Posts tagged #cardiology

Symptomatic Bradycardia: Considering the Differential Diagnosis

Written by: Keara Kilbane (NUEM ‘25) Edited by: Eric Power (NUEM ‘24)
Expert Commentary by: Seth Trueger, MD, MPH, FACEP


THE HEART CONDUCTION SYSTEM

"Normal” adult heart rates range from 60-100 beats per minute (BPM), with bradycardia defined as a heart rate of less than 60 BPM. Electrical impulses for each heartbeat begin at the sinoatrial (SA) node, then propagate through the atrium to the atrioventricular (AV) node, continuing down the Bundle of His, and lastly to each bundle branch, causing the ventricles to contract. Bradycardia can be physiologic, such as in individuals who have high levels of cardiovascular training. However, pathologic and/or symptomatic bradycardia results from a disruption in this electrical circuit [1].

What is symptomatic bradycardia [1-2]?

Defined as the presence of bradycardia, resulting in debilitating symptoms with lack of alternate explanation. 

The most common symptoms include: 

  • Lightheadedness

  • Syncope 

  • Chest pain

  • Exercise intolerance 

  • Fatigue

**Important note: The heart rate at which patients experience symptoms may vary based on their ability to increase stroke volume. 

CARDIAC OUTPUT = STROKE VOLUME X HEART RATE

Treatment Algorithm for Symptomatic Bradycardia [2-4]:


What are common causes of symptomatic bradycardia [2]?

  1. Myocardial Infarction

  2. Medication

  3. Sinus node dysfunction

  4. Infectious Disease

  5. Hypothermia

  6. Metabolic Abnormalities (hypothyroidism, hyperkalemia, ect.)

  7. Elevated intracranial pressure (ICP)

  8. Genetic Conditions

Myocardial Infarction

Bradyarrhythmias occur in up to 25% of patients with an acute myocardial infarction, especially those involving the right coronary artery (RCA) which supplies the SA node in up to 60% of patients. 

Treatment for bradycardia secondary to myocardial infarction is standard care for an occlusive MI, including emergent cardiology consult and cath lab activation, and loading the patient with anti-platelet medications [5-7]. 

Common Medications and Mechanisms of Causing Bradyarrhythmias

  • Beta Blockers and Non-Dihydropyridine Calcium Channel Blockers (Diltiazem and Verapamil)

    • Inhibit the automaticity of the SA node 

  • Antiarrhythmics (Amiodarone, Adenosine, Flecainide) 

    • Inhibits the SA and AV node 

  • Acetylcholinesterase inhibitors  (Donepezil, Neostigmine, Pyrodostigmine, Physostigmine)

    • Activates the parasympathetic nervous system which leads to inhibition of the automaticity of the SA node 

  • Clonidine

    • Stimulation of central alpha-2-receptors, reducing the norepinephrine

  • Antidepressants (Citalopram, Escitalopram, Fluoxetine)

    • Sodium and calcium channel inhibition

  • Digoxin

    • Increases vagal tone 

  • Anesthetics (Bupivacaine, Propofol) 

    • Reduces sympathetic activity 

Treatment depends on the medication involved. If high suspicion or known overdose, involve and consult your local Poison Center [8]. 

Sinus Node Dysfunction (Sick Sinus Syndrome) [9-10]: 

Sick sinus syndrome is most commonly due to aging of the sinus node and surrounding atrial myocytes. It is often associated with severe bradycardia (HR<50 bpm. It is also associated with sinus pauses, arrests, and SA node block, and or a junctional escape rhythm. Treatment includes  permanent pacemaker placement [9].

Hypothermia

Moderate to severe hypothermia can cause significant bradycardia leading to hypotension. Treatment includes removing all wet clothing, externally rewarming with bair huggers and warm blankets, administering warm IV fluids, active core rewarming including bladder and thoracic irrigation with warmed fluids). It is also important to remember that the differential to hypothermia itself is broad itself and not just limited to environmental exposure. For example, hypothyroidism, adrenal insufficiency, sepsis, neuromuscular disease, malnutrition, thiamine deficiency, hypoglycemia can all lead to hypothermia [11-13]. 

 Decompensated Hypothyroidism (Myxedema Coma)        

Classic symptoms of myxedema coma include: 

  • Decreased mentation or delirium

  • Hypothermia 

  • Bradycardia 

  • Hyponatremia 

  • Hypoglycemia 

  • Hypoventilation

  • Hypotension

Common triggering events:  

  • Infection 

  • Medication non-adherence 

  • Surgery or trauma

  • Myocardial infarction

  • CHF exacerbation 

  • Cerebral Vascular Accident 

  • GI bleed 

Treatment includes IV atropine if unstable while treating the underlying condition (IV steroids, IV levothyroxine) [14]. 

Increased Intracranial Pressure

Classic triad of bradycardia, respiratory depression, and hypertension (Cushing reflex), concerning for brainstem compression and/or herniation [15]. 

 Treatment includes treating the underlying condition, and stabilization through maneuvers including [15]:

  • Hyperventilation 

  • Head of the bed elevation to maximize venous outflow

  • Ensure neck braces (c-collar) is appropriately placed (not too tight)

  • Hypertonic solutions like mannitol or hypertonic saline 

  • Emergent craniotomy

Other Etiologies of Symptomatic Bradycardia [15-16]

  • Prolonged hypoxia

  • Severe electrolyte derangements (hyperkalemia)

  • Vagal response 

  • Severe obstructive sleep apnea

  • Genetic channelopathies 

References: 

  1. Spodick, D. H., Raju, P., Bishop, R. L., & Rifkin, R. D. (1992). Operational definition of normal sinus heart rate. The American Journal of Cardiology, 69(14), 1245–1246. https://doi.org/10.1016/0002-9149(92)90947-w

  2. UpToDate. (n.d.). Www.uptodate.com. https://www.uptodate.com/contents/sinus-bradycardia?search=Bradycardia&source=search_result&selectedTitle=1~150&usage_type=default&disp

  3. Spodick, D. H. (1992). Normal sinus heart rate: Sinus tachycardia and sinus bradycardia redefined. American Heart Journal, 124(4), 1119–1121. https://doi.org/10.1016/0002-8703(92)91012-p

  4. ACLS Bradycardia Algorithm. (n.d.). ACLS Medical Training. https://www.aclsmedicaltraining.com/adult-bradycardia-algorithm/

  5. A. A. J. Adgey, Geddes, J. S., Mulholland, H., Keegan, D., & Pantridge, J. F. (1968). INCIDENCE, SIGNIFICANCE, AND MANAGEMENT OF EARLY BRADYARRHYTHMIA COMPLICATING ACUTE MYOCARDIAL INFARCTION. The Lancet, 292(7578), 1097–1101. https://doi.org/10.1016/s0140-6736(68)91577-8

  6. UpToDate. (n.d.). Www.uptodate.com. Retrieved June 11, 2024, from https://www.uptodate.com/contents/sinus-node-dysfunction-clinical-manifestations-diagnosis-and-evaluation?search=bradycardia&source=

  7. ROTMAN, M., WAGNER, G. S., & WALLACE, A. G. (1972). Bradyarrhythmias in Acute Myocardial Infarction. Circulation, 45(3), 703–722. https://doi.org/10.1161/01.cir.45.3.703

  8. Tisdale, J. E., Chung, M. K., Campbell, K. B., Hammadah, M., Joglar, J. A., Leclerc, J., & Rajagopalan, B. (2020). Drug-Induced arrhythmias: A scientific statement from the american heart association. Circulation, 142(15). https://doi.org/10.1161/cir.0000000000000905

  9. Kusumoto, F. M., Schoenfeld, M. H., Barrett, C., Edgerton, J. R., Ellenbogen, K. A., Gold, M. R., Goldschlager, N. F., Hamilton, R. M., Joglar, J. A., Kim, R. J., Lee, R., Marine, J. E., McLeod, C. J., Oken, K. R., Patton, K. K., Pellegrini, C. N., Selzman, K. A., Thompson, A., & Varosy, P. D. (2019). 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and

  10. Cardiac Conduction Delay. Journal of the American College of Cardiology, 74(7), e51–e156. https://doi.org/10.1016/j.jacc.2018.10.044

  11. Farkas, J. (2021, October 1). Hypothermia. EMCrit Project. https://emcrit.org/ibcc/hypothermia/

  12. UpToDate. (n.d.). Www.uptodate.com. Retrieved June 11, 2024, from https://www.uptodate.com/contents/accidental-hypothermia-in-adults?search=hypothermia&source=search_result&selectedTitle=1~150&usage_type=default&display_r

  13. Näyhä, S. (2005). Environmental temperature and mortality. International Journal of Circumpolar Health, 64(5), 451–458. https://doi.org/10.3402/ijch.v64i5.18026

  14. Decompensated Hypothyroidism (“Myxedema Coma”). (n.d.). EMCrit Project. https://emcrit.org/ibcc/myxedema/#treatment_of_cause

  15. UpToDate. (n.d.). Www.uptodate.com. Retrieved June 11, 2024, from https://www.uptodate.com/contents/evaluation-and-management-of-elevated-intracranial-pressure-in-adults?search=increased%20intracranial%20pressure&source=search_result&selectedTitle=2~150&usage

  16. UpToDate. (n.d.). Www.uptodate.com. https://www.uptodate.com/contents/sinus-bradycardia?search=Bradycardia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=

Expert Commentary

Thank you for this nice review of the differential diagnosis of bradycardia. As emergency physicians, it’s easy to slip into the default of “symptomatic/unstable” vs “asymptomatic/stable” and slip past the underlying causes, and with bradycardia (as with many things), patients are often not divided quite so neatly.

Similarly, the context matters considerably: what resources are available? Is a cardiologist who can place a permanent pacer upstairs and ready with a staffed lab? Or is “definitive care” hours away (eg, requires transfer, or the cardiology team needs to come in from home). A patient with bradycardia from an acute MI will need the cath lab regardless, but in settings that require a transfer that may require transvenous pacemaker prior to transfer. On the other hand, a patient being whisked upstairs to a cath lab requires a different conversation with the cardiology team, eg preparing for transcutaneous pacing while getting the patient from the door to the balloon in a handful of minutes.

The differential can also be helpful when considering other logistics. For example, while I am happy to place a transvenous pacemaker for a patient who needs it for, say, a high degree AV block from Lyme disease, I may consider if the patient is stable enough to have a transvenous pacer placed more elegantly by the cardiology team as the patient may keep the TVP for 2 weeks but not need a permanent pacemaker.

Of course there are also secondary causes of bradycardia that need other, non-cardiac, definitive treatments, eg, overdose, hypothermia, Cushing’s response, and of course, hyperkalemia; keeping the differential in mind is part of the reason why we have not yet been replaced by robots.

Seth Trueger, MD, MPH, FACEP

Associate Professor of Emergency Medicine

Northwestern Memorial Hospital


How To Cite This Post:

[Peer-Reviewed, Web Publication] Kilbane, K. Power, E. (2024, Jun 17). Symptomatic Bradycardia: Considering the Differential Diagnosis. [NUEM Blog. Expert Commentary by Trueger, S]. Retrieved from http://www.nuemblog.com/blog/symptomatic-bradycardia


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