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Lidocaine, also known as lignocaine, belongs to class 1B of antiarrhythmic (Bursell, Ratzan, & Smally, 2009). Other drugs that belong to this class include phenytoin, tocainide and mexiletine (Lippincott Williams & Wilkins, 2009; Acosta, 2009). The three drugs are mainly used to provide treatment for ventricular ectopic (irregular or abnormal) beats, ventricular fibrillation and acute ventricular arrhythmias (Acosta, 2009). They are primarily used to provide treatment for ventricular arrhythmias for the reason that they generally affect the myocardial cells and Purkinje fibers (subendocardial branches or Purkyne tissue) in the ventricles (Acosta, 2009). These drugs are commonly used in acute care because they are not capable of producing instant severe adverse reactions.
The drugs of this class are in most cases administered orally except lidocaine, and are quickly absorbed from the gastrointestinal (GI) tract. Lidocaine is administered through intramuscular (IM) injection into the patient’s tissues, injected into an existing intravenous (IV) line or it can be infused as an intravenous solution (Tashjian & Armstrong, 2011). These drugs are pure sodium channel blockers and, by blocking the rapid influx of sodium ions, they reduce the refractory period of the heart, which in turn minimizes the risk of arrhythmia.
Taking these drugs together with other antiarrhythmic agents such as quinidine, procainamide, propranolol and phenytoin may improve or worsen the effects of class 1B drugs. Class 1B drugs are absorbed in the liver and eliminated through the urine. Elimination of mexiletine can also occur through the breast milk. Adverse reactions associated with the class 1B antiarrhythmic drugs include bradycardia (anomalous slow heartbeat), hypotension, sensory disturbances, paresthesia (prickly-feeling or tingling skin), light-headedness and drowsiness (Acosta, 2009; Lippincott Williams & Wilkins, 2009).
The Mechanism of Action of Lidocaine
Lidocaine is regularly used to provide treatment for ventricular arrhythmias in emergency conditions. Lidocain cannot be used to provide treatment for supraventricular arrhythmias (Lippincott Williams & Wilkins, 2009). This drug has an estimated 20 minutes plasma half-life and it is quickly metabolized from the liver (Tashjian & Armstrong, 2011). The metabolism of lidocaine is controlled by two major factors namely: the liver cytochrome P450 activity and liver blood flow. After being administered, this drug is widely distributed all over the body, as well as in the brain. Lidocaine acts upon ischemic or injured myocardial cells to slow down sodium influx and fix cardiac rhythm.
Under normal conditions, the ventricles respond to an impulse from the SA (sinoatrial) node by contracting. However, when there is tissue damage in the ventricles, ischemic cells have the capability of creating an ectopic pacemaker, which may induce ventricular arrhythmias (Lippincott Williams & Wilkins, 2009). Lidocaine increases the electrical stimulation threshold (EST) of the cells by retarding sodium influx. The raised EST decreases excitability, automaticity and depolarization in the ischemic cells (Bursell, Ratzan, & Smally, 2009) and maintains control to the heart’s primary pacemaker, SA node.
In therapeutic doses, lidocaine does not alter absolute refractory period, atrioventricular (AV) conduction velocity, systolic arterial blood pressure or contractility (Acosta, 2009). Ventricular arrhythmias are commonly caused by acute myocardial infarction. When lidocaine is administered to someone who has developed myocardial infarction, it inhibits ventricular ectopy and raises the ventricular fibrillation threshold (Lippincott Williams & Wilkins, 2009). It stops premature ventricular contractions (PVCs) from causing ventricular fibrillation. Lidocaine is the most preferable drug to curb ventricular arrhythmias and should be used only when the amount of drug in the blood is in the interval of 1.5 to 6.0 mcg per ml of blood (Papastylianou & Mentzelopoulos, 2012).
The Reason why Lidocaine was Indicated in This Patient
Lidocaine was indicated in this patient mainly because the ventricular tachycardia was stable. The ventricular tachycardia in this patient is conssidered to be stable because he is not experiencing symptoms of haemodynamic decompensation (Papastylianou & Mentzelopoulos, 2012). If the ventricular tachycardia was unstable and became an emergency condition, the best drug to use would be amiodarone. Lidocaine is also indicated in refractory ventricular tachycardia if amiodarone is not available (Papastylianou & Mentzelopoulos, 2012).
Lidocaine is useful in providing treatment for stable monomorphic ventricular tachycardia with preserved ventricular function. This drug is also used to treat stable polymorphic ventricular tachycardia with a correction of electrolyte imbalances, normal QT interval and preserved left ventricular (Papastylianou & Mentzelopoulos, 2012). The doctor must have determined that the patient was experiencing the stable ventricular tachycardia condition to administer lidocaine. The drug is also used in patients with long QT syndrome.
The Side Effects of Lidocaine
It is advisable to use lidocaine with caution as it may lead to negative cardiovascular effects such as cardiac arrest, arrhythmias, bradycardia, slow heartbeat, twitching or tremors, ringing in ears, vomiting or nausea, blurred or double vision and hypotension (Tashjian & Armstrong, 2011). Several of these adverse effects may occur due to hypoxemia that may be caused by respiratory depression. Since lidocaine may block sodium ions in the central nervous system, it may cause central nervous system adverse effects such as seizures, dizziness, and confusion (Tashjian & Armstrong, 2011).
Symptoms associated with lidocaine toxicity progress using an identifiable pattern. The first symptoms to appear in case of toxicity include tongue numbness, visual disturbances and lightheadedness. They are the followed by seizures, unconsciousness and muscle twitching. Finally, the concluding symptoms include cardiovascular depression, respiratory arrest and coma (Tashjian & Armstrong, 2011). Conditions that increase the risk for lidocaine toxicity include acidosis, low protein and liver dysfunction. Older patients are also prone to adverse side effects of this drug (Lippincott Williams & Wilkins, 2009).