Sinus node arrhythmias

Most bedside monitoring systems allow for simultaneous monitoring of two leads, such as lead II with or MCL. Lead II or the lead that clearly shows the P waves and QRS complex may be used for sinus node arrhythmias, PACs, and AV block. The precordial leads V. and Vg or the bipolar leads MCL. and MCLg are the best leads for monitoring rhythms with wide QRS complexes and for differentiating VT from SVT with aberrancy. 

Useful for P wave identification detecting sinus node arrhythmia, atrial arrhythmia, and monitoring the inferior wall of the left ventricle. 

Lead II or the best lead that clearly shows P waves and the QRS complex may be used for sinus node arrhythmias, premature atrial contractions, and atrioventricular block... 

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

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). 

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. 

Mechanism of Action A cardiac agent that prolongs duration of myocardial cell action potential and refractory period by acting directly on all cardiac tissue. Decreases AV and sinus node function. Therapeutic Effect Suppresses arrhythmias. Pharmacokinetics ... 

Mechanism of Action An antiarrhythmicthat prolongs both atrial and ventricular action potential duration and increases the atrial and ventricular refractory period. Activates slow, inward current (mostly of sodium), produces mild slowing of sinus node rate and AV conduction, and causes dose-related prolongation of QT interval. Therapeutic Effect Converts arrhythmias to sinus rhythm. 

This is a class IB drug used primarily for the emergency treatment of ventricular arrhythmias. It has little effect on sinus node automaticity but depresses normal and abnormal forms of automaticity in Purkinje fibres. It is generally ineffective against supraventricular and accessory pathway-induced (e.g. WPW syndrome) arrhythmias. Lidocaine is relatively safe and free from adverse cardiovascular side effects. It causes minimal cardiodepression, although high doses can cause heart block. The most common side effect is a dose-related CNS toxicity. It is given intravenously as a bolus of 1 mg-kg-1 followed by an infusion of 20-50 pg-kg-l-min-1. 

Succinylcholine may cause tachycardia, cardiac arrhythmias, and hypertension, which is brought about by stimulation of the sympathetic ganglia. It may also provoke bradycardia, caused by stimulation of muscarinic receptor sites in the sinus node of the heart. This effect is more pronounced following a second dose of succinylcholine. The bradycardia may be blocked by thiopental, atropine, and ganglionic blocking agents. 

Contraindications are hypertrophic obstructive cardiomyopathy (increase in inotropism can increase outflow tract obstruction), AF in WPW syndrome (can cause precipitation of the arrhythmia to ventricular fibrillation (VF) by preferential conduction over the accessory pathway), significant AV-block or sick sinus syndrome, hypokalemia (causes increased digoxin sensitivity and supraventricular/ventricular arrhythmia), thyreotoxicosis, postinfarction status (increased mortality). Caution should be exerted in renal failure, and coadministration of other drugs depressing sinus node or AV-nodal function. 

Although cardiac arrhythmias involve the electrical conduction system of the heart including the sinus node, atrioventricular... 

BETA-BLOCKERS - SOTALOL IVABRADINE Risk of arrhythmias Additive effect ivabradine slows the sinus node Monitor ECG closely... 

Salbutamol, fenoterol, rimiterol, reproterol, pir-buterol, salmeterol, ritodrine and terbutaline are P-adrenoceptor agonists that are relatively selective for p2-receptors, so that cardiac (chiefly p -receptor) effects are less prominent. Tachycardia still occurs because of atrial (sinus node) p -receptor stimulation the P2-adrenoceptors are less numerous in the ventricle and there is probably less risk of serious ventricular arrhythmias than with the use of nonselective catecholamines. The synthetic agonists are also longer-acting than isoprenaline because they are not substrates for catechol-O-methyltransferase, which methylates catecholamines in the liver. They are used principally in asthma, and to reduce uterine contractions in premature labour. 

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