IB Agents

HPI BB is a 72-year-old man who presents to the ED with complaints of palpitations. PMH includes anterior myocardial infarction (Ml), hypertension (HTN), and depression. 

PE Vital signs BP 105/75 mm Hg, HR 160 beats/min, RR 14 breaths/min. ECG showed sustained ventricular tachycardia (SuVT). 

Sustained ventricular tachycardia is defined as consecutive premature ventricular contractions lasting more than 30 seconds. Nonsustained ventricular tachycardia (VT) usually self-terminates and lasts for less than 30 seconds. The acute treatment of SuVT depends on the hemodynamic stability and symptoms of the patient. Unstable patients should receive immediate cardioversion. If patients are stable with mild symptoms, they can be treated with IV antiarrhythmics. 

The antiarrhythmic of choice for SuVT is lidocaine because of its fast onset and ease of administration. Lidocaine is a class IB antiarrhythmic that inhibits sodium ion channels, decreasing the action potential duration and effective 

Side effects should be monitored after the initiation of lidocaine. The most common adverse reactions are drowsiness, dizziness, paresthesia, and euphoria. Patients also may experience serious central nervous system (CNS) side effects such as confusion, agitation, psychosis, seizures, and coma, but usually only at supratherapeutic levels. The active metabolites of lidocaine are responsible for most of the CNS toxicities. Cardiovascular side effects, including atrioventricular block, hypotension, and circulatory collapse, are not as well correlated to lidocaine levels. 

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The Class I antiarrhythmic agents inactivate the fast sodium channel, thereby slowing the movement of Na" across the cell membrane (1,2). This is reflected as a decrease in the rate of development of phase 0 (upstroke) depolarization of the action potential (1,2). The Class I agents have potent local anesthetic effects. These compounds have been further subdivided into Classes lA, IB, and IC based on recovery time from blockade of sodium channels (11). Class IB agents have the shortest recovery times (t1 ) Class lA compounds have moderate recovery times (t 2 usually <9 s) and Class IC have the longest recovery times (t 2 usually >9 s). 

Glass IB Antiarrhythmic Agents. Class IB antiarrhythmic agents produce less inhibition of the inward sodium current than Class lA agents. In normal myocardial tissue, phase 0 may be unaffected or minimally depressed. However, in ischemic or infarcted tissue, phase 0 is depressed. Myocardial tissue exposed to Class IB agents exhibits decreased automaticity, shortened action potential duration, ie, shortened repolarization, and shortened refractory period. Excitability of the myocardium is not affected and conduction velocity is increased or not modified. The refractory period is shortened less than its action potential duration, thus the ratio of refractory period to action potential duration is increased by these agents. The net effect is increased refractoriness. The PR and QT intervals of the ECG are shortened and the QRS interval is unchanged (1,2). 

Class IB agents (Sodium channel blockers) [73-78-9] C H23C1N20 H2O Xylocaine, Dalcaine... 

At the cellular level, the major electrophysiological effect appears to be rate-dependent blockade of sodium channels [22]. The onset for this Class I effect (64 + 9% of the final depression of between the first and second beat of the train) was similar to that for Class IB agents [23]. The offset rate (recovery of from rate-dependent depression) for amiodarone was 1.48 s. This value falls between those seen for Class IB agents (200-500 ms) and lA agents (2.3-12.2 s) [23]. Amiodarone inhibited the binding of pH]ba-trochotoxinin A 20a-benzoate to the sodium channel, suggesting that it binds to inactivated sodium channels [24]. 

Moricizine exerts electrophysiological effects that are common to both class lA and IB agents. However, it does not belong in any of the existing drug classes. 

Lidocaine (Xylocaine) was introduced as a local anesthetic and is still used extensively for that purpose (see Chapter 27). Lidocaine is an effective sodium channel blocker, binding to channels in the inactivated state. Lidocaine, like other IB agents, acts preferentially in diseased (ischemic) tissue, causing conduction block and interrupting reentrant tachycardias. 

Mechanism of Action An anti-irritable bowel syndrome (IBS) agent that binds to 5-HT receptors in the GI tract. Therapeutic Effect Triggers a peristaltic reflex in the gut, increasing bowel motility. 

Although categorized separately, type Ib drugs probably act similarly to type la drugs, except that type Ib agents are considerably more effective in ventricular than supraventricular arrhythmias. 

Other class Ib agents, e.g. tocainide and mexiletine, are administered p.o. for treatment of ventricular arrhythmias in humans and dogs but have not yet been evaluated for use in the horse and appear to offer no significant advantages over procainamide in this species. 

Class I drugs are Na+ channel blockers. Class la drugs have little effect on SA node automaticity, while most other antiarrhythmics reduce SA node automaticity. Class la drugs slow conduction velocity and tend to be more effective than other classes in prolonging the refractory period. No clear generalizations can be made of Class Ib agents. 

Many patients undergoing ICD implantations are also on antiarrhythmic drug (AAD) therapy, and the effects of AADs on DFTs should be taken into consideration. Class IC and IB agents, such as encainide, flecainide, lidocaine, and... 

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