Approach to bradycardia: Clinical sciences

Bradycardia is typically defined as a heart rate below 60 beats per minute, or bpm, although in some instances it can be considered below 50 bpm. Bradycardia may originate from physiologic changes in vagal tone, pathologic changes to the cardiac conduction system, infectious causes, or medication effects.

The severity might range from completely asymptomatic to life-threatening, and based on 12-lead ECG findings, you can determine if the bradycardia is physiologic, or if it’s due to sinus or sinoatrial or SA node dysfunction, or even atrioventricular or AV node dysfunction.

Now, if a patient presents with bradycardia, you should first perform an ABCDE assessment to determine if they are unstable or stable. If they’re unstable and there’s a detectable pulse, follow the ACLS guidelines for Bradycardia with a Pulse.

First stabilize their airway, breathing, and circulation. Provide supplemental oxygen if they’re hypoxemic, to maintain oxygen saturation above 90%. Next, obtain IV access and put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry.

Now let's go back to the ABCDE assessment and discuss the approach to a stable patient. First, perform a focused history and physical examination. Your patient may report exercise intolerance, lightheadedness, or even syncope, and some patients may experience ischemic-type chest pain or nausea.

Additionally, on a physical exam, cardiac auscultation and pulse palpation will reveal a slower than normal heart rate. Moreover, if the heart rate is below 60 beats per minute, you can diagnose bradycardia.

Here’s a clinical pearl! The typical definition of a normal heart rate is between 60 and 100 bpm. However, although technically anything below 60 bpm should be considered bradycardia, you may find it defined as below 50 bpm, since most patients with a heart rate in the 50s are actually asymptomatic and require no treatment.

Next, obtain a 12-lead electrocardiogram, or ECG. If ECG reveals a regular rhythm, upright and uniform P waves before each QRS complex, normal PR interval, and normal P wave morphology, you can diagnose sinus bradycardia.

Now that you know that the slow heart rate is originating from the sinus node, first you should consider SA node dysfunction.

Common causes of SA node dysfunction include sinus pause or sinoatrial exit block, chronotropic incompetence, or tachy-brady syndrome. If the ECG demonstrates periods of sinus bradycardia interrupted by periods of electrical inactivity, without P waves or QRS complexes, this suggests sinus pause or sinoatrial exit block. Moreover, this is the most common cause of sinus node dysfunction, which typically occurs due to age-related fibrosis of the SA node.

Next, if your patient reports exercise intolerance, order an exercise stress test. If the HR fails to increase with exertion, you can diagnose chronotropic incompetence.

Finally, if the sinus bradycardia observed at baseline is interrupted by periods of paroxysmal supraventricular tachycardia, suspect tachy-brady syndrome, also known as sick sinus syndrome.

Now, here’s a clinical pearl to keep in mind! In some individuals, sinus bradycardia occurs only during sleep, but that does not mean it’s benign. The apneic episodes associated with sleep apnea may result in hypoxia, which in turn causes bradycardia. If sleep apnea is suspected, you should order a polysomnogram to further evaluate.

Now if you’re considering SA dysfunction and find that no SA node dysfunction is present.

Then your next step is to assess for physiologic and reversible cause of sinus bradycardia. These causes can be broadly categorized as neurogenic, cardiogenic, or metabolic.

Let’s begin with neurogenic causes. If the bradycardia is at rest, or in a highly conditioned athlete, it is likely a normal response to increased vagal tone, and doesn’t require further evaluation if there are no associated symptoms.

Alternatively, if an individual has a history of syncope related to identifiable triggers, like putting on a tie, changing positions abruptly, or coughing.

Then perform ambulatory ECG monitoring. If episodes of bradycardia correlate with syncopal events, the diagnosis is neurally-mediated bradycardia, such as carotid sinus hypersensitivity, vasovagal syncope, or cough-micturition syndrome.

Next, if your patient has a head injury, stroke or other intracranial pathology that might be interrupting autonomic tracts involved in heart rate response,

perform a physical exam and check for Cushing’s triad which includes a decreased heart rate along with a widened pulse pressure and irregular respirations. If present, suspect increased intracranial pressure as a possible cause of the bradycardia.

Now let’s go over cardiogenic causes of bradycardia. Your patient may report chest pain and the ECG will have ischemic changes in the inferior leads on the 12 lead ECG, such as II, III, and aVF. These leads reflect the right coronary artery, which supplies the SA node, so occlusion leading to acute myocardial ischemia here can cause bradycardia.

Ischemic changes may include pathologic Q waves, ST segment deviations like elevation, and depression, or T wave inversion.

If there’s elevation, you can diagnose a STEMI. On the other hand, if there’s ST depression or no ST changes, you should confirm by checking a serum troponin level.