Canonical Question
CVS – Responses
Master answer
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.
\[ CBF \; = \; {{MAP \; – \; (CVP \; or \; ICP)} \over {CVR}} \; \; \; {{\leftarrow \leftarrow arterial \; baroreflex} \over {\leftarrow \leftarrow pressure \; autoregulation}}\]
- Activity: Mm pump further augments VR
- in conjunction with the one-way valves in the veins to prevents further venous pooling
JC 2019
Exam appearances
| Exam | Exact wording | Relationship | Success |
|---|---|---|---|
| 2017B Q19 | Describe the physiology of a vasovagal syncope | historical_member | — |