Approach to bradycardia: Clinical sciences

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Introduction0:00–0:49

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.

Unstable patient0:49–1:31

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.

Stable patient1:31–2:35

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.

Sinus bradycardia2:35–2:56

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.

Sinus node dysfunction2:56–4:41

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.

Physiologic/reversible causes4:41–5:06

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.

Neurogenic causes5:06–6:28

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.

Cardiogenic causes6:28–7:56

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.
Elevated troponin levels are highly suggestive of acute myocardial infarction, so you can diagnose an NSTEMI. Lastly, normal troponin levels would indicate myocardial ischemia without infarction, which is consistent with unstable angina.On the other hand, if your patient is taking a beta-blocker, a calcium channel blocker, or digoxin, keep in mind that these medications are known to have negative chronotropic effects, and you are likely dealing with a medication-induced bradycardia.
Lastly, let’s go over metabolic causes of bradycardia. If your patient reports fatigue, weight gain, and cold intolerance, check a TSH and free T4.

Metabolic causes7:56–8:57

If the TSH is elevated and the free T4 is low, your patient has hypothyroidism.Next, if your patient is hypoxic, hypothermic or hypoventilating, pacemaker activity of the SA node can be reduced, causing reversible physiologic bradycardia.Finally, if your patient reports palpitations, and their 12 lead ECG reveals U waves, or tall peaked T waves, consider electrolyte imbalance and order a CMP.
If the serum potassium is below the lower limit of normal or above the upper limit of normal, consider hypokalemia or hyperkalemia as the cause of bradycardia.Alright, now that we’ve considered physiologic and reversible causes of sinus bradycardia, let's go back, revisit our 12 lead ECG, and discuss patients who have evidence of an atrioventricular Block.

AV block8:57–12:12

The patients will have a prolonged PR interval, P waves that are not always followed by a QRS, or evidence of complete AV dissociation.
If you see any of these findings, suspect an atrioventricular block or AV block for short. If there’s a prolonged PR interval, that is greater than 200 milliseconds with P waves that precede each QRS complex, this is first degree AV block.
Alternatively, if there’s progressive lengthening of the PR interval followed by a missing QRS complex, diagnose Mobitz Type 1 second-degree AV block, which is also called Wenckebach phenomenon.
On the other hand, if there’s an unpredictable pattern of non-conducted P waves, but the interval between P waves remains constant, diagnose Mobitz Type II second-degree AV block.
Finally, if there’s wide QRS complexes, indicating ventricular origin, with no relation to the P waves, there’s complete AV dissociation and you can diagnose third degree, or complete, AV block.
If this is the case, there will be a regular P-P interval and a regular R-R interval, but they will be different lengths, usually with the R-R interval being the longer of the two.Now, here's a high-yield fact!
Lyme carditis, a manifestation of Lyme disease, commonly presents with AV nodal block, which can manifest as first, second, or third degree, and may even fluctuate in severity.
Luckily, most cases have relatively mild symptoms, which are transient and improve with appropriate antibiotic treatment of the underlying infection.
Other less common infectious and reversible causes of AV block include viral myocarditis, infective endocarditis, toxoplasmosis, and Chagas disease.And here's another clinical pearl to keep in mind!
Much like the sinoatrial node, the atrioventricular node can be affected by physiologic and reversible causes of bradycardia.
These also include increased vagal tone, as seen in athletes and young persons at rest; ischemia, like in an inferior wall MI; as well as with the use of medications that slow cardiac conduction, like beta blockers.
Additionally, electrolyte abnormalities, like hypokalemia and hyperkalemia can also affect the atrioventricular node. Finally, some causes of AV nodal disease are irreversible, like cardiac sarcoidosis or cardiac amyloidosis, where pathologic fibrosis and protein deposition cause progressive destruction of the cardiac conduction system.
Alright, as a quick recap… When approaching a patient with bradycardia, first perform the ABCDE assessment to determine if your patient is unstable or stable.

Review12:12–14:08

If unstable with a detectable pulse, follow the ACLS guidelines for Bradycardia with a Pulse. On the other hand, if stable, obtain a 12-lead ECG.
If ECG reveals a regular rhythm, upright and uniform P waves before each QRS complex, normal PR interval, and normal P wave morphology, diagnose sinus bradycardia and consider SA node dysfunction.
Important conditions associated with SA node dysfunction include sinus pause or sinoatrial exit block, as well as chronotropic incompetence and Tachy-Brady syndrome.
However, if there’s no SA node dysfunction consider physiological and reversible causes, which can be neurogenic, cardiogenic, or metabolic.
Neurogenic causes include increased vagal tone, neurally-mediated bradycardia, and increased intracranial pressure. Cardiogenic causes include acute myocardial ischemia and medication-induced bradycardia.
Metabolic causes include hypothyroidism, reversible physiologic bradycardia from hypoxia, hypothermia, or hypoventilation, and electrolyte abnormalities, primarily hypo- and hyperkalemia.
Lastly, if 12 lead ECG reveals a prolonged PR interval, P waves that are not always followed by a QRS, or evidence of complete AV dissociation, consider AV block, which can be further classified as first degree, second degree Mobitz I or II, and finally third degree or complete AV block.