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Bradycardia
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Sinus arrest, or sinus pause, is a disorder of automaticity in which no impulses are generated within the sinus node and may last from seconds to several minutes. The length of the pause is not an exact multiple of the P–P interval, suggesting that the mechanism is loss of automaticity of sinus node and not conduction block. On the contrary, a third-degree sinoatrial (SA) block is a disorder of sinus impulse conduction and electrocardiographically manifests as a sudden pause with the pause being an exact multiple of the basic P–P interval. However it must be emphasized that, this condition can be diagnosed only when the sinus rate is relatively regular before and after the pause. SA exit block can be divided into type I (SA Wenkebach), type II (SA Mobitz II), and high-degree SA block (Figure 4.1). Type I SA block can be recognized electrocardiographically as a group beating of P waves with shortening of the P–P intervals and pauses that amount to less than twice the shortest P–P cycle. In contrast, type II SA block demonstrates intermittent failure of conduction of the sinus impulse to the atrium as manifested by fixed PP intervals with pauses that equal twice the P–P interval. Type II SA exit block with a 2:1 periodicity, manifests as an alternant sequence of shorter and longer P–P cycles, with the longer measuring the double of the shorter cycles.
Supraventricular rhythms
Published in Andrew R Houghton, Making Sense of the ECG, 2019
Sinus bradycardia and sinus tachycardia have already been described. The sinus node is normally a very reliable pacemaker. However, in sinus arrest, it sometimes fails to discharge – looking at a rhythm strip, a P wave will suddenly fail to appear in the expected place, and there is a gap, of variable length, until the sinus node fires and a P wave appears, or a junctional escape beat is generated by a ‘safety net’ subsidiary pacemaker in the AV junction (see Chapter 11, Figure 11.3). In sick sinus syndrome, it's not unusual to observe a prolonged pause after an episode of atrial tachyarrhythmia.
The Cardiologists
Published in Maria Ribeiro, Sound Diagnosis, 2018
Impending risks - exercise provokes syncope as heart rate cannot keep pace with the exercising muscles. The slow inherent ventricular rhythm is unable to respond and compensate for the bradycardia. Low cardiac output. Dizziness. Sick sinus - arrest.
Tests for the identification of reflex syncope mechanism
Published in Expert Review of Medical Devices, 2023
Michele Brignole, Giulia Rivasi, Artur Fedorowski, Marcus Ståhlberg, Antonella Groppelli, Andrea Ungar
CI susceptibility can be detected during carotid sinus massage (CSM), TT and long-term ECG monitoring, mostly by implantable loop recorder (ILR) [18]. There are two major types of asystolic reflex, the classical vasovagal reflex and low-adenosine syncope phenotype [19,20]. The former usually presents as sinus arrest or profound sinus bradycardia <40 bpm, whereas the latter is caused by sudden onset paroxysmal atrioventricular block and lacks typical prodromes. In a special form of reflex syncope, carotid sinus syndrome (CSS) which is more prevalent in older patients >60 years, the CI reflex may start abruptly before the VD reflex, and the whole duration of reflex is much shorter, usually less than 15–20 seconds [21]. Interestingly, CI reflex is less frequently associated with situational syncope [22].
The future of cardioneuroablation in cardiovascular medicine
Published in Expert Review of Cardiovascular Therapy, 2022
Tolga Aksu, Asad Khan, Henry Huang
In the ISSUE 1 study, 111 patients with syncope were implanted with an ILR. 82 patients had a negative tilt table test, and 29 patients had a positive test [42]. In the group with negative tilt table tests, 11 patients experienced prolonged sinus pauses defined as >3 seconds, mainly from sinus arrest. In almost all cases, pauses were preceded by progressive sinus bradycardia suggesting NMRS as the etiology of their syncope. In another study done by Entem et al. [43], 140 patients with unexplained syncope after conventional work-up (including tilt table testing) underwent ILR implantation from 1998 to 2006. Bradycardic arrhythmias including heart block, sinus bradycardia, and asystolic pauses were seen in 27 patients. Recently, we demonstrated the use of ILR as an effective indicator of vagal denervation by using complete and durable elimination of heart rate variability on ILR [44]. It is the authors opinion that ILRs may improve comparison between intervention and control arms after CNA by providing increased accuracy during long term follow‐up due to clustered and/or nature of VVS over time.
Long-term effect of catheter ablation on tachycardia-bradycardia syndrome: evidenced by 10 years follow up
Published in Acta Cardiologica, 2020
Shushan Zhang, Yanzong Yang, Yunlong Xia, Lianjun Gao, Xuanhe Zhang, Gary Tse, Xiaomeng Yin, Shiyu Dai, Dong Chang
Around 40–70% of atrial tachyarrhythmia are associated with sinus node dysfunction (SND) [8]. The latter comprises abnormalities, including sinus arrest, sinus bradycardia, sinoatrial block, and alternating episodes of tachycardia and bradycardia. The main feature of classical SND is sinus bradycardia and sinus arrest, in the presence or absence of atrial tachycardia. TBS is characterised by paroxysmal AF, atrial flutter (AFL), or atrial tachycardia (AT), with sinus bradycardia/junctional escape rhythm or arrest secondary to these tachyarrhythmia. Many mechanisms of TBS have been put forward. Firstly, rapid ventricular rate leading to the insufficiency of the sinus arterial supply [9], which reduces the automaticity function of the sinoatrial node (SN). Secondly, atrial tachyarrhythmia can induce the release and accumulation of acetylcholine in the atrial myocardium, thereby promoting K+ efflux and negative spontaneous depolarisation [10]. Therefore, it decreases the amplitude of spontaneous depolarisation and eventually reduces the automaticity of SN. Thirdly, TBS is also related to higher vagal activity in the context of AF [11], which can cause sinus node dysfunction. Finally, atrial tachycardia could decrease the expression of HCN4 mRNA and funny current (If), thereby resulting in electrophysiological remodelling and SND [12,13]. The above factors might account for the long pauses and bradycardia in TBS.