Dysrhythmias and Tachyarrhythmias

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.

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:

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.

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.

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.

10 Why are patients with WPW syndrome at increased risk for sudden cardiac death?

Patients who have an accessory pathway lack the protection offered by AV node refractoriness. If their accessory pathway can conduct antegrade (from the atria to the ventricles) at high frequency they are at risk for very rapid ventricular rates should AF develop. Such rapid rates can lead to VT or VF. Any patient who is initially seen with an irregularly irregular wide complex tachycardia should raise the suspicion of preexcited AF. AV nodal blocking agents should be avoided in such patients because they can increase conduction down the AP leading to increased risk for VF or VT. Drugs that slow conduction of the pathway such as procainamide or amiodarone should be considered.

11 What is the main effect of adenosine on cardiac conduction?

Adenosine’s main clinically relevant effect on cardiac conduction is transient AV nodal block. As such it can be used in the diagnosis of various narrow complex tachycardias where the P waves are difficult to discern on the surface ECG. A bolus of adenosine produces rapid-onset, short-duration AV block. This can result in unmasking of P waves previously obscured by the QRST complex. In AV node–dependent rhythms (such as AVRT and AVNRT [described later]) adenosine will cause termination of tachycardia. Thus adenosine injection can be a diagnostic and therapeutic maneuver. Termination of a narrow complex tachycardia by adenosine strongly suggests an AV node–dependent rhythm but rarely can indicate adenosine-sensitive focal atrial tachycardias. It is important always to have a 12-lead ECG running when giving adenosine. See Figure 29-3.

Figure 29-3 Example of narrow-complex tachycardia with unmasking of flutter waves once the transient AV block is achieved with adenosine (asterisk).

12 What are common causes of atrial fibrillation in a critical care patient?

Although the exact causes of atrial fibrillation are unknown, a number of factors are commonly associated with atrial fibrillation: pulmonary disease, pulmonary emboli, systemic inflammatory response, hyperthyroidism, alcohol (holiday heart), valvular heart disease, and atrial enlargement.

13 How do you treat hemodynamically stable tachycardias?

There are two issues to consider when identifying arrhythmias:

Atrial fibrillation and rapid atrial tachycardias (e.g., atrial flutter) are associated with increased risk for stroke, and measures must be taken to reduce this risk independent of whether the rhythm is controlled. In some patients (e.g., those with decreased ventricular function), VT can indicate an increased risk for sudden cardiac death. Finally, preexcitation (antegrade conduction via an accessory pathway) may indicate an increased risk for sudden death depending on the refractory properties of the accessory pathway. Such patients may require an electrophysiologic study to assess the pathway’s refractory period.

14 What drugs can be used to control ventricular response rate in a patient with hypotension and atrial fibrillation?

An unfortunate side effect of most rate-controlling medications such as β-blockers and calcium channel blockers is that they are vasodilators and negative inotropes and hence can lead to lowered systemic blood pressure. For this reason physicians are often hesitant to give these medications to a patient with AF and rapid ventricular response rate who have low pressure. In the vast majority of cases repeated small doses of intravenous (IV) medication (e.g., 5 mg of diltiazem) will reduce heart rate without decreasing blood pressure (the increased diastolic filling time offsets the vasodilatory and negative inotropic effects). Direct current cardioversion (DCCV) is the treatment of choice for hemodynamically unstable rapid AF.

15 How should you treat AF in a hemodynamically stable patient?

A patient with highly symptomatic atrial fibrillation should have attempts made at restoring and maintaining sinus rhythm. Cardioversion (chemical or electrical) is the usual first step in a patient who has new-onset atrial fibrillation of less than 48 hours. After 48 hours of AF without adequate anticoagulation, the risk for thromboembolic events increases. Under these circumstances the patient should have rate control and adequate anticoagulation for at least 4 weeks and then cardioversion. If the patient cannot tolerate AF for that period of time and if transesophageal echocardiography reveals no thrombus, cardioversion can be performed and anticoagulation started. Antiarrhythmic agents can be used for patients with symptoms either in whom DCCV has failed or who are going in and out of AF (in which case DCCV is not appropriate). Long-term management for patients with symptoms in whom antiarrhythmic therapy fails should involve consideration of AF ablation. In patients without symptoms it is reasonable to allow AF to continue and control ventricular response rates. Management of anticoagulation is independent of rhythm control.

16 Who needs anticoagulation?

In patients with new-onset AF of less than 48 hours duration the need for anticoagulation before and after cardioversion may be based on the patient’s long-term risk for thromboembolism (see Table 29-1). For patients with AF of more than 48 hours duration anticoagulation should be initiated before cardioversion (for at least 3 weeks if possible or IV heparin if requiring immediate cardioversion for hemodynamic instability) and continued for 4 weeks. The decision for long-term anticoagulation is based on the CHA₂DS₂-VASc score. Patients with a score of 1 can receive either aspirin or full anticoagulation; patients with a score of 2 or more should receive long-term anticoagulation.

^{Table 29-1} CHA₂DS₂-VASc Score

LV, Left ventricular; TE, thromboembolism; TIA, transient ischemic attack.

From Lip GY, Nieuwlaat R, Pisters R, et al: Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach—The Euro Heart Survey on Atrial Fibrillation. Chest 137:263-272, 2010.

17 Are there nonpharmacologic approaches to acute rate control with atrial tachycardias?

In patients with atrial tachycardia who have atrial pacing leads in place a nonpharmacologic alternative to AV node–blocking drugs exists for controlling ventricular response rate. In an atrial tachycardia that cannot be otherwise rate controlled, efforts can be made to pace the atria faster than the rate of the atrial tachycardia; this can lead to a higher degree of block in the AV node (i.e., 3:1 vs. 2:1) and therefore paradoxically lower the ventricular rate.

18 How do you treat rapid regular narrow-complex tachycardias?

Adenosine can be a helpful diagnostic maneuver (see earlier). Typical atrial flutter can be recognized by its characteristic appearance: “sawtooth” P waves in the inferior leads and a narrow upright P wave in V₁. This ECG pattern reliably indicates counterclockwise reentry around the tricuspid annulus, a rhythm with a very high rate of cure with catheter ablation. Other atrial tachycardias can be treated with antiarrhythmic medication or ablation. Ablation of SVT has a high success rate and low complication rate. AV nodal–blocking agents can also be used for long-term suppression of SVT.

19 How do you decide which antiarrhythmic medication to use?

The choice of antiarrhythmic medication can be complex, but one should know major contraindications to the various antiarrhythmic agents. Amiodarone is contraindicated in patients with chronic lung disease and baseline thyroid dysfunction; patients taking amiodarone should have annual chest radiographs and biannual liver and thyroid function tests. Dronedarone is contraindicated in patients with congestive heart failure. Flecainide is contraindicated in patients with coronary artery or structural heart disease. Dofetilide and sotalol should be avoided in patients with renal insufficiency; with preserved renal function, therapy should be started in the hospital where the QTc can be monitored until steady states have been achieved.

20 How are bradycardias described?

Bradycardia can result from abnormalities of impulse formation (e.g., sinus bradycardia, sinus arrest) or from failure of impulse conduction (i.e., AV node or HP system disease).

21 How do you describe the different degrees of AV block?

22 Which type of second-degree heart block is worrisome and why?

Second-degree AV block is rarely symptomatic and by itself is not dangerous. The question is whether second-degree block indicates increased risk for complete AV block, and if so whether asystole is likely to occur. AV node block rarely progresses to third-degree block and often has a reliable escape rhythm if it does. HP block is more likely to progress to complete block and is more likely to result in asystole. AV node suppression typically results in Mobitz I block, whereas HP block leads to Mobitz II block. Therefore Mobitz II block is an indication for permanent pacemaker placement. In the presence of 2:1 AV block Mobitz I and II cannot be distinguished; widened QRS and normal PR interval suggest that block is at the HP level. Atropine improves AV node conduction. It has no direct effect on HP conduction but by causing increased sinus rate can paradoxically increase HP block and therefore should be avoided in this setting.

23 How would you know whether transcutaneous pacing pads are capturing?

Transcutaneous pacing is a temporary solution for hemodynamically unstable bradycardia. Electric current is delivered between the pacing/defibrillation pads on the patient’s chest. It can be difficult to assess whether myocardial capture has been achieved; the surface electrogram and telemetry are frequently obscured by a large-amplitude pacing artifact, and palpation of the pulse can be misleading because of contraction of the skeletal muscles mimicking cardiac pulsation. One can look for T waves on the cardiogram, monitor arterial blood pressure, or palpate the femoral pulse. Note: the default setting on most external pacing machines is to start pacing at the machine’s minimum output current.

Key Points Dysrhythmias and Tachyarrhythmias

1. Characteristics that point toward a wide complex tachycardia being VT

AV dissociation

Very wide QRS complex

Precordial lead concordance

Fusion beats

2. Characteristics of torsades de pointes

Long QT

Long-short coupling initiation

Twisting of the points during VT

Torsades should be distinguished from ischemic polymorphic VT because treatment is very different.

3. Second-degree Mobitz II heart block indicates conduction system disease distal to the AV node and is an indication for evaluation for permanent pacemaker.