17B19: Exam Report

Describe the physiology of a vasovagal syncope

41% of candidates passed this question.

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.

G3vii / 17B19: Describe the physiology of a vasovagal syncope

Definition

[CICM 2017B q19 examiner’s report]

  • aka neurocardiogenic syncope
  • A benign, self-limiting condition in which there is a loss of consciousness from excessive autonomic reflex activity. Whereas orthostatic hypotension is due to a failure of the autonomic reflex activity

Pathway

Pathway 1 [Guyton & Hall]

Pathway 2 [Pappano & Wier]

Trigger

Pathway 1 [Guyton & Hall]

Emotion, stress, pain

Pathway 2 [Pappano & Wier]

Vigorous ventricular contractions at a reduced filling volume (e.g. in orthostatic hypotension)

  • In a person standing quietly, ventricular filling is diminished because blood tends to pool in the veins in the abdomen & legs -> ↓CO & MAP -> ↑SNS via baroreceptor reflex -> stimulates vigorous ventricular contraction

Sensor

Pathway 1 [Guyton & Hall]

Cerebral cortex

Pathway 2 [Pappano & Wier]

Cardiac mechanoreceptors in LV (a type of cardiopulmonary baroreceptor)

Afferent pathway

Pathway 1 [Guyton & Hall]

Interneurons -> vasodilatory center of anterior hypothalamus -> vagal centers of the medulla

Pathway 2 [Pappano & Wier]

Unmyelinated vagal fibres -> Nucleus tractus solitarius

Unmyelinated sympathetic fibres -> travel with visceral afferents to enter the dorsal horn of the spinal cord before ascending to the medulla

Integrator

  • Vasodilatory center of the anterior hypothalamus
  • Vagal centers of the medulla (Nucleus Ambiguus) -> parasympathetic outflow
  • Rostro-ventrolateral medulla (RVLM) -> sympathetic outflow

Effector + Effect

  • Excessive increased parasympathetic outflow & inhibition of sympathetic outflow
    • Cardioinhibitory = ↓HR & ↓contractility -> ↓CO
    • Vasodepressor = vasodilation -> ↓SVR
    • Combined effect = ↓MAP -> ↓Cerebral blood flow -> syncope

Compensation after vasovagal syncope

There are immediate compensatory mechanisms that restore BP within seconds:
  1. Arterial baroreceptor reflex (main)
    • ↓ BP causes ↓ stretching of high-pressure baroreceptors in carotid sinus and aortic arch → ↓ firing to NTS along CN IX and X, respectively → removal of inhibition of medullary vasomotor centres → ↑ SNS outflow (and ↓ PNS outflow) which maintains BP by causing:
      1. ↑ HR and myocardial contractility → ↑ C.O.
      2. Venoconstriction of venous (capacitance) vessels → ↑ VR to ↑ C.O.
      3. Vasoconstriction of arteriolar (resistance) vessels → ↑ SVR
  2. Muscle pump in lower limbs
    • If a patient moves their lower limbs after standing, muscle contraction squeezes blood back to the heart and keeps venous pressure < 30 mmHg in feet → prevents significant venous pooling in lower limbs and promotes ↑ VR and ↑ C.O.
  3. Venous valves of lower limbs
    • Brakes up column of venous blood in lower limbs and promotes unidirectional blood flow back to the heart
  4. Thoracic pump
    • ↑ ventilation with standing causes ↑ -ve intrathoracic pressures → favours VR back to heart → ↑ C.O.

Effect on cerebral blood flow (CBF)

\( \text{CBF = } \normalsize \frac{\text{ CPP }}{\text{CVR}}  \)

CPP = MAP – CVP (or ICP)  →  due to “Starling Resistor” mechanism 

  • Vasovagal results in ↓ MAP à therefore initially ↓ ICP
  • The fall in CPP (and CBF) is partly offset by the implications of “Monroe-Kellie doctrine” (Ie. cranium is fixed volume containing brain, blood, CSF) of decreasing ICP. This response is not immediate
  • Mechanism:
    1. ↑ drainage of venous blood into the right heart (due to “Siphoning effect”) → this minimises ↓ cerebral blood volume → ↓ ICP → minimises ↓ CPP and CBF
    2. ↑ drainage of CSF from brain to spinal cord (as CSF also acts as a column of fluid subject to the effects of gravity) → this ↓ CSF volume in cranium → ↓ ICP → minimises ↓ CPP and CBF
  • Cerebral pressure autoregulation:
    • CBF is kept constant within a wide-range of MAP (50-150 mmHg) despite fluctuations in MAP within this range
    • Mechanism – ↓ arterial BP causes ↓  arteriolar wall stretching → arteriolar SM respond by dilating and ↓ arteriolar tone → this results in vasodilation and ↓  arteriolar resistance → offsets ↓  local blood flow a/w ↓ arterial BP

[Guyton & Hall 13e, pg 218]

[Pappano & Wier 11e, pg 94 & pg 170]

[Kam & Power 3e, pg 168]

Author: Huiling Tan / James Chu