Pulseless electrical activity risk factors: Difference between revisions
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* [[Syncope]]<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> | * [[Syncope]]<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> | ||
* Black race | * Black race | ||
* Pulmonary disease<ref name="pmid3988275">{{cite journal| author=Pirolo JS, Hutchins GM, Moore GW| title=Electromechanical dissociation: pathologic explanations in 50 patients. | journal=Hum Pathol | year= 1985 | volume= 16 | issue= 5 | pages= 485-7 | pmid=3988275 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3988275 }} </ref> <ref name="pmid8923578">{{cite journal| author=Herlitz J, Rosenfelt M, Bång A, Axelsson A, Ekström L, Wennerblom B et al.| title=Prognosis among patients with out-of-hospital cardiac arrest judged as being caused by deterioration of obstructive pulmonary disease. | journal=Resuscitation | year= 1996 | volume= 32 | issue= 3 | pages= 177-84 | pmid=8923578 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8923578 }} </ref> | * Pulmonary disease<ref name="pmid3988275">{{cite journal| author=Pirolo JS, Hutchins GM, Moore GW| title=Electromechanical dissociation: pathologic explanations in 50 patients. | journal=Hum Pathol | year= 1985 | volume= 16 | issue= 5 | pages= 485-7 | pmid=3988275 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3988275 }} </ref> <ref name="pmid8923578">{{cite journal| author=Herlitz J, Rosenfelt M, Bång A, Axelsson A, Ekström L, Wennerblom B et al.| title=Prognosis among patients with out-of-hospital cardiac arrest judged as being caused by deterioration of obstructive pulmonary disease. | journal=Resuscitation | year= 1996 | volume= 32 | issue= 3 | pages= 177-84 | pmid=8923578 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8923578 }} </ref> | ||
==Beta Blockers and Calcium Channel Blockers as Risk Factors for PEA== | |||
The main interrogant rewarding whether or not Beta blockers and ACE inhibitors are risk factors for presenting PEA is to determine that they are not aiding into 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>. There has been extense literature proving a decrease in the incidence of VF <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>. However, there is a need to determine whether the relative numbers of the increase of PEA as the presenting rhythm in [[sudden cardiac arrest]] are not in fact increasing because of the decrease of VF due to pharmacological treatment with beta blockers and ACE inhibitors. Or, that the use of beta blockers and ACE inhibitors is diminishing the prevalence of VF, on the behalf of converting VF to PEA or asystole. | The main interrogant rewarding whether or not Beta blockers and ACE inhibitors are risk factors for presenting PEA is to determine that they are not aiding into 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>. There has been extense literature proving a decrease in the incidence of VF <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>. However, there is a need to determine whether the relative numbers of the increase of PEA as the presenting rhythm in [[sudden cardiac arrest]] are not in fact increasing because of the decrease of VF due to pharmacological treatment with beta blockers and ACE inhibitors. Or, that the use of beta blockers and ACE inhibitors is diminishing the prevalence of VF, on the behalf of converting VF to PEA or asystole. | ||
==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. History of 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
The main interrogant rewarding whether or not Beta blockers and ACE inhibitors are risk factors for presenting PEA is to determine that they are not aiding into the conversion of ventricular fibrillation (VF) to pulseless electrical activity (PEA) [4]. There has been extense literature proving a decrease in the incidence of VF [5] [6]. However, there is a need to determine whether the relative numbers of the increase of PEA as the presenting rhythm in sudden cardiac arrest are not in fact increasing because of the decrease of VF due to pharmacological treatment with beta blockers and ACE inhibitors. Or, that the use of beta blockers and ACE inhibitors is diminishing the prevalence of VF, on the behalf of converting VF to PEA or asystole.
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.