Thought to be due to reflex inhibition of vagal nerve tone during inspiration, sinus arrhythmia is the reduction in time from one P wave to another (P-P interval) between sinus discharges, leading to an increase in heart rate during inspiration and slowing during expiration, which is thought to help improve and synchronize alveolar gas exchange [4]. As such, respiratory sinus arrhythmia is considered the sign of a healthy conduction system. Marked sinus arrhythmia may even manifest with sinus pauses for 2 seconds or longer, but is rarely pathologic by itself. Small changes in P-wave morphology and PR interval can be attributed to variation in the pacemaking site within the SA node due to differential vagal stimulation. This periodicity in the heart rate is most pronounced in the young and decreases with age. The direct impact of the autonomic nervous system on the sinus node and sinus arrhythmia is confirmed by the fact vagal tone can be abolished through parasympathetic blockade by atropine or through anatomic denervation of hearts after cardiac transplant. Autonomic system dysregulation due to microvascular disease (as in diabetes) or degeneration (as in Shy–Drager syndrome) also reduces sinus arrhythmia. Indeed, depression of respiratory sinus arrhythmia after myocardial infarction is associated with an increased risk of sudden cardiac death [5]. In contrast to respiratory sinus arrhythmia, nonrespiratory sinus arrhythmia is the change of P-P intervals varying at random and may reflect drug toxicity from digitalis, intracranial hemorrhage, or ischemic heart disease [6].

Symptomatic sinus bradycardia or sinus pauses causing reduced cardiac output or hemodynamic instability may be due to extracardiac disorders which profoundly increase vagal tone such as bowel obstruction, urinary retention, nausea and vomiting, or intracranial mass. Pharmacologic agents such as parasympathomimetic drugs, digitalis, beta-adrenergic-blocking drugs, and calcium antagonists can also exacerbate sinus bradycardia. Other disorders, such as carotid sinus hypersensitivity may also increase vagal tone and lead to transient ventricular asystole due to sinus arrest lasting up to 3 seconds or longer. Although some patients may require permanent pacemaker implantation due to recurrent, activity-related symptomatic pauses, they rarely require temporary pacemaker support as the negative chronotropic effect is relieved once pressure is removed from the carotid.

Inappropriate SA node automaticity and disordered impulse generation is called sinus node dysfunction (also described as sick sinus syndrome by Ferrer [7]). It is commonly a disorder of senescence, although can occur at any age due to destruction of sinus node cells through infiltration, collagen vascular disease, trauma, ischemia, infection, or idiopathic degeneration [8]. Sinus node dysfunction affects men and women equally, commonly in the age range of 65 to 75 years, and is the primary indication for over 50% of permanent pacemaker implants in the United States [9,10]. Indeed, sinus node dysfunction comprises of a constellation of abnormalities of the sinus node characterized by inappropriate sinus bradycardia (in the absence of drugs), sinus arrest and chronotropic incompetence. Subsidiary and latent pacemakers further downstream become active in states of such dysfunction, and can give rise to bradyarrhythmias and tachyarrhythmias. These may originate in the atrium (e.g., atrial tachycardias, multifocal atrial rhythms, paroxysmal atrial fibrillation) or ventricles (e.g., idioventricular rhythms, ventricular tachycardias [VTs]). Coexisting AV nodal disturbance and block are also common, and intermittent periods of bradycardia punctuated by tachycardia have given rise to the term “tachy–brady syndrome.” Many of these patients go on to need permanent pacemakers for effective rate control. The presentation in the intensive care setting is often due to an exacerbation of the underlying sinus node dysfunction through the use of cardioactive medications (see Table 43.1), which may result in a reduced cardiac output from diminished heart rate or unstable tachyarrhythmias. Given the diversity of potential etiologies and manifestations of sinus node dysfunction, it is often more useful to distinguish temporary or reversible causes of the syndrome (e.g., drug toxicity) from permanent etiologies (e.g., idiopathic fibrosis, degenerative changes of the conductive system) to identify the appropriate management strategy.

SA block, also called SA exit block, manifests as sinus arrest of variable length on the surface ECG. On the basis of a study of U.S. Air Force personnel, the prevalence is approximately 1% in otherwise normal subjects [11]. Considered by some to be a manifestation of sinus node dysfunction, the pathophysiology of SA block is a defect of impulse generation or propagation within the SA node. First-degree SA block cannot be detected on surface ECG as sinus node depolarization is not inscribed separately from atrial depolarization (the P wave). Type I second-degree SA block is the progressive prolongation of conduction block within the sinus node until complete exit block occurs. This manifests on surface ECG as progressive shortening of P-P intervals till a pause occurs. Type II second-degree SA block is the spontaneous block of a sinus impulse which leads to a sinus pause whose duration is an exact multiple of the preceding P-P interval. Third-degree SA block simply manifests as sinus arrest, usually with the eventual appearance of a subsidiary pacemaker rhythm such as a junctional escape. Sinus node dysfunction can be studied in the electrophysiology laboratory and quantified by techniques to specifically examine the sinus node electrograms, sinus node recovery time, and SA conduction studies. In the intensive care setting, diagnosis can be challenging, and it is usually sufficient to simply be able to recognize third-degree SA block which may necessitate temporary pacing if subsidiary pacemakers are not active or do not provide sufficient cardiac output.

AV block is frequently observed on surface electrocardiography, and may anatomically occur anywhere in the conduction system outside of the SA node. It is clinically important to attempt to distinguish AV block at the level of the AV node with block within or below the level of the His bundle, as infranodal block may be associated with instability and a worse clinical outcome. First-degree AV block is defined as a prolongation of the PR interval greater than 0.20 seconds, and is generally felt to be due to a block of impulse conduction at the level of the AV node, although when associated with bundle-branch block, may occur further down in the His–Purkinje system. In a study of over one hundred thousand airmen, the prevalence of first-degree AV block was found to be 0.65% [12]. In a 30-year longitudinal study, the association of first-degree AV block with a narrow QRS complex was thought to be largely benign [13]. More recent data from the Framingham cohort, however, suggest that significant PR prolongation may be associated with increased risks of atrial fibrillation, pacemaker implantation, and all-cause mortality over time [14]. Marked first-degree AV block may lead to hemodynamic derangement when atrial systole occurs in close proximity to the preceding ventricular systole, manifesting with symptoms similar to the pacemaker syndrome, although this is rare [15]. In the intensive care setting, second- and third-degree AV block are of greater significance.

Second-degree AV block was classified into two types by Mobitz in 1924 [16]. Mobtiz type-I second-degree AV block, or Wenckebach-type block, is characterized by progressive prolongation of the PR interval before nonconduction. Analogous to type I SA block which demonstrates shortening of P-P intervals, there is progressive shortening of the R-R intervals prior to a dropped beat in Mobitz type-I block. Irrespective of QRS width, Mobitz type-I block, or Wenckebach phenomenon, usually represents an appropriate physiologic response to increasing heart rate through decremental conduction in the AV node, and rarely requires intervention. Mobitz type-II block, on the other hand, usually represents infranodal disease, particularly when associated with a wide complex QRS. On the surface ECG, Mobitz type-II block manifests as a sudden nonconduction of an atrial impulse without change in preceding PR interval. Attention should be taken to distinguish Mobitz type-II block from block of a premature atrial complex, which is due to physiologic interference and not due to pathological involvement of the AV node. Mobitz type-II block is of significance in the clinical setting, as it may herald impending complete heart block, particularly when multiple consecutive impulses are nonconducted (often referred to as “advanced” or “high-grade” heart block). Third-degree AV block, or complete heart block, occurs with the absence of atrial impulse propagation to the ventricles and will manifest with ventricular standstill in the absence of an escape rhythm. When reversible etiologies are present, temporary pacing is critical toward providing electrical support, especially in the setting of ventricular asystole due to complete heart block. Temporary pacing is indicated when the subsidiary escape rhythm is unstable and cannot maintain hemodynamic stability, leading to cerebral hypoperfusion or further cardiac instability

Similar to sinus node dysfunction, there are myriad etiologies which may lead to AV block. In the intensive care setting, common etiologies include electrolyte disturbance, notably hyperkalemia or hypermagnesemia; drug toxicity, particularly from cardioactive drugs such as beta-adrenergic-blocking agents, nondihydropyridine calcium-channel blockers, digitalis derivatives, and antiarrhythmics; myocardial ischemia from inferior or anteroseptal infarction; infection from myocarditis or endocarditis, particularly involving the aortic valve; and trauma from cardiac surgery, catheter trauma, or radiation. Clinical history obtained from the patient is critical in determining the potential duration of the block and also prioritizing appropriate treatment modalities.

Failure in ventricular activation due to block in the His–Purkinje system may also be the cause of complete heart block. The left and right bundle branches are commonly divided into a trifascicular system, consisting of the right bundle branch and the left anterior and posterior fascicles [17]. Although a septal fascicle has also been identified in anatomic studies, ECG manifestations of septal conduction block are debated and remain to be defined [18]. Bifascicular block is present when either left anterior or left posterior fascicular block is associated with right bundle branch block. Clinically, complete heart block is most often preceded by chronic bifascicular block, although the progression is often slow [19]. However, when first-degree AV block is associated with chronic bifascicular block and symptomatic bradycardia, there is an increased risk of sudden cardiac death (this combination is sometimes erroneously referred to as “trifascicular block”). Alternating bundle branch block seen on successive ECG tracings, either manifesting with sequential right and left bundle branch block, or right bundle branch block with left anterior and left posterior fascicular block, is also associated with increased mortality and can be correctly identified as representing intermittent trifascicular block.

Similar to other forms of conduction block, there are numerous potential etiologies which may lead to intraventricular block, although ischemia in the setting of a myocardial infarction (MI) is the most common in the intensive care setting. The SA nodal artery receives its blood supply from the proximal right coronary artery in 55% of the population, from the circumflex in 35%, and from both in approximately 10%. The AV nodal artery, on the other hand, arises from the posterior descending artery in 80% of cases, 10% from the circumflex, and approximately 10% from both arteries. Although, an inferior MI may lead to varying degrees of AV block from AV nodal artery ischemia or enhanced vagal tone from exaggeration of the Bezold–Jarisch reflex, intraventricular block is
uncommon. An anterior MI, on the other hand, may cause ischemia of the fascicles directly and is associated with greater extent of left ventricular dysfunction. In the prethrombolytic era, new fascicular or bundle branch blocks were common after an MI and were associated with a significantly increased risk of mortality [20]. A simple scoring model characterizing the risk of progression to complete heart block after MI was developed by Lamas based on ECG criteria [21]. Patients with evidence of conduction block on ECG, including first or second-degree block (both type I and type II), left anterior and posterior fascicular block, right bundle branch block, or left bundle branch block had a linear relationship between their score (number of characteristics on presenting ECG) and the development of complete heart block. Patients without ECG evidence of any conduction block on presentation had a less than 4% risk of subsequent complete heart block, in contrast to those with scores of two, in whom the risk of developing complete heart block was 45%. Because of the relatively common incidence of bradycardia after MI, the American College of Cardiology (ACC) and the American Heart Association (AHA) have clear guidelines on intervention, including the use of temporary pacing, for AV and intraventricular disturbance (Table 43.2), which will also be further discussed later.