Pulseless electrical activity risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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 Ca / troponin interactions, and their inhibition of myocardial contractility. History of syncope and pulmonary disease is also associated with a higher risk of presenting PEA [1], as well as history of syncope.
Risk Factors
Beta Blockers and Calcium Channel Blockers
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) [2]. There has been extense literature proving a decrease in the incidence of VF [3] [4]. 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.
Syncope and PEA
There is a strong correlation between patients that had a syncope episode to present future PEA, than those who didn’t. Prevalence is also higher in patients that presented PEA, than those who presented VF/VT or asystolia. Findings were consistent with an odds ratio of 2.64 (Confidence interval 1.31 to 5.32) versus VF/VT and OR of 2.27 (Confidence interval of 1.08 to 4.78) versus asystole [1].
Pulmonary Disease and PEA
Teodorescu et al suggest, a strong relation between pulmonary disease and increased frequency of PEA. There are other publications supporting this association [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.
- ↑ 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.
- ↑ 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.