Chapter 33

Arrhythmias (Bradycardias)

Bradyarrhythmias, or slow heart rhythms, occur commonly in patients treated in the intensive care unit (ICU). Assessment of the critically ill patient with a bradyarrhythmia needs to take into account the clinical context and whether or not the bradyarrhythmia is causing either significant symptoms or hemodynamic compromise. Bradyarrhythmias may reflect physiologic (e.g., high vagal tone) or pathologic (e.g., high grade conduction system disease) conditions. Usually these arrhythmias resolve spontaneously or after treating the underlying cause. However, rarely, either temporary (such as a temporary pacing wire or chronotropically stimulating drugs) or permanent (such as a permanent pacemaker) interventions may be required. This chapter provides a concise approach to the ICU patient presenting with bradyarrhythmias. Bradyarrhythmias in the setting of acute myocardial infarctions are discussed in Chapter 50.

Definitions

Bradyarrhythmias refer to any disturbance in the heart rhythm in which the heart rate is abnormally slowed. Bradycardia, meanwhile, is grossly defined as any heart rate < 60 beats per minute. The limitation in using an absolute cutoff for the heart rate in categorizing pathologic arrhythmias is that a heart rate < 60 beats per minute may be physiologic and not a cause for concern in many patients. However, some patients may have a ventricular rate > 60 beats per minute, which may nevertheless be insufficient for their physiologic demands. Thus, “pathologic” bradyarrhythmias should include any heart rate that is either insufficient to meet physiologic demands, resulting in either symptoms or hemodynamic compromise, or that is associated with a high risk of progressing to a rhythm that may result in sudden death or hemodynamic collapse.

Approach to the Patient Presenting with a Bradyarrhythmia

When a patient presents with a slow heart rhythm, whether symptomatic or not, consideration must be first given to the clinical context as well as to classifying the mechanism of the arrhythmia. The clinical context is important because, in most patients, the bradyarrhythmia may be transient, such as that caused by high vagal tone during nasogastric suctioning or a hypoxic episode, or may result from cardioactive drugs, in which case the bradyarrhythmia may resolve after withdrawal of the offending agent. Sometimes, self-limited causes of a bradyarrhythmia may be identified but not readily reversible, and supportive, temporary interventions may be needed while the underlying cause resolves. In other cases, even though the underlying cause may be identified, the situation may not be reversible because of a clinical need of the offending agent to treat another condition or because of a lack of available therapies to “cure” the associated condition, and permanent interventions, such as implantation of a permanent pacemaker, may be needed.

In terms of diagnosing the mechanism, or the underlying disturbance in the conduction system leading to the bradyarrhythmia, all available resources in the ICU for documenting and reviewing the rhythm should be used. The primary ways in which the heart rate and rhythm are recorded in the ICU include pulse checks and telemetry. The limitations of each and alternative methods of diagnosing the electrophysiologic mechanism of the arrhythmia need to be considered in order to optimize decision making. In the case of pulse checks, the recorded heart rate while palpating the radial, femoral, or carotid pulse may not always reflect the number of times the heart is electrically depolarizing. For example, frequent nonperfused premature ventricular contractions may result in a QRS complex on telemetry or electrocardiography that is not noted while palpating the pulse (Figure 33.1). Thus, a pulse check in the absence of corresponding telemetry may be ineffective in establishing the diagnosis of a bradyarrhythmia in the absence of corresponding electrocardiogram (ECG) recordings.

Figure 33.1 Frequent nonperfused premature ventricular contractions. Note the six leads of electrocardiogram (ECG) at the top and the arterial pressure tracing below. The sinus beats are perfused and result in an arterial pulsation, but the premature ventricular contractions (PVCs) do not result in a significant arterial pulsation. Thus, the effective pulse rate is 35 beats per minute even though the ECG heart rate as defined by the number of electrical depolarizations occurring within a minute on ECG is ∼70 beats per minute. Recording of heart rate by pulse would thus result in a finding of bradycardia that may not correlate with the number of times the ventricle electrically depolarizes per minute and thus would be insufficient to define the cause of the low pulse rate.

In turn, telemetry offers one to three lead recordings of ECG activity. Review of telemetry alarms affords the ability to identify pauses, or periods of absence of any cardiac electrical activity, the mechanism of the pauses depending on whether the absence of activity occurs solely at the ventricular or at both the ventricular and atrial levels, and the periods immediately before and after the arrhythmia. Telemetry may be used in a similar fashion to assess periods where the heart rhythm is slowed. The episode of bradycardia needs to be further correlated with simultaneous blood pressure recordings and time of day in order to determine if there is any association with symptoms.

In some patients, because of inability to adequately see atrial activity on the limited leads available on telemetry or because of noise on telemetry that may impede interpretation, a full 12-lead ECG may be needed to diagnose the mechanism of the bradyarrhythmia. However, telemetry is generally sufficient to identify and diagnose the arrhythmia mechanism.

Once the bradyarrhythmia has been documented, classification of the bradyarrhythmia via a detailed analysis of the ECG findings is key. However, proper classification requires close, expert review of all strips with an orderly approach that involves reviewing the atrial and ventricular rhythms, identifying changes in morphology of atrial or ventricular beats that would suggest depolarizations emanating from ectopic foci, and correlating each atrial and ventricular beat to document association versus dissociation.

Classification of Bradyarrhythmias

Bradyarrhythmias may result from dysfunction of the sinus node or disturbances of atrioventricular (AV) conduction. The classification of bradyarrhythmias principally relies on documentation of a slow ventricular rate, which may or may not be generated due to a slow atrial rate. When classifying bradyarrhythmias, one should first identify the electrophysiologic mechanism and secondly whether or not a drug or another clinical event is causing the rhythm.

Sinus Node Dysfunction

The spectrum of sinus node dysfunction encompasses sinus pauses, sinus arrest, sinus bradycardia, sinus node exit block, and the tachycardia-bradycardia syndrome (sick sinus syndrome). All may result in bradycardia or pauses caused by the lack of impulse formation or propagation from the sinus node. Occasionally, not only does the sinus node fail, but “backup” subsidiary pacemakers (atrial and junctional) may also fail, and appropriate heart rate is not maintained.

Causes of sinus node dysfunction in ICU patients are listed in Box 33.1. It is important to recognize that sinus bradycardia is commonly seen in young athletic patients, during sleep, and during conditions associated with high vagal tone (pain, nausea, vomiting, endotracheal manipulation, bowel movements). These episodes are almost uniformly transient and asymptomatic. Treatment should be considered only if the bradycardia persists, is symptomatic, or results in hemodynamic compromise and the underlying cause is expected to recur or cannot be withdrawn.

BOX 33.1 Common Causes of Bradyarrhythmias in the Intensive Care Unit

Extrinsic Causes

Carotid sinus hypersensitivity

Drugs

Antiarrhythmic agents (procainamide, propafenone, amiodarone)

Beta-adrenergic blockers

Calcium channel blockers

Digoxin

Morphine

Tricyclic antidepressants

Elevated intracranial pressure

Electrolyte abnormalities (hyperkalemia, hypokalemia, hypocalcemia, hypermagnesemia)

High vagal tone (mechanical ventilation, myocardial ischemia-infarction, nausea, vomiting, pain, sleep, vasovagal reflex)

Hypothermia

Hypothyroidism

Hypoxia

Obstructive sleep apnea

Intrinsic Causes

Collagen vascular disease (systemic lupus erythematosus, rheumatoid arthritis, scleroderma)

Conduction system disease

Congenital heart disease (e.g., atrial septal defect)

Hypertensive heart disease

Infections (endocarditis, Lyme disease, viral myocarditis, diphtheria)

Infiltrative cardiomyopathy

Intrinsic sinus node disease

Myocardial ischemia or infarction

Sarcoidosis

Valvular heart disease (aortic stenosis, aortic insufficiency, mitral annular calcification)

In patients with preexisting heart disease, sinus node dysfunction may present with significant hemodynamically compromising bradyarrhythmias, particularly in the ICU setting. Ischemia, electrolyte abnormalities, drugs, hypoxia, and metabolic and endocrinologic derangements may all precipitate a clinically significant bradycardia in patients with chronic, previously stable sinus node disease. Patients with severe left ventricular systolic dysfunction are also at risk of significant sinus bradyarrhythmias, particularly in the setting of worsening heart failure. Furthermore, because inappropriately slow sinus rates may be causally related to heart failure symptoms, permanent pacing has a role in the management of these patients.

Sinus node dysfunction, particularly in the elderly, may also be associated with tachycardia-bradycardia syndrome in which symptoms may be related to the tachy- or bradyarrhythmia. Tachycardia-bradycardia syndrome is characterized by periods of atrial tachyarrhythmias (atrial flutter, atrial tachycardia, or atrial fibrillation [see Chapter 34]) interspersed with periods of sinus bradycardia or sinus arrest. Tachycardia-bradycardia syndrome is most often seen in the setting of paroxysmal atrial fibrillation when a prolonged sinus recovery time upon termination of the atrial fibrillation episode may lead to a sinus pause (“offset pause”) or a period of sinus bradycardia. Rarely, these pauses may result in syncope. Because symptoms can be due to either tachycardia or bradycardia, treatment consisting of both medication to control the fast heart rates and permanent pacing to prevent slow heart rates may be required in these patients.

Atrioventricular Conduction Disturbances

Disturbances of propagation of electrical impulses from the atria to the ventricles are classified as being secondary to different degrees of atrioventricular (AV) block (first, second, or third degree). This classification is based on the electrocardiographic pattern of the conduction disturbance which, in turn, is used to correlate with the anatomic substrate. Block occurring in the AV node generally signifies a more benign prognosis than does block resulting from disease of infranodal structures (e.g., the His-Purkinje system). Although intrinsic cardiac disease can lead to AV conduction disturbances, reversible extrinsic causes should be sought before interventions are considered (see Box 33.1). Depending on how readily the extrinsic cause may be reversed, temporary interventions to treat the bradyarrhythmia may be required. Except in cases of higher-grade conduction block at high risk of progressing to complete heart block or asystole (discussed later), acute intervention (pharmacologic or pacing) should generally be reserved for patients who are symptomatic or hemodynamically compromised. The anatomic site of block is relevant in defining which patients should receive a permanent pacemaker. However, the ultimate decision on the need for treatment is based on the presence of symptoms attributable to the bradyarrhythmia.

First-Degree Atrioventricular Block

First-degree AV block, defined as a PR interval > 200 milliseconds, rarely results in symptoms or significant hemodynamic compromise. It is most often due to delay of the electrical impulse as it traverses the AV node. Disease of the His-Purkinje system can occasionally prolong the PR interval, though generally its contribution to the PR interval is negligible. Because every impulse originating in the sinus node propagates to the ventricle, first-degree AV delay is a more accurate description of this phenomenon.

In many patients, the length of the PR interval may correlate with the heart rate. Thus, at higher heart rates the PR interval may be longer. If the PR interval is sufficiently long, patients may experience a condition where atrial depolarization occurs immediately after or concurrent with ventricular depolarization. When this happens, patients may experience headache, heart failure symptoms, or hypotension. This phenomenon is similar to that seen in patients with pacemakers in whom a “pacemaker syndrome” may occur as a result of atrial contraction occurring at a time concurrent with ventricular depolarization rather than after ventricular relaxation. In these patients, permanent pacing may be useful to better coordinate atrial and ventricular depolarization.

Second-Degree Atrioventricular Block

Second-degree AV block is divided into Mobitz I block (Wenckebach) and Mobitz II block. Mobitz I block is characterized as progressive prolongation of the PR interval until a P wave fails to propagate to the ventricle (Figure 33.2). Because the incremental PR prolongation decreases with each consecutive beat, the RR intervals progressively shorten during Mobitz I block. Generally, the simplest mechanism by which to diagnose Mobitz I block is to compare the PR interval of the beat conducted immediately after the skipped beat with the PR interval of the beat conducted immediately before the skipped beat, as successive PR intervals may only show gradual prolongation. The presence of Mobitz I block generally indicates that the site of block is in the AV node, thus portending a more benign prognosis. However, Mobitz I block can rarely occur in the infranodal structures, though intracardiac recordings are required for this diagnosis. Permanent pacemaker implantation is indicated only in patients in whom Wenckebach block has been demonstrated to cause symptoms.

Figure 33.2 Atrioventricular Wenckebach (second-degree atrioventricular [AV] block, Mobitz I) with 4:3 AV conduction. P waves marked with ^∗. Note progressive prolongation in PR interval before blocked P wave. This pattern suggests the site of block is in the AV node and implies no risk of progression to complete heart block.

Mobitz II block is defined as the sudden failure of conduction of an impulse from the atria to the ventricles and manifests on the ECG as unexpected block of a P wave without the progressive prolongation of the PR interval seen with preceding beats (Figure 33.3). Mobitz II block signifies infranodal disease and often is associated with other electrocardiographic signs of conduction system disease (e.g., bundle branch block or intraventricular conduction delays). Although a permanent pacemaker may not be absolutely indicated for patients with asymptomatic Mobitz II block, there is a risk of a sudden loss of atrioventricular conduction and, if this happens, a ventricular escape rhythm may or may not be present. Thus, the majority of patients do receive pacemakers given the relatively high risk (40% to 80%) of progression to higher-grade AV block. In particularly high-risk patients, a temporary pacing wire may be appropriate until a permanent pacemaker can be implanted.

Figure 33.3 Mobitz II block. P waves marked with ^∗. Note that the PR interval does not change on the conducted beats and the baseline bundle branch block, suggesting infra-Hisian conduction disease. This rhythm has a high risk for progression to complete heart block and would generally indicate the need for implantation of a permanent pacemaker.

Patients with 2:1 AV block, in whom every other P wave is associated with a QRS complex, may be difficult to classify as either Mobitz I or II block because there is no opportunity for the PR interval to become prolonged with successive beats (Figure 33.4). The site of block in these patients may be either AV nodal or infranodal. Clues on the ECG that suggest an infranodal site include a wide QRS (> 120 msec) on the conducted beats or an associated bundle branch or fascicular block. Furthermore, a normal PR interval on the conducted beats may support the presence of infranodal disease. In these patients, the effective heart rate (defined by the ventricular rate) is half that of the atrial rate. Findings suggestive of infranodal disease or the presence of associated symptoms should prompt consideration of placement of a temporary pacemaker and, ultimately, a permanent pacemaker in those without a definite reversible cause.