Syncope

Original Editor - Reem Ramadan Top Contributors - Reem Ramadan


Introduction[edit | edit source]

Syncope, also known as fainting, is defined as the loss of consciousness for a short period of time followed by a rapid recovery. It is a common condition with a frequency ranging between 15% and 39%[1]. It becomes more common with aging where it affects 6% of individuals above the age of 75[2].

Clinical Signs and Symptoms[edit | edit source]

  1. Nausea and/or vomiting
  2. Lightheadedness
  3. Diaphoresis (sweaty palms)
  4. Visual disturbances (tunnel vision, blurred vision)[3]
  5. Headaches
  6. Palpitations
  7. Paraesthesia[4]

Differential Diagnosis[edit | edit source]

The underlying causes of syncope can be classified into four categories:

  • Reflex-mediated: It has three different variations which are vasovagal, carotid sinus and situational. This type of syncope has no increased risk of morbidity and mortality[5]. Vasovagal syncope occurs due to an inciting event or stimulus such as stress, pain, and prolonged standing. The stimulus is often identifiable and lying down or removing the stimulus usually aborts the syncopal episode[6]. Carotid sinus syncope is associated with syncope after head-turning, shaving and wearing a tight collar and can be relieved with a carotid sinus massage[7]. Situational syncope is associated with micturition, defecation, coughing and gastrointestinal stimulation[8].
  • Cardiac-induced: Coronary artery disease, congestive heart failure, and myocarditis are all precursors of syncope[9]. Patients with cardiac disease are at greater risk for developing recurrent syncopal episodes than other patients with syncope[10]. Patients with cardiac-induced syncope have double the risk of all-cause mortality and an increased risk of fatal and nonfatal cardiovascular events[11].
  • Orthostatic causes: Orthostatic hypotension is the drop in blood pressure within 3 minutes of standing which leads to tachycardia and blood volume depletion and thus syncope[12]. It is commonly found in elderlies and exacerbated with dehydration and certain medications like anti-hypertensives, anti-depressants, and diuretic agents.
  • Cerebrovascular causes: Although syncope from cerebrovascular disease is very rare, transient ischemia may result from vertebrobasilar insufficiency and may cause syncope. Headaches, vertigo, dysarthria, and diplopia are indicative signs of syncope from neurologic causes[8].

Initial Assessment[edit | edit source]

During the initial assessment, taking the medical history of the patient and performing physical examinations are crucial to identify the cause of syncope. Syncope may be caused by a life-threatening condition such as pulmonary embolism and myocardial infarction so it's essential during taking the history of the patient to identify the circumstances just before the syncopal episode occurred, during its onset, and after the episode along with the patient's background[13]. For example, just before the onset of the syncopal attack, the diagnostic factors are: position, activity, and triggering pre-disposing events. If the patient has been standing for a prolonged period of time, the possible diagnosis would be reflex-mediated syncope whereas if the patient immediately stands and then experiences a syncopal attack, the possible diagnosis would be in this case orthostatic hypotension. Similarly, if prior to the syncopal episode, the patient was performing a certain exercise, the possible diagnosis would probably be syncope of cardiac origin. As for predisposing factors, if the environment around the patient is crowded or warm, the possible diagnosis would be a reflex-mediated syncope[14]. To be able to diagnose syncope during the onset of the syncopal episode, the diagnostic factors are the manner of falling and the skin color of the patient. For instance, if the patient suddenly collapses during the syncopal episode, the possible diagnosis would be that the syncope is of cardiac origin whereas if the patient kneels over, the most probable diagnosis for identifying the cause of syncope would be either reflex-mediated or orthostatic hypotension. In addition to that, if the patient was flushing or turned pale during syncopal attack, the diagnosis is reflex-mediated syncope whereas if there's a brief change in skin color, the possible diagnosis would be of cardiac-origin[13]. Furthermore, in order to assess the initial cause of syncope, it is crucial to check if the patient has a history of cardiac disorders such as aortic stenosis, neurologic disorders such as Parkinson's Disease, metabolic disorders such as diabetes and if the patient takes certain medications.

Additional Testing[edit | edit source]

The choice of diagnostic tool depends on both the history of the patient and the findings in the physical examination. Normally, the patient arriving to the emergency room is required to have a blood test and an ECG, electrocardiogram. Abnormal ECG readings occur in approximately 90 percent of patients with cardiac-induced syncope but in only 6 percent of patients with neurally-mediated syncope[15]. Holter electrocardiographic monitor, a device used to record heart rhythms, is used when there's a suspicion of an arrhythmic cause of syncope. This type of diagnostic tool is specifically important with patients with known or suspected heart disease, patients who experienced palpitations after syncopal episode and patients who experience syncope after exertion or after lying in supine position[16]. In addition to that, an echocardiography is beneficial in case of cardiac-induced syncope after the patient's history indicates that he has a history of heart disease or after abnormal ECG findings. Patients who experienced syncope with a heart murmur, are specifically required to have an echocardiography to rule out hypertrophic or valvular causes of cardiac disease[17]. Another form of testing would be the head-up tilt-table testing (HUTT), which is used when a patient has an unexplained syncopal episode with no known cause specifically with patients with normal heart beats. This form of testing uses changes in position to reproduce symptoms of syncopal event. During the test, the patient's vital signs including the blood pressure, heart rate and rhythm will be constantly monitored while the patient sitting upright is first tilted by a monitored table to 30 degrees then 45 degrees for a minimum of 2 minutes followed by a 70 degrees tilt for a total of 45 minutes[18]. Significant changes in blood pressure, heart rate, and rhythm indicate that there is a positive tilt table test while no change in blood pressure, heart rate and rhythm or exacerbation of symptoms after the test indicate a negative tilt table test. This test is contraindicated for pregnant patients and patients with positive stress test, 45 or older in men and 55 or older in women[14].

Treatment[edit | edit source]

Vasovagal Syncope: Avoiding situations that trigger a syncopal attack, tilt training which involve exercise sessions with prolonged upright posture[19] and the use of salt and fluid which would help prevent the drop in blood pressure which in return allows bringing enough oxygen to the brain tissue and thus prevent reoccurrence of syncope[20] and in case conservative measures fail, drug therapy using beta blockers and other medications can be used. Pacemaker implantation is an invasive, permanent procedure, it should be considered only in patients with the greatest benefit-to-risk ratio specifically patients older than 40 years of age with recurrent syncope causing injury and decreased quality of life.[21]

Orthostatic Hypotension: Avoid rising quickly from supine or sitting position, avoid medications that trigger orthostatic hypotension such as diuretics and vasodilators and use compression stockings in order to improve venous return[22].

Cardiac-induced Syncope: The treatment depends on the underlying cardiac condition.

References[edit | edit source]

  1. Da Silva RM. Syncope: epidemiology, etiology, and prognosis. Frontiers in physiology. 2014:471.
  2. Syncope: Symptoms, causes & treatments. Cleveland Clinic. Available from: https://my.clevelandclinic.org/health/diseases/17536-syncope (accessed 9/1/2023)
  3. Syncope (fainting). RWJBarnabas Health. Available from: https://www.rwjbh.org/treatment-care/heart-and-vascular-care/diseases-conditions/syncope-fainting-/ (accessed 9/1/2023)
  4. White CM, Tsikouris JP. A review of pathophysiology and therapy of patients with vasovagal syncope. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy. 2000 Feb;20(2):158-65.
  5. Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin EJ, Levy D. Incidence and prognosis of syncope. New England Journal of Medicine. 2002 Sep 19;347(12):878-85.
  6. Kaufmann H. Neurally mediated syncope: pathogenesis, diagnosis, and treatment. Neurology. 1995 Apr 1;45(5):12-8.
  7. Puggioni E, Guiducci V, Brignole M, Menozzi C, Oddone D, Donateo P, Croci F, Solano A, Lolli G, Tomasi C, Bottoni N. Results and complications of the carotid sinus massage performed according to the “method of symptoms”. American Journal of Cardiology. 2002 Mar 1;89(5):599-601.
  8. 8.0 8.1 Arthur W, Kaye GC. The pathophysiology of common causes of syncope. Postgraduate medical journal. 2000 Dec 1;76(902):750-3.
  9. Alboni P, Brignole M, Menozzi C, Raviele A, Del Rosso A, Dinelli M, Solano A, Bottoni N. Diagnostic value of history in patients with syncope with or without heart disease. Journal of the American College of Cardiology. 2001 Jun 1;37(7):1921-8.
  10. Alboni P, Brignole M, Menozzi C, Raviele A, Del Rosso A, Dinelli M, Solano A, Bottoni N. Diagnostic value of history in patients with syncope with or without heart disease. Journal of the American College of Cardiology. 2001 Jun 1;37(7):1921-8.
  11. Benditt DG, Van Dijk JG, Sutton R, Wieling W, Lin JC, Sakaguchi S, Lu F. Syncope. Current problems in cardiology. 2004 Apr 1;29(4):152-229.
  12. Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology. 1996 May;46(5):1470.
  13. 13.0 13.1 Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, van Dijk JG, Fitzpatrick A, Hohnloser S, Janousek J, Kapoor W. Guidelines on management (diagnosis and treatment) of syncope. European heart journal. 2001 Aug 1;22(15):1256-306.
  14. 14.0 14.1 Linzer M, Yang EH, Estes NA. 3, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 1: Value of history, physical examination, and electrophysiology: clinical efficacy assessment project of the American College of physicians. Ann Intern Med. 1997;126:989-6.
  15. Sarasin FP, Louis-Simonet M, Carballo D, Slama S, Rajeswaran A, Metzger JT, Lovis C, Unger PF, Junod AF. Prospective evaluation of patients with syncope: a population-based study. The American journal of medicine. 2001 Aug 15;111(3):177-84.
  16. Benditt DG, Blanc JJ, Brignole M, Sutton R, editors. The evaluation and treatment of syncope: a handbook for clinical practice. John Wiley & Sons; 2009 Feb 12.
  17. Mieszczanska H, Ibrahim B, Cohen TJ. Initial clinical experience with implantable loop recorders. The Journal of Invasive Cardiology. 2001 Dec 1;13(12):802-4.
  18. Tilt Table test. Cleveland Clinic. Available at: https://my.clevelandclinic.org/health/diagnostics/17043-tilt-table-test (accessed 21/1/2023)
  19. Kinay O, Yazici M, Nazli C, Acar G, Gedikli O, Altinbas A, Kahraman H, Dogan A, Ozaydin M, Tuzun N, Ergene O. Tilt Training for Recurrent Neurocardiogenic Syncope Effectiveness, Patient Compliance, and Scheduling the Frequency of Training Sessions. Japanese heart journal. 2004;45(5):833-43.
  20. 5G salt recommendation. Cleveland Clinic. Available at: https://my.clevelandclinic.org/health/drugs/17537-syncope-5g-salt-recommendation (accessed 21/1/2023)
  21. Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. Bmj. 2004 Aug 5;329(7461):336-41.
  22. Figueroa JJ, Basford JR, Low PA. Preventing and treating orthostatic hypotension: as easy as A, B, C. Cleveland Clinic journal of medicine. 2010 May;77(5):298.