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Chapter 21 Arrhythmias

Disorders of cardiac rhythm are common in the intensive care unit (ICU). Life-threatening arrhythmias such as ventricular tachycardia and complete heart block require immediate intervention. Even arrhythmias such as atrial fibrillation can cause marked hemodynamic instability in cardiac surgery patients. Arrhythmias are commonly a manifestation of underlying cardiac pathology; ventricular fibrillation may be due to acute myocardial ischemia, whereas atrial fibrillation may reflect raised atrial pressure due to ventricular dysfunction. Thus, it is essential that treatment be directed to the underlying cause as well as to the suppression of the arrhythmia.

In this chapter the pathophysiology, diagnosis, and treatment of cardiac arrhythmias, including the use of temporary pacing for the treatment of bradyarrhythmias, are reviewed. The physiology of cardiac conduction and the pharmacology of antiarrhythmic agents are discussed in Chapters 1 and Chapter 3, respectively. The interpretation of an electrocardiogram (ECG) is reviewed in Chapter 8.


Tachyarrhythmias arise due to abnormal impulse generation or reentry. Abnormal impulse generation is caused by automaticity or triggered activity.

Enhanced and Abnormal Automaticity

Cells of the sinoatrial (SA) node and around the atrioventricular (AV) node normally undergo spontaneous depolarization during phase 4 of the action potential. Any factor that increases the slope of phase 4 (such as β1-adrenoreceptor stimulation) causes the threshold potential to be reached earlier, increasing the rate of action-potential generation (see Fig. 1-2). This is called normal automaticity. If the firing rate of a subsidiary pacemaker is abnormally increased such that sinus node dominance is usurped, it is termed enhanced automaticity, and accelerated junctional rhythm is an example of this. When cells that are normally quiescent become partially depolarized, and resting membrane potential rises to −60 or −50 mV, pathologic pacemaker activity may occur. This is called abnormal automaticity, and it is the basis of some atrial tachycardias.


Reentry is the basis of most arrhythmias encountered clinically. Reentry is continuous circulating electricity in which an impulse reenters and repetitively excites a region of the heart. Three requirements are necessary for reentry to occur: (1) an abnormal electrical circuit; (2) slow conduction; and (3) unidirectional block (Fig. 21-1). These conditions may arise because of a fixed anatomic structure such as that which occurs in the Wolff-Parkinson-White syndrome, but more commonly, the conditions for reentry arise due to abnormal physiologic states. For instance, dynamic circuits with unidirectional block may develop due to variability in recovery times (dispersion of refractoriness) among various regions of myocardium. Slow conduction may occur because of partial membrane depolarization or loss of gap junctions.

For reentry to occur, the circulating impulse must not encounter refractory myocardium. Thus, there is a critical relationship between the length of the circuit, the conduction speed, and the refractory period. Antiarrhythmic drugs act by interrupting reentry either by prolonging the refractory period (class I and III) or by further impairing conduction (class I), converting an area of unidirectional block into an area of bidirectional block.

Proarrhythmic Factors


Narrow-complex tachycardia may be defined as a heart rate greater than 100 per minute and a QRS duration less than 0.12 seconds (3 small squares on the ECG). Narrow-complex tachycardias activate the ventricles in a normal manner unless bundle branch block is present (see later material).

Approach to the Patient With Narrow-Complex Tachycardia

A careful review of the 12-lead ECG provides important clues to the diagnosis:

Sinus Tachycardia

Sinus tachycardia is common in the ICU and has a number of causes, including pain, myocardial ischemia, surgical stress, low cardiac output or hypotension, and exogenously administered catecholamines. Maximal sympathetic stimulation can increase the heart rate up to 200 beats per minute, but it is rare for the rate to be greater than 160 beats per minute in adults who are not exercising. The PR interval tends to shorten as heart rate increases because increased sympathetic tone speeds conduction through the AV node.

Sinus tachycardia is a physiologic response to an underlying condition and not an arrhythmia per se, so treatment must be directed at the underlying cause. Sinus tachycardia must be distinguished from other, regular narrow-complex tachycardias, such as accelerated junctional rhythm and atrial flutter with 2:1 block. The presence of regular P waves and a normal PR interval suggests sinus tachycardia, whereas a long PR interval suggests atrial flutter with 2:1 block. Sinus tachycardia has a gradual onset and offset, but atrial flutter and AV nodal reentry tachycardia have abrupt onsets and offsets. The QRS morphology is normal in sinus tachycardia unless there is an abnormality of intraventricular conduction; one potential source of confusion is that patients may develop intraventricular conduction delay at high heart rates (rate-dependent bundle branch block), which may erroneously lead to the diagnosis of ventricular tachycardia (see subsequent material). An atrial ECG is helpful when the diagnosis of sinus tachycardia is uncertain.

Atrial Fibrillation

Atrial fibrillation following cardiac surgery is very common, with most series reporting an incidence of between 30% and 60%.1,2 The peak incidence is on the second postoperative day. Postoperative atrial fibrillation is not benign; it prolongs ICU and hospital stay, increases costs, and is associated with an increased incidence of stroke.2

The arrhythmia is characterized by the abrupt onset of an irregularly irregular narrow-complex tachycardia (Fig. 21-3), often with varying R wave amplitude. Heart rate varies widely, depending on adrenergic tone, but is typically between 120 and 160 beats per minute. In cardiac surgery patients, the onset of atrial fibrillation may cause marked hypotension.


Atrial fibrillation was regarded for a long time as a classic example of random reentry due to multiple wandering wavelets.1 However, it is now recognized that in many patients the atria are only passively involved and that the initiating trigger is rapid focal discharges from cells located in the muscle sleeves of the pulmonary veins.3

Sustained atrial fibrillation leads to mechanical and electrical remodeling of the atria, with loss of contractility (atrial stunning) and shortening of refractory periods. Atrial stunning persists for several weeks after reestablishment of sinus rhythm, increasing the risk for atrial thrombus formation, especially in the left atrial appendage. The shortening of atrial refractory periods results in reinforcement of the arrhythmia the longer it remains untreated.4 Furthermore, patients are very vulnerable to reinduction of atrial fibrillation immediately after reversion to sinus rhythm. For these reasons, after successful cardioversion of atrial fibrillation of more than 48 hours’ duration, anticoagulation and antiarrhythmic therapy should continue for at least 30 days.5


β Blockers (metoprolol, carvedilol, and sotalol) and amiodarone reduce the incidence of atrial fibrillation by as much as 50%.69 The combination of amiodarone and a β blocker appears to be more effective than either agent alone.10 Other drugs such as magnesium and diltiazem may also be useful for prophylaxis but data are inconclusive.9 Standard (right atrial) pacing may have a small protective effect against atrial fibrillation, but the benefit is greater if simultaneous left and right atrial pacing is used.11,12 Digoxin is not indicated for prophylaxis of postoperative atrial fibrillation.7,9

Prophylaxis against atrial fibrillation should include avoiding β-blocker withdrawal in patients chronically treated with them. For patients at increased risk for atrial fibrillation, routine prophylaxis with a β blocker or amiodarone is appropriate.9 Prophylactic biatrial pacing should also be considered in high-risk patients.12

The preoperative administration of 600 mg per day of amiodarone for 1 week prior to surgery has been shown to be effective8 but may not be feasible. A practical alternative is intraoperative dosing of 5 mg/kg intravenously followed by oral treatment of 400 mg three times daily for 2 days, 200 mg twice daily for 2 days, and then 200 mg daily until hospital discharge. Amiodarone should be withheld in the presence of sick sinus syndrome, bradycardia (heart rate <50 beats per minute), or marked first-degree AV block (PR interval >0.30 seconds). In patients with paroxysmal atrial fibrillation who are chronically treated with amiodarone, low-dose oral sotalol (40 to 80 mg twice daily) may be commenced postoperatively, with careful monitoring for excessive bradycardia or QT prolongation. When atrial fibrillation is associated with planned mitral valve surgery, a surgical maze procedure should be considered (see Chapter 10).


Atrial fibrillation that is associated with hemodynamic compromise should be treated aggressively. The success rate for primary cardioversion is low—less than 20% in one study.13 The success rate of electrical cardioversion may be increased by the use of biphasic energy (with an energy level of 200 joules) and the prior correction of hypokalemia and hypomagnesemia. If atrial pressures are elevated, an echocardiogram should be considered to rule out ventricular dysfunction and pericardial tamponade. If cardioversion is unsuccessful, it may be repeated following intravenous amiodarone (a bolus dose of 5 mg/kg over 30 minutes or an infusion of 2 mg/min for 4 hours). Amiodarone provides acute control of heart rate through its β-blocker actions and may itself result in pharmacologic cardioversion. Following successful cardioversion, an infusion of amiodarone (1 mg/min) should be administered until the patient is able to take oral amiodarone or a β blocker. Atrial pacing (AAI mode at 80 to 90 beats per minute for 24 to 48 hours) should be instituted to minimize the chance of recurrence. Intravenous sotalol or ibutilide may be used as an alternative in patients with good left ventricular function.14 If, despite these measures, the patient remains in rapid atrial fibrillation, pharmacologic control of heart rate may be achieved by an intravenous β blocker or diltiazem.15 In patients with unstable hemodynamics, intravenous digoxin may be tried, but it has limited efficacy in the setting of heightened adrenergic tone.15

In extubated patients who are not hemodynamically compromised it is reasonable to attempt pharmacologic cardioversion initially with intravenous amiodarone or a β blocker. If atrial fibrillation persists at 24 hours, the patient should be electively cardioverted (200 joules biphasic energy) followed by atrial pacing. If cardioversion is unsuccessful or atrial fibrillation is recurrent, pharmacologic rate control may be achieved with digoxin in combination with either a β blocker or diltiazem.

Pharmacologic treatment for atrial fibrillation should be continued for 4 to 6 weeks following surgery, even if the patient reverts to sinus rhythm.15 If atrial fibrillation persists at 6 weeks following surgery, a choice should be made between repeat cardioversion and permanent rate control and anticoagulation. The latter strategy is favored by the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study, which did not show a better outcome for older patients with attempted maintenance of sinus rhythm by antiarrhythmic drugs.16

Cardioversion Guided by Transesophageal Echocardiography

Cardioversion should not be performed without the guidance of transesophageal echocardiography in patients who have experienced atrial fibrillation for more than 48 hours and are not undergoing therapeutic anticoagulation. This is so because of the risk for systemic embolization of intracardiac thrombi.17 If left atrial thrombus is present on transesophageal echocardiography (TEE) examination, the patient should be given anticoagulants with heparin and warfarin, and cardioversion should be performed 4 weeks later if repeat (TEE) shows resolution of the thrombus. If thrombus is not present, cardioversion may proceed immediately, after which the patient should undergo anticoagulation with warfarin for 4 to 6 weeks (see subsequent material).

Anticoagulation for Atrial Fibrillation

If there are no contraindications, patients with sustained or paroxysmal atrial fibrillation for more than 24 to 48 hours after cardiac surgery should be given an anticoagulant with warfarin, aiming for an International Normalised Ratio (INR, see Chapter 30) between 2 and 3. Warfarin should be continued for 4 to 6 weeks following surgery, at which time, if the patient is in sinus rhythm, it may be stopped.5 However, if there are factors predictive of recurrence, such as a history of paroxysmal atrial fibrillation, a left atrial diameter greater than 5 cm, or mitral valve surgery, warfarin should be continued.

Patients at increased risk for thromboembolic complications, notably those with documented atrial thrombus, a history of systemic embolization, or a prosthetic mitral or aortic valve, should also be given anticoagulants with unfractionated heparin, which should be continued until the patient has a therapeutic INR.5 Compared with warfarin, aspirin is less effective in reducing stroke frequency in patients with atrial fibrillation,18,19 and it is therefore not usually an acceptable alternative.

Nonpharmacologic Treatment of Atrial Fibrillation

A number of catheter-based techniques involving isolation of the triggering foci around the pulmonary veins and ablation of fractionated atrial potentials have been developed for the treatment of chronic atrial fibrillation.20,21 In older patients, radiofrequency ablation of the bundle of His with permanent pacemaker implantation provides good symptom relief, although the need for anticoagulation remains. These techniques have a minimal role in the management of postoperative atrial fibrillation.

Atrial Flutter

Risk factors for atrial flutter are similar to those of atrial fibrillation, although atrial flutter is far less common than atrial fibrillation.

Atrial flutter is usually caused by a reentry circuit around the tricuspid valve with an area of slow conduction near the orifice of the coronary sinus, which results in abnormal flutter waves on the ECG that have a characteristic sawtooth pattern at a rate of between 250 and 330 per minute. Because of the long refractory period of the AV node, usually only a proportion of the flutter waves are conducted to the ventricles; typically in a ratio of 2:1 (Fig. 21-4), resulting in a heart rate of about 150. Higher ratios of AV block (e.g., 3:1 or 4:1) resulting in slower heart rates are also seen (Fig. 21-5). Postoperative atrial flutter typically has 2:1 conduction. If antiarrhythmic drugs have been given as part of routine prophylaxis, the ventricular rate with 2:1 block may be less (125 to 150 beats per minute). Atrial flutter with 2:1 AV block can be difficult to distinguish from other, regular narrow-complex tachycardias because one of the flutter waves may be concealed within the QRS complex; the rhythm may be mistaken for sinus tachycardia with first-degree AV block. Negative flutter waves on the inferior ECG leads and a fixed heart rate of 140 to 150 per minute usually confirm the diagnosis, but if doubt persists, an atrial ECG should be performed if possible (Fig. 21-6). Alternatively, adenosine (6 or 12 mg) as a rapid intravenous bolus will cause temporary AV block, exposing the characteristic flutter waves.

Technique of Overdrive Pacing for Atrial Flutter

Within a reentry circuit, at any point in time a portion of the circuit is not being activated. This is the distance between the advancing head of the circulating wave front and the tail of depolarized cells; it is called the excitable gap. Pacing impulses can invade the circuit via this gap and, by colliding with the arrhythmia wave front, eliminate the arrhythmia (Fig. 21-7). This technique is known as overdrive pacing and is useful for certain reentry arrhythmias, including ventricular tachycardia and AV nodal reentry tachycardia, but it is particularly useful for atrial flutter.

When two atrial epicardial wires are in situ, each wire should be tested to confirm that it is recording only an atrial ECG and to measure the atrial rate. The pacing pulse width should be increased to 2 ms and pacing begun at 20 mA at 100 beats per minute to confirm the absence of ventricular capture. The pacing rate should be increased to 20 beats faster than the intrinsic atrial rate (typical atrial rates are 250 to 280 beats per minute but may be as high as 330 beats per minute), and the ECG should be observed to confirm atrial capture. After 30 seconds, the pacing rate should be increased by a further 20 beats per minute. Atrial capture is confirmed by: (1) an increase in heart rate as the pacing rate is increased; (2) a subsequent abrupt fall in heart rate as the AV conduction ratio increases (from 2:1 to 3:1 or 4:1); and (3) a constant relationship between the pacing spikes and the flutter waves. Pacing is abruptly stopped after 1 to 2 minutes of atrial capture, which typically results in the establishment of sinus rhythm. If sinus rhythm is not present, the process should be repeated after reversal of atrial lead polarity. If it is still unsuccessful, deliberate induction of atrial fibrillation should be attempted by burst pacing at rates of 600 per minute for 30 seconds or until atrial fibrillation ensues. Pacing-induced atrial fibrillation is typically unstable and frequently reverts spontaneously to sinus rhythm, though reorganization to atrial flutter is possible.