Pulseless electrical activity risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]
Overview
The administration of beta blockers and calcium channel blockers is associated with an increased risk of PEA. This may be due to their effect on the interactions between calcium and troponin and their inhibition of myocardial contractility. Syncope and pulmonary disease is also associated with a higher risk of PEA.[1]
Risk Factors
The following are the major common risk factors for the PEA(pulseless electrical activity):[2] [3][4][2] [3][5] [6][1][7][8][1]
- Age
- Black race
- Female gender
- Heart failure
- Pulmonary disease
- Syncope
Beta Blockers and Calcium Channel Blockers as Risk Factors for PEA
It is not yet well established why beta blockers and ACE inhibitors are risk factors for PEA. One possible explanation is that the use of beta blockers and ACE inhibitors in the context of ventricular fibrillation might lead to the conversion of ventricular fibrillation (VF) to pulseless electrical activity (PEA).[9] Another explanation for the association is that the pharmacological treatment with beta blockers and ACE inhibitors of patients with VF have lead to a decrease in the prevalence of VF and subsequent relative increase in the incidence of PEA among patients with SCA.[10] [11]
References
- ↑ 1.0 1.1 1.2 Teodorescu C, Reinier K, Dervan C, Uy-Evanado A, Samara M, Mariani R; et al. (2010). "Factors associated with pulseless electric activity versus ventricular fibrillation: the Oregon sudden unexpected death study". Circulation. 122 (21): 2116–22. doi:10.1161/CIRCULATIONAHA.110.966333. PMID 21060069.
- ↑ 2.0 2.1 Becker LB, Han BH, Meyer PM, Wright FA, Rhodes KV, Smith DW; et al. (1993). "Racial differences in the incidence of cardiac arrest and subsequent survival. The CPR Chicago Project". N Engl J Med. 329 (9): 600–6. doi:10.1056/NEJM199308263290902. PMID 8341333.
- ↑ 3.0 3.1 Chu K, Swor R, Jackson R, Domeier R, Sadler E, Basse E; et al. (1998). "Race and survival after out-of-hospital cardiac arrest in a suburban community". Ann Emerg Med. 31 (4): 478–82. PMID 9546017.
- ↑ Jayaraman R, Reinier K, Nair S, Aro AL, Uy-Evanado A, Rusinaru C, Stecker EC, Gunson K, Jui J, Chugh SS (April 2018). "Risk Factors of Sudden Cardiac Death in the Young: Multiple-Year Community-Wide Assessment". Circulation. 137 (15): 1561–1570. doi:10.1161/CIRCULATIONAHA.117.031262. PMC 5918307. PMID 29269388.
- ↑ Pirolo JS, Hutchins GM, Moore GW (1985). "Electromechanical dissociation: pathologic explanations in 50 patients". Hum Pathol. 16 (5): 485–7. PMID 3988275.
- ↑ Herlitz J, Rosenfelt M, Bång A, Axelsson A, Ekström L, Wennerblom B; et al. (1996). "Prognosis among patients with out-of-hospital cardiac arrest judged as being caused by deterioration of obstructive pulmonary disease". Resuscitation. 32 (3): 177–84. PMID 8923578.
- ↑ Allan KS, Morrison LJ, Pinter A, Tu JV, Dorian P (January 2019). "Unexpected High Prevalence of Cardiovascular Disease Risk Factors and Psychiatric Disease Among Young People With Sudden Cardiac Arrest". J Am Heart Assoc. 8 (2): e010330. doi:10.1161/JAHA.118.010330. PMC 6497342. PMID 30661423.
- ↑ Sadeghi R, Adnani N, Sohrabi MR, Alipour Parsa S (September 2013). "Risk of sudden cardiac death". ARYA Atheroscler. 9 (5): 274–9. PMC 3845694. PMID 24302935.
- ↑ Gessman LJ (2009). "Do beta-blockers and ACE inhibitors decrease the duration of ventricular fibrillation, or cause spontaneous conversion of ventricular fibrillation?". Crit Care Med. 37 (1): 329–30. doi:10.1097/CCM.0b013e3181930578. PMID 19112286.
- ↑ Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK (2002). "Changing incidence of out-of-hospital ventricular fibrillation, 1980-2000". JAMA. 288 (23): 3008–13. PMID 12479765.
- ↑ Herlitz J, Andersson E, Bång A, Engdahl J, Holmberg M, lindqvist J; et al. (2000). "Experiences from treatment of out-of-hospital cardiac arrest during 17 years in Göteborg". Eur Heart J. 21 (15): 1251–8. doi:10.1053/euhj.2000.2150. PMID 10924315.