Overview

Recommendations for acute treatment can come only after a rapid but accurate assessment of the arrhythmia, its consequences, and its potential causes (Box 34.1). Whereas the hemodynamic consequences of the tachycardia dictate the urgency of treatment, timely assessment of multiple other factors is also essential.

Most tachyarrhythmias in the ICU setting are precipitated or potentiated by metabolic and hemodynamic derangements, electrolyte imbalances, or drug effects. These include sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, automatic atrial and junctional tachycardias, and polymorphic VT. In contrast, sustained monomorphic VT, atrioventricular (AV) nodal reentrant tachycardia (AVNRT), reentrant atrial tachycardia, and atrioventricular reentrant tachycardia (AVRT)—which uses the atria, AV nodal tissue, ventricles, and an accessory pathway—occur in the setting of a predisposing structural substrate. Even with such a substrate, however, a metabolic or hemodynamic factor may be responsible for the initiation and maintenance of the tachycardia. Furthermore, reversal of these underlying abnormalities may control the tachycardia and prevent its recurrence despite the presence of a substrate abnormality.

Diagnostic Tools

The appropriate intervention for a tachyarrhythmia depends on obtaining adequate information to arrive at the correct ECG diagnosis (Table 34.1). A reference or baseline 12-lead ECG during sinus rhythm should be sought immediately. This may provide important information regarding underlying heart disease, conduction abnormalities, and baseline P wave morphology. A 12-lead ECG during the tachycardia provides further information regarding the AV relationship during tachycardia, morphologic features of the QRS complex, and P wave morphology. Long telemetry rhythm strips are also helpful in determining the AV relationship, regularity of the ventricular response, and initiation and termination of the tachycardia (Table 34.2). Additional information regarding the AV relationship may be obtained by recording directly from epicardial pacing leads in the postoperative cardiac patient or from permanent endocardial pacing leads.

Many tachycardias are short-lived or require immediate cardioversion, making it difficult to obtain a 12-lead ECG during the event. In these cases, telemetry recordings from the appropriate leads are crucial. The V₁ precordial lead is the most helpful lead in assessing bundle branch block (BBB) morphology and suspected VT. Based on morphologic criteria, V₁ may also be useful in localizing the arrhythmia and guiding pharmacologic and ablative treatment. It is important to note that V₁ and MCL₁ (modified chest lead 1—the bipolar telemetry vector of left arm negative and right chest wall positive) recordings are not equivalent. Although the two leads may appear identical during sinus rhythm, they may be very different during wide complex tachycardias.

As a rule, the inferior limb leads (II, III, aVF) are good starting points for supraventricular tachycardias because P waves and atrial flutter waves are often well seen in these leads. If the telemetry system allows simultaneous monitoring of two leads, V₁ and an inferior limb lead provide the greatest amount of information. If only one lead can be monitored at a time, lead selection should be based on the arrhythmic information sought for an individual patient.

Interventions during tachycardia can also provide useful information. Slowing AV nodal conduction with vagal maneuvers or pharmacologic agents can reveal previously masked flutter waves or the P waves of atrial tachycardia (Figure 34.1). Adenosine, an endogenous nucleoside, interacts with specific receptors on the extracellular membrane acutely slowing AV conduction. Because adenosine has a half-life of only 0.5 to 5 seconds, doses (6 mg and then 12 mg) must be given in a rapid IV bolus injection followed by a flush. Even administration through a peripheral intravenous line can attenuate its effects. The short-lived adverse effects of adenosine include facial flushing, chest pain or pressure, bronchospasm, and dyspnea. By briefly but effectively blocking the AV node, adenosine is capable of terminating AVNRTs. Adenosine is not a perfect diagnostic tool, however, because it may also terminate some episodes of focal triggered atrial tachycardia and VT.

The “When in Doubt, Knock It Out” Rule

Severe hemodynamic instability resulting from a tachycardia warrants prompt electrical cardioversion. Before cardioversion, however, one needs to consider that the tachycardia may be sinus tachycardia or multifocal atrial tachycardia, neither of which responds to electrical cardioversion. In addition, the hemodynamic instability may be due to a separate cause, such as blood loss or sepsis, and the tachyarrhythmia is just a secondary event. Once the decision is made to perform electrical cardioversion, patient comfort should be ensured by administering a short-acting IV benzodiazepine, such as midazolam, or the anesthetic agent propofol (see Chapter 5).

One must choose a mode of delivery (synchronous or asynchronous) and an energy level. Delivery of shock energy for ventricular fibrillation (VF) and polymorphic VT should be performed in the asynchronous mode. For all other arrhythmias, energy should be delivered in the synchronous mode to decrease the risk of causing arrhythmia degeneration or VF. For any rhythm with dire hemodynamic consequences, energy output should begin at 200 joules and then should be increased to 300 joules or the maximum available dose from the defibrillator if the initial attempts fail (see Appendix D for Advanced Cardiac Life Support [ACLS] algorithms). Only in the stable patient should lower energy levels be attempted.

One always should anticipate adverse consequences when performing electrical cardioversion or defibrillation. Even in the stable patient, synchronous cardioversion can precipitate VF. Because bradycardia and significant sinus pauses are not unusual after cardioversion, IV atropine should always be immediately available, and ready access to an external pacing unit is desirable.

Sinus Tachycardia

The most common SVT encountered in the ICU is sinus tachycardia, which occurs in response to underlying conditions such as pain, fever, infection, anemia, pulmonary embolism, thyrotoxicosis, myocardial ischemia, and congestive heart failure (CHF) (see Figure 34.2A). Autonomic dysfunction may also play a role, particularly in certain neurologic disorders, such as Guillain-Barré syndrome. The clinical challenge lies in making the diagnosis of sinus tachycardia and recognizing its significance as a secondary problem. It should be viewed as a warning sign of underlying abnormalities and prompt a thorough evaluation. Treatment is directed toward the underlying cause.

Atrial Fibrillation and Atrial Flutter

Atrial fibrillation and atrial flutter are similar arrhythmias that occur commonly in the ICU (see Figure 34.2B and C). Risk factors for the development of atrial fibrillation include advanced age, CHF and valvular heart disease, systemic hypertension, pulmonary disease, sleep apnea, and thyrotoxicosis. Acute respiratory failure and high sympathetic tone, particularly in patients with other risk factors, can precipitate a paroxysm of atrial fibrillation or flutter. On the 12-lead ECG, atrial fibrillation is marked by the replacement of organized atrial activity with an irregular undulating baseline of variable amplitude. At times, the undulations may be coarse and mimic atrial activity; however, these coarse waves are not truly cyclical: the RR interval is always irregular and characteristically some will occur < 200 msec apart.

In contrast, atrial flutter is due to a reentrant mechanism within the atria and results in regular flutter waves (typically at a rate of 240 to 300 beats per minute [bpm]) on the 12-lead ECG. In the absence of medications, the ventricular rate is typically regular, with 2:1 conduction of flutter waves, resulting in a typical regular ventricular rate of 130 to 150 bpm. In fact, when encountering a regular, narrow complex tachycardia at the rate of 130 to 150 bpm, one should always first consider the diagnosis of atrial flutter. It is frequently more difficult to control the ventricular rate in atrial flutter than in atrial fibrillation because of the slower and more organized impulses reaching the AV node. Flutter waves can be easily overlooked, and blocking conduction in the AV node can help unmask them (see Figure 34.1). If atrial wires/leads (temporary or permanent) are present, direct recordings from these wires can help clarify the diagnosis.

Acutely, these arrhythmias can result in a rapid ventricular rate, loss of effective atrial contraction, and hypotension. In this situation, the treatment is electrical cardioversion. If the patient is stable, management is directed at controlling the ventricular rate, converting the arrhythmia to sinus rhythm, maintaining sinus rhythm, and preventing embolic sequelae.

A number of pharmacologic agents are available to control the ventricular response during atrial fibrillation and flutter (Table 34.3). Once the rate is controlled and the patient is hemodynamically stable, cardioversion to sinus rhythm can be pursued on an elective basis. The timing of elective cardioversion is largely determined by the need to reduce the risk of thromboembolic complications. The lack of organized atrial activity associated with atrial fibrillation leads to circulatory stasis within the atria and can result in formation of atrial thrombi and embolism into the systemic circulation. Even in new-onset atrial fibrillation, there is some embolic risk. If a patient has no contraindications, anticoagulation should be started as soon as possible, certainly within 24 to 48 hours if spontaneous conversion to sinus rhythm has not occurred. If a patient cannot receive anticoagulation, prompt cardioversion within 24 to 48 hours should be considered. In addition, patients with known risk factors for stroke who are in atrial fibrillation for over 24 hours may require a transesophageal echocardiogram to exclude the presence of a thrombus in the left atrial appendage before cardioversion.

When the duration of atrial fibrillation is unclear, one must assume that it has been present for > 48 hours. In this case, conventional therapy has consisted of anticoagulation for 4 to 6 weeks before cardioversion. A transesophageal echocardiogram can be used to rule out the presence of thrombus located in the left atrial appendage, but the absence of thrombus does not preclude the need for immediate postcardioversion heparin therapy and anticoagulation for several weeks thereafter. Anticoagulation is essential during this period because atrial stunning from intracellular calcium accumulation during atrial fibrillation may lead to thrombus formation despite restoration of sinus rhythm. Atrial stunning is a persistent mechanical atrial dysfunction despite restored bioelectric function and can take 4 to 6 weeks to resolve. Patients with atrial flutter are at a similar risk for embolic phenomena as those with atrial fibrillation and should also receive anticoagulation.

Once the decision is made to proceed to cardioversion, several options exist, particularly for atrial flutter. Because atrial flutter is a reentrant arrhythmia, overdrive pacing by means of a permanent or temporary pacing wire or an esophageal electrode can terminate the tachycardia. Overdrive pacing, however, can result in atrial fibrillation rather than sinus rhythm.

Atrial fibrillation and flutter respond to the same antiarrhythmic drugs outlined in Table 34.4. In fact, atrial fibrillation frequently organizes into stable atrial flutter on these medications. It is common, however, for these arrhythmias to resist pharmacologic interventions and require electrical cardioversion. Despite this, the use of antiarrhythmic agents before electrical cardioversion is indicated because drug treatment may help maintain sinus rhythm after cardioversion. In patients whose condition is stable, electrical cardioversion of atrial fibrillation typically begins at 200 joules, but higher doses of energy may be required. It is always performed in the QRS synchronous mode. Cardioversion of atrial flutter generally requires significantly lower energies, usually 50 to 100 joules, and again should always be delivered in the synchronous mode. An amnestic agent, such as midazolam, should always be given beforehand.

Some patients have a clear precipitating factor for atrial fibrillation, such as pulmonary embolism or pneumonia, and do not require long-term medical management. Spontaneous conversion to sinus rhythm may occur as the patient recovers from the acute insult. Other patients who have underlying risk factors remain at risk for recurrence and may require chronic antiarrhythmic management and anticoagulation. The patient with atrial fibrillation and the WPW syndrome is discussed later.