Pulseless electrical activity

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2]

Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are respiratory failure and hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19. PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. Absence of palpable pulse is the main finding. Echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. ECG findings shows sinus rhythm or sinus tachycardia, with discernible P waves and QRS complexes. Sometimes there is a bradycardia, with or without P waves, and often there is a wide QRS complex. According to the current American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines CPR is the mainstay of treatment in all patients. Administering 100% oxygen to reverse hypoxia, intubate the patient, establishing IV access should be the priority. The mainstay of drug therapy for PEA is epinephrine 1mg every 3–5 minutes. Immediately after administering epinephrine attention should be directed to reverse any possible causes of PEA as they are the most common causes like hypovolemia (i.e. hypovolemic shock) which should be treated with IV fluidsor packed red blood cell transfusion.

Pulseless electrical activity as the main approach for sudden cardiac arrest (SCA) was not completely studied until the middle of the 1980’s. The explanation for this, is that ventricular fibrillation (VF) and ventricular tachycardia (VT), were the main causes for the morbidity and mortality of SCA. However there has been a change in approaching the causes of SCA, pointing to PEA as the initial rhythm leading to SCA.

PEA( pulseless electrical activity) usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral with loss of cardiac output; hypotension, loss of consciousness and apnea rapidly ensue. Other possible mechanisms for pulseless electrical activity include Elevated Afterload, Electromechanical Dissociation, Reduced Contractility, Parasympathetic theory.

Common causes of PEA include respiratory failure in 40% to 50% of cases, and hypovolemia. Hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19.

PEA(Pulseless electrical activity) should be differentiated from asystole, ventricular fibrillation, Ventricular flutter, Torsade de Pointes. In asystole, there is cessation of any cardiac activity and lack of cardiac output on this basis. In Ventricular fibrillation there is no organized electrical activity present, while there are only fine fibrillatory waves. Peripheral arterial disease can also present with inability to feel a peripheral pulse so it should be differentiated based on other findings as well.

The incidence of SCA ranges between 300,000 to 370,000 cases per year, 50% of which are due to PEA. PEA accounts for approximately 20% of out-hospital cardiac arrests and for a third of the in-hospital cardiac arrests. There is a slight female preponderance for PEA in addition, PEA is associated with increased age and black race.

The administration of beta blockers and calcium channel blockers is associated with an increased risk of PEA. This may be due to their effect on Ca / troponin interactions, and their inhibition of myocardial contractility.

PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%. The survival for out of hospital occurrence of PEA is higher (19.5%) than for in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest. The survival of PEA as a presenting rhythm is poorer than ventricular tachycardia or ventricular fibrillation.

Absence of palpable pulse is the main finding. Depending upon the cause of pulseless electrical activity the following might be found, Tracheal deviation or the unilateral absence of breath sounds in case of tension pneumothorax, decreased skin turgor, Cool extremities, Tachycardia in case of hypotension, traumatic chest, , Cyanosis etc

A rapid beside echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. Elevated right heart filling pressures suggest pulmonary embolism. Tension pneumothorax can also be observed on a bedside echocardiogram.

Athough there are no diagnostic laboratory findings associated with PEA(pulseless electrical activity) testing should be ordered to rule out the most common reversible causes of PEA(pulseless electrical activity) like Hyperkalemia or Hypokalemia, hypoxia and acidosis which can be seen withABG, exsanguination hematocrit.

The appearance of the electrocardiogram in the setting of PEA varies, but several common patterns exist. There may be a normal sinus rhythm or sinus tachycardia, with discernible P waves and QRS complexes. Sometimes there is a bradycardia, with or without P waves, and often there is a wide QRS complex. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The EKG should be carefully evaluated for signs of Hyperkalemia, ST segment elevation MI, hypothermia, QRS interval prolongation suggests tricyclic antidepressant overdose

There are no CT scan findings associated with pulseless electrical activity. However it can be used to identify some of the causes of pulseless electrical activity like cardiac tamponade, tension pneumothorax.Superior vena cava andInferior vena cava enlargement, Hepatic and renal vein enlargment, Periportal edema, Compression of coronary sinus, Angulation of interventricular septum,Pericardial thickening, Collapse of the right atrium, Aortic blood contrast level these are seen in cardiac tamponade CT.

The current American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines advise the following be undertaken in all patients start CPR immediately, administer 100% oxygen to reverse hypoxia,Intubate the patient, establish IV access.The mainstay of drug therapy for PEA is epinephrine 1mg every 3–5 minutes.Higher doses of epinephrine can be administered in patients with suspected beta blocker and calcium channel blocker overdose.Immediately after administering epinephrine attention should be directed to reverse any possible causes of PEA as they are the most common causes like hypovolemia (i.e. hypovolemic shock) which should be treated with IV fluidsor packed red blood cell transfusion. Others like electrolyte abnormalities including hyper/hypokalemia should be corrected immediately as they can be life threatening as well as tension pneumothorax.

External and internal pacing have not been shown to improve outcome and are not recommended. There may be capture of the signals, but there is no improvement in contractility.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

Pulseless electrical activity as the main approach for sudden cardiac arrest (SCA) was not completely studied until the middle of the 1980’s. The explanation for this, is that ventricular fibrillation (VF) and ventricular tachycardia (VT), were the main causes for the morbidity and mortality of SCA. However there has been a change in approaching the causes of SCA, pointing to PEA as the initial rhythm leading to SCA.

The first approach against trying to decrease mortality due to SCA, was to target tachyarrhythmias, especially ventricular fibrillation (VF) and ventricular tachycardia (VT). This was mainly achieved by the improvements in CPR techniques, the availability of defibrillators to lay responders and the use of implantable cardioverter- defibrillators. Nevertheless, there is and increase in prevalence of PEA and asystolia, which makes them now more frequent than VT and VF. There is still not clear if this can be due to a proportional increase, rather than an absolute increase in cases of PEA. Studies suggest that there is a need to change this approach, because of the increased proportion of PEA cases, and mainly because of the better outcomes for survival in PEA patients, than those with VF/VT ^{[1] [2]}. Deeper studies will achieve ultimately a better therapeutic strategy, leading to better patient outcomes and a subsequent impact in overall mortality due to SCA.

There was a workshop created by Myerburg from a National Heart, Lung, and Blood Institute ^[2] as an attempt to record the current knowledge and direct the future research in the field. This workshop also described some of the pathophysiology of PEA, which may translate to improved clinical care.

• Although the ECG findings of Brugada syndrome were first reported among survivors of cardiac arrest in 1989, it was only in 1992 that the Brugada brothers recognized it as a distinct clinical entity, causing sudden death by causing ventricular fibrillation^[3][4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

PEA can be classified as cardiac and non cardiac depending on the initial underlying etiology. Cardiac PEA can be further classified as primary and secondary to a preceding ventricular tachycardia or ventricular fibrillation.^[1] Pulseless electrical activity can be classified either by the intensity of cardiac contractions or their electrical manifestations (true or psuedo PEA). There can be found different electrocardiographic patterns in each of the electrical manifestations classification.^[2] There is also one type of pulseless electrical activity seen in a post- shock EKG, which should not be classified, and therefore approached as a true PEA.

According to waveform morphology PEA can be classified from a normal QRS width, with isolectric ST and P waves, to waveforms beyond QRS, P and T wave recognition. Waveform analysis has been studied for ultimately predict treatment outcomes, specially regarding ROSC (return of spontaneous circulation) as the final goal. In a study made by Dragsund et al in Norway, they mainly studied waveforms for ventricular fibrillation but they hypothesize that the outcome may be similar for PEA. They suggest that PEA waveforms can be categorized quantitatively depending on the rhythm they spontaneously transformed to before they transitioned to either ROSC or asystole.

There are no cardiac contractions despite electrical activity.

There are very weak cardiac contractions present that fail to generate a blood pressure compatible with systemic perfusion and life despite electrical activity. Pseudo PEA is characterized by narrow QRS complexes, short RR intervals, and a faster rate than true PEA. Pseudo PEA has been associated with a better response to treatment compared to true PEA.

Following defibrillation, there can be a period of electromechanical dissociation where electrocardiographic complexes do not generate a pulse. Post defibrillator PEA can result either from myocardial injury or from the termination of the ventricular tachycardia or ventricular fibrillation.^[1] As a result of post defibrillation PEA, it is often useful to continue CPR for up to one minute following restoration of a perfusing rhythm.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

PEA( pulseless electrical activity) usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral with loss of cardiac output, hypotension, loss of consciousness and apnea rapidly ensue. Other possible mechanisms for pulseless electrical activity include elevated afterload, electromechanical dissociation, reduced contractility, parasympathetic theory.

Pulseless electrical activity is nothing but the loss of cardiac muscle to generate adequate force in response to electrical depolarization. It usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. The more and more the inotropic state of the cardiac muscle gets compromised it leads to insufficient mechanical activity, despite the presence of electrical activity. It causes degeneration of cardiac rhythm, and eventually, death follows. Respiratory failure leading to hypoxia is one of the most common causes of pulseless electrical activity. The following are other possible mechanisms for pulseless electrical activity:^{[1][2][3][4][5][6][7]}

PEA may be due to inadequate filling of the left ventricle with blood to stretch the cardiac sarcomeres adequately to result in a cardiac contraction (i.e. there is inadequate preload). Examples include rapid fluid or blood loss as occurs in major trauma and ruptured aortic aneurysm. Cardiac tamponade, pneumothorax, and pulmonary embolism are other conditions associated with decreased preload, predisposing to PEA.

Elevated afterload is rarely a cause of PEA.

In some cases, PEA may be caused by electromechanical dissociation. The normal condition when electrical activation of muscle cells precedes mechanical contraction is known as electromechanical coupling. This coupling is lost in some forms of PEA, and this is known as electromechanical dissociation.^{[8][9][10][11]}

Contraction of the myocardium depends upon the integrity of the troponin subunits.

Calcium binding to troponin is required for contractility. This binding can be reduced in calcium channel blocker overdoses.

In the setting of hypoxia, calcium binds less avidly to troponin.

There is a theory suggested by DeBehnke in which a vagotomy was performed after PEA provoked by asphyxia. Vagotomy was performed in randomized canines. All of them were managed first with CPR and chemical cardioversion with epinephrine (0.02 mg/kg every five minutes). He found that ROSC (Return of Spontaneous Circulation) was achieved in 13% of canines with no vagotomy, versus a 75% in those with vagotomy (P = .02). There were also performed hemodynamic and arterial blood gas values at 5, 10 and 15 minutes after ROSC with no significant differences between the 16 canines. 16 canines were induced by asphyxia until PEA presented ^[12][13].^[7].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahmoud Sakr, M.D. [2]

Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. Pulseless electrical activity is a life-threatening condition and must be treated as such irrespective of the causes. Common causes of PEA include respiratory failure in 40% to 50% of cases, and hypovolemia. Hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19.

Pulseless electrical activity is a life-threatening condition and must be treated as such irrespective of the causes. Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated.^[1][2]

Common causes of PEA include the following: The common causes of PEA can be remembered using the mnemonic “The Hs and Ts”.^{[3][4][5][2][6][7]}

• Hypovolemia
• Hypoxia
• Hydrogen ions (Acidosis)
• Hypothermia
• Hyperkalemia or Hypokalemia
• Hypoglycemia
• Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants
• Tamponade
• Tension pneumothorax
• Thrombosis (Myocardial infarction)
• Thrombosis (Pulmonary embolism)
• Trauma (Hypovolemia from blood loss)
• Covid-19

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2]

PEA(Pulseless electrical activity) should be differentiated from asystole and ventricular fibrillation, Ventricular flutter, Torsade de Pointes, Asystole etc.

• Asystole: In asystole, there is cessation of any cardiac activity and lack of cardiac output on this basis. In PEA, electrical activity is present.
• Ventricular fibrillation: There is no organized electrical activity present. There are only fine fibrillatory waves present in ventricular fibrillation. In PEA, there is organized electrical activity.
• Peripheral arterial disease: The inability to feel a peripheral pulse may be due to severe peripheral arterial disease.

The table below provides information on the differential diagnosis of pulseless electrical activity in terms of ECG appearance:

Disease Name	Causes	ECG Characteristics	ECG view
Ventricular tachycardia [1][2][3][4][5]	Ischemic heart disease Illicit drug use such as cocaine and methamphetamine Structural heart diseases Electrolyte disturbances Congestive heart failure Myocarditis Obstructive sleep apnea Pulmonary artery catheter Long QT syndrome	Ventricular tachycardia originates from a ventricular focus. Lasts more than 30 seconds. Broad QRS complexes: rate of >90 BPM.	[6]
Ventricular fibrillation [7][8][9][10]	Acute coronary ischemia Cardiomyopathies Congenital heart disease Myocardial infarction Heart surgery Electrolyte abnormalities	Poorly identifiable QRS complexes and absent P waves The heart rate is >300 BPM Rhythm is irregular	[11]
Ventricular flutter [12][13][14]	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm	[15]
Asystole [16][17]	Hypovolemia Hypoxia Acidosis Hypothermia Hyperkalemia or Hypokalemia Hypoglycemia Cardiac Tamponade Tension pneumothorax Thrombosis Myocardial infarction Thrombosis Pulmonary embolism Cardiogenic shock Degeneration of the sinoatrial or atrioventricular nodes Ischemic stroke	There is no electrical activity in the asystole	[18]
Pulseless electrical activity [19][20][21][22]	Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hypothermia Electrolyte disturbances Hypoglycemia Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers Tamponade Tension pneumothorax Thrombosis (Myocardial infarction) Thrombosis (Pulmonary embolism) Trauma (Hypovolemia from blood loss)	Several pattern are possible including: Normal sinus rhythm Sinus tachycardia, with discernible P waves and QRS complexes Bradycardia, with or without P waves	[23]
Torsade de Pointes [24][25][26]	*Electrolyte disturbances Medications such as: Amiodarone Azithromycin Clozapine Famotidine Flecainide Foscarnet Levofloxacin Lithium Mirtazapine Quetiapine Risperidone Tacrolimus Tamoxifen Ziprasidone	Paroxysms of VT with irregular RR intervals. A ventricular rate between 200 and 250 beats per minute. Two or more cycles of QRS complexes with alternating polarity. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion. Prolongation of the QT interval. Is often initiated by a PVC with a long coupling interval, R on T phenomenon. There are usually 5 to 20 complexes in each cycle.	[27]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

Over the last three decades, the incidence of PEA has increased in parallel to a decrease in the incidence of VF and VT.^[1] There is a slight female preponderance of PEA. In addition, PEA is associated with increased age and black race.^[2][3]

• The incidence of SCA ranges between 300,000 to 370,000 cases per year, 50% of which are due to PEA.^[1][4]

• PEA accounts for approximately 20% of out-hospital cardiac arrests and for a third of the in-hospital cardiac arrests.^[5] PEA is responsible for 10% of in-hospital deaths.^[6]

• The decrease in the prevalence of VF and VT has been accompanied by a parallel relative increase in the incidence of PEA among patients with SCA.^[1] In fact, following adequate management of VF and VT, the prevalence of VT/VF has dropped by 20% while the prevalence of PEA increased by 11% between 1979 and 2000.^[7]

• There is a slight female preponderance of PEA. In addition, PEA is associated with increased age and black race.^[2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

The administration of beta blockers and calcium channel blockers is associated with an increased risk of PEA. This may be due to their effect on the interactions between calcium and troponin and their inhibition of myocardial contractility. Syncope and pulmonary disease is also associated with a higher risk of PEA.

The following are the major common risk factors for the PEA(pulseless electrical activity):^{[1] [2][3][1] [2][4] [5][6][7][8][6]}

• Age
• Black race
• Female gender
• Heart failure
• Pulmonary disease
• Syncope

It is not yet well established why beta blockers and ACE inhibitors are risk factors for PEA. One possible explanation is that the use of beta blockers and ACE inhibitors in the context of ventricular fibrillation might lead to the conversion of ventricular fibrillation (VF) to pulseless electrical activity (PEA).^[9] Another explanation for the association is that the pharmacological treatment with beta blockers and ACE inhibitors of patients with VF have lead to a decrease in the prevalence of VF and subsequent relative increase in the incidence of PEA among patients with SCA.^{[10] [11]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identified and treated. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The survival of patients with PEA as a presenting rhythm for sudden cardiac arrest is poorer than ventricular tachycardia or ventricular fibrillation.^[1]

• The symptoms of (disease name) usually develop in the first/ second/ third decade of life, and start with symptoms such as ___.
• The symptoms of (disease name) typically develop ___ years after exposure to ___.
• If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

• Common complications of [disease name] include:
  • [Complication 1]
  • [Complication 2]
  • [Complication 3]

• Prognosis is generally poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [–]%.
• Depending on the extent of the [tumor/disease progression] at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.
• The presence of [characteristic of disease] is associated with a particularly [good/poor] prognosis among patients with [disease/malignancy].
• The prognosis varies with the [characteristic] of tumor; [subtype of disease/malignancy] have the most favorable prognosis.

• The survival of patients with out of hospital occurrence of PEA is 19.5% compared to 11.2% among patients with in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest.^[1][2][3]

• Among 11,963 patients with PEA, only 11% survived, 62% of which had good neurological outcomes.^[4]

• According to the Resuscitation Outcomes Consortium, the survival of patients with SCA during hospitalization is 8% among subjects with PEA compared to 30.5% for subjects with VT or VF; therefore, strategies for improving survival after PEA due to SCA should be implemented.

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