How do tricyclic antidepressants affect heart?

How do tricyclic antidepressants affect heart?

2 The TCAs have important effects on the heart, related to their anticholinergic and quinidine-like properties. The major side effects in therapeutic dosage include heart rate increase, postural hypotension and slight prolongation of the intraventricular conduction time and QT interval.

Can TCA cause cardiac arrhythmias?

Tricyclic antidepressant overdose is widely felt to be associated with cardiac arrhythmias which may occur without warning, some- times late in the clinical course.

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.

Are tricyclic antidepressants cardiotoxic?

The cardiotoxic effect of TCA overdose is the most pronounced complication. Multiple rhythm disturbances may occur in the presence of a TCA overdose. The greatest number of adverse cardiac symptoms and electrocardiographic changes are likely to occur within the first 24 hours after overdose.

What is the mechanism of action of tricyclic antidepressants?

Mechanism of Action Tricyclic antidepressants act on approximately five different neurotransmitter pathways to achieve their effects. They block the reuptake of serotonin and norepinephrine in presynaptic terminals, which leads to increased concentration of these neurotransmitters in the synaptic cleft.

Why does TCA overdose cause tachycardia?

Because of the anticholinergic effects of TCA’s, a sinus tachycardia is expected in mild to moderate overdoses in the absence of co-ingestants that would slow heart rate. By blockade of myocardial sodium channels a progressive QRS prolongation, QT prolongation, and PR prolongation result.

How does TCA overdose cause acidosis?

The amount of unbound tricyclic may also increase if the overdose causes respiratory depression resulting in an acidosis, which reduces protein binding. The toxic effects of tricyclics are caused by four main pharmacological properties: Inhibition of norepinephrine reuptake at nerve terminals.

What is a tricyclic overdose?

Tricyclic antidepressant overdose is poisoning caused by excessive medication of the tricyclic antidepressant (TCA) type. Symptoms may include elevated body temperature, blurred vision, dilated pupils, sleepiness, confusion, seizures, rapid heart rate, and cardiac arrest.

Why are tricyclic antidepressants cardiotoxic?

TCAs have anticholinergic effects, cause excessive blockade of norepinephrine reuptake at the preganglionic synapse, direct alpha adrenergic blockade, and importantly they block sodium membrane channels with slowing of membrane depolarization, thus having quinidine-like effects on the myocardium.

What is the cause of tricyclic antidepressant overdose?

Tricyclic antidepressant overdose. Tricyclic antidepressant overdose is poisoning caused by excessive medication of the tricyclic antidepressant (TCA) type.

Is there a role for physostigmine in tricyclic overdose?

Physostigmine is a short acting cholinesterase inhibitor that was proposed in the 1970s as a treatment for arrhythmias. Since then, however, it has been described as causing asystole 72 and seizures. 73 There is no role for its use in the management of tricyclic toxicity.

How does tricyclic antidepressant affect the myocardium?

TCAs have anticholinergic effects, cause excessive blockade of norepinephrine reuptake at the preganglionic synapse, direct alpha adrenergic blockade, and importantly they block sodium membrane channels with slowing of membrane depolarization, thus having quinidine -like effects on the myocardium.

When was tricyclic antidepressant first used in clinical use?

CAs were first used in the 1950s to treat clinical depression. The first report of the adverse effects of tricyclic antidepressant (TCA) overdose came within 2 years of their entry into clinical use.