Pulseless Electrical Activity 

Updated: Mar 27, 2018
Author: Sandy N Shah, DO, MBA, FACC, FACP, FACOI; Chief Editor: Jose M Dizon, MD 



Pulseless electrical activity (PEA) is a clinical condition characterized by unresponsiveness and the lack of a palpable pulse in the presence of organized cardiac electrical activity. Pulseless electrical activity has previously been referred to as electromechanical dissociation (EMD). (See Etiology.)

Although a lack of ventricular electrical activity always implies a lack of ventricular mechanical activity (asystole),[1] the reverse is not always true. That is, electrical activity is a necessary, but not sufficient, condition for mechanical activity. In a situation of cardiac arrest, the presence of organized ventricular electrical activity is not necessarily accompanied by meaningful ventricular mechanical activity. The qualifier “meaningful” is used to describe a degree of ventricular mechanical activity that is sufficient to generate a palpable pulse.

PEA does not mean mechanical quiescence. Patients may have weak ventricular contractions and recordable aortic pressure ("pseudo-PEA"). True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity. PEA encompasses a number of organized cardiac rhythms, including supraventricular rhythms (sinus versus nonsinus) and ventricular rhythms (accelerated idioventricular or escape). The absence of peripheral pulses should not be equated with PEA, as it may be due to severe peripheral vascular disease. (See Etiology, Presentation, and Workup.)


Pulseless electrical activity (PEA) occurs when a major cardiovascular, respiratory, or metabolic derangement results in the inability of cardiac muscle to generate sufficient force in response to electrical depolarization. PEA is always caused by a profound cardiovascular insult (eg, severe prolonged hypoxia or acidosis or extreme hypovolemia or flow-restricting pulmonary embolus).

The initial insult weakens cardiac contraction, and this situation is exacerbated by worsening acidosis, hypoxia, and increasing vagal tone. Further compromise of the inotropic state of the cardiac muscle leads to inadequate mechanical activity, despite the presence of electrical activity. This event creates a vicious cycle, causing degeneration of the rhythm and subsequent death of the patient.

Transient coronary occlusion usually does not cause PEA, unless hypotension or other arrhythmias are involved.

Hypoxia secondary to respiratory failure is probably the most common cause of PEA, with respiratory insufficiency accompanying 40-50% of PEA cases. Situations that cause sudden changes in preload, afterload, or contractility often result in PEA.

The use of antipsychotic agents has been found to be a significant and independent predictor of PEA.[2]

Decreased preload

Cardiac sarcomeres require an optimal length (ie, preload) for an efficient contraction. If this length is unattainable because of volume loss or pulmonary embolus (causing decreased venous return to the left atrium), the left ventricle is unable to generate sufficient pressure to overcome its afterload. Volume loss resulting in PEA is most likely to occur in cases of major trauma. In these situations, rapid blood loss and subsequent hypovolemia can exhaust cardiovascular compensatory mechanisms, culminating in PEA. Cardiac tamponade may also cause decreased ventricular filling.

Increased afterload

Afterload is inversely related to cardiac output. Severe increases in afterload pressure cause a decrease in cardiac output. However, this mechanism is rarely solely responsible for PEA.

Decreased contractility

Optimal myocardial contractility is dependent on an optimal filling pressure, afterload, and the presence and availability of inotropic substances (eg, epinephrine, norepinephrine, or calcium). Calcium influx and binding to troponin C is essential for cardiac contraction. If calcium is not available (eg, calcium channel blocker overdose) or if calcium's affinity to troponin C is decreased (as in hypoxia), contractility suffers.

Depletion of intracellular adenosine triphosphate (ATP) reserves causes an increase in adenosine diphosphate (ADP) levels, which can bind calcium, further reducing energy reserves. Excess intracellular calcium can result in reperfusion injury by causing severe damage to the intracellular structures, predominantly the mitochondria.

Additional etiologic factors

Additional factors contribute to the etiolgy of PEA, including the following mnemonic of “Hs and Ts” favored by the American Heart Association (AHA) and European Resuscitation Council (ERC)[3, 4] :

The "3 and 3 rule" of Desbiens[5] is of more practical use, because it allows easy recall of the most common correctable causes of PEA. This rule organizes PEA causes into three major ones:

  • Severe hypovolemia
  • Pump failure
  • Obstruction to circulation

The three main causes of obstruction to circulation are as follows:

  • Tension pneumothorax [6]
  • Cardiac tamponade [7]
  • Massive pulmonary embolus [8]

Pump failure is the result of massive myocardial infarction, with or without cardiac rupture, and severe heart failure. Major trauma can be responsible for hypovolemia, tension pneumothorax, or cardiac tamponade.

Metabolic derangements (acidosis, hyperkalemia, hypokalemia), although rarely the initiators of PEA, are common contributing factors. Drug overdose (tricyclic antidepressants, digitalis, calcium channel blockers, beta blockers) or toxins are also rare causes of PEA.[9] Hypothermia should be considered in the appropriate clinical context of out-of-hospital PEA.

Postdefibrillation PEA is characterized by the presence of organized electrical activity, occurring immediately after electrical cardioversion in the absence of a palpable pulse. Postdefibrillation PEA may be associated with a better prognosis than continued ventricular fibrillation. A spontaneous return of pulse is likely, and cardiopulmonary resuscitation should be continued for as long as 1 minute to allow for spontaneous recovery.


United States data

The frequency of pulseless electrical activity (PEA) varies among different US patient populations. This condition accounts for approximately 20% of cardiac arrests that occur outside of the hospital setting.

Raizes et al found that PEA was responsible for 68% of monitored in-hospital deaths and 10% of all in-hospital deaths.[10] Because of the increased disease acuity observed in patients who are admitted, PEA may be more likely to occur in patients who are hospitalized. Also, these patients are more likely to have pulmonary emboli and such conditions as ventilator-induced auto–PEEP (positive–end-expiratory pressure). PEA is the first documented rhythm in 32-37% of adults with in-hospital cardiac arrest.[11, 12]

The use of beta blockers and calcium channel blockers may increase the frequency of PEA, presumably by interfering with cardiac contractility.

Sex- and age-related demographics

Females are more likely to develop PEA than males. The reasons for this predilection are unclear but may relate to different etiologies of cardiac arrest.

Patients older than 70 years are more likely to have PEA as an etiology of cardiac arrest. Whether the patient outcome differs based on age is not known; however, advanced age is likely associated with a worse outcome.


The overall prognosis for patients with pulseless electrical activity (PEA) is poor unless a rapidly reversible cause is identified and corrected. Evidence suggests that electrocardiographic (ECG) characteristics are related to the patient's prognosis. The more abnormal the ECG characteristics, the less likely the patient is to recover from PEA; patients with a wider QRS (>0.2 sec) fare worse.

Interestingly, patients with out-of-hospital cardiac arrest (OHCA) in PEA are more likely to recover than are patients who develop this condition in the hospital. In a study, 98 of 503 (19.5%) patients survived OHCA PEA.[13] This difference is likely because of different etiologies and severity of illness. Patients who are not in the hospital are more likely to have reversible etiologies (eg, hypothermia).

In addition, the rate of electrical activity and QRS width do not appear to correlate with survival or neurologic outcome in patients who present with PEA-associated OHCA.[14]

Overall, PEA remains a poorly understood entity with a dismal prognosis. Reversing this otherwise lethal condition may be possible by aggressively seeking and promptly correcting reversible causes.

The Oregon Sudden Unexpected Death Study, which included more than 1,000 cases of patients who presented with PEA (vs ventricular fibrillation), indicated a significantly higher prevalence of syncope that was distinct from cases of ventricular fibrillation. Potential links between future manifestations of PEA and syncope require further investigatation.[15]


A systematic review and meta-analysis of 12 studies comprising 1,108,281 OHCA patients with initial nonshockable cardiac rhythms revealed that conversion to shockable rhythms, particularly when occurring early, was associated with higher likelihoods of prehospital return of spontaneous circulation (ROSC), 1-month survival, and 1-month favorable neurologic outcome, but not with survival to hospital discharge (SHD).[16] Shockable rhythm conversion from asystole, but not PEA, was associated with prehospital ROSC and SHD.

The overall mortality rate is high in patients in whom PEA is the initial rhythm during cardiac arrest. In a study by Nadkarni et al, only 11.2% of patients who had PEA as their first documented rhythm survived to hospital discharge.[11] In a study by Meaney et al, patients with PEA as the first documented rhythm had a lower rate of survival to discharge than did patients who had ventricular fibrillation or ventricular tachycardia as their first documented rhythm.[12]

In a study of 314 cases of OHCA that assessed the futility of resuscitative efforts, no resuscitation was attempted in 34 cases for futility, and 74 cases were partial resuscitation attempts that were quickly discontinued owing to dismal prognostic factors.[17] Among the factors associated with partial attempts were asystole or PEA as the initial rhythm, multiple trauma, unwitnessed OHCA, and a first-response unit being the first unit on scene. The calculated SHD rate was 14% when partial resuscitation attempts were included (there was a 5% increase when partial resuscitation attempts were excluded). Positive factors associated with survival were shockable initial rhythm, public location, and bystander cardiopulmonary resuscitation (CPR).[17]

Data from the American Heart Association's Get With The Guidelines Resuscitation registry (2001-2011) of 1-year survival trends overall and by rhythm in 45,567 Medicare beneficiaries (age ≥65 years) with in-hospital cardiac arrest (IHCA) revealed an unadjusted 1-year survival of 9.4%; it was 6.2% among 36,344 patients with PEA or asystole and 21.8% in 9,223 patients with ventricular fibrillation or pulseless ventricular tachycardia.[18]  However, overall adjusted 1-year survival rates for IHCA improved from 8.9% in 2000-2001 to 15.2% in 2011; for the same time points, they improved from 4.7% to 10.2% for PEA/asystole, and 19.4% to 25.6% for ventricular fibrillation or pulseless ventricular tachycardia.[18]

Given these grim outlooks, the rapid initiation of advanced cardiac life support (ACLS) and swift identification of a reversible cause are critical. Initiation of ACLS may improve patient outcome if a reversible cause is identified and rapidly corrected.



History and Physical Examination


Knowledge of the patient's prior medical conditions allows prompt identification and correction of reversible causes. For example, a debilitated patient who develops acute respiratory failure follwed by pulseless electrical activity (PEA) may have a pulmonary embolus. If an elderly woman develops PEA 2-5 days after a myocardial infarction, a cardiac etiology should be considered (ie, cardiac rupture, recurrent infarction). History of previous drug intake is crucial, enabling prompt treatment of patients in whom drug overdose is suspected. The presence of PEA in the setting of trauma makes hemorrhage (hypovolemia), tension pneumothorax, and cardiac tamponade the more likely causes.

Physical examination

By definition, patients with PEA have no pulse in the presence of organized electrical activity. Therefore, the physical examination should focus on identification of reversible causes; for example, tracheal shift or the unilateral absence of breath sounds indicates tension pneumothorax, whereas normal lung sounds and distended jugular veins point to cardiac tamponade.



Diagnostic Considerations

In out-of-hospital pulseless electrical activity (PEA) cardiac arrests, Ho et al reported that characteristics of presenting prehospital electrocardiograms (ECGs) do not appear to be prognostic for survival to hospital discharge (SHD) or return of spontaneous circulation (ROSC) and therefore should not be used to guide termination of resuscitation.[19]  Prognostic factors included location of arrest for SHD, as well as advanced life support paramedics on scene and successful intubation for ROSC. Atropine use was a negative predictor for SHD and for ROSC.[19]

There are ongoing attempts at developing automatic methods for retrospective data analysis of cardiac rhythms in resuscitation episodes. Unfortunately, although they appear to be successful at automaticaly classifying resuscitation cardiac rhythms, their accuracy and sensitivity for PEA and/or pulse-generating rhythm have been low.[20, 21]

Differential Diagnoses



Approach Considerations

The clinical scenario usually provides useful information in a patient with pulseless electrical activity (PEA). For example, in a previously intubated patient, tension pneumothorax and auto ̶ positive end-expiratory pressure (PEEP) are more likely to occur, whereas in a patient with prior myocardial infarction or congestive heart failure (CHF), myocardial dysfunction is likely. In a patient on dialysis, consider hyperkalemia.

A core temperature should always be obtained if the patient is thought to have hypothermia. In patients diagnosed with hypothermia, resuscitative efforts should be continued at least until the patient is rewarmed, because patient survival is possible even after prolonged resuscitation.[22]

Measure QRS duration, as it has prognostic significance. Patients with a QRS duration shorter than 0.2 second are more likely to recover, and high-dose epinephrine may be administered. Acute rightward axis shifts can suggest possible a pulmonary embolus.

Because of the emergent nature of the problem, laboratory tests are not likely to be helpful in the immediate management of a patient with PEA. If rapidly available, however, values for arterial blood gases (ABGs) and serum electrolyte levels may provide information regarding serum pH, oxygenation, and serum potassium concentration. Glucose evaluation can also be useful.

Invasive monitoring (eg, arterial line) may be placed if it does not cause a delay in delivering standard advanced cardiac life support (ACLS) care. Placement of an arterial line may identify patients with a recordable (but very low) blood pressure; these patients are likely to have a better outcome if given aggressive resuscitation.

Electrocardiographic (ECG) changes on continous telemetry that appear to precede in-hospital cardiac arrest include ST-segment changes, atrial tachyarrhythmias, bradyarrhythmias, P-wave axis changes, QRS prolongation, PR prolongation, isorhythmic dissociation, nonsustained ventricular tachycardia, and PR shortening.[23] The main causes of these changes are respiratory or multiorgan failure.[23]

A 12-lead ECG is difficult to obtain during ongoing resuscitation but, if available, can provide clues to the presence of hyperkalemia (eg, peaked T waves, complete heart block, ventricular escape rhythm) or acute myocardial infarction. Hypothermia, if not already diagnosed, may be suspected by the presence of Osborne waves. Certain drug overdoses (eg, tricyclic antidepressants) prolong QRS duration.


Bedside echocardiography may rapidly identify reversible cardiac problems (eg, cardiac tamponade, tension pneumothorax, massive myocardial infarction, severe hypovolemia).[7, 24] The protocol proposed by Testa et al employs the acronym PEA in reference to pulmonary, epigastric, and abdominal scans used in the assessment for causes of pulseless electrical activity (PEA).[25]

Echocardiography also identifies patients with weak cardiac contractions who have pseudo-PEA. This group of patients is more likely to benefit from aggressive resuscitation,[7] and they may have a rapidly reversible cause (eg, auto–positive-end-expiratory pressure [PEEP]), hypovolemia).

Echocardiography is also invaluable in identifying right ventricular enlargement, pulmonary hypertension suggestive of pulmonary emboli, and ventricular septal rupture.

Bedside ultrasonography appears to have the potential to identify a subset of patients who have different responses to advanced cardiac life support (ACLS) interventions. Secondary analysis of data from 225 patients from the Real-time Evaluation and Assessment Sonography Outcomes Network (REASON) trial who were in PEA cardiac arrest and had cardiac activity on bedside ultrasonography revealed that those with organized cardiac activity had an overall higher survival than patients with disorganized cardiac activity.[26]  The investigators noted improved survival to hospital admission in patients with PEA with organized cardiac activity that was treated with standard ACLS interventions and with continuous adrenergic agents during the resuscitation and before the return of spontaneous circulation compared to individuals who did not receive these treatments.[26] ​



Approach Considerations

Once reversible causes of pulseless electrical activity (PEA) are identified, they should be corrected immediately. This process may involve needle decompression of pneumothorax, pericardiocentesis for tamponade, volume infusion, correction of body temperature, administration of thrombolytics, or surgical embolectomy for pulmonary embolus.


Once the cause of PEA is identified and the patient's condition is stabilized, consultation with appropriate services may be obtained. A cardiothoracic surgery consult may be appropriate for a pulmonary embolectomy in patients with a large pulmonary embolus. In patients with drug overdose, consultation with the toxicology department or the local poison center may be useful after restoration of hemodynamic stability.


Some institutions may not have the capability to provide specialized care (eg, cardiac surgery, pulmonary embolectomy). Once stabilized, patients in these centers may be transferred to tertiary care centers for definitive care.


The following measures may prevent some cases of in-hospital PEA:

  • Patients who have been on prolonged bed rest should receive deep venous thrombosis (DVT) prophylaxis.
  • Patients who are on ventilators should be monitored carefully for the development of auto–positive-end-expiratory pressure (PEEP).
  • Hypovolemia should be treated aggressively, especially in patients with active bleeding.

Pharmacologic Therapy

Resuscitative pharmacology includes epinephrine and atropine.[27] Epinephrine should be administered in 1-mg doses intravenously/intraosseously (IV/IO) every 3-5 minutes during pulseless electrical activity (PEA) arrest. Higher doses of epinephrine have been studied and show no improvement in survival or neurologic outcomes in most patients. Special populations of patients, such as those who have overdosed on beta blockers or calcium channel blockers, may benefit from higher-dose epinephrine. 

If the underlying rhythm is bradycardia (ie, heart rate < 60 bpm) associated with hypotension, then atropine (1 mg IV q3-5 min, up to three doses) should be administered. This is considered the total vagolytic dose, beyond which no further benefit will occur. Note that atropine may cause pupillary dilation—therefore, this sign cannot then be used to assess neurologic function.

Sodium bicarbonate may be administered only in patients with severe, systemic acidosis, hyperkalemia, or a tricyclic antidepressant overdose. The dose is 1 mEq/kg. Routine administration of sodium bicarbonate is discouraged, because it worsens intracellular and intracerebral acidosis and does not appear to alter the mortality rate.

Surgical Care

Pericardiocentesis and emergent cardiac surgery may be lifesaving procedures in appropriate patients with pulseless electrical activity (PEA). In refractory cases, if the patient has suffered chest trauma, a thoracotomy may be performed, provided adequate expertise is available.

Prompt initiation of a cardiopulmonary bypass may have a role in carefully selected patients. This maneuver requires the availability of expertise and support services. Patient selection is paramount because cardiopulmonary bypass should be used only in patients who have an easily reversible etiology of cardiac dysfunction. In an animal model, initiation of prompt cardiopulmonary bypass resulted in a higher rate of success in returning circulation than administration of high- or standard-dose epinephrine. Cardiac pacing can result in electrical capture but does not necessarily increase the incidence of mechanical contractions; hence, this procedure is not recommended.

Near PEA, or a profound low-output state, may also be addressed with different means of circulatory assist (eg, intraaortic balloon pump, extracorporeal membrane oxygenation,[28] cardiopulmonary bypass, ventricular assist device).



Guidelines Summary

Advanced cardiac life support guidelines

Updated cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) guidelines were issued in 2015 by the following organizations:

  • American Heart Association (AHA) [3]
  • European Resuscitation Council (ERC) [4]
  • The International Liaison Committee on Resuscitation (ILCOR) [29]

Overall, the three guidelines concur that the recommendations for a patient in whom pulseless electrical activity (PEA) is suspected are the following[3, 4, 29] :

  • Activate the emergency response system.
  • Initiate CPR, and give oxygen when available.
  • Place an intravenous (IV) line.
  • Intubate the patient.

Once these basic measures are in place, reversible causes should be sought and corrected. These include the following:

  • Hypovolemia
  • Hypoxia
  • Acidosis
  • Hypokalemia/hyperkalemia
  • Hypoglycemia
  • Hypothermia
  • Toxins (eg, tricyclic antidepressants, digoxin, calcium channel blocker, beta-blockers)
  • Cardiac tamponade
  • Tension pneumothorax
  • Massive pulmonary embolus
  • Acute myocardial infarction

Adjuncts for airway control and ventilation

The AHA guidelines also provide the following recommendations for airway control and ventilation[3, 30] :

  • Advanced airway placement in cardiac arrest should not delay initial CPR and defibrillation for ventricular fibrillation arrest. (Class I)
  • If advanced airway placement will interrupt chest compressions, consider deferring insertion of the airway until the patient fails to respond to initial CPR and defibrillation attempts or demonstrates return of spontaneous circulation (ROSC). (Class IIb)
  • The routine use of cricoid pressure in cardiac arrest is not recommended. (Class III)
  • Either a bag-mask device or an advanced airway may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital setting. (Class IIb) The choice of bag-mask device versus advanced airway insertion should be determined by the skill and experience of the provider.
  • For healthcare providers trained in their use, either an supraglottic airway (SGA) device or an endotracheal tube (ETT) may be used as the initial advanced airway during CPR. (Class IIb)
  • Providers who perform endotracheal intubation should undergo frequent retraining (Class I)
  • To facilitate delivery of ventilations with a bag-mask device, oropharyngeal airways can be used in unconscious (unresponsive) patients with no cough or gag reflex and should be inserted only by trained personnel. (Class IIa)
  • In the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred. (Class IIa)
  • Continuous waveform capnography in addition to clinical assessment is the most reliable method of confirming and monitoring correct placement of an ETT. (Class I)
  • If continuous waveform capnometry is not available, a nonwaveform CO 2 detector, esophageal detector device, or ultrasound used by an experienced operator is a reasonable alternative. (Class IIa)
  • After placement of an advanced airway, it is reasonable for the provider to deliver 1 breath every 6 seconds (10 breaths/min) while continuous chest compressions are performed. (Class IIb)
  • Automatic transport ventilators (ATVs) can be useful for ventilation of adult patients in noncardiac arrest who have an advanced airway in place in both out-of-hospital and in-hospital settings. (Class IIb)

There are no significant differences in the recommendations from the ERC or ILCOR.[4, 29]

Medication management

The 2015 AHA guidelines offers the following recommendations for the administration of drugs[3, 30] :

  • Atropine during PEA or asystole is unlikely to have a therapeutic benefit. (Class IIb)
  • There is insufficient evidence for or against the routine initiation or continuation of other antiarrhythmic medications after ROSC from cardiac arrest.
  • Standard-dose epinephrine (1 mg every 3-5 minutes) may be reasonable for patients in cardiac arrest. (Class IIb); high-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III)
  • It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial nonshockable rhythm. (Class IIb)
  • Vasopressin has been removed from the adult cardiac arrest algorithm as it offers no advantage in combination with epinephrine nor as a substitute for standard-dose epinephrine. (Class IIb for both)


Medication Summary

Inotropic, anticholinergic, and alkalinizing agents are used in the treatment of pulseless electrical activity (PEA). As previously stated, resuscitative pharmacology includes epinephrine and atropine. If the underlying rhythm is bradycardia (ie, heart rate < 60 bpm) associated with hypotension, then atropine should be administered. Sodium bicarbonate may be administered only in patients with severe, systemic acidosis; hyperkalemia; or a tricyclic antidepressant overdose.

Inotropic Agents

Class Summary

Inotropic agents increase the central aortic pressure and counter myocardial depression. Their main therapeutic effects are cardiac stimulation, bronchial smooth muscle relaxation, and dilatation of skeletal muscle vasculature.

Epinephrine (Adrenalin)

Epinephrine has alpha-agonist effects that include increased peripheral vascular resistance and reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Anticholinergic Agents

Class Summary

Anticholinergic agents improve conduction through the atrioventricular (AV) node by reducing vagal tone via muscarinic receptor blockade.

Atropine IV/IM (Isopto)

Atropine should be used only in the presence of bradycardia and is not a routine medication for pulseless electrical activity. It works to increase heart rate through vagolytic effects, causing increase in cardiac output. Total vagolytic dose is 2 mg; doses of under 0.5 mg may exacerbate bradycardia

Alkalinizing Agents

Class Summary

These are useful in the alkalinization of urine. Routine administration of sodium bicarbonate is discouraged because it worsens intracellular and intracerebral acidosis and is not proven to reduce mortality rate.

Sodium bicarbonate (Neut)

Sodium bicarbonate is used only when the patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, or tricyclic antidepressant or phenobarbital overdose. Routine use is not recommended.


Questions & Answers


What is pulseless electrical activity (PEA)?

What is the 3 and 3 rule of pulseless electrical activity (PEA) etiology?

What causes pulseless electrical activity (PEA)?

What is the role of decreased preload in the etiology of pulseless electrical activity (PEA)?

What is the role of increased afterload in the etiology of pulseless electrical activity (PEA)?

What is the role of decreased myocardial contractility in the etiology of pulseless electrical activity (PEA)?

What are the risk factors for pulseless electrical activity (PEA)?

What causes obstruction to circulation in pulseless electrical activity (PEA)?

What is the role of myocardial infarction in the etiology of pulseless electrical activity (PEA)?

What is the prevalence of pulseless electrical activity (PEA) in the US?

Which patient groups have the highest prevalence of pulseless electrical activity (PEA)?

What is the prognosis of pulseless electrical activity (PEA)?

What are the mortality rates for pulseless electrical activity (PEA)?


Which physical findings are characteristic of pulseless electrical activity (PEA)?

Which clinical history findings are characteristic of pulseless electrical activity (PEA)?


Which conditions should be included in the differential diagnoses of pulseless electrical activity (PEA)?

What are the differential diagnoses for Pulseless Electrical Activity?


What is included in the workup of pulseless electrical activity (PEA)?

What is the role of echocardiography in the workup of pulseless electrical activity (PEA)?


How is pulseless electrical activity (PEA) treated?

Which specialist consultations are beneficial to patients with pulseless electrical activity (PEA)?

When is patient transfer indicated for the treatment of pulseless electrical activity (PEA)?

How is pulseless electrical activity (PEA) prevented?

What is the role of pharmacologic therapy in the treatment of pulseless electrical activity (PEA)?

What is the role of surgery in the treatment of pulseless electrical activity (PEA)?


Which organizations have issued pulseless electrical activity (PEA) guidelines?

What are the clinical guidelines for the initial treatment of pulseless electrical activity (PEA)?

What are the reversible causes of pulseless electrical activity (PEA)?

What are the AHA guidelines for airway control and ventilation in patients with pulseless electrical activity (PEA)?

What are the AHA guidelines for medication management in patients with pulseless electrical activity (PEA)?


Which medications are used in the treatment of pulseless electrical activity (PEA)?

Which medications in the drug class Alkalinizing Agents are used in the treatment of Pulseless Electrical Activity?

Which medications in the drug class Anticholinergic Agents are used in the treatment of Pulseless Electrical Activity?

Which medications in the drug class Inotropic Agents are used in the treatment of Pulseless Electrical Activity?