Continuing Education Activity

Pulseless electrical activity (PEA), also known as electromechanical dissociation, is a clinical condition characterized by unresponsiveness and impalpable pulse in the presence of sufficient electrical discharge. A lack of ventricular impulse often points to the absence of ventricular contraction, but the contrary is not always true. It means that the electrical activity is pertinent, but not sufficient, condition for contraction. In the case of cardiac arrest, the organized ventricular electrical activity does not usually follow sufficient ventricular response. This activity reviews pulseless electrical activity, its causes, its pathophysiology, management, and prognosis of this entity.

Objectives:

• Describe the etiology of pulseless electrical activity.
• Explain the pathophysiology of pulseless electrical activity.
• Review the diagnosis and management of pulseless electrical activity.
• Explain the importance of interprofessional team effort in the successful resuscitation of a patient with pulseless electrical activity.

Introduction

Pulseless electrical activity (PEA), also known as electromechanical dissociation, is a clinical condition characterized by unresponsiveness and impalpable pulse in the presence of sufficient electrical discharge. A lack of ventricular impulse often points to the absence of ventricular contraction, but the contrary is not always true. It means that the electrical activity is pertinent, but not sufficient, condition for contraction. In the case of cardiac arrest, the organized ventricular electrical activity does not usually follow sufficient ventricular response. The word “sufficient” is being used to describe a degree of ventricular mechanical activity that is adequate to generate a palpable pulse.

Pulseless electrical activity does not necessarily mean the lack of mechanical activity. There can be ventricular contractions and detectable pressures in the aorta, which are also known as pseudo-PEA.[1] True pulseless electrical activity is a state in which cardiac contractions are lacking in the presence of coordinated electrical impulses. Pulseless electrical activity can include a number of organized cardiac rhythms that may be supraventricular in origin, sinus versus non sinus, or ventricular in origin such as accelerated idioventricular or escape. An impalpable pulse should not always be taken as a pulseless electrical activity because it may be due to severe peripheral vascular abnormality.[2][3][4]

Etiology

The etiology of pulseless electrical activity is classified into primary i.e., cardiac, and secondary i.e., noncardiac causes.

Primary pulseless electrical activity, often caused by or related to cardiac arrest, is due to the depletion of myocardial energy reserves. It responds poorly to therapy.[5][6][7]

Causes of secondary pulseless electrical activity include the famous "5 Hs and 5 Ts." These are as follows:

5 Hs

1. Hypovolemia
2. Hypoxia
3. Hydrogen ion (acidosis)
4. Hypo/hyperkalemia
5. Hypothermia

5 Ts

1. Tension pneumothorax
2. Trauma
3. Tamponade
4. Thrombosis, pulmonary
5. Thrombosis, coronary

Epidemiology

The incidence of pulseless electrical activity varies among different the United States patient populations. It accounts for approximately 20% of sudden cardiac deaths outside of the hospital setting.[8][9]

A study found that 68% of the recorded in-hospital deaths and 10% of all in-hospital deaths were attributed to pulseless electrical activity. In addition, hospitalized patients are more likely to have a pulmonary embolism, among other complications. Pulseless electrical activity is the first documented rhythm in 30 to 38% of adults with in-hospital cardiac arrest. Beta-blockers and calcium channel blockers may alter contractility, leading to increased susceptibility and resistance to treatment.[10] Women are more likely to develop pulseless electrical activity as compared to the male population. The risk of pulseless electrical activity increases over the age of 70, especially in the female population.

Pathophysiology

Pulseless electrical activity occurs when an insult involving the cardiovascular, gastrointestinal, or respiratory system results in the inability of the cardiac muscle to generate adequate force in response to electrical depolarization. This adverse event decreases cardiac contractility, and the situation gets severe by potential acidosis, hypoxia, and worsening vagal tone. More compromise of the inotropic state of the cardiac muscle leads to insufficient mechanical activity, despite the presence of electrical activity. It causes degeneration of cardiac rhythm, and eventually, death follows.[11]

Transient coronary occlusion usually does not cause pulseless electrical activity unless hypotension or other arrhythmias are involved. Respiratory failure leading to hypoxia is one of the most common causes of pulseless electrical activity, responsible for about half of the PEA cases. The following are other mechanisms for pulseless electrical activity:

• Decreased preload
• Increased afterload
• Decreased contractility

Decreased cardiac contractility has been related to changes in intracellular calcium levels, which explains why patients with beta-blockers or calcium channel blockers are more prone to developing pulseless electrical activity and may become unresponsive to therapy.[12][13][14]

History and Physical

A thorough yet quick history should be reviewed while paying special attention to the following:

• Risk factors for myocardial infarction or pulmonary embolism
• Any trauma
• Severe fluid loss
• Exposure to low temperatures
• Risk of metabolic derangements

Physical findings, as the name indicates, include an absence of palpable pulses is the foremost finding.

Depending upon the cause, one may see the following:

• Tracheal deviation
• Decreased skin turgor
• Traumatic chest
• Cool extremities
• Tachycardia
• Cyanosis[15]

Evaluation

Investigations should include an electrocardiogram (EKG), arterial blood gas analysis, serum electrolytes, core body temperature, chest radiograph, and echocardiogram.[16]

Treatment / Management

The first step in managing pulseless electrical activity is to begin chest compressions according to the advanced cardiac life support (ACLS) protocol followed by administrating epinephrine every 3 to 5 minutes, while simultaneously looking for any reversible causes. Once a diagnosis is made, begin immediate, specific management, i.e., decompression of pneumothorax, pericardial drain for tamponade, fluids infusion for hypovolemia, correction of body temperature for hypothermia, administration of thrombolytics for myocardial infarction or pulmonary embolism. An arterial blood gas and serum electrolytes should be obtained during the resuscitation process.

Epinephrine should be administered in 1 mg doses intravenously (IV)/intraosseously (IO) every 3 to 5 minutes during pulseless electrical activity arrest. Each dose should be followed by 20 ml of flush and elevating the arm for 10 to 20 seconds for better perfusion. Higher doses of epinephrine have not been shown to improve survival or neurologic outcomes in most patients. Selected patients, like those with beta-blockers or calcium channel blockers overdose, may benefit from higher-dose epinephrine. It can also be given via an endotracheal tube after mixing 2 mg in 10 ml of normal saline.[17]

If the detected rhythm is bradycardia that is associated with hypotension, then atropine (1 mg IV every 3-5 min, up to three doses) should be administered. This is considered the optimal dose, beyond which no further benefit will occur. Note that atropine may cause pupillary dilation; therefore, this sign cannot be used to assess neurologic function.[18]

Sodium bicarbonate may be used only in patients with severe, systemic acidosis, hyperkalemia, or tricarboxylic acid overdose. The dose is 1 mEq/kg. Avoid routine administration of sodium bicarbonate as it worsens intracellular and intracerebral acidosis without affecting mortality. 

Pericardial drainage and emergent surgery may be lifesaving in appropriate patients with pulseless electrical activity. In a patient with a refractory case and chest trauma, a thoracotomy may be performed. Near pulseless electrical activity or a very low-output state may also be managed with circulatory assistance (e.g., intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiopulmonary bypass, and ventricular assist device).

The chances of a successful outcome depend on a very coordinated resuscitation process. There should be a specific person responsible for specific steps and a good team leader.

Differential Diagnosis

• Accelerated idioventricular rhythm
• Acidosis
• Cardiac tamponade
• Drug overdose
• Hypokalemia
• Hypothermia
• Hypovolemia
• Hypoxemia
• Myocardial ischemia
• Pulmonary embolism
• Syncope
• Tension pneumothorax
• Ventricular fibrillation[19]

Prognosis

Patients who have sudden cardiac arrest due to pulseless electrical activity have a poor outcome. In one study of 150 such patients, 23% were resuscitated and survived until hospital admission; only 11% survived until hospital discharge.

Unfortunately, despite optimal cardiopulmonary resuscitation, pulseless electrical activity still carries a high mortality rate.[20][21]

Complications

The following complications are likely to be seen in pulseless electrical activity:

• Rib fracture due to chest compression
• Ischemia of extremities due to poor perfusion
• Anoxic injury to the brain[22]

Consultations

The following consultations may be requested to detect and manage the underlying causes of pulseless electrical activity:

• Usually, patients are sent to the intensive care unit (ICU) and managed by the intensivist provider.
• Vascular surgery consult if a large pulmonary embolus is detected.
• A toxicologist for suspected poisoning.
• Cardiothoracic surgery consult for cardiac tamponade.
• Cardiologist for myocardial infarction.

Deterrence and Patient Education

Most of the cardiac arrests are preceded by changes in vital signs, including tachycardia, hypoxia, and tachypnea. Health care professionals should pay attention to such changes and look into the causes and treat them to prevent a potential cardiac arrest due to PEA.

Pearls and Other Issues

• Pulseless electrical activity is a significant cause of mortality, especially in hospitalized, elderly patients.
• Immediate evaluation to look for the cause is warranted.
• Good quality cardiopulmonary resuscitation is the first step after the activation of the emergency response system.
• Epinephrine should be used in conjunction with cardiopulmonary resuscitation.
• The foremost priority is the hemodynamic stability of the patient.
• A six-person, high-performance cardiac arrest team, is best to manage patients with PEA.

Enhancing Healthcare Team Outcomes

All healthcare workers, especially emergency department physicians, nurses, urgent care workers, internists, intensivists, and trauma specialists, must be certified in ACLS. While there are many causes of cardiac arrest, one needs to be aware of pulseless electrical activity, which carries a high mortality rate.

The first step in managing pulseless electrical activity is to start chest compressions according to the ACLS protocol along with using epinephrine, while simultaneously looking for any reversible causes. Once a diagnosis is made, begin immediate management, i.e., decompression of pneumothorax, pericardial drain for tamponade, fluids infusion, correction of body temperature, administration of thrombolytics, or surgical embolectomy for pulmonary embolus. A successful outcome very much depends on the combined efforts of an interprofessional team.