State of the art paper The trigeminocardiac reflex – a comparison with the diving reflex in humans

Lemaître, F.; Chowdhury, Tumul; Schaller, Bernhard

doi:10.5114/aoms.2015.50974

Cited by 47 publications

(50 citation statements)

References 57 publications

(83 reference statements)

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“…; Lemaitre et al . ). However, it appears that the activation of the trigeminal nerve has a greater responsibility for blood redistribution (from the periphery to the brain) and bradycardia, without directly influencing the CMRO 2 (Reis et al .…”

Section: Discussionmentioning

confidence: 97%

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Bain

Ainslie

Hoiland

et al. 2016

The Journal of Physiology

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Key points The present study describes the cerebral oxidative and non‐oxidative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that generates extremely low levels of blood oxygen and high levels of carbon dioxide. The cerebral oxidative metabolism, measured from the product of cerebral blood flow and the radial artery‐jugular venous oxygen content difference, was reduced by ∼29% at the termination of apnoea, although there was no change in the non‐oxidative metabolism. A subset study with mild and severe hypercapnic breathing at the same level of hypoxia suggests that hypercapnia can partly explain the cerebral metabolic reduction near the apnoea breakpoint. A hypercapnia‐induced oxygen‐conserving response may protect the brain against severe oxygen deprivation associated with prolonged apnoea. Abstract Prolonged apnoea in humans is reflected in progressive hypoxaemia and hypercapnia. In the present study, we explore the cerebral metabolic responses under extreme hypoxia and hypercapnia associated with prolonged apnoea. We hypothesized that the cerebral metabolic rate for oxygen (CMRO2) will be reduced near the termination of apnoea, attributed in part to the hypercapnia. Fourteen elite apnoea‐divers performed a maximal apnoea (range 3 min 36 s to 7 min 26 s) under dry laboratory conditions. In a subset study with the same divers, the impact of hypercapnia on cerebral metabolism was determined using varying levels of hypercapnic breathing, against the background of similar hypoxia. In both studies, the CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery‐internal jugular venous oxygen content difference. Non‐oxidative cerebral metabolism was calculated from the ratio of oxygen and carbohydrate (lactate and glucose) metabolism. The CMRO2 was reduced by ∼29% (P < 0.01, Cohen's d = 1.18) near the termination of apnoea compared to baseline, although non‐oxidative metabolism remained unaltered. In the subset study, in similar backgrounds of hypoxia (arterial O2 tension: ∼38.4 mmHg), severe hypercapnia (arterial CO2 tension: ∼58.7 mmHg), but not mild‐hypercapnia (arterial CO2 tension: ∼46.3 mmHg), depressed the CMRO2 (∼17%, P = 0.04, Cohen's d = 0.87). Similarly to the apnoea, there was no change in the non‐oxidative metabolism. These data indicate that hypercapnia can partly explain the reduction in CMRO2 near the apnoea breakpoint. This hypercapnic‐induced oxygen conservation may protect the brain against severe hypoxaemia associated with prolonged apnoea.

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Section: Discussionmentioning

confidence: 97%

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Bain

Ainslie

Hoiland

et al. 2016

The Journal of Physiology

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“…This reflex is most often transient, but sometimes may be pronounced and sustainable, particularly, in infants. The diving reflex (DR) (a subtype of TCR) is triggered as a result of stimulation of one of the sensory branches of the trigeminal nerve and leads to inhibition of cardiorespiratory center, thereby causes bradycardia and apnea (16–19). An exaggerated response to hypoxia (i.e., augmented TCR response) causing lethal bradycardia and apnea can be accused of sudden death in the victims of SIDS.…”

Section: Introductionmentioning

confidence: 99%

Sudden Infant Death Syndrome – Role of Trigeminocardiac Reflex: A Review

et al. 2016

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Sudden infant death syndrome (SIDS) is an unexplained death in infants, which usually occurs during sleep. The cause of SIDS remains unknown and multifactorial. In this regard, the diving reflex (DR), a peripheral subtype of trigeminocardiac reflex (TCR), is also hypothesized as one of the possible mechanisms for this condition. The TCR is a well-established neurogenic reflex that manifests as bradycardia, hypotension, apnea, and gastric hypermotility. The TCR shares many similarities with the DR, which is a significant physiological adaptation to withstand hypoxia during apnea in many animal species including humans in clinical manifestation and mechanism of action. The DR is characterized by breath holding (apnea), bradycardia, and vasoconstriction, leading to increase in blood pressure. Several studies have described congenital anomalies of autonomic nervous system in the pathogenesis of SIDS such as hypoplasia, delayed neuronal maturation, or decreased neuronal density of arcuate nucleus, hypoplasia, and neuronal immaturity of the hypoglossal nucleus. The abnormalities of autonomic nervous system in SIDS may explain the role of TCR in this syndrome involving sympathetic and parasympathetic nervous system. We reviewed the available literature to identify the role of TCR in the etiopathogenesis of SIDS and the pathways and cellular mechanism involved in it. This synthesis will help to update our knowledge and improve our understanding about this mysterious, yet common condition and will open the door for further research in this field.

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“…This reflex occurs in response to breathholding and is further augmented with subsequent contact of the face with cold water. It consists of apnea, bradycardia, and peripheral vasoconstriction, decreased cardiac output and increased mean arterial blood pressure (MABP) [10]. These responses conserve oxygen for vital organs such as the heart and brain.…”

Section: Discussionmentioning

confidence: 99%

Trigemino-Cardiac Reflex and High-Degree Atrioventricular Block in Recurrent Epistaxis

Richler¹,

Morales-Mangual²,

Chera³

et al. 2018

J Med Cases

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We present a case of a 55-year-old male who presented to emergency department with recurrent epistaxis. After placement of a 16-French Foley catheter in his right nare to tamponade the bleeding, the patient subsequently developed two episodes of syncope. Review of the telemetry rhythm strips showed that he had developed PR interval prolongation followed by complete atrioventricular block. Our case was likely secondary to stimulation of the trigemino-cardiac reflex, a neuro-cardiogenic reflex, that can occur after stimulation of the trigeminal nerve, whether centrally or peripherally. Patients can develop severe bradycardia, hypotension, asystole, and even death. The relatively common occurrence of epistaxis and its treatment with direct nasal tamponade require an increased awareness and possibly a requirement for telemetry monitoring to prevent complications from stimulation of this reflex.

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State of the art paper The trigeminocardiac reflex – a comparison with the diving reflex in humans

Cited by 47 publications

References 57 publications

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Sudden Infant Death Syndrome – Role of Trigeminocardiac Reflex: A Review

Trigemino-Cardiac Reflex and High-Degree Atrioventricular Block in Recurrent Epistaxis

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