Sinus Node

The normal heartbeat arises from the SA node that serves as the pacemaker of the heart under normal conditions. Bradycardia resulting form SA node dysfunction originates from either failure of impulse generation or failure of impulse conduction. In the past, the term “sick sinus syndrome” has been used to describe a variety of sinus bradyarrhythmias with many etiologies. More appropriate classification of SA node dysfunction includes inappropriate sinus bradycardia, sinus pause or arrest, sinus exit block, and bradycardia-tachycardia syndrome.

Sinus bradycardia (heart rate <60) does not necessarily imply SA node dysfunction, and even a heart rate less than 40 at rest can be asymptomatic in well-trained athletes. Sinus bradycardia is considered pathologic when patients are symptomatic or when there is failure to appropriately increase heart rate during activity or exercise. Sinus pause or arrest occurs when the SA node transiently fails to exhibit automaticity and does not fire. Sinus exit block similarly results in a pause but the SA node does fire. The impulse is either delayed or fails to propagate beyond the SA node, resulting in failure of atrial depolarization. Bradycardia-tachycardia syndrome refers to sinus node dysfunction with both bradycardia and tachycardia. Typically bradycardia episodes follow the termination of tachycardia events and can be associated with clinical symptoms of presyncope or syncope. Management can be challenging, as pharmacotherapy to treat fast rhythms predisposes to slow ones and vice versa. Commonly, insertion of a pacemaker for the symptomatic bradycardia, in conjunction with pharmacological treatment for the tachycardia, is required.

Treatment for SA node dysfunction depends on the clinical status of the patient and presumed etiology. If the bradycardia is transient and not associated with hemodynamic compromise, no therapy is necessary. Correction of any metabolic abnormalities, minimizing vagal-inducing maneuvers, and removal or dose reduction of medications such as beta-blockers, calcium channel antagonists, and lithium may be necessary. If the bradycardia is sustained or severe enough to cause hemodynamic instability, therapy with anti-muscarinic agents (atropine) or beta-agonist (isoproterenol) may be initiated. Percutaneous or transvenous pacing may be necessary in some patients in the acute setting and can be a bridge to permanent pacemaker placement. Patients that are relatively stable but are symptomatic from sinus node dysfunction virtually always require permanent pacing.

Atrioventricular Node

Disturbances in conduction through the AV node or His-Purkinje system are classified as atrioventricular blocks. These may be temporary or permanent, depending on the etiology of the delayed conduction. In adults, the most common causes are drug toxicity, coronary artery disease, and degenerative disease of the conduction system. Many other conditions, such as electrolyte disturbances, myocarditis, sarcoidosis, scleroderma, and hypervagal responses, can cause AV block. The P-R interval is a measure of the conduction time through the AV node and bundle of His. When the P-R interval is prolonged (>210 milliseconds), a patient has first-degree AV block. Second-degree AV block is when intermittent failure of the conduction of the impulse to the ventricles occurs. In Mobitz type I, second-degree AV block (Wenckebach block), there is progressive prolongation of the P-R interval until failure of conduction to the ventricle occurs (Figure 1). The P-R interval then shortens following the dropped beat. This failure in conduction originates from the AV node itself and the QRS complex remains narrow. In Mobitz type II, second-degree AV block, there is intermittent failure of conduction reaching the ventricles that is not associated with progressive prolongation of the P-R interval. There is not a shortened P-R interval following the dropped beat. This failure in conduction is considered “infranodal” and originates from the His-Purkinje system. The QRS complex may be prolonged, and this type of AV block is more concerning. There is a significant likelihood of progression to complete heart block associated with inadequate ventricular response with this rhythm. Third-degree or complete heart block results from failure of all impulses through the AV node and His-Purkinje system, resulting in atrioventricular disassociation. The ventricles rely on their innate automaticity which produces a typical wide QRS escape rhythm between 40 and 50 beats per minute. The atrial rate is commonly faster, producing multiple P waves with no relationship to the ventricular QRS complexes (Figure 2).

Figure 1 Rhythm strip shows progressive P-R prolongation and a subsequent “dropped” QRS complex, followed by shortening of the P-R interval which is diagnostic of Mobitz type I, second-degree AV block.

Figure 2 Rhythm strip shows atrial P waves and ventricular QRS complexes occurring at different rates and with no relationship between them, which is characteristic of third-degree AV block.

Management of AV block depends on the hemodynamic stability of the patient, the transient nature of the dysrhythmia, and where the focus originates from within the conduction system. Acute pharmacotherapy relies upon atropine and isoproterenol. Isoproterenol use should be avoided in patients with ischemia heart disease because of the associated increase in myocardial oxygen demand. There is no long-term pharmacotherapy for AV block, and removal of any of the common offending agents, such as digitalis or beta-blockers, should first be attempted. Temporary pacing is used for those with ongoing instability, and permanent pacing is typically required for Mobitz type II second-degree AV block and third-degree AV block.

Sinus Tachycardia

Sinus tachycardia should be considered a physiological reflex rather than a true dysrhythmia, but it is an important sign for which the etiology must be sought. Fever, hypovolemia, and anemia all appropriately increase heart rate to at least maintain or increase cardiac output. Blunting this reflex with pharmacotherapy without knowledge of the etiology can be dangerous. Thyrotoxicosis, pheochromocytomas, or side effects of sympathomimetic drugs also cause sinus tachycardia without regard for reflex mechanisms. The primary goal for management of sinus tachycardia is to find and appropriately treat the confounding condition. Sinus tachycardia will resolve with resolution of this inciting process.

Paroxysmal Supraventricular Tachycardia

The term “paroxysmal supraventricular tachycardia” actually describes a diverse group of tachyarrhythmias, the two most common being atrioventricular nodal re-entry tachycardia (AVNRT) and atrioventricular re-entry tachycardia (AVRT). They both have in common dual conduction pathways, each with different rates of conduction. As described previously, this allows for the possibility of re-entry and the potential for a self-propagating tachyarrhythmia focus. In AVNRT, the two pathways reside in or around the AV node itself. Antegrade conduction typically occurs through the slower pathway, while the retrograde conduction occurs through the faster pathway. Rates of 140–220 beats/min are typical, and P waves are not seen on ECG since retrograde atrial activation and antegrade ventricular activation occur simultaneously. The QRS complex is typically narrow because the antegrade conduction to the ventricles uses the normal AV node and His-Purkinje system. In comparison, AVRT also has two conduction pathways, but the additional pathway is remote from the AV node and resides in the atrioventricular groove, where it is commonly referred to as an “accessory pathway.” Similar to AVNRT, antegrade conduction occurs through the AV node and His-Purkinje system, while retrograde conduction occurs via the accessory pathway. The QRS complex for AVRT is also narrow, and since the accessory pathway only conducts retrograde, it is not seen on ECG and is considered “concealed.”

Acute management depends on the stability of the patients with paroxysmal supraventricular tachycardia. Urgent direct-current cardioversion is indicated when myocardial ischemia, acute heart failure, or hypotension result. In hemodynamically stable patients, pharmacological intervention with the intent to slow or break AV nodal conduction is the mainstay of treatment. Intravenous adenosine is the first-line drug of choice due to its potent yet short-lived depressant effects on AV nodal conduction. Adenosine will successfully terminate greater than 90% of tachyarrhythmias due to AVNRT and AVRT. Calcium channel blockers or beta-blockers (verapamil/diltiazem or metoprolol) are also useful, particularly when adenosine is not successful, although they should be used with caution due to possible hypotensive and bradycardic effects.

When the accessory pathway has the potential for antegrade conduction, the QRS complex will be wide, since conduction occurs between the ventricular myocytes themselves rather than the His-Purkinje system. Wolfe-Parkinson-White syndrome occurs when the accessory pathway allows both antegrade and retrograde conduction, and commonly a delta wave or pre-excitation can be seen in the early QRS complex (Figure 4). This syndrome can present in early adulthood, and the initial presentation can be ventricular fibrillation. Management in these patients where conduction occurs antegrade through the accessory pathway varies from narrow complex AVRT as described previously. Adenosine will only be effective if the antegrade conduction occurs through the AV node. Otherwise it can precipitate atrial fibrillation, which can result in degeneration to ventricular fibrillation when an antegrade accessory pathway exists in these patients. Calcium channel blockers and digoxin are contraindicated, because they will slow conduction in the AV node and enhance conduction through the accessory pathway. Class I and class III antiarrhythmics, which include flecainide, procainamide, and ibutilide, are able to depress the conduction across the accessory pathway, decrease the ventricular rate, and likely terminate the wide QRS tachyarrythmia. Direct-current cardioversion is used with hemodynamic instability or if failure of antiarrhythmic therapy occurs.

Figure 4 Lead II in this ECG shows a prominent delta wave consistent with the diagnosis of Wolfe-Parkinson-White syndrome.

Multifocal Atrial Tachycardia

Multifocal atrial tachycardia is thought to be due to abnormal automaticity and is commonly associated with chronic respiratory disease, congestive heart failure, and pulmonary embolus. It has an irregular rate and rhythm that is characterized by the presence of three or more morphological different P waves on ECG, and rates of 110–140 beat/min (Figure 5). It can easily be confused with atrial fibrillation if P waves are not prominent on a rhythm strip. First-line therapy consists of treating the underlying condition, correction of hypercarbia or hypoxia, and electrolyte repletion. Calcium channel blockers typically can provide rate control but beta-blockers should be used with caution in those with obstructive pulmonary disease. Amiodarone can be helpful in patients refractory to first-line therapies.

Figure 5 Rhythm strip shows an irregular tachycardia with greater than three morphologically different P waves, characteristic of multifocal atrial tachycardia (MAT).

Atrial Flutter

Atrial flutter is due to a re-entrant circuit from within atrial tissue and is associated with atrial enlargement. It is commonly grouped with atrial fibrillation due to similar associated causes and similar treatment regimens. Atrial rates of 250–350 beats/min are typical. The AV node refractory period allows only a proportion of these atrial beats to pass to the ventricle, typically in a 2:1 ratio. When a ventricular pulse rate is measured to be 150 beats per minute, atrial flutter should be considered. By increasing AV nodal delay with adenosine or beta-blockade, the atrial “flutter waves,” characterized by a saw-tooth appearance, can usually be seen on a rhythm strip (Figure 6). Adenosine may be useful for diagnosis, but as with atrial fibrillation, it rarely converts the rhythm back to sinus. Beta-blockers and calcium channel blockers allow ventricular rate control, but more commonly the use of antiarrythmic drug therapy and or electrical cardioversion is required if the rhythm remains persistent.

Figure 6 Lead II in this ECG shows the characteristic “saw-tooth” flutter wave of atrial flutter with 2:1 conduction. The rate is approximately 150 beats per minute.

Atrial Fibrillation

Atrial fibrillation (AF) is the most common supraventricular tachyarrhythmia with a concerning amount of possible detrimental consequences. Atrial fibrillation and flutter account for greater than 60% of the supraventricular tachyarrhythmias in noncardiac surgical patients and affect up to 40% of patients following cardiac surgery. It is commonly associated with left atrial distension, whether from acute fluid shifts or chronic dilatation secondary to structural heart disease. Other associations that must be ruled out include electrolyte imbalances, myocardial ischemia, hyperthyroidism, hypoxia/hypercarbia, pulmonary embolus, and pneumonia. It is an “irregularly irregular” rhythm with an absence of P waves on ECG (Figure 7). It is thought to arise from multiple shifting re-entrant circuits that bombard the AV node with a multitude of impulses, from which only a proportion initiate ventricular contraction, 110–190 beats/min. Patients without structural heart disease tolerate the loss of the atrial component of ventricular filling quite well, but in those with this history, hypotension, acute congestive failure, and myocardial ischemia can be precipitated. Another concerning consequence is the possibility of mural thrombus formation, and the associated embolic risk, from within the noncontracting left atrium. Thrombus can occur in up to 10% of patients, with new-onset AF lasting longer than 3 days.

Figure 7 Rhythm strip shows an irregular, normal complex tachycardia without P waves, consistent with atrial fibrillation.

The overall goals of treatment include ventricular rate control, resumption and maintenance of sinus rhythm, and prevention of embolic events. Acutely, if the patient is hemodynamically unstable, in acute heart failure, or the rhythm is precipitating myocardial ischemia, direct-current cardioversion should be performed. This is successful in restoring sinus rhythm in up to 90% of patients with recent-onset AF. In the hemodynamically stable patients, ventricular rate control should be the main priority. Calcium channel blockers, beta-blockers, amiodarone, and digoxin are all shown to be of benefit due to enhancement of the AV nodal refractory period. Secondary hypotension can be a common side effect, which may require concomitant fluid administration and calcium infusion. Digoxin is not associated with hypotension, but the slow mechanism of action of digoxin limits it usefulness in the semiurgent setting.

A variety of treatment methods may be used to terminate AF and restore sinus rhythm. Common options include the use of antiarrythmic drugs, alone or in conjunction with electrical cardioversion, but these must be tailored to each individual case. Therapy with class III antiarrhythmic drugs such as amiodarone, ibutilide, dofetilide, and propafenone have been shown to terminate AF, alone or in conjunction with electrical cardioversion, in 30%–80% of cases if initiated within 7 days of onset. The use of antiarrhythmic therapy must keep in mind the side-effect profile of this class of drugs, including the risk of drug-induced torsades de pointes ventricular tachycardia and other serious dysrhythmias. Controversy exists concerning what emphasis should be placed on pharmacological or electrical cardioversion of AF back into sinus rhythm. The recent results from the AFFIRM study have shown no difference in the long-term outcome in those patients treated with ventricular rate control versus rhythm control. Despite these controversies, up to one-third of patients with new-onset AF spontaneously convert to sinus rhythm without antiarrhythmic therapy in the perioperative period. In those where AF continues unabated, options include pharmacological and/or electrical cardioversion, versus ventricular rate control alone.

The risk of atrial thrombus and emboli become more concerning over time in AF, and anticoagulation therapy should be considered if return to sinus rhythm has not occurred after 48–72 hours. The potential benefits of anticoagulation must be weighed against the risk of postoperative bleeding. The embolic risk is increased when transition occurs from AF to sinus rhythm and vice versa. Typically, anticoagulation is recommended for 3–4 weeks prior to elective electrical cardioversion. If earlier cardioversion is required, it can be performed safely with only 48 hours of anticoagulation if atrial thrombus is ruled out via transesophageal echocardiogram. If this test is positive for atrial thrombus, anticoagulation should be continued for 4–6 weeks, and resolution of thrombus should be proven prior to elective cardioversion.

Ventricular Tachyarrhythmias

Appropriate management of newly diagnosed ventricular tachyarrhythmias depends on accurate rhythm classification and patient risk factor stratification so that appropriate therapy can be provided in a timely fashion. Serious ventricular tachyarrhythmias occur in less than 2% of patients following cardiac surgery, and in noncardiac surgery they are most commonly associated with postoperative myocardial ischemia and significant structural heart disease. The position of intravascular hardware should always be evaluated because dislodgement can be associated with mechanically induced dysrhythmias. Metabolic, acid-base, and oxygenation disturbances in the context of myocardial ischemia and exogenous or endogenous catecholamine excess have all been implicated in promoting triggered activity, abnormal automaticity, and re-entry phenomenon in ventricular tissue. The presence of significant structural heart disease is the most important predictor of future malignant ventricular tachyarrhythmias and sudden cardiac death. A typical ECG will show a wide QRS complex tachycardia, which can originate from a supraventricular source, or more commonly, is due to ventricular tachycardia (VT). If differentiation is not feasible, a wide complex tachycardia should be treated as probable VT. Attention to the QT interval is imperative because treatment without regard for QT prolongation can have drastic consequences. The majority, if not all, antiarrhythmic drugs are “proarrhythmic” themselves. Torsades de pointes accounts for the majority of these drug-induced ventricular tachyarrhythmias. Because of this, it is most advantageous to use single antiarrhythmic drug therapy and avoid the proarrhythmia effects of combination therapy. Ventricular fibrillation (VF) is an inherently unstable rhythm, and a detailed discussion on advanced cardiovascular life support (ACLS) is not the focus of this chapter. More pertinent is an understanding of the rhythms with the propensity to degenerate into VF, and the ability to intervene in an appropriate fashion to prevent this from happening.

Ventricular tachycardia (VT) is classified into monomorphic and polymorphic subtypes. Monomorphic VT is thought to originate from a single ventricular focus and has a wide QRS pattern, each with similar morphology (Figure 8). Polymorphic VT, in contrast, is characterized by an irregular, undulating appearance, with significant variation in QRS morphology. Differentiation is important because polymorphic VT commonly degenerates to VF. Further classification is determined by the persistence of the rhythm. Compared with sustained VT, nonsustained VT typically lasts less than 30 seconds and spontaneously terminates.

Figure 8 Rhythm strip shows a classic wide QRS tachycardia with similar QRS morphology characteristic of sustained monomorphic ventricular tachycardia.

Premature Ventricular Contractions

Premature ventricular contractions (PVCs) are common in postoperative critical care patients. They can be unifocal, present as couplets, or as bigeminy. They are associated with many electrolyte imbalances and metabolic abnormalities, such as hypokalemia, hypomagnesemia, alkalosis, hypoxia, and catecholamine excess. Correction of these abnormalities, along with the use of beta-blockers, commonly eliminates the majority of PVCs. In asymptomatic patients without structural heart disease, further treatment or suppression of PVCs is rarely required, and there are no associated short- or long-term consequences. In patients with coronary artery disease, history of myocardial infarction, or impaired left ventricular function (ejection fraction [EF] < 40%), PVCs may be a sign of more malignant dysrhythmias to come. Correction of any reversible precipitating factors, including myocardial ischemia, should first be performed, followed with attempts to reduce vasopressor or inotropic support. In symptomatic patients that do not generate sufficient stroke volumes in the face of multiple PVCs, temporary suppression with antiarrythmic drug therapy may be of benefit in critically ill patients.

Monomorphic Ventricular Tachycardia

Nonsustained monomorphic VT can be considered as a prolonged version of PVCs. The rhythm is associated with similar electrolyte and metabolic abnormalities that promote or initiate triggered activity, abnormal automaticity, or re-entry mechanisms. Beta-blockade, and reversal of any of the above precipitating factors, will reduce the frequency and duration of this rhythm. The use of antiarrythmic drug therapy or electric cardioversion is only required for those patients who manifest symptoms or hemodynamic compromise. The long-term prognosis associated with nonsustained monomorphic VT again depends on the presence of structural heart disease. There is an overall increased risk of sudden cardiac death in those with coronary artery disease and left ventricular dysfunction (EF < 40%). Due to this association, patients with structural heart disease should be referred for electrophysiologic (EP) testing. Patients found to have an inducible rhythm at the time of EP testing benefit from placement of an implantable cardioverter-defibrillator (ICD). In patients without structural heart disease, nonsustained monomorphic VT carries no added long-term risk.

The most common mechanism causing sustained monomorphic VT is re-entry. This rhythm is most commonly due to a healed scar from a prior myocardial infarction, which allows a re-entry circuit to occur. Because of this, sustained monomorphic VT is commonly recurrent and portends a poor prognosis. In-hospital mortality rates exceed 40% following surgery, with recurrence in more than 30% of patients who initially survive. As many as 20% discharged from the hospital will succumb to cardiac death within 24 months. Because the substrate for sustained monomorphic VT persists, in those that survive their acute illness, EP testing and subsequent ICD placement is similarly recommended.

The acute management for monomorphic VT is dependent on the hemodynamic status of the patient. Direct-current cardioversion is the mainstay of treatment for those symptomatic or unstable. Electric cardioversion is highly effective and is also recommended for hemodynamically stable VT in conjunction with adequate short-term anesthesia. In those patients who are stable, or where electric cardioversion is not appropriate or available, either intravenous procainamide, sotalol, or amiodarone are the current antiarrhythmic drug recommendations. Amiodarone is the drug of choice for those patients with impaired cardiac function. An important change from the most recent ACLS guidelines is that lidocaine is no longer recommended as a first-line treatment. Antitachycardia pacing is also an option in those with transvenous or an internal pacemaker already in place, although the potential for tachycardia acceleration exists and a defibrillator should be at the bedside if attempted.

Polymorphic Ventricular Tachycardia

Polymorphic ventricular tachycardia has a significant predisposition to degenerate into ventricular fibrillation. The distinction between nonsustained and sustained is less pertinent, because short bursts of this rhythm commonly evolve into sustained polymorphic VT. This rhythm is invariably symptomatic and requires prompt directcurrent cardioversion. The most important step once the patient’s condition is more stable is the determination of the QT interval by ECG analysis. In patients without QT prolongation, the most likely cause is acute cardiac ischemia and associated severe left ventricular dysfunction. Correction of any associated electrolyte and metabolic abnormalities must occur. Minimization of exogenous catecholamine support and beta-blockade should be initiated, and in those with severe coronary vascular disease, revascularization or intraaortic balloon counterpulsation may be required. Antiarrhythmic drug therapy with intravenous amiodarone, procainamide, or sotalol can promote maintenance of sinus rhythm, but emphasis should be placed on treating the underlying cardiac ischemia. Prognosis depends on the hemodynamic status of the patient rather than the presence of ongoing VT. In those that acutely recover, ICD placement has been shown to improve long-term outcome.

Polymorphic VT in the setting of a prolonged QT interval (QT 460 milliseconds) is commonly referred to as the syndrome of torsades de pointes or “twisting of the points.” The ECG shows a wide QRS tachycardia that appears to twist around the ECG baseline. This syndrome requires a different management algorithm because the mechanism is attributed to triggered activity secondary to early after-depolarizations rather than re-entry. Acquired QT prolongation can result from many electrolyte abnormalities and a myriad of medications. Common causes seen in an ICU setting include hypokalemia, hypomagnesemia, specific antibiotics and psychoactive drugs, and, most importantly, class I and III antiarrhythmics (Table 2). The first priority in the management of torsades is identification and removal of the offending agent concurrent with correction of any electrolyte abnormalities. Direct-current cardioversion is used for the hemodynamically unstable, and it is important that any medication that could further prolong the QT interval not be given. Intravenous magnesium should be given to all patients with suspected torsades. Because the length of the QT interval is proportional to the R-R interval (time between each beat), patients benefit from overdrive pacing with isoproterenol or transvenous pacing. Isoproterenol should be used with caution in patients with coronary vascular disease. Antiarrythmic drugs that do not prolong the QT internal can be used and include lidocaine and phenytoin. Long-term management depends on avoiding the use of drugs that prolong the QT interval. The overall prognosis is good, and no long-term therapy is typically recommended.

Table 2 Common ICU Drugs That Can Promote Torsades de Pointes

Adapted from Parrillo J, Dellinger R, editors: Critical Care Medicine: Principles of Diagnosis and Management in the Adult, 2nd ed. St. Louis, Mosby, 2001.