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Bioelectric and Biomagnetic Signal Analysis
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
The SA-node excites the right-atrium, and sends an electrical signal to the left-atrium through a bundle of fibers called Bachmann bundle. The excitation by the SA-node initiated electric pulse selectively, opens time-dependent sodium ion-channels for Na+ ions to enter the cell. The voltage inside the cell quickly reaches above −40 mV. At this time, Ca++ (calcium ion) ion-channels open; the time-dependent Na+ channels automatically close to avoid the influx of excessive charge in the cell. The Ca++ ion-channels remain open to take voltage above 0 mV for the contraction to occur. At this point, some K+ channels open briefly. K+ leaks out of the cell down its concentration gradient. The outward flow of K+ returns the trans-membrane potential to 0 mV. Ca++ channels are still open, and there is a small inward current of Ca++. These two counter-currents are balanced, and trans-membrane potential is maintained at 0 mV. Ca++ channels are gradually inactivated. Persistent outflow of K+ ions brings the potential back to −90 mV (the resting potential) to prepare the cell for new cycle. The voltage change inside the cell is illustrated in Figure 7.3.
The heart
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
An internodal conduction pathway (or Bachmann’s bundle) also extends from the SA node and transmits the impulse directly to the AV node. This node is located at the base of the right atrium near the interventricular septum, which is the wall of myocardium separating the two ventricles. The atria and the ventricles are separated from each other by fibrous connective tissue referred to as the fibrous skeleton of the heart. Therefore, the electrical impulse cannot spread directly to the ventricles. Instead, the AV node serves as the only pathway through which the impulse can be transmitted to the ventricles. The speed of conduction through the AV node is slowed, resulting in a slight delay (0.1 s). The cause of this AV nodal delay is partly due to the smaller fibers of the AV node. More importantly, however, there are fewer gap junctions between the cells of the node, which increases the resistance to current flow. The physiological advantage of the AV nodal delay is that it allows the atria to complete their contraction before ventricular contraction begins. This timing ensures proper filling of the ventricles prior to contraction.
Cardiovascular physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
From the SA node, the cardiac impulse spreads through atrial muscle at a rate of 1 m/s. The cardiac action potential is conducted from the SA node to the left atrium by a special pathway, Bachmann’s bundle, and to the AV node by the anterior, middle and posterior internodal pathways.
Advanced interatrial block predicts ineffective cardioversion of atrial fibrillation: a FinCV2 cohort study
Published in Annals of Medicine, 2021
Arto Relander, Tapio Hellman, Tuija Vasankari, Ilpo Nuotio, Juhani K. E. Airaksinen, Tuomas Kiviniemi
The main limitation of this study is its retrospective nature. Nevertheless, the data were collected from electronic patient records where data on baseline, peri-CV, and outcomes are reported in detail. A structured case report form was used to ensure the uniformity of reporting. It should also be noted that the ECGs for CV failure patients were collected before or after the CV, while the rest were immediately post-CV. However, this study setting relies on the assumption that underlying atrial conduction pathologies are ongoing and non-regressing processes because underlying fibrosis and damage to the Bachmann bundle are thought to cause AIAB [9]. It is not known how fast AIABs may develop and therefore the results of this study are applicable only to those with a recent (within 60 months) SR recording. The stability of atrial ECG findings in short term (within a month of index CV) was also examined and found to be true by studying extra recordings in an attempt to rule out the possible effect of atrial stunning.
The prevalence and prognostic significance of interatrial block in the general population
Published in Annals of Medicine, 2020
Tiia Istolahti, Antti Eranti, Heini Huhtala, Leo-Pekka Lyytikäinen, Mika Kähönen, Terho Lehtimäki, Markku Eskola, Ismo Anttila, Antti Jula, Antoni Bayés de Luna, Kjell Nikus, Jussi Hernesniemi
Interatrial block (IAB) is a distinct electrocardiographic (ECG) pattern that has been studied with growing interest since it was first described in 1979 by Bayés de Luna [1]. IAB is caused by conduction delay between the right and left atrium, probably resulting from local fibrosis. When the conduction through the Bachmann’s bundle is blocked, the electrical activation to the left atrium takes an alternative route through the lower parts of the interatrial septum resulting in caudo-cranial activation in the left atrium [2]. This is reflected in the surface ECG as a biphasic morphology of the P wave in the inferior leads (II, III and aVF). This together with a P-wave duration ≥120 ms is considered as advanced IAB (Figure 1). P-wave duration ≥120 ms with normal P-wave morphology is defined as partial IAB and delayed conduction via the interatrial septum through Bachmann’s bundle is considered as the background pathology for this ECG phenomenon [3].
Advances in atrioventricular and interventricular optimization of cardiac resynchronization therapy – what’s the gold standard?
Published in Expert Review of Cardiovascular Therapy, 2018
Matthew K. Rowe, Gerald C. Kaye
In HF patients, approximately 20% of cardiac output during sinus rhythm is related to synchronous atrial contraction [22]. In normal hearts, a precise series of electromechanical events occurs, aligning left atrial (LA) contraction and LV filling before LV systolic contraction. In sinus rhythm the electrical impulse spreads from right to left atrium via Bachmann’s bundle as it also conducts into the ventricles via the AV node [23]. During atrial pacing this process is altered, resulting in prolongation of LA activation and subsequent disruption to LA-LV synchrony [24]. The importance of an optimal AV interval (or AV delay) lies in allowing the maximal time for LV diastolic filling to occur, increasing LV preload, stroke volume and cardiac output. In an optimal cardiac cycle this involves allowing passive filling of the LV to complete (observed on echocardiogram as the mitral inflow E wave), followed by active filling from LA contraction (mitral inflow A wave) without creating an AV interval so long that there is diastolic mitral regurgitation (MR), or so short that active filling is truncated by ventricular contraction and mitral valve closure (Figure 2). Optimization of the AV interval also prevents intrinsic, dyssynchronous, LV activation through the native conduction system, maximizing the amount of biventricular (BiV) pacing [25].