Vasovagal syncope and Darwinian fitness

  title={Vasovagal syncope and Darwinian fitness},
  author={Rolf R Diehl},
  journal={Clinical Autonomic Research},
  • R. Diehl
  • Published 1 April 2005
  • Biology, Medicine
  • Clinical Autonomic Research
Vasovagal syncope, although often seen as a disease, is the result of a neurophysiological reflex which can be induced in most healthy people after a 30 % reduction in blood volume either by venous pooling or by hemorrhage. Studies in mammals showed that the activation of certain brainstem nuclei including the caudal midline medulla is responsible for hypotension and bradycardia following central hypovolemia. The hypothesis is presented that vasovagal fainting developed during the evolution in… 

Pathophysiology of Vasovagal Syncope: Conclusive Remarks

Adenosine and B-type natriuretic peptides are promising markers to be used in typifying clinical forms of VVS, their aetiology and prognosis.

Vasovagal Syncope As A Manifestation Of An Evolutionary Selected Trait.

It is suggested that typical VVS should be regarded as a selected response, which probably evolved in the ancient past as a defense mechanism of the organism within some ancestral group(s) of vertebrates.

Origine ed evoluzione della sincope vasovagale

The most likely hypothesis is a defense mechanism of the heart during stressful and possible dangerous heart conditions and the slowing of heart rate induced by the vasovagal reflex may constitute a beneficial break of cardiac pump and permit better diastolic filling and coronary perfusion.

Typical vasovagal syncope as a “defense mechanism” for the heart by contrasting sympathetic overactivity

Many observations suggest that typical (emotional or orthostatic) vasovagal syncope (VVS) is not a disease, but rather a manifestation of a non-pathological trait, and a few theories have been postulated.

The target of vasovagal syncope is hemostasis and not heart protection

  • R. Diehl
  • Biology, Psychology
    Clinical Autonomic Research
  • 2017
Four reasons against the validity of the HDT and in favor of the clot production theory (CPT), which was only briefly mentioned in this review.

Vasovagal syncope in humans and protective reactions in animals.

  • J. BlancP. AlboniD. Benditt
  • Biology
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
  • 2015
A review of computer databases addressing VVS pathophysiology and origins, spontaneous transient loss of consciousness in animals, and comparative physiology concluded that the faint causes the body to assume a gravitationally neutral position, thereby offering a better chance of restoring brain blood supply and preserving brain function.

Vasovagal fainting as an evolutionary remnant of the fight against hemorrhage

  • M. Levi
  • Medicine
    Clinical Autonomic Research
  • 2005
This issue of Clinical Autonomic Research proposes an interesting explanation for the occurrence of vasovagal syncope, as a mechanism that was originally developed as a protective strategy against exsanguination upon major bleeding in mammals and is supported by various physiological and clinical observations.

The origin of vasovagal syncope: to protect the heart or to escape predation?

It is suggested that VVS in humans involves physiological mechanisms similar to those found in other vertebrates, and that this may indicate a common evolutionary root.

Vasovagal Syncope: Hypothesis Focusing on Its Being a Clinical Feature Unique to Humans

A new hypothesis (the “brain theory”) is suggested to try to address the question of why humans, to the exclusion of other species, remain susceptible to vasovagal syncope, and suggests that VVS evolved to offer protection to the brain's functional integrity under certain conditions of severe threat.

Origin and Evolution of the Vasovagal Reflex

Two processes which appear relevant for the investigation of VVS evolution are found: fear/threat bradycardia in animals, mainly during tonic immobility and vasovagal reflex during hemorrhagic shock (thoracic hypovolemia) both in animals and humans.



The vasovagal response.

The vasovagal response is the development of inappropriate cardiac slowing and arteriolar dilatation. Vasovagal responses reflect autonomic neural changes: bradycardia results from sudden

Why do we faint?

The most frequent cause of unexplained transient loss of consciousness is vasovagal syncope, popularly referred to as fainting, and the mechanisms responsible for vasodilation are not well understood.

Orthostatic tolerance in patients with unexplained syncope

It is concluded that the new combined test is able to discriminate patients who have poor orthostatic tolerance and is likely to be of value in assessing the effects of treatment regimes.

Clinical Disorders of the Autonomic Nervous System Associated with Orthostatic Intolerance: An Overview of Classification, Clinical Evaluation, and Management

  • B. GrubbB. Karas
  • Medicine, Psychology
    Pacing and clinical electrophysiology : PACE
  • 1999
On going studies will continue to help better define the broad spectrum of these disorders, and to elaborate better diagnostic and treatment modalities.

Hemodynamic and neurohumoral responses to acute hypovolemia in conscious mammals.

In conscious mammals including humans, the neurohumoral and hemodynamic responses to progressive acute hypovolemia have two distinct phases. There is an initial arterial baroreceptor-mediated phase

Methysergide delays the decompensatory responses to severe hemorrhage by activating 5-HT(1A) receptors.

Data indicate that methysergide stimulates 5-HT(1A) receptors to delay the decompensatory responses to hemorrhage, and selective blockade of 5- HT(1B/1D) receptors nor stimulation of 7-OH-DPAT receptors had any effect on hemorrhage responses.