Sinus node

Arrhythmias Originating in the Sinus Node Sinus bradycardia Sick sinus syndrome Sinus tachycardia Disorders of Impulseformation ... 

Indeca.inide. Indecainide hydrochloride is a po active antiarrhythmic agent that received PDA approval in 1989, but it has not been marketed as of this writing. Chemically, it is 9-[3-(isopropylamino)propyl]fiuorine-9-carboxamide [74517-78-5]. The dmg has potent activity against premature ventricular complexes (PVCs) and ventricular tachycardias. Indecainide has no effect on sinus node function, atrial or ventricular effective refractory periods (32,33). 

Normal rhythmic activity is the result of the activity of the sinus node generating action potentials that are conducted via the atria to the atrioventricular node, which delays further conduction to the His-Tawara-Purkinje system. From the Purkinje fibres, action potentials propagate to the ventricular myocardium. Arrhythmia means a disturbance of the normal rhythm either resulting in a faster rhythm (tachycardia, still rhythmic) or faster arrhythmia (tachyarrhythmia) or slowed rhythm (bradycardia, bradyarrhythmia). 

Inhibition of the Na+/K+-ATPase leads to a loss of potassium and an increase of sodium within the cell. Secondary intracellular calcium is increased via the Na VCa -exchanger. This results in a positive inotropic effect in the myocardium, with an increase of peak force and a decrease in time to peak tension. Besides this, cardiac glycosides increase vagal activity by effects on the central vagal nuclei, the nodose ganglion and increase in sensitivity of the sinus node to acetylcholine. 

The sinus rhythm is the heart rhythm in which the sinus node generates an electrical impulse that travels through specialized cells (that form a conduction system) and leads to a ventricular contraction. 

The LVA channels are expressed in a wide variety of tissues. In the cardiac sinus node and the thalamus, activation of LVA channels seems to be necessary to generate action potentials upon depolarising the membrane. 

Many individuals, particularly those who partake in regular vigorous exercise, have heart rates less than 60 bpm. For those individuals, sinus bradycardia is normal and healthy, and does not require evaluation or treatment. However, some individuals develop symptomatic sinus node dysfunction. In the absence of correctable underlying causes, idiopathic sinus node dysfunction is referred to as sick sinus syndrome,12 and occurs with greater frequency with advancing age. The prevalence of sick sinus syndrome is approximately 1 in 600 individuals over the age of 65 years.12... 

Sick sinus syndrome leading to sinus bradycardia may be caused by degenerative changes in the sinus node that occur with advancing age. However, there are other possible etiologies of sinus bradycardia, including drugs (Table 6-2).13... 

Sick sinus syndrome Idiopathic sinus node dysfunction leading to symptomatic sinus bradycardia. 

Sympathetic (sympatholytic) Heart Sinus node Atrioventricular (AV node) Slowing Increased refractory period Bradycardia Dysrhythmias, conduction block... 

Asymptomatic sinus bradyarrhythmias (heart rate less than 60 beats/min) are common especially in young, athletically active individuals. However, some patients have sinus node dysfunction (sick sinus syndrome) because of underlying organic heart disease and the normal aging process, which... 

Treatment of sinus node dysfunction involves elimination of symptomatic bradycardia and possibly managing alternating tachycardias such as AF. Asymptomatic sinus bradyarrhythmias usually do not require therapeutic intervention. 

Ivabradine is used in the treatment of angina in patients in normal sinus rhythm. It acts on the sinus node resulting in a reduction of the heart rate. It is contraindicated in severe bradycardia (heart rate lower than 60 beats/ minute), cardiogenic shock, acute myocardial infarction, moderate-to-severe heart failure, immediately after a cerebrovascular accident, second and third-degree heart block and patients with unstable angina or a pacemaker. Side-effects include bradycardia, first-degree heart block, ventricular extrasystoles, headache, dizziness and visual disturbances, including blurred vision. 

The a-subunit of some G-proteins may induce opening of a channel protein. In this manner, IC channels can be activated (e.g., ACh effect on sinus node, p. 100 opioid action on neural impulse transmission, p. 210). 

Indications. Verapamil is used as an antiarrhythmic drug in supraventricular tachyarrhythmias. In atrial flutter or fibrillation, it is effective in reducing ventricular rate by virtue of inhibiting AV-conduction. Verapamil is also employed in the prophylaxis of angina pectoris attacks (p. 308) and the treatment of hypertension (p. 312). Adverse effects Because of verapamil s effects on the sinus node, a drop in blood pressure fails to evoke a reflex tachycardia Heart rate hardly changes bradycardia may even develop. AV-block and myocardial insufficiency can occur. Patients frequently complain of constipation. 

Impulses originating at loci outside the sinus node are seen in supraventricular or ventricular extrasystoles, tachycardia, atrial or ventricular flutter, and fibrillation. In these forms of rhythm disorders, antiarrhythmics of the local anesthet-Ltillmann, Color Atlas of Pharmacology... 

Propranolol is a prototype of this series of drugs and is the oldest and most widely used nonselective )3-adrenoblocker. It possesses antianginal, hypotensive, and antiarrhythmic action. Propranolol is a cardiac depressant that acts on the mechanic and electrophysio-logical properties of the myocardium. It can block atrioventricular conductivity and potential automatism of sinus nodes as well as adrenergic stimulation caused by catecholamines nevertheless, it lowers myocardial contractility, heart rate, blood pressure, and the myocardial requirement of oxygen. 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

Amiodarone s antiarrhythmic action is connected to its ability to block K, Na, and Ca channels while noncompetitively blocking a- and j3-adrenergic receptors of the heart, thus prolonging the action potential and effective refractive period of atrial cells, atrioventricular junctions, and ventricles of the heart, which is accompanied by decreased automatism of sinus node and slowing of atrioventricular conductivity. 

Sinus node disease andAVbiock The drug may cause severe sinus bradycardia or sinoatrial block in patients with preexisting sinus node disease and may cause advanced or complete heart block in patients with preexisting incomplete AV block. Consider inserting a pacemaker before treatment with digoxin. 

Uncontrolled CHF cardiogenic shock sinoatrial, AV and intraventricular disorders of impulse generation or conduction (eg, sick sinus node syndrome, AV block) in the absence of an artificial pacemaker bradycardia marked hypotension bronchospastic disorders manifest electrolyte imbalance hypersensitivity to the drug. 

Cardiovascular effects If a ventricular pacemaker is operative, patients with seconder third-degree heart block may be treated with mexiletine if continuously monitored. Exercise caution in such patients or in patients with preexisting sinus node dysfunction or intraventricular conduction abnormalities. 

Oral Severe sinus-node dysfunction, causing marked sinus bradycardia second-and third-degree AV block when episodes of bradycardia have caused syncope (except when used in conjunction with a pacemaker). 

Chronic heart failure is associated with intrinsic sinus node dysfunction that can be demonstrated on careful electrophysiologic studies [22, 23]. Patients with chronic heart failure have longer intrinsic sinus cycle... 

Ideally, if symptomatic sinus node dysfunction occurs in the presence of drugs known to impair sinus node function, the first treatment is to discontinue the offending drug [29]. However, this is typically not feasible in patients with heart failure who are dependent on several medications to improve long-term outcomes, or may need antiarrhythmic drug therapy for symptomatic arrhythmias. Accordingly, the treatment usually becomes a question of whether to apply pacing to increase heart rate. This is further complicated by the appropriate pacemaker prescription once the decision to pace has been made. 

In the normal situation, the sinus node initiates a wave of depolarization that spreads rapidly throughout both atria. The atria contract followed shortly thereafter by contraction of the... 

Benditt DG, Sakaguchi S, Goldstein MA, et al. Sinus node dysfunction, pathophysiology, clinical features, evaluation, and treatment. In Zipes DP, Jalife J, eds. Cardiac electrophysiology from cell to bedside. 2nd ed. Philadelphia WB Saunders, 1995 1215-47. 

Becker AE. Relationship between structure and function of the sinus node general comments. In Bonke FI, ed. The sinus node. The Hague Martinus Nijhoff, 1978 212-22. 

Sanders P, Kistler PM, Morton JB, Spence SJ, Kalman JM. Remodeling of sinus node function in patients with congestive heart failure reduction in sinus node reserve. Circulation 2004 110 897-903. 

The therapeutic efficacy in the treatment of tachyarrhythmias is based upon the reduction of the influence of endogenous catechol-amines on the sinus node and the AV node. 

Antiarrhythmic activity (verapamil, possibly also diltiazem) impairment of AV conduction and to a lesser degree also that of sinus node activity. 

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