Bradycardia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M.Umer Tariq [2] Ibtisam Ashraf, M.B.B.S.[3]
Overview
It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia. There are generally two types of problems that result in bradycardia: Sinus node dysfunction and AV node dysfunction. However other pathophysiologic conditions can also result in bradycardia such as Acute Myocardial infarction, Obstructive sleep apnea, Exaggerated vagal activity, Increased intracranial pressure and infectious diseases such as Lyme disease, rocky mountain spotted fever, Chagas disease, psittacosis, Q fever and typhoid fever.
Pathophysiology
It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia. However, the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker.
There are generally two types of problems that result in bradycardia:
Disorders of the sinus node
- Impaired automaticity - Sinus node dysfunction/sick sinus syndrome)[1]
- Exit block - Impaired conduction of the impulse from the sinus node into the surrounding atrial tissue
Disorders of the atrioventricular node (AV node)
- Atrioventricular conduction disturbances (1o AV block, 2o type I AV block, 2o type II AV block, 3o AV block) may result from impaired conduction in the AV node, or anywhere below it, such as in the bundle of HIS.
Sinus bradycardia can also be seen in these pathophysiologic settings:
Acute Myocardial infarction
- Patients with acute myocardial infarction, especially those with the right coronary artery, as it supplies the SA node are affected by bradycardia.[2]
Obstructive sleep apnea
- Those with obstructive sleep apnea also have sinus bradycardia, which can be extreme (< 30 beats per minute) during apnea.[3]
Exaggerated vagal activity
- Vasovagal responses may be associated with severe bradycardia due to elevated parasympathetic involvement and sympathetic suppression of the SA node. These stimuli include carotid sinus stimulation, vomiting, coughing, and Valsalva maneuver.
Increased intracranial pressure
- Increased intracranial pressure should be excluded when sinus bradycardia arises in a patient with neurological dysfunction.Sinus bradycardia is often associated with damage to the cervical or thoracic spine, where the sympathetic denervation of the heart leaves an uncontested parasympathetic tone.[4]
Infectious causes
- Infectious agents associated with relative sinus bradycardia include Lyme disease, Chagas disease, legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis, malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic fevers, trichinosis, and Rocky Mountain Spotted fever. [5][6]
References
- ↑ Alpert MA, Flaker GC (1983). "Arrhythmias associated with sinus node dysfunction. Pathogenesis, recognition, and management". JAMA. 250 (16): 2160–6. PMID 6620520.
- ↑ Davis WT, Montrief T, Koyfman A, Long B (August 2019). "Dysrhythmias and heart failure complicating acute myocardial infarction: An emergency medicine review". Am J Emerg Med. 37 (8): 1554–1561. doi:10.1016/j.ajem.2019.04.047. PMID 31060863.
- ↑ Caples SM, Rosen CL, Shen WK, Gami AS, Cotts W, Adams M; et al. (2007). "The scoring of cardiac events during sleep". J Clin Sleep Med. 3 (2): 147–54. PMID 17557424.
- ↑ Gilson GJ, Miller AC, Clevenger FW, Curet LB (1995). "Acute spinal cord injury and neurogenic shock in pregnancy". Obstet Gynecol Surv. 50 (7): 556–60. doi:10.1097/00006254-199507000-00022. PMID 7566833.
- ↑ Cunha BA (2000). "The diagnostic significance of relative bradycardia in infectious disease". Clin Microbiol Infect. 6 (12): 633–4. doi:10.1046/j.1469-0691.2000.0194f.x. PMID 11284920.
- ↑ Puljiz I, Beus A, Kuzman I, Seiwerth S (2005). "Electrocardiographic changes and myocarditis in trichinellosis: a retrospective study of 154 patients". Ann Trop Med Parasitol. 99 (4): 403–11. doi:10.1179/136485905X36307. PMID 15949188.