Review

Authors: Sunjeet Sidhu, Joseph E Marine

Bradycardia is a commonly observed arrhythmia and a frequent occasion for cardiac consultation. Defined as a heart rate of less than 50-60 bpm, bradycardia can be observed as a normal phenomenon in young athletic individuals, and in patients as part of normal aging or disease (Table 1). Pathology that produces bradycardia may occur within the sinus node, atrioventricular (AV) nodal tissue, and the specialized His-Purkinje conduction system. Given the overlap of heart rate ranges with non-pathologic changes, assessment of symptoms is a critical component in the evaluation and management of bradycardia. Treatment should rarely be prescribed solely on the basis of a heart rate lower than an arbitrary cutoff or a pause above certain duration. In the 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay (referred to hereafter as the 2018 Bradycardia Guideline), there was a significant shift in emphasis from prior guidelines that emphasized device-based implantation recommendations to a focus on evaluation and management of disease states [1,2]. In this review, we will highlight the changes in the new guideline as well as describe the key elements in evaluation and management of patients presenting with bradycardia.

Topics: Action Potentials; Atrioventricular Block; Bradycardia; Cardiac Pacing, Artificial; Clinical Decision-Making; Heart Conduction System; Heart Rate; Humans; Pacemaker, Artificial; Patient Selection; Sick Sinus Syndrome; Treatment Outcome

PubMed: 31311698
DOI: 10.1016/j.tcm.2019.07.001

Review

Authors: Paul Grossman

The polyvagal collection of hypotheses is based upon five essential premises, as stated by its author (Porges, 2011). Polyvagal conjectures rest on a primary assumption that brainstem ventral and dorsal vagal regions in mammals each have their own unique mediating effects upon control of heart rate. The polyvagal hypotheses link these putative dorsal- vs. ventral-vagal differences to socioemotional behavior (e.g. defensive immobilization, and social affiliative behaviors, respectively), as well as to trends in the evolution of the vagus nerve (e.g. Porges, 2011 & 2021a). Additionally, it is essential to note that only one measurable phenomenon-as index of vagal processes-serves as the linchpin for virtually every premise. That phenomenon is respiratory sinus arrhythmia (RSA), heart-rate changes coordinated to phase of respiration (i.e. inspiration vs. expiration), often employed as an index of vagally, or parasympathetically, mediated control of heart rate. The polyvagal hypotheses assume that RSA is a mammalian phenomenon, since Porges (2011) states "RSA has not been observed in reptiles." I will here briefly document how each of these basic premises have been shown to be either untenable or highly implausible based on the available scientific literature. I will also argue that the polyvagal reliance upon RSA as equivalent to general vagal tone or even cardiac vagal tone is conceptually a category mistake (Ryle, 1949), confusing an approximate index (i.e. RSA) of a phenomenon (some general vagal process) with the phenomenon, itself.

Topics: Animals; Humans; Vagus Nerve; Heart; Arrhythmia, Sinus; Respiratory Sinus Arrhythmia; Respiration; Heart Rate; Mammals

PubMed: 37230290
DOI: 10.1016/j.biopsycho.2023.108589

Review

Authors: Michael Semelka, Jerome Gera, Saif Usman...

Sick sinus syndrome refers to a collection of disorders marked by the heart's inability to perform its pacemaking function. Predominantly affecting older adults, sick sinus syndrome comprises various arrhythmias, including bradyarrhythmias with or without accompanying tachyarrhythmias. At least 50 percent of patients with sick sinus syndrome develop alternating bradycardia and tachycardia, also known as tachy-brady syndrome. Sick sinus syndrome results from intrinsic causes, or may be exacerbated or mimicked by extrinsic factors. Intrinsic causes include degenerative fibrosis, ion channel dysfunction, and remodeling of the sinoatrial node. Extrinsic factors can be pharmacologic, metabolic, or autonomic. Signs and symptoms are often subtle early on and become more obvious as the disease progresses. They are commonly related to end-organ hypoperfusion. Cerebral hypoperfusion is most common, with syncope or near-fainting occurring in about one-half of patients. Diagnosis may be challenging, and is ultimately made by electrocardiographic identification of the arrhythmia in conjunction with the presence of symptoms. If electrocardiography does not yield a diagnosis, inpatient telemetry monitoring, outpatient Holter monitoring, event monitoring, or loop monitoring may be used. Electrophysiologic studies also may be used but are not routinely needed. Treatment of sick sinus syndrome includes removing extrinsic factors, when possible, and pacemaker placement. Pacemakers do not reduce mortality, but they can decrease symptoms and improve quality of life.

Topics: Electrocardiography; Humans; Pacemaker, Artificial; Sick Sinus Syndrome

PubMed: 23939447
DOI: No ID Found

Review

Authors: Stephen W Porges

The polyvagal theory introduced a new perspective relating autonomic function to behavior, that included an appreciation of the autonomic nervous system as a "system," the identification of neural circuits involved in the regulation of autonomic state, and an interpretation of autonomic reactivity as adaptive within the context of the phylogeny of the vertebrate autonomic nervous system. The paper has two objectives: first, to provide an explicit statement of the theory; and second, to introduce the features of a polyvagal perspective. The polyvagal perspective emphasizes how an understanding of neurophysiological mechanisms and phylogenetic shifts in neural regulation leads to different questions, paradigms, explanations, and conclusions regarding autonomic function in biobehavioral processes than peripheral models. Foremost, the polyvagal perspective emphasizes the importance of phylogenetic changes in the neural structures regulating the autonomic nervous system and how these phylogenetic shifts provide insights into the adaptive function and the neural regulation of the two vagal systems.

Topics: Adaptation, Physiological; Arrhythmia, Sinus; Autonomic Nervous System; Brain Stem; Cerebral Cortex; Environment; Heart Rate; Humans; Limbic System; Nerve Net; Parasympathetic Nervous System; Peripheral Nervous System; Phylogeny; Pressoreceptors; Psychomotor Performance; Vagus Nerve

PubMed: 17049418
DOI: 10.1016/j.biopsycho.2006.06.009

Review

Authors: M J Parkes

This article reviews the basic properties of breath-holding in humans and the possible causes of the breath at breakpoint. The simplest objective measure of breath-holding is its duration, but even this is highly variable. Breath-holding is a voluntary act, but normal subjects appear unable to breath-hold to unconsciousness. A powerful involuntary mechanism normally overrides voluntary breath-holding and causes the breath that defines the breakpoint. The occurrence of the breakpoint breath does not appear to be caused solely by a mechanism involving lung or chest shrinkage, partial pressures of blood gases or the carotid arterial chemoreceptors. This is despite the well-known properties of breath-hold duration being prolonged by large lung inflations, hyperoxia and hypocapnia and being shortened by the converse manoeuvres and by increased metabolic rate. Breath-holding has, however, two much less well-known but important properties. First, the central respiratory rhythm appears to continue throughout breath-holding. Humans cannot therefore stop their central respiratory rhythm voluntarily. Instead, they merely suppress expression of their central respiratory rhythm and voluntarily 'hold' the chest at a chosen volume, possibly assisted by some tonic diaphragm activity. Second, breath-hold duration is prolonged by bilateral paralysis of the phrenic or vagus nerves. Possibly the contribution to the breakpoint from stimulation of diaphragm muscle chemoreceptors is greater than has previously been considered. At present there is no simple explanation for the breakpoint that encompasses all these properties.

Topics: Arrhythmia, Sinus; Carbon Dioxide; Diaphragm; Homeostasis; Humans; Lung; Muscle Contraction; Oxygen; Partial Pressure; Phrenic Nerve; Proprioception; Respiration; Respiratory Center; Respiratory Mechanics; Respiratory Muscles; Vagus Nerve

PubMed: 16272264
DOI: 10.1113/expphysiol.2005.031625

Authors: Han Ouyang, Zhuo Liu, Ning Li...

Self-powered implantable medical electronic devices that harvest biomechanical energy from cardiac motion, respiratory movement and blood flow are part of a paradigm shift that is on the horizon. Here, we demonstrate a fully implanted symbiotic pacemaker based on an implantable triboelectric nanogenerator, which achieves energy harvesting and storage as well as cardiac pacing on a large-animal scale. The symbiotic pacemaker successfully corrects sinus arrhythmia and prevents deterioration. The open circuit voltage of an implantable triboelectric nanogenerator reaches up to 65.2 V. The energy harvested from each cardiac motion cycle is 0.495 μJ, which is higher than the required endocardial pacing threshold energy (0.377 μJ). Implantable triboelectric nanogenerators for implantable medical devices offer advantages of excellent output performance, high power density, and good durability, and are expected to find application in fields of treatment and diagnosis as in vivo symbiotic bioelectronics.

Topics: Animals; Arrhythmia, Sinus; Cardiac Surgical Procedures; Cell Line; Dimethylpolysiloxanes; Disease Models, Animal; Electrophysiological Phenomena; Equipment Design; Heart; Male; Mice; Nanomedicine; Nylons; Pacemaker, Artificial; Polytetrafluoroethylene; Prosthesis Implantation; Sus scrofa

PubMed: 31015519
DOI: 10.1038/s41467-019-09851-1

Review

Authors: Paul Grossman

Linchpin to the entire area of psychophysiological research and discussion of the vagus is the respiratory and cardiovascular phenomenon known as respiratory sinus arrhythmia (RSA; often synonymous with high-frequency heart-rate variability when it is specifically linked to respiratory frequency), i.e. rhythmic fluctuations in heart rate synchronized to inspiration and expiration. This article aims 1) to clarify concepts, terms and measures commonly employed during the last half century in the scientific literature, which relate vagal function to psychological processes and general aspects of health; and 2) to expand upon an earlier theoretical model, emphasizing the importance of RSA well beyond the current focus upon parasympathetic mechanisms. A close examination of RSA and its relations to the vagus may 1) dispel certain commonly held beliefs about associations between psychological functioning, RSA and the parasympathetic nervous system (for which the vagus nerve plays a major role), and 2) offer fresh perspectives about the likely functions and adaptive significance of RSA, as well as RSA's relationship to vagal control. RSA is neither an invariably reliable index of cardiac vagal tone nor of central vagal outflow to the heart. The model here presented posits that RSA represents an evolutionarily entrenched, cardiovascular and respiratory phenomenon that significantly contributes to meeting continuously changing metabolic, energy and behavioral demands.

Topics: Humans; Respiratory Sinus Arrhythmia; Vagus Nerve; Arrhythmia, Sinus; Heart; Parasympathetic Nervous System; Heart Rate

PubMed: 38151156
DOI: 10.1016/j.biopsycho.2023.108739

Review

Authors: Xingqun Liang, Sylvia M Evans, Yunfu Sun...

The sinoatrial node (SAN) is the dominant pacemaker of the heart. Abnormalities in SAN formation and function can cause sinus arrhythmia, including sick sinus syndrome and sudden death. A better understanding of genes and signaling pathways that regulate SAN development and function is essential to develop more effective treatment to sinus arrhythmia, including biological pacemakers. In this review, we briefly summarize the key processes of SAN morphogenesis during development, and focus on the transcriptional network that drives SAN development.

Topics: Arrhythmia, Sinus; Heart Diseases; Homeodomain Proteins; Humans; LIM-Homeodomain Proteins; Pacemaker, Artificial; Sinoatrial Node; T-Box Domain Proteins; Transcription Factors

PubMed: 27770149
DOI: 10.1007/s00018-016-2400-1

Authors: Pascale Calabrese, Sophie Lambert-Lacroix

Breathing and ECG were recorded in 33 healthy human subjects at rest. The RR interval was labeled according to its occurrence in the respiratory phases: II (both R waves during inspiration), IE (first R wave in inspiration and following R wave in expiration), EE (both R waves during expiration), and EI (first R wave in expiration and following R wave in inspiration). For each subject, II and EE intervals were plotted versus normalized mean inspiratory duration and normalized mean expiratory duration, respectively, and correlation coefficients and slopes of regression lines were calculated. Statistical analyses were conducted to compare these slopes between and within individuals. These relationships appeared to be linear in most cases, although neither the decrease nor the increase in heart rate occurred at the same rate for all subjects. Overall, the slope associated with II intervals was not higher, in terms of absolute values, than the slope associated with EE intervals for the same subject. Our results underscore the difference between inspiratory and expiratory sinus arrhythmia and suggest that the effects of any stimulation presumed to induce changes in vagal cardiac activity should primarily be sought during expiration.

Topics: Humans; Male; Female; Adult; Exhalation; Inhalation; Heart Rate; Electrocardiography; Respiratory Sinus Arrhythmia; Middle Aged; Young Adult; Arrhythmia, Sinus

PubMed: 40173080
DOI: 10.14814/phy2.70245

Authors: Lauren E Philbrook, Mina Shimizu, Stephen A Erath...

Sleep and autonomic nervous system functioning are important bioregulatory systems. Poor sleep and low baseline respiratory sinus arrhythmia (RSA), a measure of parasympathetic nervous system activity, are associated with externalizing behaviors and depressive symptoms in youth. Rarely, however, have measures of these systems been examined conjointly. The present study examined baseline RSA (RSA-B) as a moderator of longitudinal relations between adolescent sleep and adjustment. Participants were 256 adolescents (52% girls, 66% White/European American, 34% Black/African American) from small towns and surrounding rural communities in the southeastern United States. Sleep (minutes, efficiency, variability in minutes and efficiency) was assessed at age 15 via actigraphs across seven nights. RSA-B was derived from electrocardiogram data collected at rest. Adolescents self-reported externalizing problems and depressive symptoms at ages 15 and 17. Controlling for age 15 adjustment, findings generally demonstrated that sleep predicted age 17 adjustment particularly at higher (rather than lower) levels of RSA-B, such that adolescents with good sleep (more minutes and lower variability) and high RSA-B were at lowest risk for maladjustment. The results highlight the value of examining multiple bioregulatory processes conjointly and suggest that promoting good sleep habits and regulation of physiological arousal should support adolescent adjustment.

Topics: Adolescent; Adolescent Behavior; Arrhythmia, Sinus; Female; Humans; Male; Parasympathetic Nervous System; Respiratory Sinus Arrhythmia; Sleep

PubMed: 34964495
DOI: 10.1002/dev.22220