Lidocaine Classification, Mechanism, Indication and Effect

1. Running head: LIDOCAINE-CLASSIFICATION, MECHANISM, INDICATION 1






Lidocaine-Classification, Mechanism, Indication and Effect
José F. Pereira
Herzing University Online

2. LIDOCAINE-CLASSIFICATION, MECHANISM, INDICATION 2

Lidocaine-Classification, Mechanism, Indication and Effect
Today, lidocaine has found much use in the medical practice in treating arrhythmias
particularly in patients with cardiac disease (Marzlin & Webner, 2012). However, clinicians need
to understand various intricacies of the drug while trying to use it in antiarrhythmia management.
The following is an analysis of lidocaine as a kind of antiarrhythmic medication in a patient with
ventricular tachycardia. The details presented include its classification, action
mechanism/pharmacodynamics, indications, and side effects.
Classification
To begin with, the first aspect to understand about the drug is its classification. Ideally,
other than being a typical local anesthetic, lidocaine equally falls under the antiarrhythmic drugs
(Sharma, 2007). Specifically, it is a class Ib antiarrhythmic, mostly used for the purpose after
initiation of defibrillation, vasopressors and CPR.
Mechanism
As an antiarrhythmic, lidocaine’s action mechanism involves alteration of conduction of
signals in the neurons through the blocking of voltage-gated kinds of sodium channels. These
channels are located in the cell membrane of the neuron and function to propagate the neuronal
signals. When the blockage of the aforementioned channels is sufficient, the postsynaptic
neuron’s membrane fails to depolarize hence hindering the transmission of the action potential
(Homoud, 2008). Careful titration helps to create some higher selectivity degree in blocking of
the sensory neurons while higher concentrations tend to affect other neuronal signaling
modalities.

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Therefore, when lidocaine acts on a person’s heart, it blocks the sodium voltage gated
channels in the heart’s muscle cells and conduction system hence raising the heart’s
depolarization threshold. Consequently, when the depolarization threshold is raised, the heart
cannot begin or conduct some early action potentials, which may cause arrhythmias. In simple
terms, to expound on the aforementioned action, lidocaine generally exerts its antiarrhythmic
effect through increasing the threshold of electrical stimulation of a patient’s ventricle during the
diastolic episode. In other words, it blocks activated, as well as inactivated kinds of sodium
channels (Suzer, 2009). However, in the normal therapeutic doses, the drug may not produce
any change in the arterial pressure, myocardial contractility, or refractory period. This means
that for lidocaine to exact its aforementioned action mechanism, the clinician has to understand
the proper dosage at which the drug can produce the desired effects on a patient.
Indication in a case study patient
A good example of the utilization of lidocaine is in treating ventricular tachycardia. In
the presented case of a male patient aged 70 years who has developed myocardial infarction,
intravenous lidocaine bolus and intravenous infusion of lidocaine serves to prevent
antiarrhythmia development and treat any arrhythmic episode especially in the emergencies. As
highlighted, the patient presented in the case study has a history of recurrent ventricular
tachycardia episodes. Therefore, considering that the patient is already on a beta-blocker that
suppresses the ventricular arrhythmia, lidocaine serves to compliment the role of the beta-
blocker (Marzlin & Webner, 2012). Ideally, ventricular tachycardia refers to a fast heartbeat
starting in a person’s ventricles. The fact that the ventricles work as the heart’s major pumping
chambers means that such a pathology that touches on them is possible life threatening because it
can cause ventricular fibrillation, trigger asystole or lead to sudden death.

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More often than not, lidocaine administration in the case study patient will function to
prevent or manage monomorphic kind of ventricular tachycardia (Marzlin & Webner, 2012).
Research indicates that one of the most noted etiology of the monomorphic kind of ventricular
tachycardia is myocardial scarring that develops secondary to a previous case of myocardial
infarction in a person. Specifically, the scar that develops after myocardial infarction cannot
conduct any electrical activity and thus creates a circuit, which results in tachycardia. Perhaps,
this is especially why lidocaine utilization is relevant to the presented case, in which the
ventricular tachycardia developed after myocardial infarction in the patient. Therefore, if such a
patient receives an appropriate dosage of lidocaine, any pending or threatening tachycardia will
not develop as the drug blocks the patient’s voltage-gated kinds of sodium channels hence
hindering the transmission of the action potential.
Lidocaine’s side effects
Ideally, compared with other sodium blockers, lidocaine is least cardiotoxic in nature.
However, some rare proarrhythmic effects may be reported including worsening of an already
impaired conduction, arrest of the sinoatrial node, and worsening of an arrhythmia. Moreover, in
very large doses, particularly in a patient with a long history of heart failure, the drug can cause
hypotension through the depressing of myocardial contractility (Suzer, 2009). Other than the
effects on the cardiac, lidocaine can have some extracardiac effects including paresthesia,
nausea, tremor, seizures, lightheadedness, slurred speech, convulsions, and hearing disturbances.
However, such aforementioned neurologic effects mainly affect the vulnerable patients like the
elderly particularly following rapid administration of a lidocaine bolus. Nevertheless, the effects
tend to be short-lived and dose-related, with seizures responding very well to the intravenous
diazepam.

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Concisely, from the above discussion, it is clear that lidocaine not only serves as an
anesthetic, but also plays a major role in managing arrhythmia. However, it is imperative for any
clinician to understand its pharmacodynamics, indications, and potential adverse effects in order
to guarantee the patient the appropriate outcomes after the drug administration.

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References
Homoud, M. (2008). Introduction to antiarrhythmic agents. Tufts-New England Medical Center ,
2, 1-21. Retrieved from http://ocw.tufts.edu/data/50/636944.pdf
Marzlin, K., & Webner, C. (2012). Antiarrhythmic pharmacology: Linking pharmacological
treatment to the patient and the rhythm. CNEA/Key Choice , 1, 1-37. Retrieved from
http://www.cardionursing.com/pdfs/AHCourse/Antiarrhythmic%20Pharmacology%202-
12.pdf
Sharma, S. (2007). Antiarrhythmic drugs: Present and future. Supplement of JAPI , 55, 43-47.
Retrieved from http://www.japi.org/april2007/suppliment/Suppliment_43-
46.pdf?origin=publication_detail
Suzer, O. (2009). Antiarrhythmic drugs. Suzer Farmakoloji , 1, 1-23. Retrieved from
http://www.ctf.edu.tr/farma/onersuzer/pdf/ing/14_Antiarrhythmics_2002.pdf