Atrioventricular reentrant tachycardia (AVRT), or atrioventricular reciprocating tachycardia, is a type of abnormal fast heart rhythm and is classified as a type of supraventricular tachycardia (SVT). AVRT is most commonly associated with Wolff–Parkinson–White syndrome, but is also seen in permanent junctional reentrant tachycardia (PJRT). In AVRT, an accessory pathway allows electrical signals from the hearts ventricles to enter the atria and cause earlier than normal contraction, which leads to repeated stimulation of the atrioventricular node. Signs and symptoms
An episode of SVT may present with palpitations, dizziness, shortness of breath, or losing consciousness (fainting). The electrocardiogram (ECG) would appear as a narrow-complex SVT. Between episodes of tachycardia the affected person is likely to be asymptomatic; however, the ECG would demonstrate the classic delta wave in Wolff–Parkinson–White syndrome. Pathophysiology
Two distinct pathways are involved: the normal atrioventricular conduction system, and an accessory pathway. During AVRT, the electrical signal passes in the normal manner from the AV node into the ventricles. Then, the electrical impulse pathologically passes back into the atria via the accessory pathway, causing atrial contraction, and returns to the AV node to complete the reentrant circuit (see figure). Once initiated, the cycle may continue causing the heart to beat faster than usual.Initiation of AVRT may be through a premature impulse of atrial, junctional, or ventricular origin. Treatment
Acute management is as for SVT in general. The aim is to interrupt the circuit. In the shocked patient, DC cardioversion may be necessary. In the absence of shock, inhibition at the AV node is attempted.
Blockage prevents the activation of the H1 receptors by histamine, preventing the symptoms associated with allergies from occurring. Fexofenadine does not readily cross the blood–brain barrier, so is less likely to cause drowsiness in comparison to other antihistamines that readily cross that barrier (i.e., first-generation antihistamines such as diphenhydramine). In general, fexofenadine takes about an hour to take effect, though this may be affected by the choice of dosage form and the presence of certain foods.Fexofenadine also exhibits no anticholinergic, antidopaminergic, alpha 1-adrenergic, or beta-adrenergic receptor-blocking effects. Pharmacokinetics
Absorption: After oral application, maximum plasma concentrations are reached after 2–3 hours. Fexofenadine should not be taken with a high-fat meal, as mean concentrations of fexofenadine in the bloodstream are seen to be reduced from 20 to 60% depending on form of medication (tablet, ODT, or suspension). Distribution: Fexofenadine is 60–70% bound to plasma proteins, mostly albumin. Metabolism: Fexofenadine is a substrate of CYP3A4, but only about 5% is metabolized by the liver, indicating that hepatic metabolism is relatively minor in clearance from the body. Elimination: Most of the substance is eliminated unchanged via the feces (80%) and urine (11–12%). Interactions
Taking erythromycin or ketoconazole while taking fexofenadine does increase the plasma levels of fexofenadine, but this increase does not influence the QT interval. The reason for this effect is likely due to transport-related effects, specifically involving p-glycoprotein (p-gp). Both erythromycin and ketoconazole are inhibitors of p-gp, a transporter protein involved in preventing the intestinal absorption of fexofenadine.