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Investigation of Sudden Cardiac Death
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
The sinoatrial node is subject to a number of pathological processes which include an age-related loss of the number of P-cells, amyloidosis, occlusion of the nodal artery by coronary atheroma, myocarditis etc. With the exception of the age-related change, none of these processes is specific for the node. SA nodal disease leads to sinoatrial block or the sick sinus syndrome. The node intermittently ceases to discharge, causing a syncopal attack; these attacks are, however, very rarely fatal because an escape rhythm is initiated by other pacing cells in the AV nodal area. Sinoatrial node disease does not therefore figure in any consideration of SCD.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Sinus bradycardia is a regular heart beat that originates from the sinoatrial node, but at a rate lower than 60 beats per minute (please see Figure 6.24). Whilst in a healthy heart this may not cause problems with cardiac output, as there is a corresponding increase in stroke volume, in the diseased heart, sinus bradycardia may cause circulatory compromise. If the patient becomes symptomatic, feels dizzy, faints, experiences chest pain, has a low blood pressure or becomes breathless, treatment will be required. Supplemental oxygen to maintain saturations between an agreed target range of 94–98% (or 88–92%, if at risk of hypercapnia) should be commenced. IV access will be needed and atropine 500mcg IV may be prescribed, as this inhibits the effect of the parasympathetic vagus nerve and allows the sinus node to increase the heart rate. If the bradycardia is extreme, then a temporary pacemaker may be indicated. It is important that the medications the patient is taking are reviewed, as common cardiac drugs such as beta blockers, digoxin and calcium antagonists such as diltiazem can cause a reduction in heart rate.
Thorax
Published in Bobby Krishnachetty, Abdul Syed, Harriet Scott, Applied Anatomy for the FRCA, 2020
Bobby Krishnachetty, Abdul Syed, Harriet Scott
The conducting system is the unique tissue specific to the heart and has specialised cardiac muscle. It generates and transmits impulses that regulate cardiac contraction. The sinoatrial node (SA node) is situated in the upper part of the crista terminalis, within the myocardium, to the right of the SVC opening. It is also called the pacemaker of the heart as it initiates and modulates the heart rate and transmits impulses to the atria and the ventricles.The atrioventricular node (AV node) is situated in the endocardium, near the atrial septum, immediately above the opening of the coronary sinus. It receives electrical impulses that originate in the SA node and transmits them to the bundle of His.The atrioventricular bundle of His transmits impulses to the walls of the ventricles. It first transits along the membranous part of the interventricular septum and then divides at the junction of the muscular and membranous parts of the interventricular septum. The subendocardial branches are the Purkinje fibres, specialised cardiac fibres, which then ascend within the muscular walls of the ventricles.
Attitude towards sexuality and sexual behaviors among men with heart rhythm disorders
Published in The Aging Male, 2020
Rafal Mlynarski, Agnieszka Mlynarska, Krzysztof S. Golba
Cardiac arrhythmias are one of the biggest problems in modern cardiology. People all over the world have many symptoms that are connected with arrhythmias such as fluttering in the chest, tachycardia or bradycardia, dizziness or in the most advanced symptoms – syncope [1,2]. Due to the nature of these symptoms, they can all negatively affect the quality of life, which has been documented many times [3,4]. There are two main types of heart rhythm disorders – sinus node dysfunction and different types of atrioventricular blocks. Sinus node dysfunction, or sinoatrial node disease, is a group of abnormal heart rhythms that are caused by a malfunction of the sinus node, the heart’s primary pacemaker [5]. Atrioventricular blocks (AV block) are a type of heart block in which the conduction between the atria and the ventricles of the heart is impaired [6].
Ivabradine, the hyperpolarization-activated cyclic nucleotide-gated channel blocker, elicits relaxation of the human corpus cavernosum: a potential option for erectile dysfunction treatment
Published in The Aging Male, 2020
Serap Gur, Laith Alzweri, Didem Yilmaz-Oral, Ecem Kaya-Sezginer, Asim B. Abdel-Mageed, Suresh C. Sikka, Wayne J. G. Hellstrom
Also, in this study, the specific type Ca2+ channel blocker, nifedipine, and the nonselective K+ channel blocker, TEA, significantly inhibited ivabradine-induced relaxation in HCC. Thus, it can be proposed that other mechanisms, such as the effect on Ca2+ and K+ channels in penile smooth muscle, may play a prominent role. Ivabradine partially facilitates HCC muscle relaxation through different mechanisms, depending on several ion channels and independent of the classical NO/sGC pathway. Ca2+-related pathways may enable persistent activity at the single-cell level through hyperpolarization-activated HCN channels [38,39]. The HCN channel releases Ca2+ from the sarcoplasmic reticulum in atrioventricular node conduction. The inhibition of If channels blocked Ca2+ release and delayed conduction in functional experiments [40]. Also, silencing of HCN4 channel caused altered Ca2+ release and Ca2+ handling in the sinoatrial node, which leads to impaired pacemaker activity and symptoms characteristic of human pacemaking [41]. Previous studies have demonstrated that the If channel improved membrane potential and contributed to the generation of rhythmic cardiac activity, which reveals a mixed permeability to both Na+ and K+ channels[42,43].
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.