Question 19

College Answer

Generally, there was a lack of knowledge about this topic with many candidates confusing
vasovagal syncope with a Valsalva or orthostatic hypotension. A “vasovagal” is from excessive
autonomic reflex activity in contrast to orthostatic hypotension which is a failure of the
autonomic reflex response.
A good place to start was with a description of vasovagal syncope, also known as
neurocardiogenic syncope. It is benign, self-limiting and caused by an abnormal or exaggerated
autonomic response to various stimuli (which should have been listed). The mechanism should
have been described including the various receptors involved.

Discussion

Interestingly, though the official CICM answer draws a distinction between vasovagal syncope and orthostatic hypotension ("which is a failure of the autonomic reflex response"), orthostatic causes are listed in the 2018 ESC guidelines for the management of syncope. In fact they separated vasovagal syncope into "orthostatic" and "emotional", alongside several other forms of reflexive neurally mediated syncopes. 

• Description:
  • ​​V​​​​asovagal syncope, or neurocardiogenic syncope, is a transient loss of consciousness due to global cerebral hypoperfusion, which occurs as the result of an autonomic reflex response to various stimuli
• Stimulus:  
  • For "true" vasovagal syncope:
    • Emotional distress
    • Orthostatic changes (decreased preload with changes in posture)
  • For "situational" neurocardigenic syncope:
    • Micturition
    • Increased intrathoracic pressure:
      • Defaecation
      • Cough, sneeze, laughter, playing a brass instrument 
      • Following exercise
    • "Carotid sinus syndrome"
• Sensors: Central (descending) as well as peripheral
  • Mechanoreceptors located in the wall of the left ventricle, the aorta, atria and the pulmonary trunk
  • Numerous other strecth receptors, eg. splanchnic, bowel, 
• Afferent nerves: Unknown! Presumably, both central nervous system and peripheral sensory nerves are involved
• Processor: Unknown! Presumably at some stage the nucleus of the solitary tract and the nucleus ambiguus are involved.
• Efferent nerves: 
  • Vagus nerve, via the cardiac ganglion
  • Sympathetic nervous system
• Effector:  SA node, AV node, peripheral smooth muscle
• Effects:
  • Vagal: bradycardia
  • Sympathetic: systemic vasodilation (mainly muscles)
  • Vasovagal syncope is thought to have four distint phases:
    • phase 1: early stabilization (by normal baroreceptor reflex)
    • phase 2: circulatory instability (baroreflex vasoconstriction)
    • phase 3: terminal hypotension (bradycardia, cerebral hypoperfusion, systemic vasodilation)
    • phase 4: recovery

Jardine, David L., et al. "The pathophysiology of the vasovagal response." Heart Rhythm 15.6 (2018): 921-929.

Brignole, Michele, et al. "2018 ESC Guidelines for the diagnosis and management of syncope." European heart journal 39.21 (2018): 1883-1948.

Alboni, Paolo, Marco Alboni, and Giorgio Bertorelle. "The origin of vasovagal syncope: to protect the heart or to escape predation?." Clinical Autonomic Research 18.4 (2008): 170-178.

van Dijk, J. Gert, and Robert Sheldon. "Is there any point to vasovagal syncope?." Clinical Autonomic Research 18.4 (2008): 167.

Berntson, Gary G., John T. Cacioppo, and Karen S. Quigley. "Respiratory sinus arrhythmia: autonomic origins, physiological mechanisms, and psychophysiological implications." Psychophysiology 30.2 (1993): 183-196.

Hayano, Junichiro, et al. "Respiratory sinus arrhythmia: a phenomenon improving pulmonary gas exchange and circulatory efficiency." Circulation 94.4 (1996): 842-847.

Braga, Simona Sarzi, Raffaele Manni, and Roberto FE Pedretti. "Laughter-induced syncope." The Lancet 366.9483 (2005): 426.

Faulkner, Maurice, and E. P. Sharpey-Schafer. "Circulatory effects of trumpet playing." British medical journal 1.5123 (1959): 685.