Pulseless electrical activity overview

Jump to navigation Jump to search

Pulseless electrical activity Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Pulseless Electrical Activity from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-Ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Pulseless electrical activity overview On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Pulseless electrical activity overview

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Pulseless electrical activity overview

CDC on Pulseless electrical activity overview

Pulseless electrical activity overview in the news

Blogs on Pulseless electrical activity overview

Directions to Hospitals Treating Pulseless electrical activity

Risk calculators and risk factors for Pulseless electrical activity overview

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.

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 tacycardia 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

  1. 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)
  2. 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)

Template:WH Template:WS