Sudden cardiac death pathophysiology: Difference between revisions
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{{Sudden cardiac death}} | {{Sudden cardiac death}} | ||
{{CMG}} {{AE}} {{Sara.Zand}} {{Jose}} {{EdzelCo}} | |||
==Overview== | ==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== | ==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 [[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 | *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]].<ref name="OsmanTan2019">{{cite journal|last1=Osman|first1=Junaida|last2=Tan|first2=Shing Cheng|last3=Lee|first3=Pey Yee|last4=Low|first4=Teck Yew|last5=Jamal|first5=Rahman|title=Sudden Cardiac Death (SCD) – risk stratification and prediction with molecular biomarkers|journal=Journal of Biomedical Science|volume=26|issue=1|year=2019|issn=1423-0127|doi=10.1186/s12929-019-0535-8}}</ref><ref name="MehtaCurwin1997">{{cite journal|last1=Mehta|first1=Davendra|last2=Curwin|first2=Jay|last3=Gomes|first3=J. Anthony|last4=Fuster|first4=Valentin|title=Sudden Death in Coronary Artery Disease|journal=Circulation|volume=96|issue=9|year=1997|pages=3215–3223|issn=0009-7322|doi=10.1161/01.CIR.96.9.3215}}</ref><ref name="Akhtar1991">{{cite journal|last1=Akhtar|first1=Masood|title=Sudden Cardiac Death: Management of High-Risk Patients|journal=Annals of Internal Medicine|volume=114|issue=6|year=1991|pages=499|issn=0003-4819|doi=10.7326/0003-4819-114-6-499}}</ref> | ||
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*Profound [[bradycardia]] | *Profound [[bradycardia]] | ||
*[[Asystole]] | *[[Asystole]] | ||
*[[Pulseless electrical activity]]|}} | *[[Pulseless electrical activity]]|}} | ||
{{Family tree/end}} | {{Family tree/end}} | ||
* The [[pathogenesis]] of [[cardiac arrest]] during [[defecation]] in [[patients]] with [[advanced cardiomyopathy]] and [[poor cardiac reserve]] is defined as [[increased parasympathetic tone]] during [[defecation]] rather than [[conduction system]] abnormalities leading to [[defecation]] induced [[bradyarrhythmia]] by these [[mechanism]]s: | |||
**Negative [[chronotropic]] and [[drotropic]] effects during [[defecation]] | |||
**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.<ref name="pmid33464284">{{cite journal| author=Tsushima T, Patel TR, Sahadevan J| title=Unusual Cause of Cardiac Arrest. | journal=JAMA Intern Med | year= 2021 | volume= 181 | issue= 4 | pages= 542-543 | pmid=33464284 | doi=10.1001/jamainternmed.2020.8370 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33464284 }} </ref> | |||
==References== | |||
{{reflist|2}} | |||
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Latest revision as of 19:12, 19 July 2023
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Risk calculators and risk factors for Sudden cardiac death pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] José Eduardo Riceto Loyola Junior, M.D.[3] Edzel Lorraine Co, DMD, MD[4]
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
| ||||||||||||||||||||||||||||||||||||
- The pathogenesis of cardiac arrest during defecation in patients with advanced cardiomyopathy and poor cardiac reserve is defined as increased parasympathetic tone during defecation rather than conduction system abnormalities leading to defecation induced bradyarrhythmia by these mechanisms:
- Negative chronotropic and drotropic effects during defecation
- 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
|pmid=value (help).