Bradycardia (bradyarrhythmias)

I. Problem/Condition.

Bradycardia is a slow heart rate, traditionally defined as a heart rate less than 60 beats per minute. Due to intrinsic variability in heart rate among individuals and during different times of day, it is difficult to ascertain how common bradycardia is in the general population. Given the variety of underlying etiologies in hospitalized patients, bradycardia requires thoughtful evaluation to determine the appropriate treatment.

II. Diagnostic Approach

A. What is the differential diagnosis for this problem?

See Figure 1, ’The evaluation and management of bradycardia’.

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Figure 1.

Differential diagnosis

B. Describe a diagnostic approach/method to the patient with this problem

The diagnostic approach to bradycardia begins with a thorough history. Patients should be queried about new medications or changed doses of existing medications. Clinicians should screen for potential drug-drug interactions and multiple drugs within the same class (i.e. atrioventricular (AV) nodal blocking agents). Questions should also focus on systemic findings the patient may have in addition to the bradycardia.

For example, a patient with symptoms suggestive of systemic lupus erythematosus (SLE) should have further questioning and diagnostic testing geared towards SLE as a possible cause of the bradycardia.

1. Historical information important in the diagnosis of this problem.

  • Have you had any episodes of “passing out”?

  • Do you ever have any associated symptoms when you notice your heart rate is low – do you feel “dizzy” or “sweaty” or have tunnel vision?

  • Are you taking any new medications?

  • Have there been any changes to your medications?

  • Do you get sleepy during the daytime?

  • Have you ever been told by a sleep partner that you snore?

  • Do you ever have palpitations or feel your heart fluttering?

  • Have you had any fevers or other systemic complaints?

  • Do you drink alcoholic beverages regularly? If you do, have you ever been managed for alcohol intoxication/withdrawal and get low potassium/magnesium levels?

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

In patients in whom the possibility of endocarditis exists based upon the history. Careful physical examination may disclose skin or mucosal lesions in about 50% of cases (See Figure 5). These include subconjunctival and soft palate petechiae, hemorrhages within the nail beds (splinter hemorrhages), painful subcutaneous nodules on the palms or soles (Osler’s nodes), and generalized rashes. Patients may also present with painful embolic lesions on the fingers or toes, which may be visible.

Typically, an endocarditis associated murmur should be carefully auscultated in the mitral or aortic valve position. The vegetations cause typical aortic regurgitation (usually characterized as blowing, decrescendo, and heard best in the third left intercostal space; in severe regurgitation, it may be holodiastolic, sounding lub-dub-shhh, radiating widely along the left sternal border) or mitral insufficiency (typically systolic murmur, sounding lub-shhh-dub in the apical area). One symptom may be intolerance to exercise, because it is difficult to increase the cardiac output. Also, with mitral insufficiency, pulmonary pressures are elevated, possibly creating pulmonary edema. New or changing murmurs in patients with preexisting murmurs are noted in about 30% of cases. A widening of the pulse pressure may be a sign of aortic valve dehiscence, an indication for urgent surgical intervention. Similarly, bradycardia progressing to complete heart block can be caused by a septal abscess, which also requires open surgical débridement and drainage.

Clinicians should also evaluate patients for signs of hypothyroidism, any infiltrative disease (e.g., sarcoidosis or amyloidosis) or rheumatologic diseases if the patient’s history is suggestive of these processes as the underlying etiology of the bradycardia.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

A 12-lead electrocardiogram (ECG) should be performed on all individuals with bradycardia. Further diagnostic testing depends upon the patient’s clinical scenario. Specific causes of bradycardia – acute myocardial infarction, elevated intracranial pressure, medication toxicity and metabolic derangements (i.e. potassium) – must be rapidly excluded from the differential diagnosis.

Specific ECGs offer insight into the underlying cause of a patient’s bradycardia (Figure 2, Figure 3, Figure 4).

Figure 2.

Second degree AV block, Mobitz I

Figure 3.

Second degree AV block, Mobitz II

Figure 4.

Third degree AV block

Figure 5.

Skin or mucosal lesions.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Please refer to the AV block chapter for further information.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Much like syncope, the diagnostic evaluation for patients with bradycardia should be directed by the patient’s history and physical examination findings. All patients should have a 12-lead ECG performed, but other testing is strictly limited based upon the clinician’s impression.

III. Management while the Diagnostic Process is Proceeding

A. Management of bradycardia.

The management of bradycardia depends upon the patient’s degree of symptoms. An asymptomatic patient who is hemodynamically stable may be observed with close outpatient follow-up. If the patient does have symptoms that relate to the bradycardia, they should be admitted for further evaluation. These patients should be placed on telemetry monitoring to evaluate for changes in heart rate, including tachycardic episodes that might suggest tachy-brady syndrome.

Any patient with hemodynamic compromise must be admitted to an intensive care unit for potential temporary pacing or hemodynamic support with parenteral medications. Patients with bradycardia referable to medication overdoses or interactions should have the offending agents stopped and appropriate therapies instituted (e.g., glucagon for beta-blocker overdose).

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

Clinicians are advised to follow the advanced cardiac life support algorithm for symptomatic bradycardia.


Intravenous (IV) atropine may be given at a dose of 0.5 milligrams (mg) and repeated to a maximum cumulative dose of 3 mg. This drug may be effective in symptomatic sinus bradycardia or bradycardia-related to the tachy-brady syndrome. However, patients with high-grade AV blocks may not respond to this medication and will require a pacemaker as the definitive treatment.

Other medications that may prove effective are epinephrine, isoproterenol and dopamine. The doses of these medications will vary as they are titrated to hemodynamic stability. All three medications are a bridge to the placement of a temporary or permanent pacemaker.

For more details regarding the treatment of high grade AV blocks and pacemakers, please refer to those respective chapters.

IV. What’s the Evidence?