Sudden cardiac death pathophysiology: Difference between revisions
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*Profound [[bradycardia]] | *Profound [[bradycardia]] | ||
*[[Asystole]] | *[[Asystole]] | ||
*[[Pulseless electrical activity]]|}} | *[[Pulseless electrical activity]]|}} | ||
{{Family tree/end}} | {{Family tree/end}} | ||
* A recently published case report described the case of a patient that had [[cardiac arrest]] after defecating. He underwent many [[ECG]] changes before presenting with [[asystolia]]. It has been theorized that [[defecation]] the pathophysiologic development leading to this event is: | * A recently published case report described the case of a patient that had [[cardiac arrest]] after defecating. He underwent many [[ECG]] changes before presenting with [[asystolia]]. It has been theorized that [[defecation]] the pathophysiologic development leading to this event is: |
Revision as of 03:54, 7 June 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2]
Overview
The pathogenesis of cardiac arrest is characterized by the myocardial inflammatory process in the setting of atherosclerosis, structural heart disease, genetic disorders, and environmental factors. The SCN5A, KCNH2, KCNQ1, RYR2, MYBPC3, PKP2, DSP genes mutation are associated with the development of inherited causes of cardiac arrest and sudden cardiac death.
Pathophysiology
- The pathogenesis of cardiac arrest is characterized by the myocardial inflammatory process in the setting of atherosclerosis, structural heart disease, genetic disorders, and environmental factors.
- The SCN5A, KCNH2, KCNQ1, RYR2, MYBPC3, PKP2, DSP genes mutation are associated with the development of inherited causes of cardiac arrest and sudden cardiac death.[1][2][3]
Structural and functional causes of sudden cardiac death | Trigger
| Arrhythmia mechanism
| Fatal arrhythmia
| ||||||||||||||||||||||||||||||||||||
- A recently published case report described the case of a patient that had cardiac arrest after defecating. He underwent many ECG changes before presenting with asystolia. It has been theorized that defecation the pathophysiologic development leading to this event is:
- reduced venous return to the heart;
- Reduced cardiac output;
- Sympathetic efferent reflex stimulation by arterial baroreceptors to compensate for such changes;
- Inappropriate stimulation of cardiac mechanoreceptors (C-fibers) due to sympathetic response in a volume-depleted ventricle;
- C-fiber signal activates vasopressor neurons in the medulla causing parasympathetic stimulation and sympathetic withdraw;
- Parasympathetic stimulation results not only in negative chronotropic, dromnotropic and inotropic effects but also vascular tone instability.[5]
References
- ↑ Osman, Junaida; Tan, Shing Cheng; Lee, Pey Yee; Low, Teck Yew; Jamal, Rahman (2019). "Sudden Cardiac Death (SCD) – risk stratification and prediction with molecular biomarkers". Journal of Biomedical Science. 26 (1). doi:10.1186/s12929-019-0535-8. ISSN 1423-0127.
- ↑ Mehta, Davendra; Curwin, Jay; Gomes, J. Anthony; Fuster, Valentin (1997). "Sudden Death in Coronary Artery Disease". Circulation. 96 (9): 3215–3223. doi:10.1161/01.CIR.96.9.3215. ISSN 0009-7322.
- ↑ Akhtar, Masood (1991). "Sudden Cardiac Death: Management of High-Risk Patients". Annals of Internal Medicine. 114 (6): 499. doi:10.7326/0003-4819-114-6-499. ISSN 0003-4819.
- ↑ Basso, Cristina; Perazzolo Marra, Martina; Rizzo, Stefania; De Lazzari, Manuel; Giorgi, Benedetta; Cipriani, Alberto; Frigo, Anna Chiara; Rigato, Ilaria; Migliore, Federico; Pilichou, Kalliopi; Bertaglia, Emanuele; Cacciavillani, Luisa; Bauce, Barbara; Corrado, Domenico; Thiene, Gaetano; Iliceto, Sabino (2015). "Arrhythmic Mitral Valve Prolapse and Sudden Cardiac Death". Circulation. 132 (7): 556–566. doi:10.1161/CIRCULATIONAHA.115.016291. ISSN 0009-7322.
- ↑ Tsushima T, Patel TR, Sahadevan J (2021). "Unusual Cause of Cardiac Arrest". JAMA Intern Med. 181 (4): 542–543. doi:10.1001/jamainternmed.2020.8370. PMID 33464284 Check
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value (help).