Dysrhythmias and Tachyarrhythmias

Chapter 29 Dysrhythmias and Tachyarrhythmias



Pierre Znojkiewicz, MD , Peter S. Spector, MD




1 How do you treat tachycardia in the intensive care unit (ICU)?


The first step in treating an arrhythmia in the ICU is determination of the urgency with which it must be resolved; hemodynamically unstable rhythms require immediate treatment at times not affording the clinician the luxury of full diagnostic assessment. Even in the patient whose condition is unstable a very quick look at a telemetry recording allows one to answer several key questions: Is this a wide (QRS > 120 ms) or narrow complex rhythm? Is the rhythm irregular or regular? Unstable rhythms can be electrically cardioverted or defibrillated. With better-tolerated rhythms it is important to gather some diagnostic information that may be required for both short- and long-term arrhythmia management.



2 How do you determine the cause of wide complex tachycardias?


Whenever possible, a 12-lead electrocardiogram (ECG) should be obtained. The first distinction to make is between supraventricular and ventricular arrhythmias. A detailed description of how to make this distinction is beyond the scope of this chapter, but a few rules of thumb can be helpful. Narrow complexes indicate that the ventricles are being depolarized via the conduction system (His-Purkinje [HP]). A wide QRS complex indicates that ventricular activation is not entirely via the conduction system. This can occur with ventricular tachycardia (VT), ventricular pacing, bundle branch block (BBB), accessory pathway conduction, or rarely with ventricular conduction delay (e.g., hyperkalemia).



3 How do you differentiate a VT from an aberrantly conducted supraventricular tachycardia (SVT)?


In wide complex tachycardia, one must distinguish SVT with aberrancy from VT. Step 1 is to identify P waves and assess the relationship between atrial and ventricular activation. A 1:1 relationship can occur with conduction between atria and ventricles (or vice versa and therefore does not distinguish SVT from VT). Atrioventricular (AV) dissociation, on the other hand, can identify VT (V faster than A) or SVT with aberrancy (A faster than V). Other indicators that suggest VT (though not definitively) are a very wide QRS (> 160 ms), precordial concordance (leads V1-V6 all positive or all negative), and fusion beats (indicating intermittent conduction via the HP system during VT). Finally, inspection of an old ECG can help identify the prior presence of BBB or preexcitation. Irregularly irregular rhythms are likely to be atrial fibrillation.



4 What rhythms produce a wide complex tachycardia that can be mistaken for VT?


SVTs that are conducted with BBB (preexisting or rate related) are referred to as SVT with aberrancy. In patients with an accessory pathway (AP) conduction from atria to ventricles over the AP will produce a wide complex. This will occur whether the AP is part of the arrhythmia circuit (antidromic AV reentrant tachycardia [AVRT]; conduction antegrade over the AP and retrograde over the AV node) or a bystander that simply conducts activation resulting from some other arrhythmia (e.g., atrial flutter).



5 What should you think of when you see a very wide QRS (and no P waves)?


Hyperkalemia leads to baseline depolarization of cardiac cell membranes. This in turn results in an increased proportion of inactivated sodium channels. The global consequence of increased inactivation is decreased conduction velocity. In the atria this creates long low-amplitude P waves (which can be difficult to see), and in the ventricle it creates a very wide QRS. With sufficient hyperkalemia a sine wave–appearing rhythm can result. If the underlying rhythm is fast (e.g., sinus tachycardia) the wide QRS and apparent lack of P waves can be mistaken for VT. It is critical not to give sodium channel blocking antiarrhythmics (e.g., lidocaine) in this setting because they further increase sodium channel inactivation and can result in asystole and death. Treatment should be aimed at stabilizing the cell membrane (calcium) and reducing potassium (insulin, glucose, Kayexalate, and/or dialysis). See Figure 29-1.


image

Figure 29-1 Example of a wide complex tachycardia in a patient with hyperkalemia. Note how this could easily be mistaken for VT.



6 What is torsades de pointes, and what predisposes a patient to it?


Torsades de pointes, French for twisting of the points, is a specific polymorphic VT that is frequently self-limiting but can degenerate into ventricular fibrillation (VF). It must be distinguished from polymorphic VT due to ischemia. Torsades is defined by the following:



image Constellation of one long QT interval (QTc > 440 ms in men and > 460 ms in women)


image Initiation with a long-short interval (tachycardia begins after a pause [long cycle])


image Premature ventricular contraction that begins during the T wave (short cycle)


Long QT (and torsade) can result from a congenital ion channel abnormality or ion channel blocking medication (see Fig. 29-2) and can be exacerbated by hypomagnesemia, hypokalemia, and hypocalcemia.


image

Figure 29-2 Example of torsades de pointes. Notice the long QT, long-short interval (asterisk), and self-limited run of polymorphic VT with twisting of the points.



7 What drugs commonly used in the ICU can cause QT prolongation?


See Box 29-1. See also www.torsades.org.



Box 29-1 Drugs Commonly Used in the ICU that Can Cause QT Prolongation




















Amiodarone Quinidine
Clarithromycin Sotalol
Amitriptyline Moxifloxacin
Haloperidol Lithium
Methadone Risperidone


8 What is the Wolff-Parkinson-White (WPW) syndrome?


WPW syndrome occurs in patients who have an abnormal extra connection between the atria and the ventricles: an AP. This can result in evidence of preexcitation on surface ECG. The atrial wave front travels down the AP and begins depolarizing ventricular tissue before ventricular activation through the HP system, resulting in a short PR interval and initial slurring of the QRS (delta wave). This is followed by rapid activation of the remaining ventricular tissue through the HP system. A patient with preexcitation and documented AVRT is said to have WPW syndrome. Note that a subset of APs will only conduct retrograde and will not produce evident preexcitation; these are so-called concealed accessory pathways.



9 What are the two forms of AV reentrant tachycardia (AVRT)?


In patients with an AP, a well-timed premature atrial contraction or premature ventricular contraction that conducts up or down through only one of the AV connections (either the AV node or the AP) but blocks in the other can then set up a reentrant arrhythmia called AVRT (not to be confused with AV nodal reentrant tachycardia [AVNRT]). The two forms of AVRT are described by the conduction through the AV node as either orthodromic, meaning that the tachycardia propagates down the AV node and back up to the atria via the AP, or antidromic when conducting down to the ventricles via the AP and retrograde over the AV node.


Note: Orthodromic AVRT will produce a narrow complex tachycardia with loss of preexcitation; antidromic AVRT will produce a wide complex tachycardia.

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Jul 6, 2016 | Posted by in CRITICAL CARE | Comments Off on Dysrhythmias and Tachyarrhythmias

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