Sudden cardiac death pathophysiology
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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] Nehal Eid, M.D.[5]
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
- Arrhythmias that cease cardiac mechanical activity[1] include tachyarrhythmias such as ventricular tachycardia (VT) and ventricular fibrillation(VF),and bradyarrhythmias.Such arrythmias are acutely reversible with defibrillation or pacing and may be caused by myocardial injury via acquired cardiac disease (eg, ischemia, inflammation, pressure overload), inherited cardiac disease (eg, arrhythmia syndromes and structural heart diseases), acute electrolyte imbalance(eg,hyperkalemia due to kidney failure),or autonomic dysregulation.
- Approximately 10% of persons who have had outside the hospital cardiac arrests have pulseless electrical activity,[2] defined by absence of palpable pulse in an unconscious person with organized electrical activity other than VT or VF on ECG[3]. Possible underlying causes include acute heart failure, cardiac tamponade, acidosis, hemorrhage, hypoxia, or tension pneumothorax. Asystole is characterized by complete absence of electrical and mechanical cardiac activity.
- These terminal rhythms can be due to:
- Unrecognized underlying structural heart disease such as CAD or cardiomyopathy, arrhythmia syndromes such as long QT syndrome(LQTS) or Brugada syndrome, and conditions that predispose to arrhythmias such as muscular dystrophies[4]
- Noncardiac conditions such as neurocardiogenic VF due to intracranial hemorrhage,[5]bradyarrhythmias secondary to opioid overdose,[6]and serum electrolyte disorders.[7]
- Opioids, stimulants (eg, cocaine), or supplements (eg,herbal medications,energy drinks)[8][9]can also cause sudden cardiac arrest via QT prolongation,[10] predisposing to polymorphic VT, also called torsades de pointes.
- Congenital conditions such as anomalous coronary artery origin with a course between the aorta and pulmonary artery can predispose to cardiac arrest via myocardial ischemia.[11]
- 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.[12][13][14]
| Structural and functional causes of sudden cardiac death | Trigger
| Arrhythmia mechanism
| Fatal arrhythmia
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- 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.[16]
References
- ↑ Nichol G,Rumsfeld J,Eigel B,et al; American Heart Association Emergency Cardiovascular Care Committee;American Heart Association Council on Cardiopulmonary, Perioperative, and Critical Care; American Heart Association Council on Cardiovascular Nursing; American Heart Association Council on Clinical Cardiology; Quality of Care and Outcomes Research Interdisciplinary Working Group.Essential features of designating out-of-hospital cardiac arrest as a reportable event: a scientific statement from the American Heart Association Emergency Cardiovascular Care Committee;Council on Cardiopulmonary, Perioperative, and Critical Care; Council on Cardiovascular Nursing; Council on Clinical Cardiology; and Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2008;117(17):2299-2308. doi:10.1161/ CIRCULATIONAHA.107.189472
- ↑ KitamuraT,Iwami T,Nichol G,et al;Utstein Osaka Project. Reduction in incidence and fatality of out-of-hospital cardiac arrest in females of the reproductive age. Eur Heart J. 2010;31(11):1365-1372. doi:10.1093/eurheartj/ehq059
- ↑ Myerburg RJ,Halperin H,Egan DA,et al. Pulseless electric activity: definition, causes, mechanisms,management,and research priorities for the next decade:report from a NationalHeart, Lung, and BloodI nstitute workshop. Circulation. 2013;128(23):2532-2541. doi:10.1161/ CIRCULATIONAHA.113.004490
- ↑ Groh WJ,Groh MR,Saha C,et al. Electrocardiographic abnormalities and sudden death in myotonic dystrophy type1.N Engl J Med. 2008;358(25):2688-2697.doi:10.1056/ NEJMoa062800
- ↑ Kim AS,Moffatt E,Ursell PC,Devinsky O, Olgin J, Tseng ZH.Sudden neurologic death masquerading as out-of-hospital sudden cardiac death. Neurology. 2016;87(16):1669-1673. doi:10. 1212/WNL.0000000000003238
- ↑ Tseng ZH,Olgin JE,Vittinghoff E, et al. Prospective countywide surveillance and autopsy characterization of sudden cardiac death: POST SCD study.Circulation. 2018;137(25):2689-2700. doi:10.1161/CIRCULATIONAHA.117.033427
- ↑ Siscovick DS, RaghunathanTE,Psaty BM,et al. Diuretic therapy for hypertension and the risk of primary cardiac arrest. N Engl J Med. 1994;330(26): 1852-1857. doi:10.1056/NEJM199406303302603
- ↑ Liperoti R, Vetrano DL,BernabeiR,OnderG. Herbal medications in cardiovascular medicine. J AmCollCardiol. 2017;69(9):1188-1199. doi:10. 1016/j.jacc.2016.11.078
- ↑ Shah SA,Szeto AH,Farewell R,et al.Impact of high volume energy drink consumptionon electrocardiographic and blood pressure parameters: a randomized trial. J AmHeartAssoc. 2019;8(11):e011318. doi:10.1161/JAHA.118.011318
- ↑ Orkin AM,Zhan C,Buick JE,et al. Out-of-hospital cardiac arrest survival in drug-related versus cardiac causes in Ontario: a retrospective cohort study. PLoS One. 2017;12(4): e0176441. doi:10.1371/journal.pone.0176441
- ↑ Gentile F, Castiglione V, De Caterina R. Coronary artery anomalies. Circulation. 2021;144 (12):983-996. doi:10.1161/CIRCULATIONAHA.121. 055347
- ↑ 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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