Sudden cardiac death pathophysiology: Difference between revisions

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__NOTOC__
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{{Sudden cardiac death}}
{{Sudden cardiac death}}
{{CMG}} {{AE}} {{Sara.Zand}}
{{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]].
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 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>
*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}}


* 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:
* 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:  
**reduced venous return to the heart;
**Negative [[chronotropic]] and [[drotropic]] effects during [[defecation]]
**Reduced [[cardiac output]];
**Reduced [[venous return]] to the [[heart]]
**[[Sympathetic efferent reflex]] stimulation by arterial [[baroreceptors]] to compensate for such changes;
**Reduced [[cardiac output]]
**Inappropriate stimulation of [[cardiac mechanoreceptors]] (C-fibers) due to sympathetic response in a volume-depleted ventricle;
**[[Sympathetic efferent reflex]] stimulation by [[arterial]] [[baroreceptors]] to compensate for such changes
**[[C-fiber]] signal activates [[vasopressor neurons]] in the [[medulla]] causing [[parasympathetic stimulation]] and [[sympathetic]] withdraw;
**Inappropriate stimulation of [[cardiac mechanoreceptors]] ([[C-fibers]]) due to [[sympathetic]] response in a volume-depleted [[ventricle]]
**[[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>
**[[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==
==References==

Latest revision as of 19:12, 19 July 2023

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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] 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



 
 
 
Structural and functional causes of sudden cardiac death
 
Trigger
  • Myocardial infarction
  • Myocardial ischemia/reperfusion
  • Emotional, physical stress
  • Hemodynamic decompensation
  • Electrolyte imbalance
  • Hypoxemia,acidosis
  • Neurophysiological interactions
  • Drugs
    •  
    		Arrhythmia mechanism
  • Re-entry
  • Automaticity
  • Triggered activity
  • Conduction block
  •  
    		Fatal arrhythmia
  • Monomorphic ventricular tachycardia
  • Polymorphic ventricular tachycardia
  • Ventricular fibrillation
  • Profound bradycardia
  • Asystole
  • Pulseless electrical activity
    •  
     
     
     

    References

    1. ↑ 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.
    2. ↑ 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.
    3. ↑ 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.
    4. ↑ 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.
    5. ↑ 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).

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