Fainting in animals

Abstract

Fainting (syncope) is unconsciousness due to insufficient cerebral circulation in the context of a temporary failure of the systemic circulation. This paper firstly aims to discuss fainting in animals, and secondly to discuss animal physiology to broaden the understanding of human fainting. Of the three major syncope types (cardiac, orthostatic and reflex syncope), only cardiac syncope occurs in animals as in man, through arrhythmia or output failure. Man's orthostatic fainting tendency has been blamed on his upright posture. A comparison with animals shows that giraffes, tree climbing snakes, and animals that quickly raise and lower their heads face more serious gravitational circulatory challenges than man, but do not appear to faint. Merely carrying the brain above the heart does not explain a fainting tendency, as the human heart-to-brain height is smaller than that of many mammals with similar blood pressure. Two evolutionary novelties may be to blame: the proportion of cardiac output going upwards to the brain is much larger than in apes, and man's large legs suggest that the volume lost to venous pooling is also larger. Emotional factors play a role in many reflex syncope events. Tonic immobility ('feigning death','playing possum') is not a good model, as it concerns immobility as a survival strategy of an attentive brain, rather than unconsciousness due to circulatory breakdown. Whether orienting and defense responses form a valid model remains to be proven. Emotional fainting may be uniquely human; how mental processes can shut down the circulation and thereby the brain needs serious study, as it may hold the key to syncope prevention.

Electrodermal activity in patients with neurally mediated syncope

“…NMS is a uniquely human phenomenon, the trigger of which is poorly understood [24]. Although many still accept the notion that activation of ventricular afferents evokes the bradycardia and hypotension of syncope there is little objective evidence to support this notion [14,18,19].…”

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

“…Recently, van Dijk [65] offered a possible explanation based on some anatomical or physiological traits recently evolved in the human lineage: (1) the metabolic demand of the brain is much higher in humans than in other species; in man, about 20% of cardiac output is destined for the brain, while in apes (gorillas, chimpanzees) the proportion of cardiac output that needs to be pumped upwards is only 4%-7%; consequently, cerebral hypoperfusion (severe enough to elicit loss of consciousness) would be more likely in humans compared to other animals; (2) human legs are more robust than hind legs in other primates and the muscle pump appears to be less active; gravity would therefore cause more venous pooling in the human legs and, consequently, more orthostatic difficulties.…”

Is there any point to vasovagal syncope?

“…There is significant intraspecies aggression in chimpanzees as well (and possibly also in earlier hominoids), but fainting has never been witnessed in chimpanzees [12]. Moreover, at the time when VVS is supposed to have evolved, Homo sapiens may have had the ability to mimic death in a much smarter and more immediately applicable way than through VVS.…”

“…The article by Alboni et al in this issue [1] makes just this contribution, and should be read with reviews on why animals do not faint [12], and on a possible paleolithic origin of syncope in the human genetic lineage [4]. Together they provide insights into possible animal origins of syncope, on why animals do not mount a complete vasovagal response, and on what might have turned us into a species with many members who lose consciousness when stressed.…”