What happens when phenytoin given with TCAs?

What happens when phenytoin given with TCAs?

Phenytoin may act through a similar mechanism as lidocaine, although experimental studies suggest that it does not compete directly for the same sodium channel binding site as TCAs. Allosteric modulation of the TCA binding site may occur in the setting of phenytoin use.

Why is it important to apply ECG monitoring on all tricyclic antidepressants TCA overdose?

The ECG is a vital tool in the prompt diagnosis of poisoning with sodium-channel blocking medications such as tricyclic antidepressants (TCA), which cause CNS and cardiovascular toxicity in overdose in the form of seizures and ventricular dysrhythmias.

Why does TCA overdose cause seizures?

They also block alpha receptors peripherally and thus can cause hypotension. Furthermore, they block neurotransmitter reuptake (norepinephrine, serotonin) at central presynaptic terminals, and this may be the mechanism by which seizures are induced by TCA overdose.

What electrocardiogram changes are associated with amitriptyline toxicity?

ECG changes are a frequent manifestation of TCAs overdose and include sinus tachycardia, prolongation of the PR, QRS and QTc intervals, nons- pecific ST and T wave changes, atrioventricular block, right axis deviation, Brugada pattern and R wave changes in aVR, R/S ratio in aVR > 0.7 and ventricular arrhythmias.

Can TCA cause arrhythmia?

Tricyclic antidepressants remain a common cause of fatal drug poisoning as a result of their cardiovascular toxicity manifested by ECG abnormalities, arrhythmias and hypotension.

What is a terminal R wave ECG?

A terminal R-wave in AVR is often used to identify a TCA overdose, but what does it mean? Along with QRS prolongation, this finding is not specific to a TCA overdose; rather it is pathognomonic for a sodium channel blockade. You will see a wide R-wave in aVR that is greater than 3mm.

Why imipramine toxicity will effect on heart cause arrhythmia?

Imipramine has type 1 antiarrhythmic effects as it blocks the fast sodium channel on the myocardium. Therefore, this will lead to inhibition of depolarization of the heart action potential, which will result in QRS prolongation, which can lead to cardiac arrhythmia.

What should I monitor with TCAs?

All patients starting a TCA need screening for pre-existing cardiac conditions, including prolonged QTc intervals, heart disease, and a family history of arrhythmias.

What are signs and symptoms of a TCA overdose?

The most common clinical features are dry mouth, blurred vision, dilated pupils, sinus tachycardia, pyramidal neurological signs, and drowsiness. In severe poisoning, there may be coma, convulsions, respiratory depression, hypotension and a wide range of electrocardiographic (ECG) abnormalities.

What should I monitor with TCAS?

Can ECG detect TCA overdose?

ECG Library Homepage The ECG is a vital tool in the prompt diagnosis of poisoning with sodium-channel blocking medications such as tricyclic antidepressants (TCA), which cause CNS and cardiovascular toxicity in overdose in the form of seizures and ventricular dysrhythmias.

What is Dilantin toxicity?

Dilantin, or phenytoin, toxicity happens when you have high levels of Dilantin in your body that become harmful. Dilantin is a medicine that is used to prevent and treat seizures. Dilantin toxicity can lead to a coma. What increases my risk for Dilantin toxicity? Your risk of Dilantin toxicity is higher if you are elderly.

When is an ECG indicated in the workup of tricyclic antidepressant toxicity?

An ECG should be taken in all patients who present with a deliberate self-poisoning (or altered GCS of unknown aetiology) to screen for TCA overdose. Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to muscarinic (M1) receptor blockade

What causes QQT prolongation in TCA overdose?

QT prolongation seen in cases of TCA overdose occurs due to potassium channel blockade that may potentially cause torsades de pointes. TCAs can also exert a quinidine-like toxic effect on the myocardium that can cause decreased cardiac contractility and hypotension. [5][6][7]