Bradycardia Case File

Bradycardia Case File

Eugene C. Toy, Md, Michael d . Faulx, Md

Case 12

A 75-year-old man with a history of hypertension, hyperlipidemia, and coronary artery disease with drug-eluting stent placement 5 years ago presents with a com plaint of lightheadedness and fatigue, ongoing for the past 24 hours. He has not experienced any episodes of syncope, chest pain, shortness of breath, or palpitations. He was able to ambulate to your office, and is fully conversant with you; however, he does state that these activities were significantly more difficult to per form than usual, and he had to stop multiple times to rest coming from the parking lot to your office. He appears fatigued in general. He is afebrile with a blood pressure of 110/60 mmHg, heart rate of 30 bpm, and breathing rate of 14 times per minute. On examination, his lungs are clear, and he does not have any lower extremity edema. His cardiac examination is significant for bradycardia without murmurs, rubs, or gallops. Neck examination shows intermittent large jugular venous pulsations. Peripheral pulses are strong. Laboratory evaluation shows normal blood count, renal function, electrolytes, thyroid function tests, and no elevation in serum cardiac biomarkers. An ECG is obtained in office and is shown in Figure 12-1.

c What is the most likely diagnosis?

c What else do you need to know about his medical history?

c What is the best next step in management?

Figure 12-1. An ECG for the main subject of this case.

Answer to Case 12:

Bradycardia

Summary: A 75-year-old man with little comorbid history presents with a 1-week history of fatigue and lightheadedness, with no other significant symptoms. Examination is significant for severe bradycardia. There is no laboratory evidence of renal impairment or acute or ongoing myocardial ischemia or infarction. ECG shows abnormal conduction through the AV node, with dissociation of the atrial (P waves) and ventricular (QRS) activation.

• Most likely diagnosis: Complete heart block (third-degree AV block).
• What else is needed to know about his medical history? Medications taken by patient or recent changes in his regimen.
• Next step in management: Ventricular pacing.

ANALYSIS

Objectives

1. Know how to interpret an electrocardiogram (ECG) and identify the different types of AV block.
2. Recognize key factors that need to be identified and evaluated as part of management of patients with conduction abnormalities.
3. Understand key physical exam findings in patients with complete heart block.
4. Understand different maneuvers that can be employed in the evaluation of patients with second-degree AV block to differentiate Mobitz 1 from Mobitz 2 block.

Considerations

This 75-year-old man presents with severe bradycardia for 24 hours, with associated symptoms (lightheadedness and fatigue). The first, and most important, step in diagnosis of a patient presenting with these symptoms and exam finding of bradycardia is electrocardiogram (ECG). The ECG will provide the diagnosis of what the conduction abnormality is (sinus bradycardia vs. second-degree AV block type 1 or type 2 vs. complete heart block), where the ventricular activation is coming from if complete heart block is present (narrow complex suggesting junctional escape, wide complex suggesting ventricular escape), as well as providing other pertinent information such as the presence of active myocardial ischemia or infarction, or interventricular conduction abnormalities (right or left bundle branch block). This ECG shows complete heart block, identified by dissociation of the atrial and ventricular activation, with more P waves than QRS complexes. Further, the ventricular rate is very slow, and in the presence of symptoms, is not ultimately sustainable. The next immediate step is to stabilize the patient with temporary ventricular pacing. While this patient ultimately may require permanent pacemaker implantation, this process would not occur likely for hours at a minimum, and therefore more immediate intervention is warranted.

Transcutaneous pacing with external pads is an option, but not an ideal one as they are often uncomfortable for the patient and are typically unreliable with either complete inability to pace, or intermittent loss of capture. Transvenous temporary pacing provides more reliability, better pacing options, and aside from initial venous access, is more comfortable for the patient while further workup and planning is done; this can be performed by a trained cardiologist or intensivist.

Finally, after stabilization, baseline workup can commence. Careful review of the patient’s medication list, as well as recent changes, is needed as many medications (beta-blockers, calcium channel blockers, digoxin, antiarrhythmics) may cause AV block that can be resolved with decreasing dose, cessation, or pharmacologic reversal of the agent. Lab evaluation with complete blood count (CBC), comprehensive metabolic panel (CMP; a standardized group of 14 blood tests), and thyroid-stimulating hormone (TSH) blood tests are important to rule out end-organ dysfunction, which may result from hypoperfusion due to bradycardia, as well as ensure that electrolyte or thyroid dysfunction are not culprits in the presenting situation. Cardiac evaluation should include exclusion of myocardial infarction with serial CK, CK-MB, and troponin T or I, as active ischemia or infarct may cause AV conduction abnormalities; and an echocardiogram should be performed to evaluate for baseline LV function, wall motion, and valvular abnormalities. In patients with known severe coronary artery disease, or suspicion of disease due to concomitant symptoms (chest pain, shortness of breath, heart failure symptoms), evaluation for ischemia or severe coronary disease may be necessary with noninvasive stress testing or cardiac catheterization.

Approach To:

Bradycardia

DEFINITIONS

BRADYCARDIA: Ventricular rate <60 bpm.

COMPLETE HEART BLOCK: Dissociation of atrial and ventricular activation.

SECOND-DEGREE HEART BLOCK, MOBITZ TYPE 1: PR interval that progressively prolongs before a nonconducted P wave occurs, resulting in a “dropped” QRS for a single beat.

SECOND-DEGREE HEART BLOCK, MOBITZ TYPE 2: PR interval is consistent beat to beat, and a QRS is consistently dropped, typically at a regular interval (3:2, 4:3, etc).

CLINICAL APPROACH

Etiologies

The most common etiology of acquired AV nodal block is idiopathic fibrosis and sclerosis of the conduction system, accounting for approximately 50% of cases of new AV block. This is termed Lenègre’s disease in young patients, and it is due to slow fibrosis and associated with a slow progression to complete heart block. In the elderly, Lev’s disease is conduction disease due to progressive calcification of fibrous structures of the heart adjacent to the conduction system. This may often start as bifascicular block in the form of right bundle branch block (RBBB) with left anterior fascicular block, which then progresses to complete heart block.

Ischemic heart disease accounts for up to 40% of cases of AV block, and can result from chronic disease or acute myocardial infarction. Of patients with acute MI, 5% will develop second-degree AV block, and 6% will develop complete heart block.

Atrioventricular block can also be caused by increased vagal tone (sleep, carotid sinus massage, pain, athletic training), typically also associated with slowing of the sinus rate. Other causes of AV block include myocarditis, cardiomyopathy, infiltrative diseases, neuromuscular disorders, rheumatologic disorders, thyroid dysfunction (hyper- and hypothyroidism), cardiac tumors, and hyperkalemia. Congenital heart block is diagnosed at birth, and usually associated with a higher ventricular rate than acquired complete heart block.

Iatrogenic causes of AV block include AV nodal blocking medications (betablockers, calcium channel blockers, digoxin, amiodarone, and adenosine), cardiac surgery, or percutaneous interventions (including transcatheter valve replacement, alcohol septal ablation, catheter ablation of arrhythmias, and VSD closure).

Types of AV block

First-degree AV block is defined as a prolongation of the conduction between the atria and ventricles, as determined by a PR interval of >200 ms on ECG.

Second-degree AV block comes in two varieties: Mobitz type 1 (or Wenckebach) and Mobitz type 2. Mobitz type 1 AV block is defined by a progressive PR prolongation with eventual “dropped” QRS complex (Figure 12-2a). The subsequent PR interval after the dropped beat is short, and again shows progressive prolongation in subsequent beats. Mobitz type 1 block typically occurs within the AV node; therefore, maneuvers that improve AV conduction will improve the block (exercise, atropine), whereas maneuvers which decrease AV conduction will worsen the degree of block (carotid sinus massage). Mobitz 1 block does not typically progress to highgrade block (Mobitz II or complete heart block).

Mobitz type 2 second-degree AV block is defined by a stable PR interval in consecutive beats, with nonconduction or “dropped QRS” occurring at either regular or irregular intervals (Figure 12-2b). Mobitz 2 block typically occurs below the AV node, in the His-Purkinje system. As a result of the disease at this level, Mobitz 2 is more often associated with bundle branch block (but not the rule). Maneuvers that improve conduction through the AV node actually worsen Mobitz 2 block, as this decreases recovery time for the His-Purkinje system (exercise, atropine); by contrast, carotid sinus massage will improve Mobitz 2 block, as this slows AV nodal conduction enough to allow the His-Purkinje system to recover and conduct more impulses. Because of instability of the His-Purkinje system in Mobitz 2 block, there is a high rate of progression to complete heart block.

Differentiation between Mobitz types 1 and 2 second-degree AV block is difficult when the ratio of AV conduction is 2:1 (Figure 12-2c). This is clinically relevant

Figure 12-2. Types of atrioventricular (AV) block: (A) second-degree AV block, Mobitz type 1

(Wenckebach); (B) second-degree AV block, Mobitz type 2; (C) second-degree AV block with 2:1 AV

conduction; (d ) third-degree (complete) AV block.

because the likelihood of progression to complete heart block is higher with Mobitz type 2 AV block and knowing the mechanism may influence management (such as the decision to place a transvenous pacing wire). In this circumstance there are some characteristics that may help one distinguish between types 1and 2 (Table 12-1). Third-degree block (complete heart block) is defined as complete dissociation of the atria and ventricles (Figure 12-2d). Typically, in complete heart block, the PP interval and the RR interval are consistent from beat to beat, but are not the same. PR interval will vary as well due to the dissociation. Typically, atrial rate will be higher than the junctional or ventricular escape rate, and more P waves will be noted than QRS complexes.

Clinical Presentation

Patients presenting with complete heart block, or even second-degree AV block, can have various symptoms at presentation. Patients typically experience symptoms consistent with decreased perfusion to end organs. Specifically, lightheadedness, dizziness, fatigue, confusion, and syncope are common. Also associated are shortness of

breath with exertion and angina-like pain. Block due to acute myocardial infarction may present with chest pain or referred pain. Onset of the symptoms may be gradual over hours, or abrupt; in some cases symptoms are not noted until the patient begins physical activity, at which point they cannot increase cardiac output enough to match oxygen demand.

The history taken should be detailed, and specifically focused on when the symptoms started, as that will likely indicate the duration of their bradyarrhythmia. Associated concerning symptoms such as chest pain should elicit evaluation for ischemic heart disease. Detailed review of medications, particularly in those with multiple comorbidities, is necessary; medications with AV nodal blocking activity need to be identified, and dosing, frequency, compliance, and changes in regimen of these medications needs to be discussed.

The physical examination should first note vitals, particularly heart rate (before pacing) and blood pressure. Some patients tolerate bradycardia well with normal blood pressure, whereas others may experience significant hypotension as well. Neck examination may reveal “cannon A waves” of the jugular venous pulsation, consistent with right atrial contraction against a closed tricuspid valve. Lung examination is typically normal, but findings consistent with heart failure such as crackles need to be addressed quickly and portend a more significant disease process. Cardiac exam will identify bradycardia, but also may note variable intensity of S1. An S3 may also identify those with volume overload due to uncoordinated atrial and ventricular conduction. Murmurs should be noted as well, as valvular endocarditis may cause regurgitant disease with infiltration of the conduction system.

Treatment

The first step in management of a patient presenting with bradycardia is determination of the rhythm. In those with symptoms consistent with their bradycardia, or high-degree block, immediate action should be taken to increase the ventricular rate, typically with temporary pacing. Once stabilized, determination of the etiology is the next step. Evaluation for electrolyte disturbance, thyroid or renal dysfunction, and myocardial ischemia should all be undertaken with initial laboratory tests. Any of these abnormalities should be treated aggressively, as correction of the underlying problem (hyperkalemia, thyroid dysfunction, etc) may improve the conduction and obviate the need for permanent pacing. Evidence of myocardial ischemia or active infarction should be addressed with cardiac catheterization and intervention if necessary. Recent cardiac surgery may cause sinus node dysfunction and subsequent bradycardia, particularly junctional bradycardia, but this often improves with time.

Careful medication review is of extreme importance in the assessment of patients with bradycardia, particularly elderly patients in whom polypharmacy is quite common. Medications that can cause AV block (and medications that may potentiate their effect) should be of particular concern. Changes in regimen and compliance (double dosing) should be noted, or changes in organ function that may cause elevated drug levels. Monitoring and withholding of the medication is often all that is required, and once levels decrease, AV function may improve. However, in extreme cases, medication reversal may be necessary with appropriate reversal agents.

Finally, in cases of persistent symptomatic bradycardia, permanent pacing may be required. Consultation with a cardiac electrophysiologist is necessary, for implant of the device, as well as selection of the appropriate type of device (single-chamber, dual-chamber, etc).

COMPREHENSION QUESTIONS

12.1 A 45-year-old woman misunderstood her physician’s instructions and took 10 pills of metoprolol instead of 1 tablet. She presents with some lethargy and a heart rate of 44 bpm and BP of 100/60 mmHg. Which of the following is the best treatment?

A. Digoxin

B. Glucagon

C. Glucose

D. Propranolol

E. Warfarin

12.2 An 86-year-old man with chlorthalidone-treated hypertension presents for evaluation of his 6-month complaint of progressive exercise intolerance. He reports a steady decrease in stamina while walking and as of late has noted dyspnea and lightheadedness after walking for a few minutes. He saw his primary care physician, who arranged for a treadmill ECG study that was nondiagnostic for myocardial ischemia because of failure to achieve target heart rate (he achieved 60% of his maximum predicted heart rate) with no ST segment deviation despite symptoms of shortness of breath and dizziness. His ECG reveals sinus bradycardia with a ventricular rate of 45 bpm and a nonspecific intraventricular conduction abnormality with leftward axis deviation and QRS duration of 122 ms. Basic laboratory data including TSH are normal, and a resting echocardiogram reveals preserved biventricular function with no significant valvular disease and stage 1 diastolic dysfunction. What is the most appropriate next step?

A. Refer for pacemaker implantation to treat symptomatic bradycardia

B. Refer for coronary angiography to exclude coronary artery disease

C. Refer for phase 2 cardiac exercise to treat deconditioning

D. Discontinue chlorthalidone because of a possible medication side effect

E. Begin beta-blockers for diastolic heart failure

12.3 Which of the following statements about second-degree AV block is most accurate?

A. Mobitz type 1 block is likely to progress to complete AV block

B. Mobitz type 2 block tends to improve when the heart rate increases

C. Mobitz type 1 block occurs within the AV node

D. Mobitz type 2 block tends to worsen with carotid sinus massage

E. Mobitz type 1 block features a normal PR interval

ANSWERS

12.1 B. Glucagon is the best antidote to beta-blocker overdose. Digoxin and propranolol are both AV nodal blocking agents that would be expected to worsen bradycardia. Glucose should have little effect on the heart rate in the absence of profound hypoglycemia, and warfarin is an anticoagulant that should have no effect on the AV node.

12.2 A. This patient has symptomatic bradycardia manifesting as chronotropic incompetence or failure of the heart rate to increase to meet physical demands. He also has conduction disease beyond the AV node, and the most appropriate treatment choice would be the implantation of a rate-responsive permanent pacemaker. Coronary angiography is not indicated as this patient does not have symptoms strongly suggestive of coronary disease. Cardiac exercise would be unlikely to help, given that his exercise capacity is limited by his slow heart rate. A thiazide-type diuretic such as chlorthalidone should not cause bradycardia, but the introduction of a beta-blocker such as metoprolol would almost certainly worsen his symptoms.

12.3 C. Mobitz type 1 block occurs within the AV node itself and is often due to dynamic inhibition of the node by drugs or increased vagal tone. The PR interval gradually increases until a QRS drops and the QRS width is normal (provided that there is no underlying distal conduction disease). Vagal maneuvers such as carotid massage tend to worsen the degree of block, whereas sympathetic stimulation or vagolytic medications such as atropine lessen the block. Mobitz type 2 block occurs just distal to the AV node, often resulting in subtle widening of the QRS. The block can handle only a fixed rate of impulses from above, so increasing the heart rate produces more block and slowing the heart rate results in less block. Mobitz type 2 is more likely to progress to complete heart block than Mobitz type 1.

CLINICAL PEARLS

C complete heart block may present with multiple symptoms, including lightheadedness, fatigue, syncope, and shortness of breath.

C The most common cause of AV block is idiopathic fibrosis and sclerosis of the conduction system. The second most common cause is ischemic heart disease.

C second-degree AV block with 2:1 conduction can complicate differentiation between type 1 (Wenckebach) and type 2 Mobitz. Maneuvers that improve AV conduction (exercise, atropine) tend to improve type 1 block while worsening type 2 block.

C Maneuvers that decrease AV conduction (carotid sinus massage) tend to worsen Mobitz 1 block but will improve type 2 block (as a result of slowed AV nodal conduction, allowing the His-Purkinje system to recover for the subsequent impulse).

C In patients with complete heart block and slow rhythms, initial management after ECG is obtained should be directed at providing ventricular pacing, preferably with transvenous temporary pacemaker wires, until possible etiology can be determined, with arrangements for long-term pacing (permanent pacemaker implant).

References

Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342: 703–709. 

Olgin JE, Zipes DP. Specific arrhythmias: Diagnosis and treatment. In: Libby P, et al. Braunwald’s Heart Disease. 8th ed. Philadelphia, PA: Saunders, Elsevier; 2008:913–920. 

Sauer WH. Etiology of atrioventricular block. UpToDate 2014. Leonard I. Ganz, Brian C. Downey, Editors. http://www.uptodate.com.

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