Pulseless electrical activity pathophysiology: Difference between revisions
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There is often a downward spiral in the pathophysiology of PEA. A severe initial insult often reduces [[cardiac output]] which may in turn cause [[myocardial ischemia]], [[left ventricular failure]], [[hypoxia]] and [[metabolic acidosis]]. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral. With loss of [[cardiac output]]; [[hypotension]], [[loss of consciousness]] and [[apnea]] rapidly ensue. | There is often a downward spiral in the pathophysiology of PEA. A severe initial insult often reduces [[cardiac output]] which may in turn cause [[myocardial ischemia]], [[left ventricular failure]], [[hypoxia]] and [[metabolic acidosis]]. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral. With loss of [[cardiac output]]; [[hypotension]], [[loss of consciousness]] and [[apnea]] rapidly ensue. | ||
===Reduced Preload and Inadequate Filling of the Left Ventricle | ===Reduced Preload and Inadequate Filling of the Left Ventricle=== | ||
PEA may be due to inadequate filling of the [[left ventricle]] with blood to stretch the cardiac sarcomeres adequately to result in a cardiac contraction (i.e. there is inadequate [[preload]]). Examples include rapid fluid or [[blood loss]] as occurs in major trauma. [[Cardiac tamponade]], [[pneumothorax]], and [[pulmonary embolism]] are other examples. | PEA may be due to inadequate filling of the [[left ventricle]] with blood to stretch the cardiac sarcomeres adequately to result in a cardiac contraction (i.e. there is inadequate [[preload]]). Examples include rapid fluid or [[blood loss]] as occurs in major trauma. [[Cardiac tamponade]], [[pneumothorax]], and [[pulmonary embolism]] are other examples. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
There is often a downward spiral in the pathophysiology of PEA. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral. With loss of cardiac output; hypotension, loss of consciousness and apnea rapidly ensue.
Reduced Preload and Inadequate Filling of the Left Ventricle
PEA may be due to inadequate filling of the left ventricle with blood to stretch the cardiac sarcomeres adequately to result in a cardiac contraction (i.e. there is inadequate preload). Examples include rapid fluid or blood loss as occurs in major trauma. Cardiac tamponade, pneumothorax, and pulmonary embolism are other examples.
Elevated Afterload
Elevated afterload is rarely a cause of PEA.
Electromechanical Dissociation
In some cases, PEA may be caused by electromechanical dissociation. The normal condition when electrical activation of muscle cells precedes mechanical contraction is known as electromechanical coupling. This coupling is lost in some forms of PEA, and this is known as electromechanical dissociation.
Reduced Contractility
Contraction of the myocardium depends upon the integrity of the troponin subunits.
Reduced Calcium Influx
Calcium binding to troponin is required for contractility. This binding can be reduced in calcium channel blocker overdoses.
Reduced Affinity of Troponin for Calcium
In the setting of hypoxia, calcium binds less avidly to troponin.
It is important to differentiate primary from secondary PEA (postshock PEA) to understand physiology of pure PEA. There were several attempts to try to study the pathophysiology of SCA due to PEA. One of them was inducing PEA by asphyxia, which is not the initial mechanism for the onset of PEA, in other than in a clinical induced scenario. In the case of postshock PEA, there is evidence that electrolyte misbalance can explain the presentation of PEA after defibrillation. Whereas on pure PEA, there are several theories that suggest its pathophysiology.
Parasympathetic Theory
There is a theory suggested by DeBehnke in which a vagotomy was performed after PEA provoked by asphyxia [1]. 16 canines were induced by asphyxia until PEA presented [2]. Vagotomy was performed in randomized canines. All of them were managed first with CPR and quemical cardioversion with epinephrine (0.02 mg/kg every five minutes). He found that ROSC was achieved in 13% of canines with no vagotomy, versus a 75% in those with vagotomy (P = .02) [3]. There were also performed hemodynamic and arterial blood gas values at 5, 10 and 15 minutes after ROSC with no significant differences between the 16 canines.
β Blockers
This theory is based on the suspicion that there has been a coincidence in the increased prevalence of SCA due to PEA, and the use of β blockers for cardiac disease [4].
References
- ↑ Myerburg RJ, Halperin H, Egan DA, Boineau R, Chugh SS, Gillis AM; et al. (2013). "Pulseless electric activity: definition, causes, mechanisms, management, and research priorities for the next decade: report from a national heart, lung, and blood institute workshop". Circulation. 128 (23): 2532–41. doi:10.1161/CIRCULATIONAHA.113.004490. PMID 24297818.
- ↑ DeBehnke DJ (1993). "Effects of vagal tone on resuscitation from experimental electromechanical dissociation". Ann Emerg Med. 22 (12): 1789–94. PMID 8239096.
- ↑ DeBehnke DJ (1993). "Atropine use in electromechanical dissociation". Am J Emerg Med. 11 (3): 312. PMID 8489681.
- ↑ 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.