Cardiovascular Responses — Vasovagal Syncope

Vasovagal Syncope

• Loss of consciousness from excessive autonomic reflex activity
• typically triggered by seeing blood, pain, emotional stress, or prolonged standing, Time varying magnetic field (i.e. transcranial magnetic stimulation)
• Underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels resulting in low blood pressure and therefore not enough blood flow to the brain
• Recovery happens without specific treatment. Prevention involves avoiding the triggers.
• Drinking sufficient fluids, salt, and exercise may also be useful.

Mechanism

Regardless of the trigger, the mechanism of syncope is similar

• The nucleus tractus solitarii of the brainstem is activated directly or indirectly by the triggering stimulus
• Results in simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone.

This results in a spectrum of hemodynamic responses:

• On one end of the spectrum is the cardioinhibitory response
  •  ↓ HR, ↓ contractility → ↓ CO → LOC
  • This response results primarily from enhancement in parasympathetic tone.
• On the other end of the spectrum is the vasodepressor response
  •  ↓ BP without change in HR.
  • This occurs due to dilation of the blood vessels, probably as a result of withdrawal of sympathetic nervous system tone.

The majority of people with vasovagal syncope have a mixed response somewhere between these two ends of the spectrum.

One account for these physiological responses is the Bezold-Jarisch reflex.

CVS Challenges

• ↓ in MAP: = due to ↓ CO
• Hydrostatic effects on CPP:
  • ↓MAP at level of brain
  • effect = immediate.
  • NB : ↓MAP at brain level is offset by a similar:
    • ↑ CVP venous side (brain circulation is like an inverted U-tube) as well as on the ↓CSF pressure.
    • CPP is further augmented by an increase in VR from the brain to the heart in the erect position
• Summary: the main challenge to the CVS (and the brain circulation) is ↓MAP

The CVS response

• baroreceptor reflex mechanism:
  • ↓ MAP ⇒ sensed by carotid (mainly) and aortic baroreceptors ⇒ ↓ traffic up to NTS ⇒ via medullary control centre ⇒ ↑ SNS outflow and ↓ PNS outflow.
  • The ↑ SNS outflow causes: [ remember: MAP (minus RAP) = CO x SVR ]
    • [↑preload] peripheral venoC ⇒ ↑ VR ⇒ ↑ CO ⇒ ↑ MAP
    • [↑afterload] peripheral vasoC ⇒ ↑ SVR ⇒ ↑ MAP (slight ↓ in SV due to afterload increase, but net effect = ⇑ MAP)
    • ↑ cardiac contractility ⇒ ↑ CO ⇒ ↑ MAP
    • ↑ Heart rate ⇒ ↑ CO ⇒ ↑ MAP

NB: Baroreflex ⇒ vasoconstriction = more effective than venoconstriction to restore MAP

 ! (not to be confused with the vascular function curves where venoconstriction shifts the curve more up than what vasoconstriction rotates it downwards)

• Cerebral pressure autoregulation: a.k.a. the myogenic mechanism:
  • effective at maintaining constant cerebral blood flow in a MAP range of 50–150 mmHg
  • It effects this by changing the CVR.
  • Onset is not immediate though.

• Activity: Mm pump further augments VR
  • in conjunction with the one-way valves in the veins to prevents further venous pooling

JC 2019

Answer by JC