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Pulseless electrical activity

Updated : December 1, 2023





Background

Pulseless electrical activity (PEA), also recognized as electromechanical dissociation, is a clinical condition marked by unresponsiveness and the absence of a palpable pulse despite sufficient electrical discharge. While the absence of ventricular impulse often indicates an absence of ventricular contraction, the reverse is not always true. In cardiac arrest situations, organized ventricular electrical activity typically fails to result in an adequate ventricular response.

Here, “sufficient” denotes a level of ventricular mechanical activity necessary to generate a palpable pulse. It is important to note that pulseless electrical activity does not necessarily imply a complete lack of mechanical activity. Pseudo-PEA can occur where there are ventricular contractions and palpable pressures in the aorta.

True PEA describes a state where cardiac contractions are absent despite coordinated electrical impulses. Various organized cardiac rhythms, whether supraventricular (sinus vs. non-sinus) or ventricular (such as escape rhythms or accelerated idioventricular rhythms), can contribute to pulseless electrical activity. It is crucial to recognize that an impalpable pulse does not always indicate pulseless electrical activity; it might be attributed to severe peripheral vascular abnormalities.

Epidemiology

The occurrence of pulseless electrical activity varies across different patient populations in the United States. It constitutes approximately 20% of sudden cardiac deaths that occur outside of the hospital. A recent study revealed that 68% of documented in-hospital deaths and 10% of all in-hospital deaths were associated with pulseless electrical activity.

Hospitalized patients face a higher likelihood of experiencing complications like pulmonary embolism. Pulseless electrical activity is the initial documented rhythm in 30 to 38% of adults experiencing in-hospital cardiac arrest.

The use of beta-blockers and calcium channel blockers can impact contractility, potentially increasing vulnerability and resistance to treatment. Women exhibit a higher predisposition to developing pulseless electrical activity compared to their male counterparts. The risk of experiencing pulseless electrical activity rises notably after the age of 70, particularly among the female population.

Anatomy

Pathophysiology

Pulseless electrical activity arises when insults affecting the gastrointestinal, cardiovascular, or respiratory systems result in the cardiac muscle’s inability to generate sufficient energy in response to electrical depolarization. This event diminishes cardiac contractility, and the situation is exacerbated by potential factors like hypoxia, acidosis, and heightened vagal tone.

Further compromise to the inotropic state of the cardiac muscle results in inadequate mechanical activity despite the presence of electrical signals, leading to a degeneration of cardiac rhythm and eventual death. Transient coronary occlusion typically does not induce pulseless electrical activity unless hypotension or other arrhythmias are involved.

Respiratory failure, often causing hypoxia, stands out as one of the most common culprits for pulseless electrical activity, contributing to approximately half of PEA cases. Other mechanisms for pulseless electrical activity include reduced preload, increased afterload, and reduced contractility.

A reduction in cardiac contractility has been linked to alterations in intracellular calcium levels, elucidating why individuals using calcium channel blockers or beta-blockers are more susceptible to develop pulseless electrical activity and may exhibit reduced responsiveness to therapy.

Etiology

Hypoxia

Hydrogen ion (acidosis)

Hypothermia

Hypovolemia

Hypokalemia

Hyperkalemia

Trauma

Thrombosis, coronary

Tension pneumothorax

Thrombosis, pulmonary

Tamponade

Genetics

Prognostic Factors

Patients experiencing sudden cardiac arrest attributed to pulseless electrical activity often face a grim prognosis. In a study encompassing 150 such cases, only 23% were successfully resuscitated and survived until hospital admission, with a mere 11% ultimately surviving until discharge.

Regrettably, even with optimal cardiopulmonary resuscitation, pulseless electrical activity continues to be associated with a substantial mortality rate.

Clinical History

Despite the presence of organized electrical activity, there is no palpable pulse, distinguishing PEA from other cardiac rhythms. The condition may be exacerbated by acidosis, contributing to the deterioration of cardiac function.

Respiratory failure, often due to hypoxia, is a common cause of PEA and can manifest as symptoms such as shortness of breath and cyanosis. Although less common, if present, transient coronary occlusion may contribute to PEA, particularly if accompanied by hypotension or other arrhythmias.

Physical Examination

The primary and most notable finding in cases of pulseless electrical activity (PEA) is the absence of palpable pulses. Depending on the underlying cause, additional signs and symptoms may manifest, including:

Tracheal Deviation: In certain instances, tracheal deviation may be observed, indicating potential respiratory or mediastinal issues.

Decreased Skin Turgor: Reduced skin turgor, indicative of dehydration or hypovolemia, may be present as a secondary sign.

Traumatic Chest: Patients with traumatic chest injuries may exhibit specific signs associated with the underlying trauma.

Cool Extremities: Peripheral vasoconstriction can lead to coolness in the extremities, highlighting impaired circulatory function.

Tachycardia: An elevated heart rate may be observed as the body attempts to compensate for the lack of effective cardiac output.

Cyanosis: Insufficient oxygen delivery to tissues can result in cyanosis.

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Acidosis

Accelerated idioventricular rhythm

Cardiac tamponade

Hypokalemia

Hypoxemia

Hypovolemia

Myocardial ischemia

Ventricular fibrillation

Syncope

Tension pneumothorax

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

The management of pulseless electrical activity (PEA) demands a systematic and prompt approach. In the event of PEA, immediate initiation of chest compressions following advanced cardiac life support (ACLS) guidelines is paramount. Simultaneously, administering epinephrine at intervals of 3 to 5 minutes is crucial, with vigilant consideration for reversible causes.

For cases involving bradycardia and hypotension, atropine may be judiciously administered. Sodium bicarbonate finds its role primarily in severe systemic acidosis, hyperkalemia, or tricarboxylic acid overdose.

In refractory situations, pericardial drainage, thoracotomy for chest trauma, or circulatory support through intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiopulmonary bypass, or ventricular assist device may be lifesaving. Success hinges on a coordinated and efficient resuscitation process, emphasizing the importance of rapid interventions and targeted therapies tailored to the specific underlying etiology of PEA.

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Pericardial drainage and urgent surgical intervention can be life-saving for suitable patients experiencing pulseless electrical activity. In cases where refractory situations coexist with chest trauma, a thoracotomy may be considered.

Near-pulseless electrical activity or a state of extremely low cardiac output can also be addressed through circulatory support methods such as an intra-aortic balloon pump, cardiopulmonary bypass, extracorporeal membrane oxygenation, and ventricular assist devices. The likelihood of a favorable outcome hinges on the effectiveness of a highly coordinated resuscitation process.

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Administration of a pharmaceutical agent

  • Epinephrine 

Epinephrine is recommended to be administered in 1 mg doses, either intravenously (IV) or intraosseously (IO), every 3 to 5 minutes during pulseless electrical activity arrest. Following each dose, it is advisable to provide 20 ml of flush and elevate the arm for 10 to 20 seconds to enhance perfusion.

Despite the lack of demonstrated improvement in survival or neurological outcomes in the majority of patients with higher doses of epinephrine, specific groups, such as those affected by beta-blockers or calcium channel blockers overdose, might benefit from elevated doses. In situations where intravenous access is challenging, epinephrine mixed with normal saline can be administered via an endotracheal tube. 

  • Atropine 

In the presence of bradycardia associated with hypotension, the recommended intervention involves administering atropine at a dosage of 1 mg intravenously every 3-5 minutes, with a maximum of three doses. It is important to note that this dosage is considered optimal, with no additional benefits anticipated beyond this point. It is worth highlighting that atropine administration may lead to pupillary dilation, rendering this sign unreliable for assessing neurological function. 

  • Sodium Bicarbonate 

Sodium bicarbonate is appropriate for use solely in patients presenting with severe hyperkalemia, systemic acidosis, or tricarboxylic acid overdose. The recommended dosage is 1 mEq/kg.

It is crucial to refrain from the routine administration of sodium bicarbonate, as it exacerbates intracerebral and intracellular acidosis without imparting any impact on mortality. 

Intervention with procedure

Chest Compressions (Immediate Intervention) 

The initial approach to addressing pulseless electrical activity involves initiating chest compressions in accordance with the advanced cardiac life support (ACLS) guidelines.

Subsequently, administering epinephrine at intervals of 3 to 5 minutes is recommended. Concurrently, healthcare providers should actively search for any reversible causes contributing to the occurrence of pulseless electrical activity. 

 

Medication

Media Gallary

References

Pulseless electrical activity

Updated : December 1, 2023




Pulseless electrical activity (PEA), also recognized as electromechanical dissociation, is a clinical condition marked by unresponsiveness and the absence of a palpable pulse despite sufficient electrical discharge. While the absence of ventricular impulse often indicates an absence of ventricular contraction, the reverse is not always true. In cardiac arrest situations, organized ventricular electrical activity typically fails to result in an adequate ventricular response.

Here, “sufficient” denotes a level of ventricular mechanical activity necessary to generate a palpable pulse. It is important to note that pulseless electrical activity does not necessarily imply a complete lack of mechanical activity. Pseudo-PEA can occur where there are ventricular contractions and palpable pressures in the aorta.

True PEA describes a state where cardiac contractions are absent despite coordinated electrical impulses. Various organized cardiac rhythms, whether supraventricular (sinus vs. non-sinus) or ventricular (such as escape rhythms or accelerated idioventricular rhythms), can contribute to pulseless electrical activity. It is crucial to recognize that an impalpable pulse does not always indicate pulseless electrical activity; it might be attributed to severe peripheral vascular abnormalities.

The occurrence of pulseless electrical activity varies across different patient populations in the United States. It constitutes approximately 20% of sudden cardiac deaths that occur outside of the hospital. A recent study revealed that 68% of documented in-hospital deaths and 10% of all in-hospital deaths were associated with pulseless electrical activity.

Hospitalized patients face a higher likelihood of experiencing complications like pulmonary embolism. Pulseless electrical activity is the initial documented rhythm in 30 to 38% of adults experiencing in-hospital cardiac arrest.

The use of beta-blockers and calcium channel blockers can impact contractility, potentially increasing vulnerability and resistance to treatment. Women exhibit a higher predisposition to developing pulseless electrical activity compared to their male counterparts. The risk of experiencing pulseless electrical activity rises notably after the age of 70, particularly among the female population.

Pulseless electrical activity arises when insults affecting the gastrointestinal, cardiovascular, or respiratory systems result in the cardiac muscle’s inability to generate sufficient energy in response to electrical depolarization. This event diminishes cardiac contractility, and the situation is exacerbated by potential factors like hypoxia, acidosis, and heightened vagal tone.

Further compromise to the inotropic state of the cardiac muscle results in inadequate mechanical activity despite the presence of electrical signals, leading to a degeneration of cardiac rhythm and eventual death. Transient coronary occlusion typically does not induce pulseless electrical activity unless hypotension or other arrhythmias are involved.

Respiratory failure, often causing hypoxia, stands out as one of the most common culprits for pulseless electrical activity, contributing to approximately half of PEA cases. Other mechanisms for pulseless electrical activity include reduced preload, increased afterload, and reduced contractility.

A reduction in cardiac contractility has been linked to alterations in intracellular calcium levels, elucidating why individuals using calcium channel blockers or beta-blockers are more susceptible to develop pulseless electrical activity and may exhibit reduced responsiveness to therapy.

Hypoxia

Hydrogen ion (acidosis)

Hypothermia

Hypovolemia

Hypokalemia

Hyperkalemia

Trauma

Thrombosis, coronary

Tension pneumothorax

Thrombosis, pulmonary

Tamponade

Patients experiencing sudden cardiac arrest attributed to pulseless electrical activity often face a grim prognosis. In a study encompassing 150 such cases, only 23% were successfully resuscitated and survived until hospital admission, with a mere 11% ultimately surviving until discharge.

Regrettably, even with optimal cardiopulmonary resuscitation, pulseless electrical activity continues to be associated with a substantial mortality rate.

Despite the presence of organized electrical activity, there is no palpable pulse, distinguishing PEA from other cardiac rhythms. The condition may be exacerbated by acidosis, contributing to the deterioration of cardiac function.

Respiratory failure, often due to hypoxia, is a common cause of PEA and can manifest as symptoms such as shortness of breath and cyanosis. Although less common, if present, transient coronary occlusion may contribute to PEA, particularly if accompanied by hypotension or other arrhythmias.

The primary and most notable finding in cases of pulseless electrical activity (PEA) is the absence of palpable pulses. Depending on the underlying cause, additional signs and symptoms may manifest, including:

Tracheal Deviation: In certain instances, tracheal deviation may be observed, indicating potential respiratory or mediastinal issues.

Decreased Skin Turgor: Reduced skin turgor, indicative of dehydration or hypovolemia, may be present as a secondary sign.

Traumatic Chest: Patients with traumatic chest injuries may exhibit specific signs associated with the underlying trauma.

Cool Extremities: Peripheral vasoconstriction can lead to coolness in the extremities, highlighting impaired circulatory function.

Tachycardia: An elevated heart rate may be observed as the body attempts to compensate for the lack of effective cardiac output.

Cyanosis: Insufficient oxygen delivery to tissues can result in cyanosis.

Acidosis

Accelerated idioventricular rhythm

Cardiac tamponade

Hypokalemia

Hypoxemia

Hypovolemia

Myocardial ischemia

Ventricular fibrillation

Syncope

Tension pneumothorax

The management of pulseless electrical activity (PEA) demands a systematic and prompt approach. In the event of PEA, immediate initiation of chest compressions following advanced cardiac life support (ACLS) guidelines is paramount. Simultaneously, administering epinephrine at intervals of 3 to 5 minutes is crucial, with vigilant consideration for reversible causes.

For cases involving bradycardia and hypotension, atropine may be judiciously administered. Sodium bicarbonate finds its role primarily in severe systemic acidosis, hyperkalemia, or tricarboxylic acid overdose.

In refractory situations, pericardial drainage, thoracotomy for chest trauma, or circulatory support through intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiopulmonary bypass, or ventricular assist device may be lifesaving. Success hinges on a coordinated and efficient resuscitation process, emphasizing the importance of rapid interventions and targeted therapies tailored to the specific underlying etiology of PEA.

Pericardial drainage and urgent surgical intervention can be life-saving for suitable patients experiencing pulseless electrical activity. In cases where refractory situations coexist with chest trauma, a thoracotomy may be considered.

Near-pulseless electrical activity or a state of extremely low cardiac output can also be addressed through circulatory support methods such as an intra-aortic balloon pump, cardiopulmonary bypass, extracorporeal membrane oxygenation, and ventricular assist devices. The likelihood of a favorable outcome hinges on the effectiveness of a highly coordinated resuscitation process.

  • Epinephrine 

Epinephrine is recommended to be administered in 1 mg doses, either intravenously (IV) or intraosseously (IO), every 3 to 5 minutes during pulseless electrical activity arrest. Following each dose, it is advisable to provide 20 ml of flush and elevate the arm for 10 to 20 seconds to enhance perfusion.

Despite the lack of demonstrated improvement in survival or neurological outcomes in the majority of patients with higher doses of epinephrine, specific groups, such as those affected by beta-blockers or calcium channel blockers overdose, might benefit from elevated doses. In situations where intravenous access is challenging, epinephrine mixed with normal saline can be administered via an endotracheal tube. 

  • Atropine 

In the presence of bradycardia associated with hypotension, the recommended intervention involves administering atropine at a dosage of 1 mg intravenously every 3-5 minutes, with a maximum of three doses. It is important to note that this dosage is considered optimal, with no additional benefits anticipated beyond this point. It is worth highlighting that atropine administration may lead to pupillary dilation, rendering this sign unreliable for assessing neurological function. 

  • Sodium Bicarbonate 

Sodium bicarbonate is appropriate for use solely in patients presenting with severe hyperkalemia, systemic acidosis, or tricarboxylic acid overdose. The recommended dosage is 1 mEq/kg.

It is crucial to refrain from the routine administration of sodium bicarbonate, as it exacerbates intracerebral and intracellular acidosis without imparting any impact on mortality. 

Chest Compressions (Immediate Intervention) 

The initial approach to addressing pulseless electrical activity involves initiating chest compressions in accordance with the advanced cardiac life support (ACLS) guidelines.

Subsequently, administering epinephrine at intervals of 3 to 5 minutes is recommended. Concurrently, healthcare providers should actively search for any reversible causes contributing to the occurrence of pulseless electrical activity.