Physiology, Diving Reflex

Issues of Concern

The dive reflex is an effective way 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 time, no data or studies support a best practice approach regarding 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.[1] 

In addition to further research needed to determine the most effective maneuver in the clinical setting to elicit the dive response, there are other study limitations for the dive reflex. Although there have been significant advancements in current research equipment and technology, the dive reflex has proven difficult to study due to the aquatic conditions in which a subject must be present 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.[2] To further research the physiologic changes within the dive reflex, advancements must be made in technology that can withstand the aquatic environment in which the dive reflex is observable.

Cellular Level

The cellular response 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, it is not entirely clear what stimulus activates these specific nerve fibers, but chemesthetic trigeminal chemoreceptors are believed to play a role.[3] Once activated, afferent neuronal signals are relayed to the brainstem, causing transmission of efferent neuronal signals that 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 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 60 mm Hg or less activates the chemoreceptor. Studies have observed that when divers hold their breath for an extended period, a robust chemoreflex activation triggers additional sympathetic peripheral vasoconstriction activity. Widespread peripheral vasoconstriction is believed to help maintain proper oxygen stores in fundamental organ systems during prolonged water submersion.[4] Overall, the cellular mechanisms involved in the dive reflex are numerous; however, the main components involve activating the sympathetic and parasympathetic nervous system using chemoreceptors and initial afferent nerve track stimulation.

Development

The diving response exists in all mammals, including humans, and it is hypothesized to aid in preserving oxygen stores for key organ systems during asphyxia. Interestingly, the reflex is found to be present in human infants as well.[5] 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 cardiorespiratory response is more intense than in adults.[5] 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.[6] 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 is only triggered by holding one's breath and immersing one's face in the water.[7] In other words, facial stimulation combined with breath-holding must be accomplished to trigger the dive response in adults completely. 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.

Organ Systems Involved

Mammals maintain physiologic homeostasis largely due to the nervous system responses that regulate heart rate, breathing, and blood pressure. However, these physiologic checks and balances are effectively modified when a mammal dives below the water. During submersion, the mammal holds its breath, the heart rate slows, and the 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.[8][9] 

Activating the peripheral receptors involving the nervous system impacts two distinct organ groups: the pulmonary and cardiovascular systems. Keeping in mind the cause-and-effect relationship of these systems at work, the major contributors to this physiologic reflex include:

• Nervous system 
• Pulmonary system
• Cardiovascular system

Function

The dive reflex has been described as a series of physiological changes in the body in response to a mammal holding its breath while submerged in water. The answer 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 increased peripheral vascular resistance, leading to a redistribution of blood flow to adequately perfuse the brain and heart while limiting flow to nonessential muscles.[3] With increased vascular resistance, the body can save oxygen stores for the vital organs, including the brain and the heart, while shunting blood away from inactive muscle groups. The additional response of bradycardia again preserves oxygen reserves by decreasing the heart rate, thus decreasing the heart's workload, which utilizes less oxygen. Though the dive reflex is a complicated process, it characterizes the simplicity of its overall goal, preserving life by physiologic adaptation in response to the current environment.

Mechanism

The dive reflex is a vast physiologic process, but its main mechanisms involve peripheral receptors, neuronal pathways, and chemoreceptors. Once a mammal holds its breath and submerges under water, two things occur: the face gets wet, and the oxygen content in the lungs becomes fixed. When mammals dive underwater, sensory information from the nasal region is relayed to the brainstem, which makes up the afferent tract of the diving reflex neural pathway.[10] Specifically, the afferent neuronal pathway is the trigeminal nerve relaying sensory information to the brainstem. The brainstem 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 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 mechanisms associated with the diving response; chemoreceptors in the carotid bodies and aorta also play a role in active physiologic changes. The carotid bodies sense the regulation of the partial pressure of oxygen in the lungs. When oxygen drops below a certain threshold, the carotid bodies send an afferent signal to the brainstem that travels on the glossopharyngeal nerve. The resultant efferent signal from the brainstem travels on several 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 is to conserve oxygen while maintaining homeostasis within the body that is suitable for sustaining life.  

Related Testing

Several tests have proven beneficial in objectively recording the changes observed during the dive reflex. In particular, the cardiovascular component of the dive reflex has been the subject of intensive study.  common research trend is to take vitals recordings before and after water submersion. Commonly tested physiologic parameters include:

• Blood pressure
• Heart rate
• Hemoglobin oxygen saturation
• Muscle sympathetic nerve activity
• Vascular resistance

In addition to the tests mentioned, current advancements in field devices have allowed 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.[2] The submersible echocardiogram has allowed additional physiologic factors to be recorded, including stroke volume, cardiac output, left atrial dimensions, and early diastolic transmitral flow deceleration time. The previously mentioned tests and devices have proven beneficial in demonstrating the observed change in physiologic factors when initiating the dive response. 

Pathophysiology

Though the dive reflex is a remarkable physiological adaptation studied and cited throughout scientific literature, a more serious medical syndrome is 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).[11] 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.[6] 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.

Clinical Significance

The dive reflex can manage and treat paroxysmal supraventricular tachycardia (PSVT). Though the therapeutic benefit of this reflex has been known 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 noninvasive maneuver for preventing PSVT.[1] Although complete facial immersion in cold water is difficult in a clinical setting, the effects of the dive reflex are reproducible using various techniques, the most common being the use of a cold stimulus applied to the subject’s face. Several studies have explored the effectiveness of different techniques and variables in triggering the dive response in a clinical setting. However, at this time, no widely accepted standardized technique is proven to be most effective. Based on current research, initiating the dive reflex is a quick, simple, and noninvasive clinical maneuver that effectively elicits increased vagal tone, which induces bradycardia and results in the termination of paroxysmal supraventricular tachycardia.