Chapter 32: Arrhythmias: Rhythm Disturbances in Critically Ill Patients

A variety of different rhythm disturbances may be seen in critically ill patients in an intensive care unit (ICU). These arrhythmias include supraventricular and ventricular tachyarrhythmias, which result from acute illness, electrolyte abnormalities, or drug use. Arrhythmias may also be preexisting and can be worsened by extrinsic factors or metabolic abnormalities in the acute setting. In addition, bradyarrhythmias may occur and may potentially be worsened by drugs or metabolic abnormalities. This chapter will review common types of bradyarrhythmias and tachyarrhythmias seen in the intensive care setting and offer diagnostic approaches and options for acute treatment.

The presenting rhythm is marked sinus bradycardia (Figure 32-1). Sinus bradycardia is defined as a heart rate less than 60 bpm. There is a P wave before every QRS complex with a constant PR interval. In this case, bradycardia may be related to medications, although underlying sinus node dysfunction cannot be excluded.

Electrical activation of the heart originates in the sinoatrial (SA) node at a rate of 60 to 100 bpm. If the SA node fails to generate an impulse, a subsidiary pacemaker (the atrioventricular [AV] node) takes over but at a slower rate (typically < 60 bpm). Bradyarrhythmias are due to either failure of impulse formation in the SA node (sinus node dysfunction) or failure of impulse conduction out of the SA node through the AV node and His-Purkinje system. In the intensive care setting, the most common manifestation of sinus node dysfunction is sinus bradycardia, which may be associated with “brady-tachy syndrome.” AV conduction abnormalities include first-degree AV block or delay, which represents slowing of conduction through the AV node and His-Purkinje system, as well as second- and third-degree AV block. The latter includes “dropped beats,” described in more detail later.

Sinus bradycardia can be a sign that the sinus node itself is dysfunctional. Sinus bradycardia can also be due to increased vagal tone, myocardial ischemia, an intracranial process (such as increased intra- cranial pressure, meningitis, or brain tumor), eye surgery, hypothermia, hypothyroidism, hypoxia, hyperkalemia, and some infectious diseases. Excessive vagal tone can occur with endotracheal suctioning, abdominal distention, vomiting, the Valsalva maneuver (straining), cervical or high thoracic spinal injuries, and pain. During sleep, heart rate can decrease to 35 to 40 bpm with pauses up to 2 seconds, which is not considered pathologic and does not necessarily require permanent pacing unless individuals also have symptomatic bradycardia while awake. Obstructive sleep apnea can also cause worsening bradycardia or promote pauses while individuals are asleep. Many drugs can also suppress the automaticity of the sinus node and slow the heart rate.

This patient is showing signs of hypoperfusion, and atropine can be used to increase the heart rate. If atropine fails to increase the heart rate, isoproterenol, transcutaneous pacing, or transvenous pacing can then be utilized. If transcutaneous pacing is needed in an urgent situation, sedation is required as this is a painful procedure. Permanent pacemaker implantation is recommended if symptomatic bradycardia persists without reversible causes. Symptoms may include lightheadedness, dizziness, presyncope, loss of consciousness, excessive fatigue, and hypotension. In this case, it is also feasible that hypotension may have led to transient cerebral hypoperfusion resulting in a transient neurologic deficit that resolved prior to arrival. Medications in this patient, including amiodarone and the β blocker, are likely contributing to bradycardia. Secondary causes of bradycardia, such as hypothyroidism, should also be excluded.

Permanent pacing may be indicated if bradycardia is the result of drug therapy considered necessary for the treatment of other disorders such as coronary artery disease or atrial arrhythmias. Indications for permanent pacing in the setting of sick sinus syndrome (SSS) are noted in Table 32-1.¹ In this case, antiarrhythmic therapy with amiodarone was necessary to treat atrial arrhythmias and β-blocker therapy was indicated for the treatment of atrial arrhythmias and coronary artery disease.

“Brady-tachy syndrome,” also known as “sick sinus syndrome,” is severe bradycardia associated with paroxysms of tachycardia, the latter of which most commonly include atrial fibrillation. After cessation of the tachycardia, there is typically a postconversion pause (Figure 32-2A). This pause may be prolonged, lasting several seconds, and may result in symptoms of lightheadedness, dizziness, fatigue, or loss of consciousness. Intermittent marked bradycardia or pauses may also occur during atrial fibrillation and can be symptomatic, requiring permanent pacing to allow continued treatment with AV nodal blocking drugs to control rapid rates during atrial fibrillation (Figure 32-2B).

Patients with “brady-tachy syndrome” require that the tachycardia rate be controlled, and this is accomplished with AV nodal blocking drugs, which slow the ventricular response during atrial fibrillation. In addition, antiarrhythmic drugs to help maintain sinus rhythm may also be utilized, which will be discussed in a later section. However, medications utilized to control the rhythm may also worsen bradycardia and promote pauses. A permanent pacemaker is indicated in this situation to prevent worsening bradycardia. Indications for permanent pacing in the setting of SSS are noted in Table 32-1.¹

First-degree AV block is defined as a fixed prolongation of the PR interval to greater than 200 milliseconds. This represents prolonged conduction, without any dropped beats (Figure 32-3).

Second-degree AV block is classified as either Mobitz type I (Wenckebach) or Mobitz type II. In Mobitz type I AV block, the PR interval progressively prolongs prior to the occurrence of a P wave that does not conduct to the ventricles (“dropped beat”) (Figure 32-4). The QRS complex is often narrow but may also be wide with preexisting underlying bundle branch block. The R-R intervals prior to the pause progressively shorten. The R-R interval after the pause is greater than the R-R interval prior to the pause. The pause is less than the preceding two R-R intervals.

Mobitz type II AV block has a fixed PR interval with one P wave that does not conduct to the ventricles (Figure 32-5).² The R-R interval of the pause is equal to two of the preceding R-R intervals. The QRS complex is usually wide, although rarely it can be narrow.

In third-degree AV block, the atria and ventricles are dissociated and firing at their own rates. Typically, the atrial rate will be faster than the ventricular rate (Figure 32-6). If the block is above the His-Purkinje system, the QRS complex is typically narrow, with a rate of 40 to 60 bpm. If the block is below the His-Purkinje system, the QRS complex will be wide, with a rate less than 40 bpm. On occasion, the level of block may occur within the His-Purkinje system (“intra-His block”) and the QRS complex may be narrow, but this is a rare finding.

In Mobitz type I AV block, the site of block is usually within the AV node. In Mobitz type II block, the site of block is typically below the AV node, either within the His-Purkinje system or within the bundle branches. Type III heart block can occur within the AV node or below the AV node.

The SA node is supplied by the right coronary artery in 60% of patients and the left circumflex artery in 40%. The AV node is supplied by the right coronary artery in 90% of patients and the left circumflex artery in 10%.³ The His bundle is supplied by the SA nodal branch of the right coronary artery and septal perforators of the left anterior descending artery. The left anterior descending artery also supplies the bundle branches. Therefore, patients who present with an acute myocardial infarction (MI) can develop sinus brachycardia or first-, second-, or third-degree heart block. Patients with AV block related to an acute inferior wall MI often have complete heart block with a narrow QRS complex, and AV conduction commonly returns within days following the MI. Transient AV block may be related to ischemia or increased vagal tone in these patients. In contrast, patients who have heart block related to an acute anterior wall MI typically have occlusion of a very proximal portion of the left anterior descending artery with a wide QRS complex and bundle branch block, signifying more severe conduction disease related to extensive myocardial damage.

Both second- and third-degree heart block can occur in young healthy individuals as a result of increased vagal tone. Ischemia and underlying heart disease can produce heart block. Drugs may be another common cause of AV block, and medications that slow conduction through the AV node include β blockers, calcium channel blockers, and digoxin. Other drugs also impact on conduction through the His-Purkinje system, including class I and III antiarrhythmic agents. Heart block can also occur after aortic or mitral valve replacement owing to extensive surgical dissection in the region of the AV conduction system.

For a hemodynamically unstable patient with heart block, temporary pacing is recommended with either transcutaneous or transvenous pacing. Atropine 1 mg intravenously every 3 to 5 minutes can be used while setting up for pacing. Care must be used, as atropine may worsen any heart block that occurs below the AV node. The presence of a wide QRS complex may indicate conduction disease below the AV node. Dopamine 5 to 20 μg/kg per minute continuous infusion can be added to enhance the heart rate. Isoproterenol infusion may also be utilized to enhance His-Purkinje conduction.

Once the patient is stabilized, an underlying cause of the heart block should be investigated, including assessment of medications. After discontinuing a drug, it should be kept in mind that it takes five half-lives for most of the drug to wash out and therefore determine if the drug caused the bradycardia. Ischemia should also be ruled out as a potential cause of the underlying conduction disturbance. Following an acute myocardial infarction, it may take hours to days for the conduction abnormality to resolve, particularly in the setting of an acute inferior wall MI. Indications for implantation of a permanent pacemaker in the setting of acquired AV block according to the American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS) guidelines are outlined in Table 32-2, and indications for permanent pacing after the acute phase of MI are outlined in Table 32-3.¹

The differential diagnosis for regular narrow complex tachycardias includes sinus tachycardia, atrial tachycardia, atrial flutter, AV nodal reentrant tachycardia, AV reciprocating tachycardia (AVRT), and junctional tachycardia.

The presence or absence of P waves on the 12-lead ECG and the relationship of the P wave to the QRS complex are useful in the diagnosis and determination of the likely mechanism of the narrow complex tachycardia (Figure 32-8).

Sinus tachycardia is due to increased automaticity within the SA node. As a result, the onset and termination of this tachycardia will be gradual. The P wave precedes the QRS complex and usually has a “long RP” interval. However, if first-degree AV conduction delay is present, the P wave could be closer to the preceding QRS with a somewhat shorter RP interval compared to the PR interval (Figure 32-9). The rate of sinus tachycardia can range from 100 to 180 bpm, depending on the age of the patient, with a maximum rate estimated to be 220 minus the patient's age. The P waves have a morphology similar to sinus rhythm, although the P waves may become more peaked as the rhythm accelerates. Taller P waves often represent a focus higher in the SA node. In most instances, the PR interval shortens with an increase in heart rate due to increased catecholamines and enhanced conduction through the AV node.

Atrial flutter is a macro-reentrant atrial arrhythmia that rotates around the coronary sinus ostium in either a counterclockwise or clockwise fashion.⁴ Flutter waves are best identified in leads II, III, aVF, and V₁. The atrial rate can range from 250 to 350 bpm with a sawtooth contour. The flutter waves are positive in V₁ and negative in leads II, III, and aVF during counterclockwise flutter (Figure 32-10). In clockwise flutter, the flutter waves are negative in V₁ and positive in leads II, III, and aVF. The ventricular rate depends on the ability of the AV node to conduct to the ventricle. If the AV node is not diseased, conduction can occur on a 2:1 basis, resulting in a ventricular rate of approximately 150 bpm. In rare circumstances, 1:1 conduction during atrial flutter may occur. If the AV node is diseased, then conduction to the ventricles can be in a 4:1 ratio, with a ventricular rate of approximately 75 bpm, or even slower. AV nodal blocking drugs will also slow the ventricular rate during atrial flutter.

Atrioventricular nodal reentrant tachycardia (AVNRT) is a narrow complex tachycardia with a rate usually ranging from 150 to 250 bpm. The AV node has two pathways, a slowly conducting pathway with a short refractory period and a fast-conducting pathway with a long refractory period (Figure 32-11A). In sinus rhythm, the fast pathway is utilized. When a precisely timed premature atrial beat occurs, it can be blocked from conducting antegrade down the fast pathway owing to refractoriness within the fast pathway. This premature atrial beat then conducts slowly down the slow pathway. By the time the impulse reaches the His-Purkinje system, the fast pathway has recovered excitability and the impulse not only travels antegrade through the His-Purkinje system to the ventricle but also conducts retrograde up the fast pathway to the atrium. This creates the slow–fast reentrant circuit otherwise known as “typical AVNRT.” Because the atria and ventricles are activated simultaneously, the P wave is buried within the narrow QRS and therefore is not easily identified on ECG. A “pseudo-r” wave in lead V₁ and “pseudo-s” wave in the inferior leads represent the retrograde P wave (Figure 32-11B). If the onset of the arrhythmia is captured, the ECG will show a long PR interval or “jump” (as illustrated in the second schematic of panel A in Figure 32-11), representing the premature atrial beat traveling down the slow pathway.⁵ The onset and termination of typical AVNRT are abrupt.

Atypical AVNRT occurs when antegrade conduction is down the fast pathway and retrograde conduction is up the slow pathway. Since ventricular activation occurs before atrial activation, the ECG demonstrates inverted P waves in the inferior leads and a long RP interval (Figure 32-12).

AV reciprocating tachycardia is a macro-reentrant tachycardia utilizing the normal His-Purkinje system in the antegrade direction and an accessory pathway in the retrograde direction. During sinus rhythm in patients with manifest Wolff-Parkinson-White (WPW) syndrome, simultaneous conduction down the accessory pathway and AV node produces a short PR interval and a delta wave (slurred upstroke of the QRS) on a 12-lead ECG (Figure 32-13). The initial slurred upstroke of the QRS complex is the delta wave, and this represents ventricular activation by the accessory pathway. However, in many cases, the accessory pathway does not conduct in the antegrade direction and can only function in a retrograde fashion. This is called a “concealed” accessory pathway and no delta wave is present in sinus rhythm. As the accessory pathway is still capable of conducting retrograde, supraventricular tachycardia (SVT) can still occur.

A premature atrial or ventricular beat can initiate AV reciprocating tachycardia, also referred to as “orthodromic tachycardia” (Figure 32-14). Orthodromic AV reciprocating tachycardia is the most common type of tachycardia using an accessory pathway. This is a narrow complex tachycardia that conducts antegrade down the AV node and retrograde activation up the accessory pathway, which produces a retrograde P wave within the ST segment. The delta wave is not seen in orthodromic AV tachycardia since the accessory pathway is being utilized in the retrograde direction. The ventricular rate typically ranges from 180 to 220 bpm.

In antidromic reciprocating tachycardia, there is antegrade conduction down the accessory pathway with retrograde conduction up the His-Purkinje system and AV node. This produces a wide QRS complex on the ECG.

Nonparoxysmal junctional tachycardia is thought to be due to enhanced automaticity in or near the bundle of His.⁶ The ventricular rate ranges from 70 to 120 bpm. The tachycardia has a gradual onset and termination. There can be retrograde conduction up the AV node to capture the atrium and ventricle simultaneously, resulting in inverted P waves in leads II, III, and aVF, which can occur before or after the QRS (Figure 32-15). When the retrograde P wave is before the QRS complex, the PR interval is short and less than 120 milliseconds. This may look similar to AV nodal reentry and often cannot be easily distinguished from this arrhythmia, especially if the onset of the tachycardia is not available.

Focal atrial tachycardia has an atrial rate ranging from 150 to 200 bpm (Figure 32-16). Focal atrial tachycardia arises from a single location in either the right or left atrium. The most common site of origin in the right atrium is from the crista terminalis.⁷ The ostium of the pulmonary veins is the most common site in the left atrium.⁸ Depending on the site of origin, the P-wave morphology may or may not be similar to the sinus P wave. If the origin is at the superior aspect of the crista terminalis, the P wave will be similar to the sinus P wave and therefore it might be difficult to distinguish this from sinus tachycardia. There is generally an abrupt onset and termination, with acceleration and deceleration occurring over 3 to 4 beats. Typically, focal atrial tachycardia has a long RP interval, but as the rhythm accelerates, this interval may shorten.

Multifocal atrial tachycardia may be seen in patients with diseased atria, who may also have acute or chronic lung disease. There are multiple areas within the atria that have abnormal or ectopic foci. The ECG will therefore have at least three morphologically different P waves. The PR interval varies because the foci that generate the P waves arise from different locations in the atria, at varying distances from the AV conduction system (Figure 32-17). The R-R interval can also vary with this rhythm, and it may often be confused with atrial fibrillation owing to its irregularity. Close observation will reveal distinct P waves of varying morphologies, distinguishing this from atrial fibrillation.

Sinus tachycardia is a physiological response by the body to stress with a “flight-or-fight” response. Other causes include fever, volume depletion, shock, sepsis, hyperthyroidism, hypoxia, anemia, chronic pulmonary disease, and acidosis, to name a few.

Atrial flutter can occur in patients with congenital heart disease (septal defects), pulmonary disease, hyperthyroidism, or myocardial infarction or after atrial fibrillation ablation. It may also be seen after cardiac surgery or can be idiopathic in the absence of known structural heart disease.

Most patients with AVNRT and AVRT do not have any underlying structural heart disease. These arrhythmias are most often seen in otherwise young, healthy individuals. However, the first detection may occur in patients who are hospitalized unexpectedly for other medical problems.

Nonparoxysmal junctional tachycardia may be a marker for a serious underlying condition. It occurs during digoxin toxicity, acute MI, myocarditis, and hypokalemia and following open-heart surgery.

Focal atrial tachycardia can occur in structurally normal or abnormal hearts (ischemic or nonischemic cardiomyopathies) and can be seen in patients with obstructive lung disease. It can occur with electrolyte abnormalities and drug toxicity, such as with digoxin or theophylline. Multifocal atrial tachycardia is often seen in patients with either acute or chronic lung diseases such as pneumonia, pulmonary embolism, or chronic obstructive pulmonary disease. Medications (theophylline), electrolyte abnormalities (hypokalemia or hypomagnesemia), myocardial infarction, and sepsis can exacerbate multifocal atrial tachycardia.

Carotid sinus massage or adenosine can slow or block conduction through the AV node, which helps identify the arrhythmia mechanism for various supraventricular arrhythmias (Figure 32-18). During these maneuvers, a 12-lead ECG or rhythm strip should be recorded continuously. If the arrhythmia terminates abruptly with adenosine, it is most likely AVNRT, AVRT, or occasionally focal atrial tachycardia. If the ventricular rated during the arrhythmia slows but fails to terminate and multiple P waves are visualized for each QRS complex, then the arrhythmia represents atrial flutter or atrial tachycardia. The tachycardia will continue in the atrium, as the ventricles are not required as part of the reentrant circuit. Adenosine or other AV blocking agents will block in the AV node, allowing better identification of the underlying P-wave or flutter-wave morphology. It should also be noted that AV block will occur when adenosine is administered in sinus rhythm. Figure 32-19 demonstrates temporary high-grade AV block after adenosine administration.

Since sinus tachycardia is a physiologic response to stress, management would involve identifying and treating the underlying cause. β Blocker therapy is generally not used to treat sinus tachycardia except in special circumstances, such as acute myocardial infarction, thyrotoxicosis, and congestive heart failure.

For a hemodynamically unstable patient with atrial flutter, emergent synchronized cardioversion with low energy (25-100 joules) may be required to convert the rhythm to sinus. Intravenous ibutilide can also emergently convert atrial flutter to sinus rhythm. Ibutilide does carry a low risk of prolonging the QT interval and causing torsades de pointes. Therefore, ibutilide should only be used by trained personnel in an intensive care or other closely monitored settings. Anticoagulation status needs to be considered before attempted conversion, as detailed below.

Most patients with atrial flutter are hemodynamically stable. Rate control can be achieved with AV nodal blocking agents. Conversion to sinus rhythm can be achieved through overdrive pacing or external direct-current (DC) cardioversion, or pharmacologically with antiarrhythmic drugs, including class IA, IC, or III agents. It should be noted that class I and class III drugs can also slow the flutter rate in the atrium, making it more likely that 1:1 atrioventricular conduction might occur. Therefore, an AV nodal blocking drug (such as a β blocker or calcium channel blocker) should typically be used with these membrane-active antiarrhythmic agents. As with atrial fibrillation, atrial flutter has been associated with thrombus formation and increased risk of stroke.^{9, 10} Therefore, patients with atrial flutter should be anticoagulated in the same manner as those with atrial fibrillation. If the duration of the atrial flutter is unknown or greater than 48 hours, anticoagulation is required 3 weeks before and 4 weeks after cardioversion, including electrical or pharmacologic conversion.¹¹ If the arrhythmia duration is unknown or longer than 48 hours and more urgent conversion is needed, transesophageal echocardiography is indicated to first exclude left atrial thrombus.

AVNRT relies on the AV node for continuation of the arrhythmia. For acute termination of the arrhythmia in an unstable patient, DC synchronized cardioversion with 150 to 200 joules may rarely be required. For a stable patient with AVNRT, blocking the AV node with vagal maneuvers (such as carotid massage or Valsalva) can terminate this arrhythmia. Adenosine works by prolonging AV nodal conduction. Adenosine 6 mg intravenous (IV) bolus followed by 12 mg IV, if the first dose is unsuccessful, usually terminates the arrhythmia. It should be noted that smaller doses may be utilized for termination of the arrhythmia if adenosine is administered centrally. The drug should be infused as close as possible to the skin (rather than through a port in an IV line far from the patient), as this drug has a very short half-life. Calcium channel blockers (such as verapamil or diltiazem) or β blockers are generally used if adenosine fails to terminate the arrhythmia. These calcium channel blockers and β blockers can also be used to prevent recurrences. For long-term treatment of AVNRT, catheter ablation is an option for “cure.”

Wolff-Parkinson-White syndrome is defined as the WPW pattern on ECG in conjunction with a tachyarrhythmia (80% AVRT, 15%-30% atrial fibrillation, 5% atrial flutter). Vagal maneuvers and adenosine slow and block the conduction through the AV node and should be used as first-line therapy to terminate orthodromic AVRT, which has a narrow QRS complex. If the patient does not have congestive heart failure, intravenous verapamil can be used with a 5-mg bolus every 10 to 15 minutes for a total of 15 mg. Direct-current cardioversion can be employed if vagal maneuvers or adenosine fails to work, although this is very rarely needed.

Accessory pathways can rapidly conduct in an antegrade fashion to the ventricles during antidromic AVRT (which has a wide complex tachycardia). If antidromic AVRT is suspected, then AV nodal blocking agents including verapamil are contraindicated. Intravenous procainamide should be given with a loading dose of 10 mg/kg over 25 minutes followed by 1 to 4 mg/min continuous infusion. As procainamide can cause hypotension, close blood pressure monitoring is required during the infusion. The dose must be adjusted for renal dysfunction. If the patient is hemodynamically unstable, immediate cardioversion should be utilized.

Atrial fibrillation can also occur in the setting of WPW syndrome and may conduct very rapidly down the accessory pathway, which can degenerate into ventricular fibrillation. Atrial fibrillation in a patient with WPW syndrome should be treated with intravenous procainamide or ibutilide. If the patient is hemodynamically unstable, DC cardioversion is recommended.

With respect to long-term treatment, catheter ablation is curative therapy for patients with Wolff-Parkinson-White syndrome and supraventricular tachycardia. For those who decline catheter ablation, antiarrhythmic drugs can be used.

The management for nonparoxysmal junctional tachycardia should be aimed at treating the underlying condition. When digoxin is the offending agent, the drug should be withheld. In the setting of digoxin toxicity, ventricular arrhythmias or AV block may occur, and digoxin-specific antibody Fab fragments should be initiated. Hyperkalemia in digoxin toxicity has a 50% mortality rate when the levels are between 5.0 and 5.5 mEq/dL.¹² Therefore, a potassium level greater than 5.0 mEq/dL is an indication for digoxin-specific antibody Fab fragment therapy. Efforts should be made to correct hypokalemia or hypomagnesemia. An accelerated junctional tachycardia can occur during or after an acute myocardial infarction; therefore, ischemia should also be ruled out as a cause of the nonparoxysmal junctional tachycardia.

Focal atrial tachycardia may be difficult to treat medically. The mechanism of this arrhythmia may be a result of abnormal automaticity, triggered activity, or reentry.¹³ Direct-current cardioversion is seldom successful. Adenosine can terminate some atrial tachycardias, depending on the arrhythmia mechanism.¹⁴ β Blockers and calcium channel blockers can be used to control the ventricular rate and may terminate the arrhythmia. Class IC (flecainide) and class III (sotalol and amiodarone) agents may be effective in terminating this arrhythmia.¹⁵ Coronary artery disease must be excluded prior to initiation of a class IC antiarrhythmic drug. Because of potential drug side effects and the high success rate of catheter ablation, ablation is often a good option for patients with incessant focal atrial tachycardia.¹¹

What Are the Risks for Developing Atrial Fibrillation?

Atrial fibrillation is the most common arrhythmia seen in the intensive care unit setting, particularly in the elderly.^{16, 17} Risk factors for developing atrial fibrillation include hypertension, coronary artery disease, diabetes, valvular heart disease, and heart failure. Atrial fibrillation can also occur in patients with structurally normal hearts. Reversible causes of atrial fibrillation include hypoxia, cardiac ischemia, infection, hyperthyroidism, electrolyte disturbances, drugs (such as theophylline and digitalis), alcohol, sleep deprivation, obesity, and increased sympathetic tone. One must always consider an acute pulmonary embolism as the cause of atrial fibrillation, and this arrhythmia may rarely be the only sign. Atrial fibrillation is frequently seen in the postoperative period following cardiac and noncardiac surgery. In one study the incidence of postoperative atrial fibrillation following noncardiac surgery was 4.1%.¹⁸ There is a 10% to 65% incidence of atrial fibrillation following open-heart surgery.¹⁹

How Is Atrial Fibrillation Classified?

According to the ACC/AHA/European Society of Cardiology (ESC) guidelines, atrial fibrillation is classified as paroxysmal, persistent, or permanent.²⁰ Paroxysmal atrial fibrillation is defined as recurrent atrial fibrillation (two or more episodes) that terminates spontaneously within 7 days. Persistent atrial fibrillation applies to recurrent atrial fibrillation with a duration of longer than 7 days that is not self-terminating. Persistent atrial fibrillation can terminate spontaneously after 7 days or can be cardioverted, either electrically or pharmacologically. Atrial fibrillation is considered “long-standing persistent” if it is present for longer than 1 year. It is considered “permanent” if cardioversion has failed or has not been attempted. The term “lone” atrial fibrillation has been used to apply to patients younger than 60 years old without evidence of structural heart disease.

How Would You Evaluate a Patient with Atrial Fibrillation?

Atrial fibrillation may be symptomatic or asymptomatic. The patient should be questioned regarding symptoms of palpitations, shortness of breath, lightheadedness, fatigue, or chest pain. History should also include the presence or absence of known heart disease, other contributing diseases, family history of atrial fibrillation, current medications, and social history (particularly alcohol intake). However, the patient may be intubated and unable to give any history.

It is important to determine the duration of the atrial fibrillation to help guide management, as this is related to the need for anticoagulation and safety of cardioversion. In addition to a 12-lead ECG, a transthoracic echocardiogram is indicated to evaluate for valvular abnormalities, left atrial size, left ventricular systolic function, and wall thickness, which will help guide medical therapy. For atrial fibrillation of unknown duration or lasting longer than 48 hours with plans for cardioversion, a transesophageal echocardiogram is recommended to exclude left atrial appendage thrombus. Transesophageal echocardiography may also occasionally aid in the diagnosis of a large pulmonary embolism. If the patient has an implantable pacemaker or defibrillator, interrogation of the device may help determine the duration of the atrial arrhythmia. A chest x-ray can also be performed to exclude an infectious process.

What Are the ECG Findings of Atrial Fibrillation?

The ECG will not show P waves, but rather “fibrillatory” waves. The ventricular rate typically ranges from 100 to 170 bpm with irregular R-R intervals in the absence of AV nodal blocking drugs. If there is normal conduction through the AV node, the QRS complex will be narrow. A wide QRS complex during atrial fibrillation represents either a preexisting bundle branch block, a rate-related aberrancy, or conduction through an accessory pathway. Comparison with an old ECG is always helpful.

How Do You Treat Atrial Fibrillation?

Indications for immediate cardioversion include hemodynamic compromise (hypotension), pulmonary edema, cardiac ischemia, or WPW syndrome with very rapid conduction down the accessory pathway. Direct-current cardioversion is painful and requires the patient to be heavily sedated with a short-acting anesthetic. The external defibrillator should be synchronized to the QRS complex to prevent induction of ventricular fibrillation during electrical conversion of atrial fibrillation. The starting energy for conversion of atrial fibrillation is 100 joules, with energies up to 360 joules if initial attempts are unsuccessful. Intravenous ibutilide can also result in conversion to sinus rhythm, but it must be administered cautiously in a monitored setting by trained personnel because of the risk of hypotension and torsades de pointes.

If the patient is hemodynamically stable, the determination of rate vs rhythm control should be made along with decisions regarding anticoagulation and timing of conversion. Anticoagulation status and the need for transesophageal echocardiography have been previously discussed in the atrial flutter section, and this also pertains to atrial fibrillation. Anticoagulation should be continued for at least 4 weeks after cardioversion. The timing and duration of anticoagulation are detailed in the ACC/AHA/ESC guidelines and summarized in Table 32-4.²⁰ Attempts at conversion to sinus rhythm are contraindicated if transesophageal echocardiography demonstrates the presence of left atrial thrombus. In this case, therapeutic anticoagulation should be continued for at least 4 weeks until the thrombus resolves. Repeat transesophageal echocardiography can be performed to document resolution of the thrombus prior to cardioversion. The risks and benefits of anticoagulation must always be taken into account when determining plans for rhythm vs rate control and whether or not cardioversion will be attempted. If a patient is not considered a candidate for even short-term anticoagulation, cardioversion should not be attempted.

If rate control is elected, a β blocker, calcium channel blocker (verapamil or diltiazem), or digoxin can be utilized. To obtain adequate rate control, more than one agent may be required. Standard drugs and dosing regimens are outlined in Table 32-5.

Digoxin is renally excreted and the dose should be adjusted based on the patient's creatinine clearance. Digoxin is less effective in states of increased sympathetic tone and therefore may not significantly slow the ventricular rate in a shock state. Calcium channel blockers have a negative inotropic effect and are therefore contraindicated in patients with decompensated congestive heart failure or severe left ventricular systolic dysfunction. β Blockers should be avoided in patients with asthma or severe chronic obstructive pulmonary disease.

Intravenous amiodarone can be used if pharmacologic cardioversion is desired. Pharmacologic cardioversion carries a similar risk of thromboembolism as electrical cardioversion. Therefore, a transesophageal echocardiogram should be performed to rule out intracardiac thrombus before initiating any antiarrhythmic drugs in the absence of an adequate duration of anticoagulation. The loading dose of amiodarone is a 150-mg bolus over 10 to 15 minutes followed by a continuous infusion of 1 mg/min for the first 6 hours, then 0.5 mg/min for the next 18 hours. Amiodarone may cause hypotension, requiring the dose to be decreased or the infusion to be discontinued. Amiodarone's potential side effects include hepatic, pulmonary, and thyroid toxicities. Baseline liver function and thyroid function tests should be performed. Pulmonary function tests would not be feasible in a critically ill patient, but a chest x-ray should be examined for any serious underlying pulmonary disease. Before beginning any antiarrhythmic medication, a cardiology or electrophysiology consultation should be considered.

Wide complex tachycardias can be either of ventricular or supraventricular origin. Supraventricular tachycardias can have a wide QRS complex if there is a preexisting bundle branch block, a rate-related bundle branch block, or an accessory pathway. Antiarrhythmic agents can also prolong the QRS duration, and sometimes greater widening of the QRS may be evident at faster heart rates, particularly if the patient is taking a class IC antiarrhythmic drug. Tachycardias of ventricular origin include monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation.

Approximately 80% of wide complex tachycardias are ventricular tachycardias (VTs), with more than 95% of these patients having had a prior MI.^{21, 22} A potentially fatal mistake is the misdiagnosis of a monomorphic ventricular tachycardia as a supraventricular tachycardia and treating it with AV nodal blocking drugs, such as calcium channel blockers. This may result in hypotension and degeneration of VT to ventricular fibrillation in a patient with VT. Therefore, whenever a wide complex tachycardia is encountered, it should be presumed to be VT until proven otherwise.

The ECG characteristics can help to distinguish VT from supraventricular tachycardia with aberrancy. Features that favor VT but that are not always seen on the ECG are AV dissociation, marked change in axis, precordial concordance, and fusion or capture beats.²³ AV dissociation, capture and fusion beats, and precordial concordance are demonstrated in Figure 32-21. If the patient is hemodynamically stable, it is important to obtain a 12-lead ECG to aid in diagnosis. A comparison with an old ECG should be attempted if one is available, although this may not always be feasible at the time of presentation.

Monomorphic VT can occur in the setting of myocardial scar, including a left ventricular aneurysm, or in the setting of a structurally normal heart. Monomorphic VT may be sustained or nonsustained. Nonsustained monomorphic VT is defined as three or more consecutive ventricular beats at a rate of greater than or equal to 100 bpm lasting less than 30 seconds. Sustained monomorphic VT lasts longer than 30 seconds or results in hemodynamic compromise prior to that time. Ventricular tachycardia arises from the ventricular myocardium and therefore has a wide QRS complex, but this is not a “typical” bundle branch block appearance compared to a supraventricular tachycardia with aberrancy or a preexisting bundle branch block.

There are certain ECG criteria to help distinguish VT from SVT with aberration²⁴ (Table 32-6). For VT with a right bundle branch morphology, the QRS duration is usually greater than 140 milliseconds with the R-to-S ratio less than 1 in V₆. VT with a left bundle branch morphology generally has a QRS duration of greater than 160 milliseconds, an R-wave duration in V₁ of less than 30 milliseconds, the onset of the R wave to the nadir of the S wave in lead V₁ greater than 60 milliseconds, or notching of the S wave in V₁ or V₂.²⁵ If the QRS complexes are either all-positive or all-negative (known as concordance) in the precordial leads (V₁-V₆), this would be more consistent with VT (Figure 32-21D). AV dissociation in VT exists because the atria and ventricles are firing at different rates without any relationship between the two (Figure 32-21A). Fusion beats represent simultaneous activation from a supraventricular and ventricular origin resulting in a QRS complex that has a combined morphology of the ventricular tachycardia and a normal sinus QRS complex (Figure 32-21B). Capture beats are sinus or supraventricular beats that conduct to the ventricle with a narrow QRS complex during ventricular tachycardia (Figure 32-21C).

An accelerated idioventricular rhythm can also frequently be seen in the ICU setting (Figure 32-22). This may be related to ischemia or reperfusion. The rate is typically less than 100 bpm and the rhythm has a wide complex. The ECG criteria used to distinguish this rhythm from SVT with aberrancy are identical to those criteria used for VT with a more rapid rate.

Polymorphic VT has wide QRS complexes that have varying morphologies and often phasic variation in axis around the baseline. The ventricular rate ranges from 150 to 250 bpm. Polymorphic VT can be associated with a normal or prolonged QT interval (Figure 32-23). When preceded by a long QT interval, this is referred to as “torsade de pointes,” or twisting of the points (Figure 32-23A). Polymorphic VT associated with ischemia may be associated with a normal QT interval (Figure 32-23B).

Prolonged QT intervals can be acquired or congenital. Certain drugs and electrolyte abnormalities can prolong the QT interval and predispose to torsades de pointes. Table 32-7 outlines some major drug categories that can lead to QT prolongation and torsades de pointes. An extensive list of drugs that can cause prolongation of the QT interval is available on the website www.torsades.org. Polymorphic VT with a long QT interval can develop during periods of bradycardia or a pause that follows a premature beat. In patients with congenital long QT syndrome, the development of polymorphic VT or torsades de pointes may occur during periods of adrenergic stress, such as sudden awakening, exertion, or emotional stress in some patients. Central nervous system injury, including brain tumor, may also result in QT prolongation with diffuse T-wave inversion.

Supraventricular tachycardia can present with a wide QRS complex and can mimic VT. When the heart rate accelerates, conduction can be delayed in one of the bundle branches, leading to right or left bundle branch block. Sometimes P waves can be seen preceding the wide QRS complexes. The relationship between P waves and QRS complexes will not be helpful if the patient is in atrial fibrillation. If atrial fibrillation conducts aberrantly, the rhythm would be irregularly irregular. On occasion, patients with WPW syndrome can also have atrial fibrillation with rapid conduction down the accessory pathway, and this may also mimic VT. However, there is often marked beat-to-beat variation in the width and morphology of the QRS complexes in patients with preexcited atrial fibrillation (Figure 32-24). The latter rhythm may be extremely rapid and potentially life threatening, as the accessory pathway does not have the normal “slowing” properties of the AV node and very rapid rates can bombard the ventricle, degenerating into ventricular fibrillation.

Electrolyte abnormalities including hypokalemia, hypomagnesemia, and hypocalcemia can, either alone or in combination, precipitate ventricular arrhythmias. Electrolytes should be aggressively repleted. A 12-lead ECG should be obtained and the QT interval measured. The patient's medication list should be checked for any QT-prolonging drugs. Ischemia, hypoxia, and acid-base disturbances should also be excluded. Some patients in the ICU setting may be receiving catecholamines for hemodynamic support. Endogenous or exogenous catecholamines are known to precipitate ventricular arrhythmias. When exogenous catecholamines are thought to be the culprit, the dose should be lowered or discontinued if feasible. Intravascular catheters should be checked for correct placement within the heart, as mechanical irritation between the catheter and the ventricular myocardium can induce ventricular ectopy, nonsustained VT, or sustained VT.

Nonsustained VT can occur in structurally abnormal hearts (ischemic heart disease, hypertrophic heart disease, valvular disease, dilated cardiomyopathy) or in structurally normal hearts. Nonsustained ventricular arrhythmias in the setting of an acute myocardial infarction may be related to ischemia or reperfusion, and this appears to have no long-term adverse prognostic significance. On the other hand, the presence of nonsustained VT occurring greater than 72 hours after an MI appears to portend a worse prognosis. Ventricular tachycardia occurring greater than 1 week after an MI on ambulatory monitoring has been associated with increased mortality rate and increased risk for sudden cardiac death.²⁶ The presence of nonsustained VT and reduced left ventricular systolic function are well-established independent predictors of mortality after an MI.²⁷

Sustained ventricular arrhythmias may be seen in patients with ischemic heart disease and acute MI. Sustained monomorphic VT occurring greater than 48 hours after an MI is a strong independent predictor of 6-week mortality.²⁸ Sustained ventricular arrhythmias complicate 2% to 20% of acute MIs and are associated with increased in-hospital mortality rate.²⁹ However, it has been suggested that sustained VT/ventricular fibrillation (VF) in the peri-infarct period (24-48 hours) is not associated with any increased long-term mortality risk, although this is still somewhat controversial.^{30, 31} Both early (< 2 days) and late (> 2 days) occurrences of sustained VT and VF were associated with a higher risk of later mortality in the Global Utilization of Streptokinase and TPA for Occluded Arteries-1 (GUSTO-1) study (P < .001).³¹ Among patients who survived hospitalization in this study, no significant difference was found in 30-day mortality rate between the VT/VF and no VT/VF groups, although after one year, the mortality rate was significantly higher in the VT alone and VT/VF groups (P < .0001).³¹

There are some types of “idiopathic” VT—right ventricular outflow tract (RVOT) VT, left ventricular outflow tract (LVOT) VT, or left ventricular fascicular VT—that may first be identified during monitoring in the ICU. These arrhythmias are considered benign in nature, with low risk of sudden cardiac death occurring in the setting of a structurally normal heart. Salvos of monomorphic VT arising from the RVOT are illustrated in Figure 32-25. These arrhythmias are often effectively treated with a β blocker or calcium channel blocker.

The primary treatment for nonsustained VT is first to evaluate for potential causes. Reversible causes, such as electrolyte abnormalities or ischemia, should first be addressed. If the VT is mildly symptomatic in the setting of a structurally normal heart without underlying coronary artery disease, a trial of a β blocker may be considered. β Blockers are also useful for primary prevention of sudden cardiac death in patients with asymptomatic ventricular ectopy or nonsustained VT in the setting of reduced left ventricular systolic function. Although membrane-active antiarrhythmic agents may be useful in suppression of ventricular ectopy, these are not recommended in the setting of underlying structural heart disease because of potential adverse effects or proarrhythmia. “Proarrhythmia” is more common in patients with underlying structural heart disease, reduced left ventricular function, or coronary disease. When antiarrhythmic agents were used to suppress ventricular ectopy in a multicenter clinical trial, Cardiac Arrhythmia Suppression Trial (CAST), the study was terminated prematurely because there was an increased mortality rate in the treated group.³² In some situations, particularly in the absence of structural heart disease or with recurrent VT requiring frequent implantable cardioverter defibrillator shock therapy, catheter ablation should be considered if medications are not tolerated or are ineffective.²²

In hemodynamically stable sustained monomorphic VT, a 12-lead ECG, history, and laboratory studies should be performed. The history should include questions regarding ischemic heart disease, prior MI, and drug therapy, particularly with antiarrhythmic drugs. Identification of reversible causes, such as ischemia or hypokalemia, should be evaluated and treated. Treatment options include synchronized DC cardioversion with sedation and/or IV antiarrhythmic drugs (amiodarone, procainamide, lidocaine). A bolus of amiodarone 150 mg over 10 minutes followed by a continuous infusion of 1.0 mg/min for 6 hours, then 0.5 mg/min may be administered. Intravenous amiodarone can cause hypotension, which requires a dose reduction or discontinuation of the drug. If VT is thought to be ischemic in nature, then IV lidocaine may be effective.³³ Lidocaine is dosed at a 1- to 1.5-mg/kg bolus over 2 to 3 minutes with a continuous infusion at 1 to 4 mg/min. Lidocaine can cause neurotoxicity, which is dose-dependent. Monitoring of daily lidocaine levels may be useful, particularly in the setting of hepatic disease or a low cardiac output state. Hemodynamically unstable monomorphic VT or pulseless VT should be treated promptly with DC cardioversion.

Sustained polymorphic VT is an unstable and hemodynamically poorly tolerated rhythm, and prompt DC cardioversion is required. Once cardioverted, the QT interval should be measured. If the QT interval is normal, acute ischemia should be suspected and urgent angiography may be considered. Administration of β blockers to reduce ischemia should also be considered. If the QT interval is prolonged, any QT-prolonging drugs should be discontinued and any electrolyte abnormalities corrected. If bradycardia or pause-dependent polymorphic VT is suspected, pacing or IV isoproterenol should be initiated. For patients with congenital long QT syndrome and torsades de pointes, β-blocker therapy should be initiated and an implantable defibrillator should be strongly considered for prevention of sudden cardiac death.

In the case presented in this section, the rhythm was effectively terminated following administration of IV amiodarone. Echocardiography following conversion revealed moderate left ventricular systolic dysfunction with a left ventricular ejection fraction of 42%, anterior hypokinesis, and mild mitral regurgitation. Diagnostic catheterization revealed no change in anatomy with patent grafts and a patent stent. The patient underwent insertion of an implantable cardioverter-defibrillator for secondary prevention of sudden cardiac death.