Pulseless electrical activity risk factors: Difference between revisions
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==Overview== | ==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]] | 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.<ref name="pmid21060069">{{cite journal| author=Teodorescu C, Reinier K, Dervan C, Uy-Evanado A, Samara M, Mariani R et al.| title=Factors associated with pulseless electric activity versus ventricular fibrillation: the Oregon sudden unexpected death study. | journal=Circulation | year= 2010 | volume= 122 | issue= 21 | pages= 2116-22 | pmid=21060069 | doi=10.1161/CIRCULATIONAHA.110.966333 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21060069 }} </ref> | ||
==Risk Factors== | ==Risk Factors== | ||
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==Beta Blockers and Calcium Channel Blockers as Risk Factors for PEA== | ==Beta Blockers and Calcium Channel Blockers as Risk Factors for PEA== | ||
It is not well established yet why [[beta blocker]]s and [[ACE inhibitor]]s are risk factors for PEA. One possible explanation is that the use of [[beta blocker]]s and [[ACE inhibitor]]s in the context of [[ventricular fibrillation]] might lead to the conversion of [[ventricular fibrillation]] (VF) to [[pulseless electrical activity]] (PEA).<ref name="pmid19112286">{{cite journal| author=Gessman LJ| title=Do beta-blockers and ACE inhibitors decrease the duration of ventricular fibrillation, or cause spontaneous conversion of ventricular fibrillation? | journal=Crit Care Med | year= 2009 | volume= 37 | issue= 1 | pages= 329-30 | pmid=19112286 | doi=10.1097/CCM.0b013e3181930578 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19112286 }} </ref> Another explanation for the association of [[beta blocker]]s and [[ACE inhibitor]]s with the increased incidence of [[PEA]] among patients with [[SCA]] 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.<ref name="pmid12479765">{{cite journal| author=Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK| title=Changing incidence of out-of-hospital ventricular fibrillation, 1980-2000. | journal=JAMA | year= 2002 | volume= 288 | issue= 23 | pages= 3008-13 | pmid=12479765 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12479765 }} </ref> <ref name="pmid10924315">{{cite journal| author=Herlitz J, Andersson E, Bång A, Engdahl J, Holmberg M, lindqvist J et al.| title=Experiences from treatment of out-of-hospital cardiac arrest during 17 years in Göteborg. | journal=Eur Heart J | year= 2000 | volume= 21 | issue= 15 | pages= 1251-8 | pmid=10924315 | doi=10.1053/euhj.2000.2150 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10924315 }} </ref> | |||
==References== | ==References== | ||
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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
- Age
- Female gender
- Heart failure
- Syncope[1]
- Black race
- Pulmonary disease[2] [3]
Beta Blockers and Calcium Channel Blockers as Risk Factors for PEA
It is not well established yet 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).[4] Another explanation for the association of beta blockers and ACE inhibitors with the increased incidence of PEA among patients with SCA 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.[5] [6]
References
- ↑ 1.0 1.1 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.
- ↑ 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.
- ↑ 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.