncope 2. Other possible mechanisms  o Bradycardia   Increased parasympathetic output from vagus nerve o Vasodilation-due to:   Post exercise withdrawal of alpha-agonist activity   Increased Beta 2 agonist activity o Increased catecholamines/dehydration during prolonged exercise can stimulate ventricular contractions   Catecholamine directly stimulates ventricles  Dehydration increases heart rate/contractility  Diagnostics 1. Detailed history of syncopal event  o Postural or exertional symptoms o Association with neurologic symptoms o History of cardiac disease o History of psychiatric illness o Family history of sudden death 2. Evaluate for structural heart disease  o EKG o ECHO   Pathological causes of syncope  Positive findings may need:   Exercise stress testing  Cardiac catheterization  Coronary angiography  Myocardial biopsy  Electrophysiology study   Neurocardiogenic Syncope Page 2 of 3    1.29.09 o Ambulatory heart monitoring   Necessary if EKG/ECHO negative but continued syncopal episodes   Possible arrhythmia   Consider cardiology consult  Holter-24 hour monitoring  Event monitor-allows up to two week monitoring 3. Neurally mediated syncope  o Carotid-sinus syncope o Psychiatric illnesses (panic, anxiety disorders, major depression)  o Carotid sinus massage   Rubbing carotid sinus stimulates baroreceptors and glossopharyngeal nerve   Can cause decreased heart rate  May slow rapid heart rate  o Atrial flutter or atrial tachycardia  Can provide diagnostic information  May be useful in older patients   Carotid-sinus syncope common in elderly  Avoid in patients with carotid bruit/known cerebrovascular disease   May dislodge thrombus/plaque  Diagnostic testing   Head up tilt table test  Increased sensitivity with provocation with isoproterenol or nitroglycerin  Therapeutics 1. Activity modification 2. Avoid sports that may cause syncopal episodes 3. Proper post exercise cool-down periods  4. Increase salt and water intake 5. Wear compression stockings 6. Reestablish cerebral perfusion  o Place athlete in Trendelenburg position o Medications:   Beta-blockers, disopyramide, SSRIs, fludrocortisone, midodrine  Prevention 1. Proper hydration 2. Cool down periods 3. Avoid provocative environments 4. Be aware of warning signs  o Lie down, cross legs, tighten leg muscles may help avoid fainting 5. Avoid alcohol  o Causes vaso-arterial dilation 6. Reduce caffeine intake 7. Increase fluid intake     Neurocardiogenic Syncope Page 3 of 3    1.29.09 8. Medications:  o B-blockers, disopyramide, SSRIs, fludrocortisone, midodrine o No protocol for athletes exist o Individual response vary 9. Pacemaker  o Currently experimental use only for neurogenic syncope  References 1. Abbiss et al. Effect of carbohydrate ingestion and ambient temperature on muscle fatigue development. J Appl Physiol. 2008; 104: 1021-1028 2. Blue, J, Pecci, M. The Collapsed Athlete. Orthopedic Clinics of North America, Vol. 33, Issue 3, July 2002. 3. Camargo, C, Simmons, FE. Anaphylaxis: Rapid recognition and treatment. UpToDate Online 16.3 Topic last update 10/10/08 4. Davis, J Mark, Alderson L, Nathan, Welsh, S Ralph. Serotonin and Central nervous system fatigue: nutritional considerations. American Journal of Clinical Nutrition, Vol. 72, No. 2, 573S-578S, August 2000. 5. Hew-Butler, T, Ayus, JC, Kipps, C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clinical Journal of Sport Medicine 2008; 18:111 6. Hosey, R, Carek, P, Goo, A. Exercise-Induced Anaphylaxis and Urticaria. American Family Physician. October 15, 2001. 7. McCaffree, J. Managing the Diabetic Athlete. Journal of America Dietetic Assn. 2006: 106 (8): 1161-2. 8. Nybo, L, Nielsen, B, Blomstrand, E, Moller, K. Secher, N. Neurohumoral responses during prolonged exercise in humans. J Appl Physiol, September 1, 2003; 95(3): 1125 - 1131. 9. Ostrowski, K, Schjerling, P, Pedersen, B. Physical activity and plasma interleukin-6 in humans: effect of intensity of exercise European. Journal of Applied Physiology 2000, vol. 83, n6, pp. 512-515  10. J. D. Fernstrom and M. H. Fernstrom. Exercise, Serum Free Tryptophan, and Central Fatigue. J. Nutr., February 1, 2006; 136(2): 553S - 559S. 11. Tang, A. A Practical Guide to Anaphylaxis. Am Fam Physician 2003; 68:1325-32, 1339-40.    Author:  Tony Chang, MD, University of Nevada FPRP  Editor:  Carol Scott, MD, University of Nevada Reno FPRP  

Exercise induced collapse: neurocardiogenic syncope

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University of Missouri: MOspace