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Physiological consequences of ionic mechanisms
Published in Burt B. Hamrell, Cardiovascular Physiology, 2018
This is the normal pacemaker of the heart because diastolic depolarization is faster than in before AV node cells and much before Purkinje fibers (self-study module Cardiac Action Potentials, Part 2: Nodal and Conduction System Myocytes). The pacemaker potential in SA node cells normally reaches threshold before the AV node cells and much before Purkinje fibers. The normal heart rhythm, driven by the SA node as the pacemaker, is called “normal sinus rhythm.” The intrinsic frequency of the SA node, in the absence of input from the autonomic nervous system, is about 100 beats/min.
Physiology of excitable cells
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
The sinoatrial node has no resting state; rather, there is a pacemaker potential that generates cardiac autorhythmicity. The maximum diastolic potential of sinus node cells is −45 to −55 mV and −50 to 65 mV in the AV node cells. Phases 1 and 2 are absent in the sinoatrial node as there is no depolarization plateau (Figure 1.18). Phase 4: From the maximum diastolic potential, spontaneous diastolic depolarization slowly shifts the membrane towards the action potential threshold (approximately −40 mV). The pacemaker potential is produced by a fall in potassium permeability (iK), a hyperpolarization-activated mixed sodium–potassium ‘funny’ current (if) and an increase in a slow inward current. The slow inward current consists of a voltage-gated increase in calcium permeability via transient calcium channels and activity of the electrogenic sodium–calcium exchange system, driven by inward movement of calcium ions. This pacemaker activity brings the cell to the threshold potential.Phase 0: Depolarization is produced by opening of long-lasting voltage-gated calcium channels (iCaL) and inward movement of positive ions. There is no sodium current involved in the sinoatrial node potential. The sinoatrial node potential reaches a peak at about 20 mV.Phase 3: Repolarization occurs as a result of a reduction in depolarizing currents (if and iCaL are inactivated by positive potentials) and an increase in repolarizing currents (iK becomes activated by positive potentials) causing a late increase in potassium permeability and outward flow of ions.
Electrical Properties of the Heart
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The maximum diastolic potential of a sinus node cell is −65 mV. Phases 1 and 2 (of the fast response cardiac action potential) are absent in the SA node as there is no depolarization plateau (Figure 24.1). Phase 4. The pacemaker current is determined by hyperpolarization-activated cyclic nucleotide (HCN)–gated channels. From the maximum diastolic potential (−65 mV), a slow, spontaneous depolarization occurs towards a threshold potential of approximately −40 mV. The pacemaker potential is produced by a fall in potassium permeability (iK) and an inward sodium ‘funny’ current (If) produced by the opening of sodium channels. The funny current is a mixed sodium–potassium current that is activated when the SA action potential is repolarized below about −40 to −50 mV and provides the inward current that is responsible for initiating the diastolic depolarization phase. The funny current is also activated by cAMP. The binding of cAMP to the If channels enhances the opening of the channels. Sympathetic stimulation increases cAMP molecules, which bind to the If channels and increase the diastolic current, resulting in an increase in the steepness of the diastolic depolarization phase. Ivabradine is a selective If inhibitor used to control tachycardia that is resistant to conventional anti-arrhythmic drugs. The slow, inward current brings the membrane to the threshold potential (−40 mV) of T-type calcium channels, which open for the upstroke. The voltage-gated increase in calcium permeability via transient calcium channels results in an inward movement of calcium ions. The SA node exhibits automaticity because it spontaneously generates action potentials without neural input.Phase 0. Depolarization is produced by the opening of long-lasting (L-type), voltage-gated calcium channels (iCaL) and inward movement of Ca++ ions. No sodium current is involved in the SA node potential. The SA node potential reaches a peak at about 20 mV.Phase 3. Repolarization is accomplished by a late increase in potassium permeability and outward flow of K+ ions. This is the result of an increase in repolarizing currents (iK becomes activated by positive potentials), causing a late increase in potassium permeability and outward flow of ions.
Ivabradine for treatment of heart failure
Published in Expert Opinion on Drug Safety, 2019
Edimar Alcides Bocchi, Vera Maria Cury Salemi
Ivabradine selectively inhibits If (funny) channels in a concentration-dependent manner reducing HR [30]. The If channels are located in the sinoatrial node, which control the slope of the diastolic depolarization. The spontaneous diastolic depolarization current determines the HR, by allowing the threshold for action potentials to be reached [31]. This is known as the If current and can be activated by voltage changes, cyclic nucleotides, and nitric oxide making it possible for the channel’s activity to be altered by both sympathetic and parasympathetic stimulations. Then, ivabradine prolongs the slow spontaneous phase of diastolic depolarization and thereby reduces HR. The activity of ivabradine is therefore dependent on the opening and closing of the If channels, with greater potency seen with faster HRs [32]. At higher concentrations, the activity of ivabradine saturates, preventing adverse reductions in the HR.
Asymptomatic bradycardia amongst endurance athletes
Published in The Physician and Sportsmedicine, 2019
Benoit Doyen, David Matelot, François Carré
Pacemaker cells are located on the superior portion of the right atrial wall at the sinoatrial node. Cyclical local depolarization results in the generation of action potentials resulting in automatism of surrounding myocardiocytes [12]. In humans, the intrinsic frequency of this process is approximately comprised between 100 and 120 bpm. The action potentials of pacemaker cells differ from those of contractile myocardial cells by the presence, in phase 4, of a spontaneous diastolic depolarization slope which is the key factor for generation of cardiac rhythm (Figure 3).
Biological therapies targeting arrhythmias: are cells and genes the answer?
Published in Expert Opinion on Biological Therapy, 2018
Debbie Falconer, Nikolaos Papageorgiou, Emmanuel Androulakis, Yasmin Alfallouji, Wei Yao Lim, Rui Providencia, Dimitris Tousoulis
Pacemaker cells possess automaticity. This refers to the ability of cardiac cells to undergo spontaneous diastolic depolarization and subsequently initiate an electrical impulse in the absence of external electric stimulation. Suppression or enhancement of automaticity leads to the development of clinical arrhythmias [11].