Epidemiology

Bradycardia is a frequent finding in clinical practice, and its significance is dependent on the underlying cause and clinical effects. The baseline heart rate in an individual patient is determined predominantly by the balance between the parasympathetic and sympathetic nervous systems, and a “normal” heart rate has been defined arbitrarily as 60 to 100 beats/min at rest. The heart rate will vary depending on age, physical condition, and time of observation. Normal ranges for a healthy asymptomatic individual will vary from 46 to 93 beats/min in men and 51 to 95 beats/min in women during the day to rates as low as 40 beats/min at night.¹ The heart rate should fluctuate with respiration, the Valsalva maneuver, and other vagal influences confirming normal autonomic control of the sinus node. Bradycardia is a frequent finding in trained athletes, in whom heart rates lower than 40 beats/min are often observed at rest.² Bradycardias of clinical significance increase in frequency with age and in the setting of illnesses or medications affecting the heart and its conduction system.

Pathophysiology

Bradyarrhythmias are the result of either (1) extrinsic factors slowing the normally functioning sinus node and conduction pathways or (2) failure of the sinus node and conduction pathways because of intrinsic causes of degeneration of the conduction system.

Extrinsic Causes

Clues to an extrinsic cause of a bradyarrhythmia are a history of a new cardioactive medication, conditions that activate vagal tone, and extreme electrolyte imbalances, specifically potassium (Table 58.1). The associated rhythms are typically those that are due to dysfunction of the sinus or atrioventricular (AV) node:

• Sinus bradycardia, arrest (Figs. 58.1 to 58.3)

• Type I second-degree AV nodal block (Fig. 58.4)

• Third-degree heart block (see Fig. 58.6)

Table 58.1 Extrinsic Causes of Bradyarrhythmias

	COMMON	UNCOMMON
Drugs	Class Ia antiarrhythmic agents Class Ic antiarrhythmic agents Beta-blocking agents Calcium channel blockers Class III antiarrhythmic agents Amiodarone and sotalol Digoxin Cholinergic agents α2-Agonists Opioids Sedative-hypnotics Organophosphates Tricyclic antidepressants	Lithium Phenothiazines Reserpine Amantadine Chloroquine Phenytoin Carbamazepine Clonidine Physostigmine Cimetidine Propoxyphene Thioridazine
Situational reflex	Neurocardiogenic syncope Maxillofacial reflex Micturition syncope Oculocardiac reflex Cough syncope	Pain syncope Defecation syncope Vomiting Swallow syncope
Metabolic	Hypokalemia Hyperkalemia Hypothyroidism	Hypermagnesemia Hypercalcemia
Ischemia and infarction	Inferior wall ischemia or infarction is associated with bradycardia and/or atrioventricular nodal conduction delays that are due to abnormal sensitivity to parasympathetic stimulation and are responsive to atropine	—
Other	Obstructive sleep apnea Hypothermia Hypoxia	—

From Ford M. Clinical toxicology. Philadelphia: Saunders; 2001. pp. 23-5.

Fig. 58.1 Rhythm strip of a patient with a bradycardia that is due to a hypervagal response.

The initial portion of the strip shows a sinus rhythm with progressive slowing to the point of sinus arrest. In addition, there is progressive prolongation of the PR interval, which indicates that atrioventricular node conduction is affected as well. This finding suggests that the cause is “external” and affecting both the sinoatrial and atrioventricular nodes and not intrinsic disease of either node.

Fig. 58.2 Sinus bradycardia with a ventricular response rate of 59 beats/min.

There is a P wave for every QRS complex and normal PR intervals.

Fig. 58.3 Sick sinus syndrome.

This syndrome has many variants, but all have the common feature of abrupt dysfunction of the sinus node. This electrocardiogram shows a normal sinus rhythm with abrupt absence of P waves.

Fig. 58.4 Mobitz type I second-degree heart block.

This is sinus rhythm at 70 beats/min with a slower ventricular rate because of a progressive delay in atrioventricular (AV) nodal conduction and, finally, a dropped beat. Note that the PR interval after the dropped beat is shorter than the PR interval just before the dropped beat. The hallmark feature of this type of second-degree AV block is the presence of a normal sinus rhythm with a progressive delay in AV nodal conduction.

Intrinsic Causes

Certain conditions result in failure of elements of the conduction system because of aging, ischemia or infarction, surgical trauma, or infiltration (Table 58.2). The latter cause encompasses a large group of conditions that include infectious and rheumatologic diseases.^3–5 The associated rhythms are typically those that indicate failure of one element of the conduction system rather than failure to generate a rhythm:

• Second-degree AV block (either type I or type II) (Fig. 58-5; also see Fig. 58.4)

• Third-degree heart block (Fig. 58.6)

• Associated fascicular or bundle branch blocks (see Fig. 58.5)

Table 58.2 Intrinsic Causes of Bradyarrhythmias

Ischemia and infarction	Inferior wall MI—sinus bradycardia, type I second-degree heart block, third-degree heart block Anterior wall MI—type II second-degree heart block, third-degree heart block
Infection	Viral—varicella, mononucleosis, hepatitis, mumps, rubella, rubeola Bacterial—endocarditis, diphtheria, Lyme disease Parasitic—Chagas disease
Malignancy	Lymphoma, sarcoma
Rheumatologic	Systemic lupus erythematosus, rheumatoid arthritis, Reiter syndrome, systemic sclerosis
Other	Sarcoid, amyloid, Lev disease (spread of fibrosis and calcification from the adjacent cardiac skeleton), Lenègre disease (idiopathic fibrotic degeneration of the His-Purkinje system)

MI, Myocardial infarction.

Fig. 58.5 Mobitz type II second-degree atrioventricular block.

Careful review of this electrocardiogram shows a sinus rhythm with a left anterior fascicular block and a right bundle branch block. Importantly, there is evidence of an anterior wall infarct with ST-segment elevation in the anterior leads. This demonstrates a significant complication of anterior wall infarcts involving the septum, with necrosis of the right bundle branch and left anterior fascicle and intermittent failure of the left bundle branch.

Fig. 58.6 Complete atrioventricular block.

This electrocardiogram shows an underlying sinus rhythm that is regular at approximately 80 to 90 beats/min. The ventricular escape rhythm is slow and regular with no apparent relationship between the P waves and the QRS complexes.

Presenting Signs and Symptoms

Cardiac output is dependent on the patient’s stroke volume and heart rate. Bradycardias are symptomatic only to the extent that they affect cardiac output, which is a product of the heart rate and stroke volume. In the setting of a normal stroke volume, heart rates as low as 20 to 30 beats/min can sustain a reasonable cardiac output. A heart rate of 40 beats/min may be physiologically normal for some individuals, whereas a rate of 60 beats/min may be inadequate for patients with conditions that compromise stroke volume, such as cardiomyopathies, bleeding, or sepsis.

Symptoms of low cardiac output are due to hypoperfusion of vital organs and muscle tissue. Mild reductions in cardiac output usually cause exertional fatigue and dyspnea. Greater reductions in cardiac output can produce signs and symptoms of cerebral ischemia, congestive heart failure, mesenteric ischemia, and renal insufficiency. Complete heart block with slow escape rhythms or bradycardia in the setting of profound reductions in stroke volume can manifest as syncope, pulmonary edema, and cardiogenic shock.

Alternatively, a profound bradycardia that does not result in hemodynamic compromise does not need to be treated but should be considered an important diagnostic clue. The classic example is a patient with intracranial hemorrhage and Cushing reflex, which will be manifested as hypertension and often profound bradycardia. In this case the bradycardia is a sign of elevated intracranial pressure, and treatment should focus on reducing it.

Differential Diagnosis and Medical Decision Making

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