The diving reflex commonly referred to as the mammalian dive reflex, diving bradycardia, and the diving response is a protective, multifaceted physiologic reaction that occurs in mammals including humans in response to water submersion. Aspects of the dive reflex were first described in 1786 by Edmund Goodwyn; however, it would take until an 1870 publication by Paul Bert for the physiologic adaptations to be recognized. The dive reflex is believed to aid in the conservation of oxygen stores in mammals by initiating several specific physiologic changes during aquatic immersion. When a human holds their breath and submerges in water, the face and nose become wet which in turn causes bradycardia, apnea, and increased peripheral vascular resistance; these three main physiologic changes are collectively referred to as the diving reflex. The cause of increased peripheral resistance is thought to redistribute blood to the vital organs while limiting oxygen consumption by non-essential muscle groups. In addition to vascular resistance, bradycardia is initiated to decrease the work of the heart and further limit unnecessary oxygen consumption. Overall, the dive reflex is an innate multi-system physiologic response present in all vertebrates that functions to preserve oxygen stores during times of water immersion.
The dive reflex has been shown to be an effective means by which to treat paroxysmal supraventricular tachycardia (PSVT). Current medical literature supports several techniques that can trigger the dive response, the most common being a cold application to the face to increase vagal tone. However, at this present time, there is no data or studies that support a best practice approach in terms of equipment to use, duration of application, or optimal temperature range for therapeutically treating PSVT. Thus, further studies and research must be conducted to provide evidence-based information that reveals the optimal methods of inducing the dive reflex to alleviate PSVT.
In addition to further research needed to determine the most effective maneuver in the clinical setting to elicit the dive response, there are other limitations of study for the dive reflex. Although there have been significant advancements in current research equipment and technology the dive reflex has proven difficult to study in its entirety due to the aquatic conditions a subject must be present in to trigger the response. Specifically, cardiovascular adaptations in mammals during water submersion are only moderately understood due to the technical difficulty of studying mammals while completely submerged in water. To further research the physiologic changes present within the dive reflex, advancements must be made in technology that can withstand the aquatic environment in which the dive reflex is observable.
The cellular response that takes place during the dive reflex is vast; however, the primary cellular mechanisms responsible for the reflex involve afferent and efferent neuron tracts along with carotid chemoreceptors. The dive response activates with the immersion of the face in water which triggers a neuronal afferent response via the trigeminal nerve. Nerve fibers innervating the anterior nasal mucosa and paranasal region are essential in triggering this autonomic reflex. However, at this present time, it is not entirely clear what stimulus activates these specific nerve fibers, but chemesthetic trigeminal chemoreceptors are believed to play a role. Once activated, afferent neuronal signals are relayed to the brainstem causing transmission of efferent neuronal signals which activate the sympathetic nervous system including alpha-1 receptors and the parasympathetic nervous system including muscarinic M2 receptors which induce peripheral vasoconstriction and bradycardia respectively.
In addition to neural tracts, the chemoreceptors located in the carotid bodies contribute to the induction of bradycardia and peripheral vascular changes. When a human holds their breath underwater, oxygen gets consumed, and carbon dioxide is produced; a decrease in oxygen of 60mm Hg or less activates the chemoreceptor. Studies have observed that when divers hold their breath for an extended period a robust chemoreflex activation aids in triggering additional sympathetic peripheral vasoconstriction activity. Widespread peripheral vasoconstriction is believed to help maintain proper oxygen stores to fundamental organ systems during times of prolonged water submersion. Overall, the cellular mechanisms involved in the dive reflex are numerous; however, the main components involve the activation of the sympathetic and parasympathetic nervous system using chemoreceptors and initial afferent nerve track stimulation.
The diving response exists in all mammals including humans, and it is hypothesized to aid in the preservation of oxygen stores for key organ systems during times of asphyxia. Interestingly, the reflex is found to be present in human infants as well. There is still speculation as to why infants demonstrate this reflex, but it is believed to be a protective response to avoid drowning. When the dive reflex activates in infants, the cardio-respiratory response is more intense than compared to adults. During the first year of life, the dive response can be fully elicited by merely immersing the infant's face in water without having them hold their breath. As humans age, the dive reflex is still present, but the vigorous response initiated from simply wetting or cooling the face in infants does not exist in adults. As an adult, the full effect of the dive response only triggers with the holding one's breath in addition to immersing their face in the water. In other words, to completely trigger the dive response in adults facial stimulation combined with breath holding must be accomplished. Though the robustness of the reflex evolves as humans age, research shows that the physiologic changes observed while submerged in water are still present throughout life.
Mammals maintain physiologic homeostasis largely due to the nervous system responses that regulate heart rate, breathing, and blood pressure. However, when a mammal dives below the water, these physiologic checks and balances are effectively modified. During submersion the mammal holds its breath, the heart rate slows down, and their peripheral vascular system constricts. These unique but separate physiologic changes are prompted by triggering peripheral receptors, and they work together to preserve the mammal’s oxygen levels.
Through activation of the peripheral receptors involving the nervous system impact two distinct organ groups: the pulmonary and cardiovascular system. Keeping in mind the cause and effect relationship of these systems at work the following list outlines the major contributors to this physiologic reflex:
The dive reflex has been described as a series of physiological changes that take place in the body in response to a mammal holding its breath while submerged in water. The answer as to why this complicated dynamic reflex takes place is quite simple: to preserve life. The diving response demonstrates a cessation of breathing, decreased heart rate, and an increase in peripheral vascular resistance leading to a redistribution of blood flow to adequately perfuse the brain and heart while limiting flow to non-essential muscles. With an increase in vascular resistance, the body can save oxygen stores for the vital organs including the brain and the heart while simultaneously shunting blood away from inactive muscle groups. The additional response of bradycardia again preserves oxygen reserves by decreasing the heart rate, thus decreasing the workload of the heart which in turn utilizes less oxygen. Though the dive reflex is a complicated process, it characterizes the simplicity of its overall goal, the preservation of life by physiologic adaptation in response to the current environment.
The dive reflex is a vast physiologic process, but its main mechanisms involve peripheral receptors, neuronal pathways, and chemoreceptors. Once a mammal holds it's breath and submerges under water two things occur: the face gets wet and the oxygen content in the lungs becomes fixed. When mammals dive under water, sensory information from the nasal region is relayed to the brainstem, making up the afferent tract of the diving reflex neural pathway. Specifically, the afferent neuronal pathway involved is the trigeminal nerve relaying sensory information back to the brainstem. The brainstem then sends efferent signals via the vagus nerve to specific target organs. The vagus nerve primarily associates with the parasympathetic nervous system, and the result of this neuronal pathway is bradycardia. The brainstem also sends out efferent signals to the peripheral vascular musculature which increases peripheral vascular resistance and results in blood shunting toward more vital organs.
The neuronal pathways previously described are not the only mechanism associated with the diving response, chemoreceptors in the carotid bodies and aorta also play a role in the active physiologic changes as well. The carotid bodies sense regulation of partial pressure of oxygen in the lungs. When oxygen drops below a certain threshold, the carotid bodies send out an afferent signal to the brainstem that travels on the glossopharyngeal nerve. The resultant efferent signal from the brainstem travels on a number of sympathetic nerves that cause a marked increase in peripheral vasoconstriction that further save blood for vital organs including the brain and heart. A synergistic relationship exists in the human body to properly activate and achieve the dive reflex. The overarching goal of the detailed mechanism previously explained is to conserve oxygen while maintaining homeostasis within the body that is suitable for sustaining life.
Several tests have proven beneficial to objectively record the changes observed during the dive reflex. In particular, the cardiovascular component of the dive reflex has been the subject of intensive study. A common trend in research is to take recordings of vitals before and after water submersion. A list of the commonly tested physiologic parameters are listed below:
In addition to the tests mentioned there has been current advancements in field devices that have allowed the obtaining more vitals and data. The recent development of a submersible echocardiograph has allowed a viable assessment of cardiac function and anatomy during a real-time dive. The submersible echocardiogram has allowed additional physiologic factors to be recorded including stroke volume, cardiac output, left atrial dimensions, and deceleration time of early diastolic transmitral flow. The previously mentioned tests and devices have proven to be beneficial in demonstrating the observed change in physiologic factors when initiating the dive response.
Though the dive reflex is a remarkable physiological adaptation that has been studied and cited throughout scientific literature, there is a more serious medical syndrome potentially associated with it. The mechanism of the dive response is one of the most frequently considered reflex-etiologies related to sudden infant death syndrome (SIDS). How the dive reflex and SIDS may be connected is explained by how the reflex gets elicited. Through the nervous system stimulation of the trigeminal nerve, the overall response triggered by the dive reflex is apnea, bradycardia, and increased peripheral vascular resistance.
Several studies suggest that diving reflex hyperreactivity could potentially be the principal cause of SIDS due to its ability to trigger bradycardia and apnea. The hypothesis is that an infant sleeping in the prone position could have their face (trigeminal nerve) stimulated by the bedding and cause the child to activate the dive reflex which would cause the child to stop breathing and ultimately lead to SIDS. Presently there is no determining factor as to what potentiates SIDS, however, at this point, there is not enough current evidence to rule out the role of the diving reflex and its contribution to sudden infant death syndrome.
The dive reflex can be used to manage and treat paroxysmal supraventricular tachycardia (PSVT). Though the therapeutic benefit of this reflex has been a known fact since the early 1970s, it is now starting to be used in prehospital settings, offering a simple management option for individuals with regular narrow complex tachyarrhythmias. When triggering the dive reflex in humans with cold water facial immersion, the primary result is a reflex bradycardia response. The resultant bradycardia and a related increase in myocardial refractoriness is useful as a non-invasive maneuver for the cessation of PSVT. Although complete facial immersion in cold water is difficult in a clinical setting the effects of the dive reflex are reproducible by a variety of techniques, the most common being the use of a cold stimulus applied to the subject’s face. There have been several studies conducted exploring the effectiveness of different techniques and variables in triggering the dive response in a clinical setting. However, at this time there is no widely accepted standardized technique proven to be most effective. Based on current research, initiating the dive reflex is shown to be a quick, simple, and non-invasive clinical maneuver that is effective in eliciting increased vagal tone which induces bradycardia and results in the termination of paroxysmal supraventricular tachycardia.
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