Pulseless electrical activity pathophysiology
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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
PEA( pulseless electrical activity) usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. 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. Other possible mechanisms for pulseless electrical activity include elevated afterload, electromechanical dissociation, reduced contractility, parasympathetic theory.
Pathophysiology
Pulseless electrical activity is nothing but the loss of cardiac muscle to generate adequate force in response to electrical depolarization. It usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. The more and more the inotropic state of the cardiac muscle gets compromised it leads to insufficient mechanical activity, despite the presence of electrical activity. It causes degeneration of cardiac rhythm, and eventually, death follows. Respiratory failure leading to hypoxia is one of the most common causes of pulseless electrical activity. The following are other possible mechanisms for pulseless electrical activity:[1][2][3][4][5][6][7]
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 and ruptured aortic aneurysm. Cardiac tamponade, pneumothorax, and pulmonary embolism are other conditions associated with decreased preload, predisposing to PEA.
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.[8][9][10][11]
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.
Parasympathetic Theory
There is a theory suggested by DeBehnke in which a vagotomy was performed after PEA provoked by asphyxia. Vagotomy was performed in randomized canines. All of them were managed first with CPR and chemical cardioversion with epinephrine (0.02 mg/kg every five minutes). He found that ROSC (Return of Spontaneous Circulation) was achieved in 13% of canines with no vagotomy, versus a 75% in those with vagotomy (P = .02). 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. 16 canines were induced by asphyxia until PEA presented [12][13].[7].
References
- ↑ Oliver TI, Sadiq U, Grossman SA. PMID 30020721. Missing or empty
|title=(help) - ↑ Saarinen S, Salo A, Boyd J, Laukkanen-Nevala P, Silfvast C, Virkkunen I, Silfvast T (November 2018). "Factors determining level of hospital care and its association with outcome after resuscitation from pre-hospital pulseless electrical activity". Scand J Trauma Resusc Emerg Med. 26 (1): 98. doi:10.1186/s13049-018-0568-0. PMC 6245922. PMID 30454005.
- ↑ Weber F, Guha R, Weinberg G, Steinbach F, Gitman M (June 2019). "Prolonged Pulseless Electrical Activity Cardiac Arrest After Intranasal Injection of Lidocaine With Epinephrine: A Case Report". A A Pract. 12 (11): 438–440. doi:10.1213/XAA.0000000000000962. PMID 30663992.
- ↑ Sillers L, Handley SC, James JR, Foglia EE (2019). "Pulseless Electrical Activity Complicating Neonatal Resuscitation". Neonatology. 115 (2): 95–98. doi:10.1159/000493357. PMID 30352434.
- ↑ Littmann L, Bustin DJ, Haley MW (2014). "A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity". Med Princ Pract. 23 (1): 1–6. doi:10.1159/000354195. PMC 5586830. PMID 23949188.
- ↑ Patil KD, Halperin HR, Becker LB (June 2015). "Cardiac arrest: resuscitation and reperfusion". Circ. Res. 116 (12): 2041–9. doi:10.1161/CIRCRESAHA.116.304495. PMC 5920653. PMID 26044255.
- ↑ 7.0 7.1 Myerburg RJ, Halperin H, Egan DA, Boineau R, Chugh SS, Gillis AM, Goldhaber JI, Lathrop DA, Liu P, Niemann JT, Ornato JP, Sopko G, Van Eyk JE, Walcott GP, Weisfeldt ML, Wright JD, Zipes DP (December 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.
- ↑ Ewy GA (September 1984). "Defining electromechanical dissociation". Ann Emerg Med. 13 (9 Pt 2): 830–2. doi:10.1016/s0196-0644(84)80452-7. PMID 6476549.
- ↑ Aufderheide TP, Thakur RK, Stueven HA, Aprahamian C, Zhu YR, Fark D, Hargarten K, Olson D (April 1989). "Electrocardiographic characteristics in EMD". Resuscitation. 17 (2): 183–93. doi:10.1016/0300-9572(89)90070-1. PMID 2546234.
- ↑ Stueven HA, Aufderheide T, Waite EM, Mateer JR (April 1989). "Electromechanical dissociation: six years prehospital experience". Resuscitation. 17 (2): 173–82. doi:10.1016/0300-9572(89)90069-5. PMID 2546233.
- ↑ Stueven HA, Aufderheide T, Thakur RK, Hargarten K, Vanags B (April 1989). "Defining electromechanical dissociation: morphologic presentation". Resuscitation. 17 (2): 195–203. doi:10.1016/0300-9572(89)90071-3. PMID 2546235.
- ↑ 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.