Roemheld Syndrome, first reported in the early 20th century by Austrian physician Ludwig von Roemheld, is usually seen in overweight, middle-aged males and was described as a set of symptoms that center around the digestive system and its proximity to the heart. These men would complain of shortness of breath, fatigue, anxiety, and vertigo while displaying cardiac-focused symptoms such as palpitations, angina pectoris, bradycardia, or sometimes tachycardia. Dr. Roemheld, even with the more primitive medicine available in his time, was almost certain that none of these patients had any true cardiac problems since the episodic symptoms only manifested soon after meals. In the ensuing 100+ years, the interconnected symptoms between heart and stomach were not seen as a comprehensive pathology, although older reports noted the practices of cardiology and gastroenterology were often related in patients complaining of both cardiac and digestive issues [1]. In modern medicine, this set of specific symptoms has evolved into the term “gastrocardiac syndrome” (hereafter GCS) and is usually treated symptomatically unless anatomic correction by surgery is possible.

Clinically, only scarce case reports exist, and no large-scale studies or exploratory literature have been published on this topic. Only recently has a connection between GCS and the autonomic nervous system been revisited. As the longest cranial nerve that connects both heart and viscera, the vagus nerve has been found to play a central mediation role between digestion and heart rate braking functions. Here, the GCS Triad (gastrointestinal system, heart, psychiatric issues, all interconnected by the vagus nerve) is detailed and dissected from an anatomical view to reveal likely causes for symptoms and comorbidities that it may exacerbate, along with suggestions for treatment.

As two names exist for this condition, the keywords “Roemheld syndrome” and “gastrocardiac syndrome” were used to search for the associated literature (reviews, case reports, etc.) in PubMed/Medline. The literature that included cardiac effects mediated by gastrointestinal pathologies were included, as were reports of the effect of the vagus nerve on both systems. Since the term “gastrocardiac” is sometimes used to describe a cardiac-adjacent location for ulcers within the stomach, these reports were excluded, as the ulcer may rarely erode into the heart myocardium, necessitating repair, and this outcome is not reliant on the GCS Triad.

In healthy people, GCS is most likely upsetting but essentially harmless as the symptoms disappear over time; however, in patients with other pathologies, GCS may be an important indicator of digestive system issues. In 2020, Mehta and colleagues encountered a representative case of a 62-year-old woman who experienced distressing heart palpitations of a moderate, fluttering, and non-radiating nature that were accompanied by mild vertigo, sweating, and shortness of breath [1]. No angina, syncope, or other severe issues were noted, but the timing always came after meals (lunch and dinner). After noting a medical history of GERD, obesity, and hiatal hernia, testing revealed over 35,000 ectopic beats per day (14.6% burden) but with a normal ejection fraction and no signs of ischemic heart disease or other cardiovascular disorders. She was then found to have a 5 cm hiatal hernia that was surgically corrected, resolving the symptoms (ectopic burden of 0.1%).

These findings are similarly reported in several other case studies that involve older, adult patients with hiatal hernias; esophageal pathologies (e.g., GERD/Barrett’s esophagus); or gastric distention/excessive flatus [2,3,4]. Thus, a picture emerges of a reproducible set of symptoms that reliably erupt when gastrointestinal pressure impinges into the thoracic cavity from the diaphragm side or affects the nerves that pass through it, especially the vagus nerve. Once these underlying issues are addressed, the cardiac symptoms are rapidly resolved. A summary of currently published cases is available in Table 1.

No current reports detail the prevalence within any population, adult or pediatric; the literature searches reveal only sparse case literature. Thus, standardized diagnostic and treatment criteria remain unestablished and treatment is based on individual symptoms.

Named for its wandering nature, cranial nerve X starts within the medulla oblongata and terminates within the small intestine, with large branches in the cardiac, pulmonary, and gastrointestinal systems. Bidirectional data flow allows for the precise parasympathetic nervous system (PNS) regulation of respiration; oxygenation; smooth muscle contractility (e.g., variable heart rate, elastic vessel tone, and rhythmic peristalsis); digestion (bile release, acid secretion, etc.); and autonomic nervous system switching (i.e., parasympathetic activation to regulate the sympathetic innervation from the spine). It is the primary and direct connection of the brain to parasympathetic regulation of the cardiopulmonary and digestive organs and also supplies innervation to the muscles that control speech near the thyroid gland and in the tongue (intrinsic larynx muscles and palatoglossus muscle) [5]. Of concern are the branches (left and right) within the cardiovascular and gastrointestinal systems, since the vagus may transduce signals from the gut to the heart. GCS, as a discrete pathology involving both systems, relies on communication between the gut and heart through the vagus nerve to generate its specific symptoms.

In the context of the GCS Triad, the vagus nerve is of primary importance as it is the braking system of the heart rate (heart-rate variability control) and also modulates the sensing of inflammation, as well as the deployment of anti-inflammatory responses via the cholinergic anti-inflammatory pathway [10]. The vagus nerve affects all parameters of heart function, as evidenced in a trial of chronic heart failure patients who received cervical vagus nerve stimulator implants in the ANTHEM-HF trial; these patients, regardless of right or left vagal location, experienced increased left ventricular ejection fraction, left ventricular end-systolic volume, and left ventricular end-systolic diameter, along with significantly improved heart rate variability and exercise stamina [11]. Heart rate and blood pressure were also shown to be affected in the INOVATE-HF and NECTAR-HF vagus stimulation implant trials, as sympathetic control of the heart (higher blood pressure, faster pulse, lowered fibrillation threshold) is countered by the boosted parasympathetic tone [12]. Thus, the vagus nerve is a critical mediator of the GCS Triad, as it may itself regulate the action of the heart, as well as transduce errant signals from the digestive organs to the heart.

The gastrointestinal system, which involves multiple organs (including the liver and pancreas), consumes up to 10% of total daily energy expenditure to assimilate nutrients and is heavily innervated by the PNS, especially the vagus nerve [13]. Separated from the thoracic cavity by the diaphragm, the abdominal cavity is heavily muscled on all sides to provide contractile action (through sympathetic nervous system [SNS] signals from the T7-T12 intercostal nerves) for defecation and vomiting, plus sneezing and coughing in concert with the diaphragm [14]. The stomach itself is controlled by the vagus (PNS); pelvic splanchnic (SNS, from the spine); and paraaortic autonomic plexuses, in addition to multiple other control centers (Figure 1). The vagus nerve also adds central control over bile release, plus acid and gastrin release through thyrotropin-releasing hormone from the medulla that transduce through the vagus via M3 cholinergic receptors and histamine [15]. Fine control of intestinal digestion and peristalsis is then provided through the parasympathetic nervous system, under control of the vagus nerve, and the myenteric/submucosal plexuses (Auerbach’s and Meissner’s plexuses) that function as a wrapped layer around the lumen to innervate the muscularis interna layer with spike-wave signals that create pulsatile contractions to move food, chyme, and other liquids unidirectionally through the gut [16]. Of note, Meissner’s plexus is primarily associated with PNS, while Auerbach’s plexus can transduce both PNS and SNS signals. Interstitial cells of Cajal in Auerbach’s plexus provide a pacemaker effect, controlling the duration and period of the contractile pulses. Biochemically, mechanical distention of the gut lumen as a bolus is passed releases 5-HT from enterochromaffin cells (synthesized from tryptophan) that is crucial for propagating peristalsis [17].

It is defects in this peristaltic system, usually considered as part of the irritable bowel syndrome (IBS) pathology, that are causative for GCS through aberrant or absent nerve signals from distension, pathologies, or infection. Essentially, pressure from the gut forces the diaphragm up, impinging into the thoracic cavity and pressing on the efferent branches of the vagus nerve, causing a negative chronotropic/dromotropic burst of parasympathetic vagal “static” that may also briefly lower thresholds for atrial fibrillation switching and reduce contractility [18]. Mechanical irritation of the atria or chemical burn-induced remodeling of the esophagus due to reflux disease may also synergistically contribute to atrial fibrillation [19]. It is this phenomenon that causes the symptoms felt and reported by GCS patients in the case literature; these symptoms disappear when the underlying gastrointestinal pathology is resolved. Thus, the “gut brain”, a term describing the collective action of the over 160 million neurons in the gastrointestinal tract that are coordinated by spinal/vagal nerve interplay, maintains a key role in GCS and modulation of GI neuronal activity and the peristalsis it controls may therefore be a key component of preventing or treating GCS in a clinical setting [20].

Outside of the brain, the gastrointestinal system is the largest concentration of neurons in the human body, and each must act in concert to keep secretion, primary/secondary peristalsis, and segmentation intact while food, gas, and liquid unidirectionally transit the digestive tract.

Of note, the digestive system is tied into CNS external threat perception directly through spinal nerves which can allow SNS activation by simply suppressing activation of the PNS. Once activated through SNS action, hormonal messengers, such as adrenaline/cortisol can suppress peristalsis, shunting blood elsewhere during the fight/flight/freeze response. Conditions that reduce or alter the level of 5-HT (such as selective serotonin reuptake inhibitors, or stress) may also ablate or stimulate peristalsis; both are considered a key element in the pathogenesis of the IBS family of symptoms (diarrhea, constipation, etc.) that can exacerbate GCS. The gut flora has also been shown to modulate enteric neurotransmitters (i.e., GABA, acetylcholine) and, as such, dysbiosis is considered a key driver of GCS [21].

The “rest and digest” function of the PNS is balanced in the gut by the SNS, which maintains peristalsis and the heart rate necessary to suffuse digestive organs with blood. Thus, PNS/SNS activation is not a binary state switching but rather a carefully controlled, analog condition with predetermined thresholds of activation to maintain rhythmic and unidirectional motion; secrete acid, gastrin, and bile; and sense nutrition in chyme. For this reason, stress perceived by the brain is transmitted through the autonomic nervous system to prepare for fight or flight by suppressing vagal action and permitting the SNS to take over. This fast-stress response activates the sympathetic–adreno–medullar axis and catecholamines (adrenaline, norepinephrine), plus cortisol, to suppress peristalsis and shunt blood to extremities while increasing respiration and heart rate. The freeze response, conversely, is mediated by the PNS when fight or flight is impossible (“terror” situations) and the body prepares to ablate the damage from danger by vagal domination and subsequent slowing of heart rate, blood pressure, and respiration to lessen the effects of bleeding [22]. The freeze effect may result in syncope or dizziness due to hypotension, but usually creates a reduction in mobility to reduce fast motion that is theorized to reduce predator threats (“playing dead”) or give time to synthesize a threat response [23]. This response is dominated by acetylcholine, which may cause spontaneous vomiting or defecation through enhanced activation of muscarinic acetylcholine receptors in the intestines, but also features the hypothalamus-pituitary-adrenal (HPA) axis release of corticotrophin-releasing hormone (CRH) and adrenocorticotropin hormone (ACTH) [24]. These two hormones have been found as key modulators of intestinal motility and excess CRH was reported to induce duodenal dysmotility in IBS patients [25]. Thus, acute stress states that lead to partial activation of any preprogrammed fear state (fight/flight/freeze) can severely disrupt the activity of the gut brain and peristalsis by increasing hormones that act on the autonomic nervous system (ANS), which controls both systemic stress response and digestion.

Recently, the chronic state of stress (as opposed to acute stress) has come into focus as a chief regulator of GI issues in the modern world since low-level but constant stress states keep a small amount of both SNS-activating hormones in the bloodstream at all times. Acute stress/anxiety has also been shown to downregulate activation of the α7-nicotinic acetylcholine receptors which are abundant in the intestines to regulate secretion of glucagon-like peptide-1 from L cells and downregulate cytokine-based inflammation that interferes with peristalsis [26,27]; anxious rats treated with vagal nerve simulation (increasing nicotinic receptor activity) experience reduced stress symptoms as well as restoration of intestinal function from stress-induced IBS [27]. Of importance, vagal nerve stimulation has the double effect of restoring normal digestion and reducing anxiety/panic by checking sympathetic activation, as well as reducing inflammation that might irritate digestive tissues [28]. Thus, the vagus nerve is a critical interface that transduces anxiety and panic from the brain to the gut and heart, but may also transmit errant signals that cause symptoms which sensitize the brain to anxiety/panic with regard to signals from IBS; this is the result of bidirectional signaling.

A state of chronic, low-level sympathetic activation (e.g., anxiety disorders) may dysregulate the vagal control of the digestive system through loss of tone, especially in anxiety/panic sufferers, and disrupt peristalsis, acetylcholinergic receptor function, acid/enzyme secretion, and anti-inflammatory activities. These collective GI symptoms from chronic stress and/or anxiety are termed irritable bowel syndrome (IBS) and 11% of the world suffers from some form of it [29]. To compare, a meta-review estimated that 39% of people with IBS also suffer from anxiety disorder; the effect of anxiety, as reflected in a loss of vagal tone and subsequent sympathetic overactivation, is therefore both a key driver and result of GCS [30]. In this syndrome, intimately related to GCS, cortisol from long-term stress can disrupt peristalsis, while ACTH and CRH promote dysmotility in the small intestine and disruptions in the migrating motor complex can push colonic flora into the small intestine, creating small intestinal bacterial overgrowth (SIBO) and large volumes of gut-distending gas that exert pressure on the vagus nerve and promote GCS episodes. As gut flora modulate gut serotonin with short-chain fatty acids and also produce ACTH/galanin-mediated cortisol release, dysbiosis can also become a chief driver of IBS symptoms, and the effect of these symptoms may increase perceived chronic stress that further disrupts the digestive system in a positive feedback loop [31]. Disruptions in ANS balance may also create conditions of excessive or insufficient acid release in the stomach, plus secretory irregularities in bile and pancreatic enzymes (bicarbonate, pancrease). Combined with dysmotility (from any source, but primarily stress), IBS symptoms may also reduce digestion efficiency, create chronic diarrhea or constipation, and errantly stimulate the vagus nerve to propagate cardiovascular symptoms of GCS. Constipation-dominant IBS (IBS-C), in particular, has been linked to GCS in popular media, due to the presence of increased methanogenic bacteria that slow peristalsis [32].

An ideal digestive system would have its own nervous system that was insensitive to stress hormones used for survival, but the economy of evolution selected for digestive systems that could be controlled by nervous branches responsive to stress as an adaptation to provide extra blood to perfuse muscles and increase physical capabilities in the face of acute danger. As the modern world is, essentially, far safer than the wild nature our ancestors roamed, most of the stress humans face is chronic and low-level, exploiting that very specific flaw to disrupt the gut brain and create a unique environment to promote GCS through psychiatric and IBS symptoms, especially IBS-C, transduced through the vagus nerve. Thus, the GCS Triad is established and reinforced.

Hiatal hernias occur when the upper section of the stomach (fundus, cardia, upper body) infiltrate into the thoracic cavity via a weakened esophageal hiatus, impinging into the lungs and relaxing the abdominal section of the esophagus, forcing open the lower esophageal sphincter. Typical hiatal hernias present with gastroesophageal reflux (GERD, especially when prone), pain, dysphagia, and feelings of fullness. Severe cases of extended reflux may also cause Barrett’s esophagus as a complicating factor. Laparoscopic surgery is usually corrective, with GI symptoms resolving soon after correction, but osteopathic manipulation in lieu of surgery was also reported to resolve a hiatal hernia in a 71-year-old female [33].

The increased intrathoracic pressure resulting from a hiatal hernia may also stimulate GCS symptoms, such as tachycardia, premature ventricular contractions, atrial fibrillation, or other arrythmias, through anterior vagal nerve stimulation, as seen in several reported cases [4,5,33]. The literature indicates that hiatal hernias are a risk factor for cardiac arrythmias, with a 2013 study by Roy and colleagues indicating a 17.5-fold (men) or 19-fold (women) increase in atrial fibrillation occurrence in populations with hiatal hernias [34]. A review by Goodwin and colleagues also points to pulmonary compression and increased pressure on the left atrium as potential causes for atrial fibrillation in hiatal hernia cases [35]. Thus, GCS symptoms in populations at risk for hiatal hernias (usually over 50 years of age, male, and obese) may point to the need for GI screening in order to simultaneously resolve both the primary hernia and GCS through surgical repair [36].

The most distressing and recurring symptoms of GCS are centered around the heart. As with all rhythmic, contractile tissues, myocardial contractility is precisely regulated by a dedicated electrical system centered in the sinoatrial node (SAN) that sends a propagating electrical wave across the heart that starts in the atria and is then conducted by His-Purkinje bundles (right and left) to the ventricles [8]. The four chambers of the heart thus fill and contract in a specific sequence (right atrium to right ventricle to the lungs via the pulmonary artery then back to the left atrium, the left ventricle and out to systemic circulation). This sequence is tightly controlled by the SAN, which itself is innervated by PNS ganglia originating in the right vagus nerve trunk. These PNS ganglia are situated around the left atrium, also infiltrating into the ventricular myocardium, and serve as a brake (via acetylcholine release) to slow heart rate, reduce atrioventricular conduction, and lower ventricular contractility without affecting the rhythmic pulses of the SAN [18]. The PNS system therefore specifically serves to generate negative chronotropic/dromotropic effects via the SAN (and alterations in conduction within the atrioventricular node), alter atrial fibrillation thresholds, create a negative ionotropic signal on the ventricular myocardium, reduce ventricular arrythmia thresholds, prevent SNS-activated heart rate increases, open up the coronary artery during exercise (via nitrous oxide release), and also maintain baroreflexive responses within the coronary artery [18,37,38,39]. As the vagus nerve is directly connected to the SAN, errant signals traveling up from the gut can activate the vagal braking system and cause the SAN to slow the heart rate; other parts of the heart conducting the previous signal may thus transduce an ectopic beat, causing palpitations that are the most common symptom of GCS [40]. As such, anything which may affect vagal signal fidelity or transmission could also affect the heart rate via these anatomic mechanisms.

The effect of anxiety/panic response may further complicate returns to cardiac homeostasis during GCS attacks as the same chronic stress response that affects the GI tract also directly acts on the cardiovascular system. Adrenaline and norepinephrine, released during anxiety, elevate systolic blood pressure, heart rate, and temporarily overcome vagal control. In addition, palpitations and variations in heart rate are common symptoms of anxiety and panic attacks. Cortisol, released under chronic stress/anxiety, increases T1 time, inducing reductions in heart rate variability (HRV) and also causing LV hypertrophy (and compensation that may further affect HRV) over long periods of exposure [41]. Conflicting signals (i.e., biochemical from adrenaline simultaneously with errant vagal activation from GCS) may therefore cause the cardiac irregularities seen in case reports and panic over perceptions of suffering cardiac arrest can sustain adrenaline/norepinephrine release for hours, overwhelming vagal control.

Repeated episodes cause enhancement of amygdala sensitivity and lower subsequent thresholds of panic activation through norepinephrine’s effect on the memory enhancing β-adrenergic receptors in the vagus nerve that then directly stimulate noradrenergic neurons in the locus coruleus [24]. This positive-feedback loop means that future GCS episodes may more easily trigger catecholamine release and the panic response since hypersensitivity in vagal afferents ablates the medulla’s ability to gate signals that cause amygdala activation and subsequent release of norepinephrine [24]. Over time, this repeated stimulation results in overactivation of the HPA axis; enhanced nociception or interoception (that may trigger fear responses, especially if pain or odd sensations are felt in the thoracic area); and hypervigilance that may resemble chronic stress with regard to somatic conditioning. Essentially, repeated GCS episodes may enhance SNS dominance, further exacerbating both IBS and anxiety/panic responses, which are then able to sustain a gut–vagus–cardiac mechanism that self-propagates through chronic stress-induced disruptions in digestion that create mechanical distention which generates vagal static. In turn, this signal propagates GCS cardiac-focused symptoms (such as palpitations) that exploit a hypersensitive amygdala which then dumps catecholamines that both maintain the loss of cardiac homeostasis, as well as lowering thresholds for the next gut-induced GCS activation [42]. In this manner, fear is amplified and ingrained into the nervous system via a positive-feedback system.

The heart has a set of reflexes that serve to maintain blood pressure, rhythmic, and functional homeostasis. These reflexes are carefully regulated feedback loops designed to coordinate with the vagus nerve and are conserved in all mammals. Therefore, disruptions transduced through the vagus nerve due to IBS pressure in the thoracic cavity or via the vagus nerve may cause GCS symptoms through manipulation of these reflexes. In humans, there are five such reflexes tied to both GCS and vagally mediated homeostasis: the baroreceptor, chemoreceptor, Bainbridge, Bezoid-Jarisch, and Valsava. Each reflex, by common ties to the vagus nerve, may have ties to GCS and contribute to the symptoms experienced during an exacerbation.

The baroreceptor reflex is a negative feedback loop that maintains higher arterial pressure in the carotid sinuses and aortic arch while lowering relative pressure in the atria, pulmonary system, and ventricles. This reflex is regulated by large, myelinated type-A vagal fibers that control pressure and heart rate second-to-second (variability) while smaller, unmyelinated type-C vagal fibers modulate tone and basal blood pressure [33]. In this reflex circuit, the carotid sinus nerve communicates directly with the vagal trunk (PNS) and cervical ganglion (SNS), and the sinus itself responds to acetylcholine. As the atrial/medullar link is through the vagus nerve, modulation of angiotensin, aldosterone, and vasopressin are affected by the PNS [43]. Thus, vagal static from GCS may cause changes in blood pressure or temporarily shift blood pressure balance via the baroreceptor reflex. This could result in the dizziness or other effects experienced during a GCS episode.

The chemoreceptor reflex specifically responds to hypoxic and hypercapnic conditions in the carotid sinus or brainstem, respectively. The carotid chemoreceptors are sensitive to oxygen, carbon dioxide, and blood pH affected by bicarbonate ions, similar to the brainstem sensors since the blood–brain barrier facilitates bicarbonate ingress [44]. Low oxygen/high carbon dioxide conditions activate the SNS through these dual receptor beds and increases breathing rate, also stimulating heart rate [45]. However, panic induced by feelings of heart-focused symptoms during GCS may drop carbon dioxide levels below homeostasis via hyperventilation, inducing an alkalotic state through reduced carbonic acid in the blood [46]. This pH shift causes a compensatory decrease in bicarbonate via lower kidney reabsorption and loss of potassium; symptoms are tingling extremities, tremors, weakness in the skeletal muscles, palpitations, sweating, and dyspnea [47]. Resolution of GCS symptoms, a return to psychological homeostasis, and increasing carbon dioxide levels (e.g., the traditional remedy of breathing into a paper bag to calm down during a panic attack) make it possible to re-establish normal blood pH.

The Bainbridge reflex opposes the Bezoid–Jarisch reflex in that it increases heart rate when atrial preload increases, as indicated by increased atrial pressure [48]. This occurs when the head is tilted far forward, when large volumes of saline are infused, the body is upside down, when legs are elevated while supine, or in reduced gravity [48]. The Bezoid–Jarisch reflex, conversely, induces reduced breath rate, bradycardia, and lower blood pressure by direct action of type-C vagal fibers, the release of neuropeptide Y receptor Y2, and afferent vagal signaling [49]. This reflex can override the baroreceptor reflex and was first observed after alkaloid injections in dogs; reduced circulation from the reflex may have evolved to provide some protection from systemic circulation of toxins [50]. This reflex can also be stimulated by nicotine (a plant alkaloid) and chronic alcohol abuse that activates the reflex via enhanced cardiac contractions due to β1-adrenergic stimulation coupled with β2-adrenergic-mediated vasodilation [51]. Clinically, it is often observed in cases of myocardial infarctions after reperfusion and is mediated by receptors localized in the right coronary artery [52]. GCS may errantly stimulate the Bezoid–Jarisch reflex, reducing respiratory rate or stimulate a premature Hering–Breuer reflex (which prevents overinflation of the lungs via vagal activation upon mechanoreception of lung stretching), which would cause a palpitation (extra systole) as the heart adapts to the new respiratory rate and pumps extra blood out with the Bainbridge reflex which activates upon sensing the extra atrial preload. Such sensations can, in hypersensitized individuals, cause panic responses that override vagal control and cause GCS symptoms via adrenaline/norepinephrine. Again, resolution of the gut-mediated vagal static and psychological symptoms allows return to homeostasis in these cases.

The Valsalva reflex is often stimulated in clinical contexts through the Valsalva maneuver, which directly activates the vagus nerve to slow the heart rate. This reflex is useful for treating supraventricular tachycardia and exists to compensate for thoracic pressure changes encountered during defecation, straining, or sustained exhalation (e.g., playing a wind instrument) [53]. It is comprised of four distinct phases that center around thoracic pressure changes: Phase I is the strain and subsequent blood pressure increase; Phase II is the withdrawal of vagal control (allowing an SNS-mediated increase in heart rate in response to reduced venous return); Phase III is a transition phase where strain is released (causing a drop in pressure via capillary bed expansion); and Phase IV is where the reversal of the previous phase leads to a temporary spike in pressure, activating the baroreceptor reflex and returning vagal tone to slow the heart rate to normal [53]. Thus, the vagus nerve plays a key role in the Valsalva reflex and interruptions in communication caused by GCS may precipitate cardiovascular symptoms as the reflex phases lose synchronicity due to vagal static that occurs from thoracic pressure increases from gas distention/tenesmus that mimic strain, errantly activating the Valsalva reflex.

Cardiovascular reflexes are hardwired to maintain pressure and flow homeostasis via interplay between interoceptive signals and the PNS/SNS, with the vagus nerve being a key controller of the PNS response. As GCS can affect the vagus nerve via stimulation or suppression, this interference could errantly activate or precipitate partial or brief full reflex responses, causing cardiac symptoms. In cases featuring hiatal hernias, the rapid and complete resolution of cardiovascular symptoms after surgical hernia repair indicates that continuous disruption of normal vagal signaling has direct effects on the heart via these coronary reflexes. Of note, hypersensitization to cardiac symptoms can trigger panic episodes that delay return to homeostasis.