Pulseless electrical activity overview: Difference between revisions
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==Overview== | ==Overview== | ||
Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are [[respiratory failure]] and [[hypovolemia]]. | Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are [[respiratory failure]] and [[hypovolemia]]. | ||
==Pathophysiology== | |||
==Risk Factors== | ==Risk Factors== | ||
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. | 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. | ||
Revision as of 22:47, 18 May 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are respiratory failure and hypovolemia.
Pathophysiology
Risk Factors
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.
Natural History, Complications and Prognosis
PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%.[1] The survival for out of hospital occurrence of PEA is higher (19.5%) than for in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest. The survival of PEA as a presenting rhythm is poorer than ventricular tachycardia or ventricular fibrillation.[2]
Diagnosis
Echocardiography
A rapid beside echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. Elevated right heart filling pressures suggest pulmonary embolism. Tension pneumothorax can also be observed on a bedside echocardiogram.
Treatment
Surgery
External and internal pacing have not been shown to improve outcome and are not recommended. There may be capture of the signals, but there is no improvement in contractility.
References
- ↑ Nadkarni VM, Larkin GL, Peberdy MA, Carey SM, Kaye W, Mancini ME, Nichol G, Lane-Truitt T, Potts J, Ornato JP, Berg RA (2006). "First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults". JAMA : the Journal of the American Medical Association. 295 (1): 50–7. doi:10.1001/jama.295.1.50. PMID 16391216. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help) - ↑ Meaney PA, Nadkarni VM, Kern KB, Indik JH, Halperin HR, Berg RA (2010). "Rhythms and outcomes of adult in-hospital cardiac arrest". Critical Care Medicine. 38 (1): 101–8. doi:10.1097/CCM.0b013e3181b43282. PMID 19770741. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help)