what’s the best course of action for sodium channel blocker toxicity with bradycardi

Sodium bicarbonate or lactate, increasing serum pH and extracellular concentration of the ion, displace the drug from its receptor sites and can be used for the treatment of cardiac toxicity in the setting of sodium-channel blocker poisoning.

Full Answer

How is sodium channel blocker toxicity treated?

Sodium bicarbonate or lactate, increasing serum pH and extracellular concentration of the ion, displace the drug from its receptor sites and can be used for the treatment of cardiac toxicity in the setting of sodium-channel blocker poisoning.

What is the treatment for calcium channel blocker overdose?

Calcium channel blocker (CCB) overdose is often lethal. Conventional medical treatment includes IV calcium, high doses of catecholamines, insulin, and glucagon. A new inotropic drug, levosimendan, should be considered in severe CCB poisoning.

What is the mechanism of action of a sodium channel blocker?

A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.

How do you reverse diltiazem overdose?

Currently, there is no specific antidote and the treatment of CCB poisoning is supportive; however, this supportive therapy is often insufficient. We present a clinical case of severe diltiazem poisoning and the therapeutic approaches that were used.

What is the reversal agent for calcium channel blockers?

Traditionally, antidotes for CCB overdose have included calcium, glucagon, adrenergic drugs, and amrinone.

How does glucagon reverse calcium channel blocker overdose?

Glucagon promotes calcium entry into cells via stimulation of a receptor that is considered to be separate from adrenergic receptors. Note that the actions of glucagon oppose those of insulin, yet both have beneficial effects in treating CCB toxicity.

What happens to action potential when sodium channels block?

Therefore, blocking sodium channels reduces the velocity of action potential transmission within the heart (reduced conduction velocity; negative dromotropy). This can serve as an important mechanism for suppressing tachycardias that are caused by abnormal conduction (e.g., reentry mechanisms).

Which class of antiarrhythmics are sodium channel blockers?

Class 1 Antiarrhythmic Drugs (Sodium Channel Blockers)

What are sodium channel blockers used to treat?

Sodium channel blockers are used as primary therapy or adjunctive treatment of processes such as trigeminal neuralgia (TN), CRPS, PDN, radicular extremity pain, chemotherapy-induced peripheral neuropathy, and PHN.

Which of the following atropine doses is correct to treat bradycardia caused by calcium channel block overdose?

For bradycardia refractory to atropine, glucagon 5-10 mg IV bolus can be administered, followed by an infusion of 5-10 mg/hour.

What is calcium The reversal for?

Calcium is given to reverse hypotension and improve cardiac conduction defects.

Does atropine work on beta-blocker overdose?

Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of beta-blocker overdose. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. These effects are unchanged by the presence of beta-receptor blocking drugs.

Why is QRS widening important?

However, QRS widening is useful because it can provide a quantitative indication of the severity of the sodium channel intoxication ( assuming that the patient has a normal baseline QRS interval; whenever possible, compare the QRS to the patient's baseline EKG).

What is a TCA?

TCAs are the original gangster of sodium channel blockade. With the increased use of selective serotonin reuptake inhibitors (SSRIs), the use of tricyclic antidepressants has decreased. Consequently, TCA intoxication has become less common.

What are the effects of inhibition of cardiac sodium channels?

Inhibition of presynaptic reuptake of dopamine, norepinephrine, and serotonin. Among these effects, inhibition of cardiac sodium channels is often the greatest life threat. Other toxic effects will generally respond to the usual supportive measures applied to critically ill patients.

What is wide complex tachycardia?

Wide-complex tachycardia often represents sinus tachycardia with a wide complex due to delayed conduction, rather than actual ventricular tachycardia. The treatments below apply only to true ventricular tachycardia (which can occur as well).

Which intoxicant inhibits sodium channels?

Tricyclic antidepressants ( TCAs) are the perhaps the most widely discussed intoxicant which inhibits sodium channels (causing a characteristic pattern of QRS widening with a tall R-wave in aVR). However, a broad variety of other xenobiotics also block sodium channels, causing a similar pattern of findings.

Is lidocaine a class IB?

Lidocaine is a class Ib antiarrhythmic, which binds to sodium channels. At first, it may be counterintuitive that giving a sodium channel blocker (lidocaine) could be beneficial for patients with sodium channel blocker intoxication.

Is isotonic bicarbonate a maintenance fluid?

Isotonic bicarbonate is most commonly used as a maintenance fluid infusion (e.g., at ~150-250 ml/hr), following initial stabilization with hypertonic sodium bicarbonate (#1 above). Isotonic bicarbonate is probably inferior to hypertonic bicarbonate, because it lacks the effect of hypertonic sodium on the cardiac sodium channels.

What are some examples of TCAs?

Specific examples include quinidine and procainamide, (class 1A antiarrhythmics), lidocaine, mexiletine, and phenytoin (class 1B), flecainide and propafenone (class 1C), carbamazepine and lamotrigine. There are many TCAs, but only imipramine and amitriptyline continue to be used in the US today. Insecticides also cause sodium channel blockade.

What drugs are used to block sodium channel?

Broadly they include Vaughn Williams Class 1 antiarrhythmics, local anesthetics, many medications used to treat neuropathic pain (including tricyclic antidepressants (TCA)), anticonvulsants, and cocaine. Specific examples include quinidine and ...

Can amitriptyline cause sodium channel blockade?

There are many TCAs, but only imipramine and amitriptyline continue to be used in the US today. Insecticides also cause sodium channel blockade. Toxicity of all these substances, whether intentional or accidental, can lead to catastrophic effects including death.

What drugs are used to treat sodium channel blockade?

Broadly they include Vaughn Williams Class 1 antiarrhythmics, local anesthetics, many medications used to treat neuropathic pain (including tricyclic antidepressants (TCA)), anticonvulsants, and cocaine . Specific examples include quinidine and procainamide, (class 1A antiarrhythmics), lidocaine, mexiletine, and phenytoin (class 1B), flecainide and propafenone (class 1C), carbamazepine and lamotrigine. There are many TCAs, but only imipramine and amitriptyline continue to be used in the US today. [1] Insecticides also cause sodium channel blockade. Toxicity of all these substances, whether intentional or accidental, can lead to catastrophic effects including death. It is essential to understand how these medications work, in order to effectively treat their toxicity and side effects.

Is there a toxidrome in sodium channel blockers?

There is no classical findings or toxidrome in the setting of sodium channel blocker toxicity. Physical exam findings vary by the substance ingested. Patients who have ingested tricyclic antidepressants often present with tachycardia, whereas those with ingestion of 'pure' sodium channel blocking medications can present with significant bradycardia. [4]

Does sodium channel blocker cause heart failure?

Broadly speaking, sodium channel blockers cause metabolic, cardiac, and neurologic symptoms. This leads to hemodynamic compromise and metabolic acidosis, potentiating the effects of the medications and causing further sodium blockade. [1] Propafenone in particular also has beta-blocking and calcium blocking activities which can worsen toxicity, leading to heart failure by decreased inotropy. [2]

Does sodium channel blockade affect AV node?

There tends to be no significant effect on the AV node as it does not depend on fast sodium channels. Instead, sodium channel blockade produces a variety of cardiac effects as demonstrated by their impact on the myocyte action potential. With varying degrees of potency, class I agents decrease the slope and amplitude of phase 0, and thereby reduce the rate of depolarization and the conduction velocity through the myocyte. This leads to a slower depolarization of the cell and is important for the desired therapeutic suppression of tachydysrhythmias through reentrant mechanisms. Concomitant anticholinergic effects of many of these drugs can complicate their sodium channel effects. [2]

Can sodium channel blocker cause overdose?

Sodium channel blocker toxicity results primarily from intentional overdose. However, patients or family members may report an inadvertent increase in medication doses or the addition of a new medication which might alter the typical elimination kinetics of the substance and lead to an unsuspected toxic dose.

Can a Na+ channel blocker cause coma?

Severe poisoning by Na + channel blockers frequently produces coma, convulsions, and respiratory depression. Securing an airway and ensuring adequate ventilation, as always, are first priority. All the specific nuances of caring for each Na+ channel blocker overdose cannot be discussed here because of diverse, additional pharmacologic effects these drugs possess. For example, beta blocker–induced hypotension and bradycardia frequently respond to glucagon. Coma from propoxyphene usually reverses with large doses of naloxone. Status epilepticus may be a problem following amoxapine overdose.

Do Na channel blockers cause sinus bradycardia?

Many Na + channel blockers possess anticholinergic (e.g., tricyclic antidepressants, diphenhydramine, phenothiazines) or adrenergic (e.g., cocaine, tricyclic antidepressants) properties that produce sinus tachycardia after overdose. Agents devoid of these effects, however, commonly produce bradyrhythmias. 18, 68 Importantly, even anticholinergic and adrenergic Na + channel blockers produce depressed automaticity with sinus bradycardia, escape junctional or ventricular rhythms, and eventual asystole after large doses.36 In Na + channel blocker poisoning by anticholinergic drugs, the combination of a wide QRS complex and bradycardia is ominous because it indicates that Na+ channel blockade is so profound that a tachycardia cannot be mounted in response to muscarinic antagonism.

Where do sodium channels reside?

Sodium channels reside in the cell membrane and comprise several subunits of long polypeptides that span the plasma membrane several times. Numerous subtypes of Na+ channels exist, and are part of a common gene superfamily, explaining their structural similarity.

Does physostigmine slow heart rate?

Sinus tachycardia rarely requires treatment. Although physostigmine slows the heart rate in patients poisoned with anticholinergic Na+ channel blockers, and such slowing may lessen Na + channel blockade, the potential for serious adverse effects prevents recommendations that physostigmine be used routinely for this purpose. Of course, physostigmine should never be given in the setting of bradycardia.

Does sodium channel blocker cause ventricular tachycardia?

Sodium channel blocker–induced monomorphic ventricular tachycardia is thought to occur by slowing intraventricular conduction to the point that unidirectional block and re-entrant circuits develop.59 Nattel et al 47 demonstrated marked slowing of intraventricular conduction and resulting ventricular tachycardia in amitriptyline-treated dog hearts. These arrhythmias did not appear to be due to an automatic increase because amitriptyline reduced the spontaneous idioventricular rate. Brugada et al8 later demonstrated the induction of functional re-entrant circuits and ventricular tachycardia in flecainide-treated rabbit hearts. These and other studies support the theory that Na + channel–blocking drugs can cause slowed intraventricular conduction, unidirectional block, the development of a re-entrant circuit, and a resulting ventricular tachycardia, 17, 70 which can degenerate into ventricular fibrillation.

Which intoxicant inhibits sodium channels?

Tricyclic antidepressants ( TCAs) are the perhaps the most widely discussed intoxicant which inhibits sodium channels (causing a characteristic pattern of QRS widening with a tall R-wave in aVR). However, a broad variety of other xenobiotics also block sodium channels, causing a similar pattern of findings.

Who is the author of the book Anticholinergic Intoxication?

In this post, I link to and excerpt the section, management of combined anticholinergic plus sodium channel blocker toxicity, from the Internet Book of Critical Care Chapter [Link is to the Table of Content], Anticholinergic Intoxication, by Dr. Josh Farkas.