Pulseless Electrical Activity


Article Author:
Tony Oliver
Usama Sadiq


Article Editor:
Shamai Grossman


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
6/4/2019 1:11:29 PM

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. 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 nonsinus) or ventricular in origin (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. [1][2][3]

Etiology

The etiology of pulseless electrical activity is classified into primary/cardiac and secondary/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. [4][5][6]

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 United States patient populations. It accounts for approximately 20% of sudden cardiac deaths outside of the hospital setting.[7][8]

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 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. 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 the 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. 

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.[9][10][11]

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

Evaluation

Investigations should include an EKG, arterial blood gas analysis, serum electrolytes, core body temperature, chest X-ray, and echocardiogram.

Treatment / Management

The first step in managing pulseless electrical activity is to begin chest compressions according to 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/intraosseously 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 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 endotracheal tube after mixing 2 mg in 10 ml of normal saline.

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.

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 the 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

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 to hospital admission; only 11% survived until hospital discharge.

Unfortunately, despite optimal CPR and resuscitation, pulseless electrical activity still carries a high mortality rate.[12][13]

Complications

Rib fracture due to chest compression

Ischemia of extremities due to poor perfusion

Anoxic injury to the brain

Consultations

Usually, patients are sent to the Intensive care and managed by the  intensivist 

Vascular surgery consult if a large pulmonary embolus is detected

Toxicologist for poisoning

Cardiothoracic surgery for tamponade

Cardiologist for Myocardial infarction

Deterrence and Patient Education

Most of the cardiac arrests are preceded by changes in the vital signs including tachycardia, hypoxia, and tachypnea.

Health care professional should pay attention to such changes and look into the causes  and treat them and prevent a potential cardiac arrest  due to PEA

Pearls and Other Issues

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

Enhancing Healthcare Team Outcomes

All healthcare workers, especially emergency department physicians, nurses, urgent care workers, internists, intensivists and trauma specialists must be certified in ALS. 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 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 the multidisciplinary team.

 


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Pulseless Electrical Activity - Questions

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A 75-year-old lady with chronic insulin dependent diabetes mellitus, chronic lymphedema, peripheral vascular disease, and history of stent placement, went into pulmonary air embolism arrest in the ED while being evaluated for fever. After 10 minutes of initial resuscitation, she was found to have an organized rhythm; however, there was no palpable pedal pulse. What is the next best step?



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A 50-year-old man with a history of chronic diabetes mellitus with poor glycemic control, the peripheral vascular disease was evaluated in the emergency room for purulent foot ulcer in the left lower leg. He was hypotensive with a BP of 70/ 40 mm Hg and tachycardic with a rate of 130 beats/ minute and had a respiratory rate of 35 breaths/minute. His lab work showed a WBC count of 24, 000 /µl, potassium of 3.9 mEq/L, urea of 60 mmol/L, bicarbonate of 12mEq/L, and creatinine of 3.5. mg/dL. He goes into cardiac arrest while in the ER. Which of the following will be the most likely rhythm in this patient?



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A 70-year-old man with a history of chronic bronchitis, nonischemic cardiomyopathy, hypertension, atrial fibrillation, chronic renal failure, systemic sclerosis who takes aspirin, metoprolol, amiodarone went into pulseless electrical activity (PEA) arrest, while he was waiting for his routine office visit with his primary care physician. Despite initiating ACLS protocol and multiple rounds of administration of adrenaline, he died. What is the most likely factor contributed to increased susceptibility and resistance to treatment to PEA?



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A 62-year-old man arrived in pulseless cardiac arrest. An organized rhythm was present on the cardiac monitor, but there was no palpable pulse. Pulseless electrical activity (PEA) was suspected. CPR was begun, and on obtaining more history from the family, it was found out that he has a history of severe chronic bronchitis, history of coronary bypass graft and stent placement several years back, end-stage renal disease on peritoneal dialysis, diabetes mellitus type 2 on insulin. He went on a week-long vacation in a camping ground in a remote area. On the third day of camping, the peritoneal catheter was blocked, and he was unable to fix it. On the fifth day, he also ran out of his insulin and aspirin. However, he continued with his camping and came to his home on the morning of admission. He was feeling very weak and was breathing rapidly on arrival and collapsed. What is the likely cause of the PEA arrest?

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    Contributed by Tammy J. Toney-Butler, AS, RN, CEN, TCRN, CPEN
Attributed To: Contributed by Tammy J. Toney-Butler, AS, RN, CEN, TCRN, CPEN



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A 62-year-old woman status post-three-vessel coronary artery bypass grafting (CABG), and TAVR is under the care of a critical care team in the intensive care unit. She was put on a ventilator due to respiratory insufficiency. The ventilator settings include FiO2 of 70, PEEP of 20, Rate of 12. She loses pulse suddenly. The EKG shows narrow QRS complexes. There is absent breath sounds on the left side with tracheal deviation on the right side. Which of the following is the next step in management after initiating CPR?



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A 35-year-old patient with no history of hypertension and DM is brought to the emergency department after he was found unresponsive by his wife in the living room. Previously he had blunt trauma to his abdomen in a bicycle crash. He had some abdominal discomfort but did not seek care. EKG shows sinus rhythm but no carotid pulses. Focused assessment with sonography for trauma (FAST) is positive. Which of the following is the most likely cause?



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A 65-year-old man becomes unresponsive in the intensive care unit. The monitor shows sinus rhythm, but the pulse is not detectable. The nurse activates the code blue. Which is the next best step in management?



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A 6-year-old boy who was living with his grandparents was brought to the emergency room with extreme fatigue followed by paralysis of both of his legs. While obtaining the history from his family, he went into pulseless electrical activity (PEA) arrest, and while ACLS protocol was being carried out, his grandfather mentioned that his pillbox was missing. Which of the following is the most likely medication responsible for this presentation?



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A 70-year-old lady with a history of diabetes mellitus, coronary artery disease, history of ovarian cancer on remission was on the orthopedic floor after an elective hip surgery. On post-op day three, she was found to have a BP of 120/85 mm Hg, heart rate of 110 beats/minute and a respiratory rate of 25 breaths/minute. She was asymptomatic and appeared to be comfortable at that time when her vital signs were checked. However, 8 hours later, she was found to be pulseless by the nurse. A CPR was started immediately followed by the ACLS protocol. She was found to be in pulseless electrical activity, and she died despite 25 minutes of CPR. Which among the following intervention might have prevented the cardiac arrest the most?



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Pulseless Electrical Activity - References

References

Solevåg AL,Luong D,Lee TF,O'Reilly M,Cheung PY,Schmölzer GM, Non-perfusing cardiac rhythms in asphyxiated newborn piglets. PloS one. 2019;     [PubMed]
Andersen LW,Holmberg MJ,Berg KM,Donnino MW,Granfeldt A, In-Hospital Cardiac Arrest: A Review. JAMA. 2019 Mar 26;     [PubMed]
de Graaf C,Beesems SG,Koster RW, Time of on-scene resuscitation in out of-hospital cardiac arrest patients transported without return of spontaneous circulation. Resuscitation. 2019 Mar 27;     [PubMed]
Mukhtar M,Hamid M,Khan MAA,Ullah W, Sudden death due to pulmonary embolism after minor ankle surgery. BMJ case reports. 2019 Mar 6;     [PubMed]
Izawa J,Komukai S,Gibo K,Okubo M,Kiyohara K,Nishiyama C,Kiguchi T,Matsuyama T,Kawamura T,Iwami T,Callaway CW,Kitamura T, Pre-hospital advanced airway management for adults with out-of-hospital cardiac arrest: nationwide cohort study. BMJ (Clinical research ed.). 2019 Feb 28;     [PubMed]
Luong D,Cheung PY,Barrington KJ,Davis PG,Unrau J,Dakshinamurti S,Schmölzer GM, Cardiac arrest with pulseless electrical activity rhythm in newborn infants: a case series. Archives of disease in childhood. Fetal and neonatal edition. 2019 Feb 22;     [PubMed]
Chia MYC,Kwa TPW,Wah W,Yap S,Doctor NE,Ng YY,Mao DR,Leong BS,Gan HN,Tham LP,Cheah SO,Ong MEH, Comparison of Outcomes and Characteristics of Emergency Medical Services (EMS)-Witnessed, Bystander-Witnessed, and Unwitnessed Out-of-Hospital Cardiac Arrests in Singapore. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors. 2019 Feb 22;     [PubMed]
Atkinson PR,Keyes AW,O'Donnell K,Beckett N,Banerjee A,Fraser J,Lewis D, Do Electrocardiogram Rhythm Findings Predict Cardiac Activity During a Cardiac Arrest? A Study from the Sonography in Cardiac Arrest and Hypotension in the Emergency Department (SHoC-ED) Investigators. Cureus. 2018 Nov 23;     [PubMed]
Weber F,Guha R,Weinberg G,Steinbach F,Gitman M, Prolonged Pulseless Electrical Activity Cardiac Arrest After Intranasal Injection of Lidocaine With Epinephrine: A Case Report. A     [PubMed]
Saarinen S,Salo A,Boyd J,Laukkanen-Nevala P,Silfvast C,Virkkunen I,Silfvast T, Factors determining level of hospital care and its association with outcome after resuscitation from pre-hospital pulseless electrical activity. Scandinavian journal of trauma, resuscitation and emergency medicine. 2018 Nov 19;     [PubMed]
Sillers L,Handley SC,James JR,Foglia EE, Pulseless Electrical Activity Complicating Neonatal Resuscitation. Neonatology. 2019;     [PubMed]
Bergström M,Schmidbauer S,Herlitz J,Rawshani A,Friberg H, Pulseless electrical activity is associated with improved survival in out-of-hospital cardiac arrest with initial non-shockable rhythm. Resuscitation. 2018 Dec;     [PubMed]
Konesky KL,Guo WA, Revisiting traumatic cardiac arrest: should CPR be initiated? European journal of trauma and emergency surgery : official publication of the European Trauma Society. 2018 Dec;     [PubMed]

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