Conduction, cardiac definition

Pre-existing cardiac conduction abnormalities, including those induced by other drugs, are a definite risk. Due consideration should be given not only to the half-life of such drugs, but also to the tissue concentrations and total clearances of the agents involved. 

Antidepressants are used to treat depressed children and adolescents because no other definitive effective therapies are currently available. Plasma concentration monitoring of TCAs is important to ensure safety. As in the adult population, plasma concentrations above 450 ng/mL are associated with increased risk of serious adverse effects including delirium, seizures, delayed cardiac conduction, and sudden death. ... 

Dead space. Anatomical dead space is equal to the volume of the conducting airways. This is determined by the physical characteristics of the lungs because, by definition, these airways do not contain alveoli to participate in gas exchange. Alveolar dead space is the volume of air that enters unperfused alveoli. In other words, these alveoli receive airflow but no blood flow with no blood flow to the alveoli, gas exchange cannot take place. Therefore, alveolar dead space is based on functional considerations rather than anatomical factors. Healthy lungs have little or no alveolar dead space. Various pathological conditions, such as low cardiac output, may result in alveolar dead space. The anatomical dead space combined with the alveolar dead space is referred to as physiological dead space ... 

General definitions relating to action potentials are given in Section 9. This section deals specifically with action potentials within the cardiac pacemaker cells and conducting system. 

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

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