Abstract 17124: Severe Bradycardia in Critically Ill Patients With COVID-19

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Julie Larue ◽  
Patrick De Jode ◽  
Jean-François Timsit ◽  
Guillaume Franchineau ◽  
Fabrice Extramiana ◽  
...  
Keyword(s):  
Heart Rate ◽  
Beta Blockers ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Cardiac Pacing ◽  
Multiple Organ ◽  
Physical Stimulation ◽  
Node Disease ◽  
Cardiac Manifestations ◽  
Mean Heart Rate

Cardiac manifestations of severe Covid19 infection are still poorly understood. From January to May 2020, 113 consecutive patients were admitted in intensive care units for severe Covid19 and 10 out of them presented an episode of bradycardia. Patients had a median age of 63 years, 6/10 were men, 7/10 were under mechanical ventilation for severe acute respiratory distress syndrome and 4/10 received a veno-venous extracorporeal membrane oxygenation. All bradycardias were due to sinus node bradycardia with a median heart rate of 36 bpm (range 10 - 45 bpm). For 6 patients, bradycardia was persistent and 3 required continuous isoprenaline infusion (Figure, patient A). Bradycardia was sudden for 4 patients and required brief resuscitation maneuvers for one (Figure, patient B) . Patients had normal baseline ECG and echocardiography, except for two patients who were under beta-blockers. For those two patients beta blockers were interrupted several days before bradycardia. A comprehensive review of patient’s files ruled out bradycardia due to drug-drug interactions, myocarditis, hyperkalemia, hypoxia or vagal physical stimulation. Holter ECG was performed for 7 patients: 3 recordings evoked vagal hyperactivity (low mean heart rate and elevated pNN50 / RMSSD, Figure Patient A), 3 others cardiac dysautonomia (SDNN<100ms, Figure Patient B). Amongst these 10 patients, 5 were discharged from ICU among which 2 returned home and five died from covid-19 associated multiple-organ failure. None of them required temporary or permanent cardiac pacing. To conclude, sinus bradycardia occurred commonly in severe Covid19 infection. This highlights the need to monitor cardiac rhythm. Even if the pathophysiology remains unclear, cardiac dysautonomia and vagal hyperactivity could be hypothesized rather than an intrinsic sinus node disease.

Bradyarrhythmias

2018 ◽  
Author(s):  
Kim Rajappan
Keyword(s):  
Heart Rate ◽  
Sick Sinus Syndrome ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Ventricular Rate ◽  
Type I ◽  
Av Block ◽  
Node Disease ◽  
Wenckebach Phenomenon ◽  
Mobitz Type

A bradyarrhythmia is defined as a rhythm disturbance that results in a heart rate of less than 60 bpm. It is important to note that many healthy people have a resting heart rate that is less than 60 bpm, most commonly due to sinus bradycardia (i.e. a rhythm arising from the sinus node but with a ventricular rate less than 60 bpm). Other forms of bradyarrhythmia are sinus node disease, sick sinus syndrome, first-degree atrioventricular (AV) block, second-degree AV block (which can be characterized as Möbitz type I (Wenckebach phenomenon) or Möbitz type II), and third-degree AV block (also known as complete heart block). This chapter discusses the bradyarrhythmias, focusing on their etiology, symptoms, demographics, diagnosis, prognosis, and treatment.

Bradyarrhythmias

2016 ◽  
Author(s):  
Inna Leybell ◽  
Liliya Abrukin
Keyword(s):  
Atrioventricular Block ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Treatment Options ◽  
Presenting Symptoms ◽  
Threatening Condition ◽  
Node Disease ◽  
Life Threatening ◽  
Sinus Node Disease ◽  
Sinoatrial Block

Bradyarrhythmias can present as an incidental electrocardiographic (ECG) finding or a life-threatening condition requiring immediate intervention. They are caused by sinus node disease or atrioventricular block. This review covers pathophysiology, stabilization and assessment, diagnosis and treatment options, and disposition and outcomes for patients with bradycardia. Figures in the review demonstrate characteristic ECG tracings. Tables list classifications of sinus node dysfunction as well as of sinoatrial and atrioventricular blocks, presenting symptoms, important information to elicit on history taking, various causes of bradycardia, and specific interventions for toxicologic etiologies. Key words: atrioventricular block, atropine, bradyarrhythmia, bradycardia, first-degree atrioventricular block, second-degree atrioventricular block, sinoatrial block, sinus bradycardia, sinus node disease, tachycardia-bradycardia syndrome, third-degree atrioventricular block This review contains 9 highly rendered figures, 7 tables, and 92 references.

Electrophysiological effects of ouabain in 6-hydroxydopamine pretreated dogs

1983 ◽  
Vol 61 (3) ◽  
pp. 229-236 ◽  
Author(s):  
Diane Godin ◽  
Claude Guimond ◽  
Réginald Nadeau
Keyword(s):  
Heart Rate ◽  
Sinus Bradycardia ◽  
Cardiac Pacing ◽  
Refractory Periods ◽  
Ventricular Extrasystoles ◽  
Additional Group ◽  
Sinus Cycle Length ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Therapeutic Doses

Chemical sympathectomy and bilateral vagotomy were used to evaluate the contribution of each division of the autonomic nervous system in the electrophysiological actions of ouabain. Intact and chemically sympathectomized dogs were given successive and cumulative doses of ouabain until toxicity became manifest (ventricular extrasystoles and (or) ventricular tachycardia). An additional group of normal and sympathectomized animals was also submitted to bilateral vagotomy in the presence of a therapeutic dose of ouabain. Sinus cycle length, AH interval of the His bundle electrogram, atrioventricular junctional effective and functional refractory periods were increased by ouabain at therapeutic doses. These effects were no different in sympathectomized dogs than in intact dogs, indicating the absence of any significant contribution of efferent sympathetic neural activity. However, our results suggested that vagal enhancement was the main mechanism whereby ouabain produced sinus bradycardia and depression of atrioventricular conduction. Sympathectomy with 6-OHDA did not modify nor abolish ouabain toxicity. However, toxic doses were significantly higher in sympathectomized animals than in normal animals. Considering that increasing heart rate by cardiac pacing or vagotomy significantly lowered toxic doses of ouabain in both intact and sympathectomized dogs, it is possible that sympathectomy could influence ouabain toxicity by altering heart rate alone.

scholarly journals Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease

2008 ◽  
Vol 105 (40) ◽  
pp. 15617-15622 ◽  
Author(s):  
Solena Le Scouarnec ◽  
Naina Bhasin ◽  
Claude Vieyres ◽  
Thomas J. Hund ◽  
Shane R. Cunha ◽  
...  
Keyword(s):  
Ion Channel ◽  
Molecular Mechanisms ◽  
Sinoatrial Node ◽  
Sinus Node ◽  
Critical Role ◽  
Cardiac Pacing ◽  
Membrane Organization ◽  
Node Disease ◽  
Sinoatrial Node Cell ◽  
Ankyrin B

The identification of nearly a dozen ion channel genes involved in the genesis of human atrial and ventricular arrhythmias has been critical for the diagnosis and treatment of fatal cardiovascular diseases. In contrast, very little is known about the genetic and molecular mechanisms underlying human sinus node dysfunction (SND). Here, we report a genetic and molecular mechanism for human SND. We mapped two families with highly penetrant and severe SND to the human ANK2 (ankyrin-B/AnkB) locus. Mice heterozygous for AnkB phenocopy human SND displayed severe bradycardia and rate variability. AnkB is essential for normal membrane organization of sinoatrial node cell channels and transporters, and AnkB is required for physiological cardiac pacing. Finally, dysfunction in AnkB-based trafficking pathways causes abnormal sinoatrial node (SAN) electrical activity and SND. Together, our findings associate abnormal channel targeting with human SND and highlight the critical role of local membrane organization for sinoatrial node excitability.

scholarly journals Electrophysiological Testing for the Investigation of Bradycardias

2017 ◽  
Vol 6 (1) ◽  
pp. 24 ◽  
Author(s):  
Demosthenes G Katritsis ◽  
Mark E Josephson ◽  
◽  
Keyword(s):  
Sinus Bradycardia ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Anatomic Site ◽  
Conduction Disturbances ◽  
Permanent Pacing ◽  
Electrophysiological Testing ◽  
Av Conduction ◽  
Node Disease

In this article we review the role of electrophysiological testing in patients presenting with bradycardia due to sinus node or atrioventricular node disease. In sinus bradycardia the role of electrophysiology studies is not established. In AV conduction disturbances, an electrophysiology study may be necessary both for the establishment of atrioventricular block as the main cause of symptoms, and for identification of the anatomic site of block that may dictate the potential need of permanent pacing.

Sinus bradycardia during injections directly into the sinus node artery

1963 ◽  
Vol 204 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Thomas N. James ◽  
Reginald A. Nadeau
Keyword(s):  
Heart Rate ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Normal Heart ◽  
Anatomic Structure ◽  
Ionic Content ◽  
Sinus Node Artery ◽  
Nutrient Artery ◽  
Normal Heart Rate ◽  
Cervical Vagotomy

In over 90% of 800 experiments in 75 dogs injection directly into the sinus node artery produced sinus bradycardia. Studies to explain this phenomenon included control of temperature, pH, osmolarity, oxygen, and ionic content of injecting solutions. Although unphysiologic variations of any of these are known to produce marked alterations in the sinus mechanism, sinus bradycardia from injection still occurred when they were controlled. Neurogenic mechanisms were excluded by bilateral cervical vagotomy, and by direct perfusion of the sinus node with atropine, hexamethonium, and trimethaphan. Because of the unique anatomic structure of the sinus node, which completely surrounds its nutrient artery, it is suggested that the sinus bradycardia may simply be the consequence of distending the sinus node artery. Implications concerning autoregulation of the normal heart rate are discussed.

Sinus node disease: ECG patterns and diagnosis

ESC CardioMed ◽  
2018 ◽  
pp. 1949-1952
Author(s):  
Tatjana Potpara
Keyword(s):  
Carotid Sinus ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Heart Rhythm ◽  
Cardiac Pacemakers ◽  
Carotid Sinus Hypersensitivity ◽  
Electrophysiological Studies ◽  
Node Disease ◽  
Structural Disease ◽  
Exit Block

A healthy sinus node (SN) is the physiological principal site of electrical impulse formation in the heart, owing to its ability to sustain a regular generation of spontaneous depolarization at faster rates than other latent cardiac pacemakers. Structural disease (or senescence) of the SN and sinoatrial junction may cause SN disease (SND). The electrocardiographic (ECG) manifestations of SND are usually intermittent and can be easily missed. The ECG patterns of SND include: (1) periods of spontaneous, often pronounced, sinus bradycardia; (2) sinus pause due to sinus arrest or sinoatrial exit block; and (3) tachycardia-bradycardia syndrome. There is no standardized set of diagnostic criteria for SND. Since the symptoms of SND are non-specific, and the initial ECG may not be diagnostic, establishing a correlation between symptoms and the underlying heart rhythm at the time of symptoms is essential for the diagnosis, provided that any potentially reversible cause(s) of transient SN dysfunction have been excluded (or identified and treated). Invasive electrophysiological studies are not routinely used for the evaluation of SND, due to a limited sensitivity, and may be considered in patients with a mismatch of symptoms and ECG findings. When reversible causes have been excluded, SND should be distinguished from ‘physiological’ bradycardia (particularly in well-trained athletes), neurocardiogenic syncope with a pronounced cardioinhibitory component, or carotid sinus hypersensitivity. Carotid sinus hypersensitivity can be established by carotid sinus massage resulting in a pause of longer than 3 s or a symptomatic drop in blood pressure, or both.

scholarly journals Functional capabilities of the heart rate depending on the characteristics of homeostasis among primary-school-age children

2021 ◽  
pp. 30-37
Author(s):  
T.B. Ihnatova ◽  
◽  
I.S. Maidan ◽  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Spectral Analysis ◽  
Sinus Rhythm ◽  
Primary School ◽  
Sinus Bradycardia ◽  
Sinus Node ◽  
Heart Rhythm ◽  
School Age ◽  
Primary School Age

One of the most common diseases of the cardiovascular system is cardiac arrhythmias. Assessment of the heart rate is one of the obligatory methods of pediatric examination and its deviation from the age norm may indicate a change in the child's health and be one of the first manifestations of the disease. Heart rhythm disturbances accompany various diseases, namely: congenital heart defects, cardiomyopathies, rheumatic and infectious diseases, intoxication, vegetative crises, endocrine diseases, diseases of the nervous system and others. Most often, in children's practice, it is not always possible to establish the cause of heart rhythm disturbances, as well as to classify the presence of organic or functional disorders without conducting morphological studies. Purpose — to study the features of heart rhythm and the state of the autonomic nervous system (ANS) among the children of primary school age with sinus bradycardia. Materials and methods. Children of primary school age with sinus bradycardia were examined (210 children). All children underwent: clinical examination, ECG at rest and after exercise, daily monitoring of ECG and heart rate, echocardiography, cardiointervalography with spectral analysis of heart rate. Results. Assessment of the cardiovascular system among children with bradycardia revealed the following features: 80.0% of children had no complaints, 68.0% of children at the age of 6–7 years and 55.0% of children at the age of 8–10 years had moderate bradycardia, 32.0% of children at the age of 6–7 years and 45.0% of children at the age of 8–10 years had significant bradycardia. After the exercise test, 71.0% of children still had bradycardia, which is typical for children at the age of 9–10 years and 29.0% of children had an acceleration of heart rate above the age norm. Holter monitoring revealed the following cardiac arrhythmias: sinus rhythm driver migration, ectopic rhythm, sinoatrial block, 2 grade atrioventricular block, atrial extrasystole and ventricular extrasystole. Different duration of sinoatrial pauses was detected: in the range from 1300–1400 ms among the most children (78.0%) to 1700–1800 ms among 1.8% of children. Data from spectral analysis of sinus rhythm showed the predominance of parasympathetic nervous system tone among the 84.0% of children, asympathicotonic (40.5%) and normal (44.9%) autonomic reactivity. Conclusions. Examination of the children of the primary school age revealed sinus bradycardia and bradyarrhythmia among the 80.7% of children. Bradyarrhythmia is typical for children at the age of 6–7 years, bradycardia — for children at the age of 9–10 years. Spectral analysis of the ANS showed an imbalance in the regulation of sinus rhythm: the predominance of the parasympathetic link, regardless of the initial state of the ANS and the violation of adaptive mechanisms. According to Holter monitoring, the duration of pauses is longer than normal for the given age (more than 1300 ms) indicates sinus node dysfunction and requires closer monitoring due to the risk of developing sinus node weakness syndrome and other threatening conditions in later life. The research was carried out in accordance with the principles of the Helsinki declaration. The study protocol was approved by the Local ethics committee of all participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors. Key words: children, bradycardia, bradyarrhythmia, vegetative homeostasis.

Sign in / Sign up

Export Citation Format

Share Document