Never Use Calcium Channel Blockers in a Wide Complex Tachycardia

It's 5:30 p.m. Phone cradled in your left shoulder, you attempt to extract a user-friendly interpretation from the radiologist while simultaneously jotting down discharge instructions and scrolling down a computer screen, wondering how a differential could precede a CBC by a full 45 minutes. An ambulance crew rolls by with a young guy on a stretcher, the monitor beeping furiously. You can't help noting what appears to be V-tach. The patient, although slightly diaphoretic, is talking and seems alert. “Room 3,” you hear behind you, as a fellow physician propels the crew down the hall. Minutes later, you suddenly notice a flurry of activity around room 3 as a code cart is urgently pushed into the room. Further investigation reveals a pulseless, apneic patient in Vfib. “Are you sure that was diltiazem?” you hear someone mutter before the team plunges forward with the resuscitation. What went wrong? The patient was given calcium channel blockers to slow a wide complex tachycardia (WCT). WCT has a variety of etiologies. The actual etiology may not be readily apparent, and making the correct diagnosis may be an elusive goal in the ED. It is important to avoid calcium channel blockers in WCT to prevent potentially disastrous consequences. A WCT is defined as an arrhythmia having a QRS complex exceeding 0.12 seconds and a rate of more than 100 beats per minute.1 There are four general etiologies of wide complex tachycardias: ventricular tachycardia, supraventricular tachycardia (SVT) with aberrant conduction, pre-excitation tachycardia with an accessory pathway, and tachycardia with QRS widening due to other causes such as tricyclic antidepressant overdose or hyperkalemia. In a hemodynamically stable patient, the therapy for WCT is entirely based on the determination of the rhythm. False interpretation can lead to potentially lethal consequences. The correct pharmacological agent to choose depends on the arrhythmia to be treated. Possibilities include lidocaine, procainamide, adenosine, and bicarbonate. Calcium channel blockers, a class of drug most emergency physicians are relatively comfortable with, is very effective in SVT, but it can be potentially disastrous if used in a ventricular or a preexcitation tachycardia and should be avoided in wide complex tachycardias. Mechanism at Play Calcium plays a vital role in cardiac conduction and contraction as well as vascular smooth muscle contraction. In the myocytes, calcium acts on phase 2 of the action potential by creating a plateau through slow calcium release. The released calcium, acting as a second messenger, opens more calcium channels, allowing for more calcium release into the cytosol. This eventually allows for actin and myosin binding, and a contraction ensues. In smooth muscle, calcium helps activate myosin by binding calmodulin, thus stimulating a kinase. This activates myosin, which in turn binds actin, and a contraction results. In addition, calcium acts in the depolarization of the action potential in the sinoatrial (SA) node, and allows normal propagation through the myocyte conduction cells and the atrioventricular (AV) node. Most calcium channel blockers act on voltage-sensitive slow calcium channels that impair calcium influx. This has several results: ▪ Decreased peripheral resistance by acting on vascular smooth muscle. ▪ Decreased cardiac contractility. ▪ Decreased myocyte conduction. ▪ Decreased heart rate by affecting SA and AV node depolarization and propagation. Importantly, it is best to consider calcium channel blockers the most effective treatment of arrhythmias that use the SA and AV nodes. Treatment Choices Where do these wide complex tachycardias originate? Ventricular tachycardia (VT) originates below the AV node and presents as either nonsustained or sustained (longer than 30 seconds, significant hemodynamic symptoms) and monomorphic or polymorphic (single-lead morphology changes with electrical axis variation).1 The treatment for VT is lidocaine (1.0–1.5 mg/kg, repeated in 5 minutes up to 3.0 mg/kg). Lidocaine is a 1b antiarrhythmic, which acts by decreasing sodium current at the start of diastole and prolonging the effective refractory period. This decreases the excitability of cells and decreases automaticity.2 The next choice is procainamide (17 mg/kg at 20 mg/min). Procainamide is a 1a antiarrhythmic, and blocks Na channels as well as potassium currents. This results in prolonged QRS, slower His-Ventricle conduction and prolonged effective refractory period.2 The next drug of choice for VT is amiodarone (5 mg/kg over 20–30min, then 1 g over 24 hours for 48–72 hours). Other drugs that may be used include bretylium and magnesium sulfate. Polymorphic VT potentially may be torsades de pointes. In that case, the treatment is magnesium sulfate. Calcium channel blockers simply should be avoided in VT. As described earlier, they are most effective when the conduction utilizes the SA or AV nodes. In VT, because the impulse originates below the AV node, blocking the node is not effective. At the same time, a patient in VT may be dependent on the increased vascular resistance to maintain adequate blood pressure. When this resistance is suddenly decreased with the calcium channel blockers, the result may be hypotension and hemodynamic instability.3 Preferred Therapy Preexcitation tachycardias with an accessory pathway also may present as a WCT. The most common is Wolff-Parkinson-White syndrome, which utilizes the Bundle of Kent as its accessory pathway. The EKG generally shows a shortened PR interval of less than 0.12 seconds, QRS interval prolongation, and a delta wave (upsloping slur of the initial portion of the QRS). The conduction down the accessory pathway can be either antegrade, retrograde (retrograde occurs in 90% of cases), or both. In antegrade conduction, or orthodromic tachycardia, propagation is down the accessory pathway and back up the AV node. In retrograde conduction, or antidromic tachycardia, the reverse is true. When the conduction is only retrograde, the QRS is narrow, the PR normal and there is often no delta wave. In this case, the treatment may include calcium channel blockers and adenosine. WPW, however, may be antegrade or a combination of retrograde and antegrade. These patients are more likely to develop atrial and ventricular fibrillation. Atrial fibrillation occurs in patients with WPW in 11.5 to 39 percent of cases.4,5 In the case of antidromic tachycardias, calcium channel blockers act by blocking the AV node, decreasing the refractory period, and thereby facilitate increased antegrade conduction. This may in turn lead to ventricular fibrillation and deterioration. Hence, in a wide complex presentation of a preexcitation tachycardia, calcium channel blockers may be lethal. In preexcitation tachycardias utilizing an accessory pathway, the preferred choice of treatment is procainamide, dosed as mentioned earlier. Supraventricular tachycardias are defined as arrhythmias originating either from the atria or from or through the AV node. These include atrial fibrillation, atrial flutter, atrial tachycardias, and reentrant tachycardias. SVT with aberrancy presents as a WCT, and occur due to a block or delay in conduction, either functional or fixed. The most common aberrancies are either right or left bundle branch blocks. These blocks may preexist or be the result of increased rate.1 In this case, a previous EKG is often very helpful, particularly if it shows a preexisting bundle branch block. Unfortunately, more often than not, old EKGs are not available. It is important to examine carefully the characteristics of the preexisting block because a new aberrancy may be superimposed and only discovered through careful inspection. SVT may be effectively treated with adenosine, 6 mg, followed if necessary by a 12 mg IV push. The next line of treatment is calcium channel blockers or beta blockers. These effectively block the AV node and slow conduction, providing rate control. It is difficult to differentiate SVT with aberrancy from VT in the ED. There are several characteristics of the history, physical exam, and EKG that may be useful. In general patients who are older (over 35) and are predisposed to coronary artery disease, VT is more likely6 because 98 percent of patients with previous myocardial infarctions will have VT as the cause of their WCT.7 The chest x-ray may reveal an enlarged heart, further supporting the history of heart disease. The physical exam in patients with VT should search for cannon A waves, beat to beat variability in blood pressure, and S1 variability as shown by evidence of AV dissociation. These are not easily noted, and the EKG becomes the important diagnostic tool. VT may show AV dissociation, capture, and fusion beats as well as negative or positive concordance in V1-V6. Furthermore if the complexes are RBBB shaped, an R:S ratio of less than 1 and a monophasic or biphasic QRS complex in V1 is more likely to be VT. In a LBBB shaped complex, V1 may show a notched S or V6 may show a qR pattern.7 Both SVT and VT may be irregular, although SVT is more likely to be. It is important to note however, that in the case of an irregular WCT, adenosine should not be given because if the etiology is preexcitation atrial fibrillation with an accessory pathway, it may cause ventricular fibrillation.7 Aside from these WCTs, QRS widening also may occur due to extrinsic causes such as electrolyte abnormalities (hyperkalemia) or drugs (TCAs or IA antiarrhythmics such as procainamide). In this case, the treatment is dependent on the cause; for example, hyperkalemia and TCA overdoses are treated primarily with sodium bicarbonate. Wide complex tachycardias often present a diagnostic dilemma on presentation to the ED. Algorithms and guidelines help differentiate between the arrhythmias. These include characteristics of the history, physical exam, radiographic findings, and finally the 12-lead electrocardiogram. These guidelines are not foolproof, however. The EKG characteristics are not always evident, and often some doubt remains. Therefore, calcium channel blockers, which are potentially lethal in cases of VT and preexcitation tachycardias should be avoided in wide complex tachycardias. Axioms in Emergency Medicine is written specifically for emergency medicine residents to dispel myths and misconceptions about different clinical entities. The column is written each month by a resident from the Emergency Medicine Residency Program at MCP Hahnemann University School of Medicine in Philadelphia.