Pulseless Electrical Activity

It is estimated that more than 250,000 deaths occur each year in Canada and the United States as the result of out-of-hospital cardiac arrests.1 Research has focused on a wide variety of topics related to cardiac arrest, from recognition of cardiac symptoms and early defibrillation to tracking patient outcomes.2,3 Pulseless electrical activity (PEA) is one potential finding in a patient in cardiac arrest that EMS?should look for. This article provides an overview of PEA as it applies to adult patients, including its etiology (cause), pathophysiology and management options.

Background, Definition & Pathology

PEA can be defined as the presence of an organized rhythm on the EKG in the absence of a palpable pulse due to a dying myocardium.4–9 In other words, any patient without a palpable pulse, yet showing electrical activity on the EKG—aside from ventricular fibrillation or tachycardia—should be considered to be in PEA. Although these definitions are broad, it is possible to be more detailed when defining PEA.10

It is becoming increasingly common for EMS providers to encounter a patient in PEA.2 It is currently estimated that PEA may occur in as many as 35% of prehospital cardiac arrests in the United States.1,2 Recent reports also suggest that the incidence of prehospital cases of PEA is increasing.2,4,5 In one review of more than 3,000 cardiac arrests, PEA was present in more than 35%, while ventricular fibrillation accounted for less than 15%.2 It has also been noted that when cases of PEA are combined with cases of asystole, they account for more than 50% of cardiac arrests in the prehospital environment.4 Clearly, EMS providers need to become familiar with the recognition and management of PEA.

Different forms of PEA may be uniquely identified. If PEA is the first rhythm identified, it may be referred to as “primary” PEA. In cases where ventricular fibrillation or tachycardia is initially identified and the patient is defibrillated into PEA, this may be referred to as “post-defibrillation PEA.” This approach helps clarify the type of PEA that is involved. It may also potentially be used when trying to predict patient outcomes. For example, primary PEA that is managed in the prehospital environment is reported to have a greater rate of restored spontaneous circulation in contrast to arrests involving prehospital post-defibrillation PEA.3,4 Having this type of background information, such as primary versus post-defibrillation PEA, may prove useful when managing immediate and long-term patient care.4,11

In addition to defining PEA, it is also appropriate to review the pathology that may be involved. PEA develops when an event such as a significant cardiac insult occurs, followed by a decrease in cardiac contractility. Contractility can be influenced by a number of factors including hypoxia, acidosis, increased vagal tone and medical conditions that influence preload and afterload. Impaired myocardial inotropy (force of contraction) may then result and lead to inadequate mechanical activity. When these events occur, they create a unique situation: Myocardial electrical activity is present; however, the myocardial contractions are not sufficient to produce palpable pulses. As a result, there is a significant, if not complete, reduction in cardiac output.2,5,10 If cardiac output is reduced to a point where carotid pulses cannot be palpated, but the patient is still actually responsive, this is referred to as “pseudo-PEA.” Table I on page 66 provides an overview of some of the more common causes of PEA.

PEA Outcomes

Survival rates from cardiac arrest in which the initial presenting rhythm was PEA range from 1%­–10%, depending on the resource consulted.4,5 Several factors appear to foreshadow outcomes in PEA. For example, a narrow QRS complex and faster QRS rate have been associated with improved outcomes. A fast and narrow complex rhythm may indicate that there is a relatively normal heart responding to a severe clinical condition, such as hypovolemia or cardiac tamponade, which may improve with a specific intervention. In such cases, a better outcome may be obtained if the cause is identified and treated appropriately. In contrast, PEA involving a wide QRS complex and a bradycardic rate may represent a dying myocardium, or may indicate the presence of a specific critical rhythm disturbance, such as can be found in hyperkalemia or tricyclic toxicity. 6–8 Similarly, post-defibrillation PEA is associated with a poor prognosis. In one report in which cases of ventricular fibrillation developed post-shock PEA rhythms, only 2% of the patients survived to hospital discharge.2

The frequency with which “reversible” causes of PEA occur may not be as common as previously thought.4 PEA is, in many cases, a terminal rhythm associated with a high mortality rate.3–5 Some authors argue that we are seeing less ventricular fibrillation and more PEA because of the attention that has been focused on the prevention and care of coronary artery disease.2 Regardless, EMS providers should strive to identify the cause of cardiac arrest, paying particular attention to potentially reversible causes. It makes sense that if a potentially reversible cause of arrest is identified and treated, the patient may benefit, and by taking such an approach, patient morbidity and mortality may be positively influenced.2,3

Additional factors can assist in promoting positive outcomes in PEA cardiac arrests. One example is bystander CPR. This component of resuscitation has been associated with improving prehospital patient outcomes, including PEA cases. One report indicates that in cases of PEA in which bystander CPR was involved, the survival rate exceeded 20%.5

Another factor that may influence PEA outcomes is the provider’s ability to accurately assess the presence or absence of a pulse during patient assessment.4,10,12 This factor may result in the question, “Was the patient really in cardiac arrest, or did the provider think the patient was in arrest?” While this seems to involve the relatively basic process of assessing the patient’s airway, breathing and, most important, circulation, it is possible for a provider to miss subtle findings. This may occur if a provider recognizes an EKG rhythm but is unable to palpate a pulse on the patient, even though one is really present. As a result, the provider might incorrectly determine the presence of PEA and proceed with treatment, despite the presence of a pulse. Given the potential for various outcomes and influencing factors, it is crucial for EMS providers to ensure that a thorough and accurate patient assessment is conducted on each case.

Assessment

As you approach the patient, note his overall appearance. Does he appear pale, gray or cyanotic (blue)? Are there any obvious signs of trauma? Do any of the clues on scene hint that a potentially reversible cause of PEA may be present? Does the patient have a medical alert tag or similar identification that might provide insight to the pathology involved? Are bystanders able to provide any additional information or assistance? If possible, consider answering the AMPLE history questions listed in Table II on page 66. This process may reveal potentially reversible causes of the cardiac arrest.

Once patient contact has been established, assess the ABCs and intervene as necessary. Is the patient’s airway open? Is he breathing? Does he have a palpable carotid, brachial or radial pulse? If you are unable to palpate a carotid pulse, consider checking the contralateral (opposite) side of the patient’s neck. The reason for this approach is to assist in locating the presence of a pulse that may be blocked by a pre-existing condition, such as a carotid artery obstruction. Depending on protocols, also check femoral pulses. Is the patient’s skin warm, pink and dry or cool, moist and pale? If any component of the ABCs is not adequate, immediate intervention is indicated.

In PEA scenarios, supporting the patient’s ABCs cannot be overemphasized. When CPR is performed, continue to assess the patient for treatment effectiveness.3,13,14 Ensure that the patient’s airway is patent, adequate ventilations are provided and chest compressions are effective. For example, with each ventilation, observe the patient’s chest for rise and fall. When chest compressions are performed, palpate for a carotid pulse. Consider the patient’s overall appearance.

Treating PEA

There is considerable discussion in the medical literature regarding the causes and treatment of PEA. The specific treatment that is provided in the prehospital setting is influenced by factors such as scene assessment, a patient assessment that includes analysis of the ECG, patient’s medical history and local protocols.2,13,14 EMS providers are encouraged to ensure that general PEA treatments are included in their treatment regimen. This includes supporting the patient’s airway (e.g., intubation), breathing (e.g., provide artificial ventilations), circulation (e.g., fluids) and medication options (e.g., epinephrine and atropine when indicated).6–9,13,14

Successful resuscitation of patients with PEA hinges on rapid diagnosis and treatment of the underlying cause. This may or may not be possible in the field. The prehospital treatment that is provided should focus on identifying causes that can be managed in the field. By taking this approach, we reduce the chance of missing an opportunity to save a patient who would otherwise very likely die.6–8 Examples of causes that can potentially be treated in the field are listed in Table III on page 68.

As we have discussed, providers should consider the potentially reversible causes of arrest whenever possible. One of the reasons for this approach is that low-pressure coronary and/or cerebral blood flow may occur during a period of pulseless electrical activity. If the cause of arrest can be identified and corrected, a positive patient outcome may result.1 For example, if hypoxia is involved, it could be managed by opening the patient’s airway and supporting his ventilations using various airway adjuncts. Hypovolemia, whether traumatic or medical in nature, may be managed with aggressive fluid replacement. A tension pneumothorax may be managed using needle chest decompression. In certain cases, acidosis and overdoses may be managed with a combination of treatment options, including airway management, ventilation and administration of etiology-specific medications like sodium bicarbonate. Hyperkalemia causing PEA may respond to fluids and/or sodium bicarbonate. Other conditions, such as cardiac tamponade and myocardial injury, may require interventions that, depending on the EMS system, can be performed in the field.3,6–8

As with any resuscitation, it is always important to reassess the patient following each intervention. This suggestion also applies to PEA, especially when specific treatments are used in an effort to rule out causes of the arrest. For example, if a fluid bolus is administered, wait for a moment following the bolus before reassessing the patient. If a tension pneumothorax was suspected and chest decompression was performed, reassess the patient to see if breath sounds have returned. By frequently re-assessing the patient, the incidence of overlooking changes in the patient’s status can be reduced. This may prove to be invaluable when managing prehospital cardiac arrests, regardless of the etiology.

Conclusion

It is becoming more common for EMS providers to encounter cardiac arrests involving PEA. By ensuring that providers are aware of the possible causes and management of such arrests, prehospital morbidity and mortality may be reduced. Providers are encouraged to consult with their local protocols and medical direction regarding the latest PEA management options. As it becomes less common for us to encounter ventricular fibrillation in the field, due to our efforts at preventing and treating coronary artery disease, more of our attention needs to focus on studying, understanding and treating PEA with the goal of improving patient outcomes.

References

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10. Schwam E. Pulseless electrical activity: When is closed chest cardiac message beneficial? American Journal of Emergency Medicine 121(2), Oxford, UK: Elsevier Science, 2003.
11.Weil M, Tang W. Cardiopulmonary resuscitation for pulseless rhythms and asystole. Special Editorial, Crit Care Med, 2002.
12. Moore E. Editorial Comment. The Journal of Trauma: Injury, Infection and Critical Care 53(5), 2002.
13. Hafen B, Karren K, Mistovich J. Prehospital Emergency Care, 5th Ed. Upper Saddle River, NJ: Simon & Schuster Co., 1996.
14. Bledsoe B, Porter R, Shade B. Paramedic Emergency Care, 3rd Ed. Upper Saddle River, NJ: Brady Prentice Hall, 1997.