In sinusitis

In the following, the cardiac action potential is explained (Fig. 1) An action potential is initiated by depolarization of the plasma membrane due to the pacemaker current (If) (carried by K+ and Na+, which can be modulated by acetylcholine and by adenosine) modulated by effects of sympathetic innervation and (3-adrenergic activation of Ca2+-influx as well as by acetylcholine- or adenosine-dependent K+-channels [in sinus nodal and atrioventricular nodal cells] or to dqjolarization of the neighbouring cell. Depolarization opens the fast Na+ channel resulting in a fast depolarization (phase 0 ofthe action potential). These channels then inactivate and can only be activated if the membrane is hyperpolarized... 

Einhaupl KM, Villringer A, Meister W, Mehraein S, Garner C, PeUkofer M, Haberl RL, Pfister HW, Schiedek P. Heparin treatment in sinus venous thrombosis. Lancet 1991 338 597-600. 

Treatment of sinus bradycardia is only necessary in patients who become symptomatic. If the patient is taking any med-ication(s) that may cause sinus bradycardia, the drug(s) should be discontinued whenever possible. If the patient remains in sinus bradycardia after discontinuation of the drug(s) and after five half-lives of the drug(s) have elapsed, then the drugs(s) can usually be excluded as the etiology of the arrhythmia. In certain circumstances, however, discontinuation of the medication(s) may be undesirable, even if it may be the cause of symptomatic sinus bradycardia. For example, if the patient has a history of myocardial infarction or HF, discontinuation of a (3-blocker is undesirable, because (3-blockers have been shown to reduce mortality and prolong life in patients with those diseases, and the benefits of therapy with... 

Role of viral infections in sinusitis and how to prevent disease transmission... 

Nasal decongestant sprays such as phenylephrine and oxymetazoline that reduce inflammation by vasoconstriction are often used in sinusitis. Use should be limited to the recommended duration of the product to prevent rebound congestion. Oral decongestants may also aid in nasal or sinus patency. To reduce mucociliary function, irrigation of the nasal cavity with saline and steam inhalation may be used to increase mucosal moisture, and mucolytics (e.g., guaifenesin) maybe used to decrease the viscosity of nasal secretions. Antihistamines should not be used for acute bacterial sinusitis in view of their anticholinergic effects that can dry mucosa and disturb clearance of mucosal secretions. 

In sinus bradycardia or incomplete heart block, lidocaine administration for the elimination of ventricular ectopy without prior acceleration in heart rate (eg, by atropine, isoproterenol or electric pacing) may promote more frequent and serious ventricular arrhythmias or complete heart block. Use with caution in patients with hypovolemia and shock, and all forms of heart block. 

IV diltiazem - If second- or third-degree AV block occurs in sinus rhythm, discontinue and institute appropriate supportive measures. 

Because of their relative - selectivity, low doses of metoprolol, acebutolol, bisoprolol, and atenolol may be used with caution in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Bradycardia Metoprolol produces a decrease in sinus heart rate in most patients this decrease is greatest among patients with high initial heart rates and least among patients with low initial heart rates. 

Phenytoin Because of its effect on ventricular automaticity, do not use phenytoin in sinus bradycardia, sino-atrial block, second- and third-degree AV block, or in patients with Adams-Stokes syndrome. 

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 direct depressant actions of disopyramide on the sinoatrial node are antagonized by its anticholinergic properties, so that at therapeutic plasma concentrations, either no change or a slight increase in sinus heart rate is observed. Both the anticholinergic and direct depressant actions of disopyramide on sinus automaticity appear to be greater than those of quinidine. 

Bretylium administration produces an initial brief increase in sinus node automaticity that is probably the result of a drug-induced release of catecholamines from sympathetic nerve terminals. No change or a slight decrease in sinus heart rate is observed after the initial phase of catecholamine release. 

There are few absolute contraindications, but several points should be considered. Medications that produce changes in sinus node or AV nodal conduction may potentiate the cardiovascular adverse effects of the a2 agonists. This may be particularly relevant for concomitant administration of beta-blockers, which, similar to the agonists, have been used to treat aggression. 

Coadministration of beta-blockers can potentiate rebound hypertension upon discontinuation of medications, and it is therefore recommended that the beta-blocker be withdrawn before the tt2 agonist (Physicians Desk Reference, 2001). Tricyclic antidepressants may also produce changes in sinus node and AV conduction, and it is recommended that they be used cautiously in combination with tt2 agonists (Physicians Desk Reference, 2001). However, in child psychiatric practice, there has been debate about whether there are adverse interactions related to concomitant use of tricyclics and tt2 agonists. Finally, the tt2 agonists may potentiate the effects of CNS depressants (e.g., barbiturates) or other medications that produce sedation, so lower doses of each may be warranted. 

As a nasal decongestant in sinusitis, in otitis media where there is evidence of obstruction of the eustachian tube especially in subacute serous otitis media and otitic barotrauma. 

The antiarrhythmic action is due to cardiac adrenergic blockade. It decreases the slope of phase 4 depolarization and automaticity in SA node, Purkinje fibres and other ectopic foci. It also prolongs the effective refractory period of AV node and impedes AV conduction. ECG shows prolonged PR interval. It is useful in sinus tachycardia, atrial and nodal extrasystoles. It is also useful in sympathetically mediated arrhythmias in pheochromocytoma and halothane anaesthesia. 

---