Asystole 

Updated: Dec 26, 2015
Author: Sandy N Shah, DO, MBA, FACC, FACP, FACOI; Chief Editor: Barry E Brenner, MD, PhD, FACEP 

Overview

Background

Asystole is also known as flatline. It is a state of cardiac standstill with no cardiac output and no ventricular depolarization, as shown in the image below; it eventually occurs in all dying patients.

Rhythm strip showing asystole. Rhythm strip showing asystole.

Pulseless electrical activity (PEA) is the term applied to a heterogeneous group of dysrhythmias unaccompanied by a detectable pulse. Bradyasystolic rhythms are slow rhythms; they can have a wide or narrow complex, with or without a pulse, and are often interspersed with periods of asystole. When discussing pulseless electrical activity, ventricular fibrillation (VF) (see the following image) and ventricular tachycardia (VT) are excluded.

Rhythm strip showing ventricular fibrillation. Rhythm strip showing ventricular fibrillation.

Pathophysiology

Asystole can be primary or secondary. Primary asystole occurs when the heart's electrical system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (ie, sclerosis) of the sinoatrial (SA) node or atrioventricular (AV) conducting system. Primary asystole is usually preceded by a bradydysrhythmia due to sinus node block-arrest, complete heart block, or both.

Reflex bradyasystole/asystole can result from ocular surgery,[1, 2] retrobulbar block, eye trauma, direct pressure on the globe, maxillofacial surgery, hypersensitive carotid sinus syndrome, or glossopharyngeal neuralgia. Episodes of asystole and bradycardia have been documented as manifestations of left temporal lobe complex partial seizures.[3, 4] These patients experienced either dizziness or syncope. No sudden deaths were reported, but the possibility exists if asystole were to persist. The longest interval was 26 seconds.

Secondary asystole occurs when factors outside of the heart's electrical conduction system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia with metabolic acidosis. Asystole or bradyasystole follows untreated ventricular fibrillation and commonly occurs after unsuccessful attempts at defibrillation. This forebodes a dismal outcome.

Etiology

Causes of primary and secondary asystole are briefly reviewed in this section.

Primary asystole

Primary asystole develops when cellular metabolic functions are no longer intact and an electrical impulse cannot be generated. With severe ischemia, pacemaker cells cannot transport the ions necessary to affect the transmembrane action potential. Implantable pacemaker failure may also be a cause of primary asystole.

Proximal occlusion of the right coronary artery can cause ischemia or infarction of both the sinoatrial (SA) and the atrioventricular (AV) nodes. Extensive infarction can cause bilateral bundle-branch block (ie, infranodal complete heart block).

Idiopathic degeneration of the SA or AV node can result in sinus arrest-block and/or AV heart block, respectively. This process is slow and progressive, but the symptoms may be acute and asystole may result. An implantable pacemaker is usually required for these conditions.

Occasionally, asystolic sudden death occurs from congenital heart block, local tumor, or cardiac trauma.[5]

Asystole can occur following an indirect lightning strike (ie, direct current [DC]) that depolarizes all the cardiac pacemakers. A rhythm may return spontaneously or shortly after cardiopulmonary resuscitation (CPR) is initiated. These patients may survive intact if given immediate attention. Alternating current (AC) from man-made sources of electrical current usually results in ventricular fibrillation (VF).

Secondary asystole

Examples of common conditions that can result in secondary asystole include suffocation, near drowning, stroke, massive pulmonary embolus, hyperkalemia, hypothermia, myocardial infarction (MI) complicated by VF or ventricular tachycardia (VT) that deteriorates to asystole, post defibrillation, and sedative-hypnotic or narcotic overdoses leading to respiratory failure.

Hypothermia is a special circumstance, because asystole can be tolerated for a longer period under such conditions and can be reversed with rapid rewarming while CPR is being performed. If available, institute cardiopulmonary bypass immediately, because it can accomplish both of these goals. Most survivors have received cardiopulmonary bypass.

Epidemiology

The number of US adults in cardiopulmonary arrest who had bradyasystole as the initial arrest rhythm is difficult to measure accurately. Reports vary and may be skewed by the patient population studied and/or by the method of reporting the initial rhythm. For example, in a 1991 study of 185 patients in cardiopulmonary arrest at the time of arrival to the emergency department, 9% had survived to hospital admission but none were discharged alive.[6] This study was not limited to patients with asystole.[6] In one study from Goteborg, Sweden, asystole was the presenting rhythm in the field in 35% of patients with cardiac arrest.[7]

Race is not a significant factor in asystole except as it relates to the underlying conditions that may lead to a cardiac arrest, such as chronic hypertension, renal failure, coronary artery disease, congestive heart failure, or cardiac dysrhythmias.

Individuals with low CAD incidence

When the incidence of coronary artery disease (CAD) in the population of a country is relatively low, asystole is relatively more common as a manifestation of cardiopulmonary arrests. This is because cardiac ischemia more frequently results in ventricular fibrillation (VF).

Children

The prevalence of asystole as the presenting cardiac rhythm is lower in adults (25-56%) than in children (90-95%). In fact, asystole is most likely to be found in cardiopulmonary arrests occurring in children; this is usually secondary to another noncardiac event (ie, respiratory arrest due to sudden infant death syndrome [SIDS], infection, choking, drowning, or poisoning).[8] Infants are more statistically likely to suffer a cardiac arrest than older children or adolescents.

The Resuscitation Outcomes Consortium Epistry-Cardiac Arrest trial, nontraumatic cardiac arrest occurred at a rate of 72.1 per 100,000 infants versus 3.73 per 100,000 in children and 7.37 per 100,000 in adolescents.[9] Investigators found the adult rate of cardiac arrest was 126.52 per 100,000 when they evaluated 25,405 adults and 624 patients younger than 20 years.

Pediatric patients with VF or ventricular tachycardia (VT) were 4 times more likely to survive an out-of-hospital cardiac arrest (20%) than those with asystole (5%), and patients younger than 20 years had an overall better survival rate than adults when all rhythms are included and traumatic arrests are excluded.[9]

Women

The frequency of asystole, as a percentage of all cardiopulmonary arrests, is higher in women than in men; however, the frequency of cardiac arrest in general is proportional to the underlying incidence of heart disease, which is more common in males until around age 75 years.

Prognosis

The prognosis in asystole depends on the etiology of the asystolic rhythm, timing of interventions, and success or failure of advanced cardiac life support (ACLS).

Resuscitation is likely to be successful only if it is secondary to an event that can be corrected immediately, such as a cardiac arrest due to choking on food (a cafe coronary), and only if an airway can be established and the patient may be rapidly reoxygenated. Occasionally, primary asystole can be reversed if it is due to pacemaker failure, which could be either intrinsic or extrinsic, and this is corrected immediately by external pacing.

Generally, the prognosis is dismal regardless of its initial cause; in particular, individuals with postcountershock asystole have an even worse survival rate.[10, 11] In the Termination of Resuscitation study, when no shock was advised in patients with unwitnessed cardiac arrest, there were no survivors.[12, 13] In the Goteborg, Sweden, study, 10% of 1,635 asystolic patients survived to hospital admission, but 2% survived to hospital discharge.[7]

The most recent American Heart Association guidelines to improve cardiocerebral resuscitation (CCR) have validated studies that show improved outcomes in all adults with out-of-hospital cardiac arrest in ventricular tachycardia and ventricular fibrillation only.[14]

Complications

Complications from asystole include permanent neurologic impairment and complications from cardiopulmonary resuscitation (CPR) or invasive procedures (eg, liver laceration, fractured ribs, pneumothorax, hemothorax, air embolus, aspiration, gastric/esophageal rupture). Death often occurs.

Patient Education

Advice about electrical storm safety and prevention of hypothermia is appropriate for those likely to be exposed to these conditions.

For patient education information, see Heart Health Center as well as Cardiopulmonary Resuscitation (CPR), Heart Attack, and Coronary Artery Disease.

 

Presentation

History

Immediate diagnosis of asystole requires the recognition of a full cardiac arrest and a confirmed flat-line rhythm in 2 perpendicular leads. Lightheadedness or syncope may precede asystole when it follows a bradyasystolic rhythm.

Physical Examination

If the rhythm is truly asystole and has been present for more than several seconds, the patient will be unconscious and unresponsive. A few agonal (final gasping) breaths may be noted, but detectable heart sounds and palpable peripheral pulses are absent.

Complications

If asystole persist for fifteen minutes or more, the brain will have been deprived of oxygen long enough to cause brain death.

 

DDx

Diagnostic Considerations

A bradyasystolic or asystolic arrest may be primary or secondary in a patient experiencing a myocardial infarction (MI). It may also be due to a failure of pacemaker generation or propagation directly because of ischemia to the sinoatrial (SA) node or the atrioventricular (AV) conducting system.

Many patients with myocardial infarction have some degree of autonomic disturbance (ie, high parasympathetic tone), resulting indirectly in bradydysrhythmias or heart block. A lack of responsiveness to sympathetic stimulation may also be present. Hypoxemia from pulmonary edema and/or poor tissue perfusion from cardiogenic shock could also lead to a secondary asystolic arrest.

Consider drug toxicity and hypoxia in the differential diagnosis. Also keep in mind that electrocardiograph (ECG) lead displacement may simulate asystole. Recheck the placement of all leads and check the patient's pulse to exclude this possibility.

Differential Diagnoses

 

Workup

Approach Considerations

Asystole is generally a diagnosis made via ongoing cardiac monitoring or electrocardiogram (ECG) and physical examination with pulselessness. Pulse oximetry may be used during resuscitation to monitor the effectiveness of forward flow or cardiopulmonary resuscitation (CPR); however, usually flow is too inadequate for the sensor to register results.

The "H's and T's of advanced cardiac life support" (ACLS) is a pneumonic that is used to help clinicians recall the major contributing factors of asystole and are as follows:

  • Hypovolemia
  • Hypoxemia
  • Hydrogen ion (acidosis)
  • Hyperkalemia, hypokalemia
  • Hypothermia
  • Toxins
  • Tamponde (cardiac)
  • Tension pneumothorax
  • Thrombosis (coronary and pulmonary)

Potassium level and ABG

A potassium level may be useful if deemed appropriate and results are immediately available.

Arterial blood gas (ABG) analysis may be used to obtain rapid reporting of potassium level in many institution's laboratories. In addition, ABG results may also help to evaluate the ventilatory and acid-base status of the patient as well as the hemoglobin level. Note that if the patient is in full arrest, a blood gas level does not accurately reflect the overall pH status of the tissues.

Echocardiography

For documentation purposes, in addition to including rhythm strips from 2 separate leads identifying asystole, bedside ultrasonography may be useful to confirm cardiac standstill. The heart may be viewed via either a subxiphoid view or an intercostal view wall motion, or lack thereof is observed. An image of 2-dimensional echocardiography taken over time in M-mode may be taken, saved, and included in the medical record. This will further document the lack of heart wall motion.

Continuous Cardiac Monitoring

Isoelectric flat line is interpreted as asystole. Immediately rule out the following as causes of isoelectric flat line not due to asystole:

  • Loose or disconnected leads
  • Loss of power to the electrocardiographic (ECG) monitor
  • Low signals gain on the ECG monitor

Asystole is best determined in 2 separate cardiac leads. This helps protect against reading a flat line due to lead malfunction incorrectly as asystole, as well as helps in differentiating fine ventricular fibrillation (VF), particularly in an isoelectric lead, from asystole (see the following images).

Rhythm strip showing asystole. Rhythm strip showing asystole.
Rhythm strip showing ventricular fibrillation. Rhythm strip showing ventricular fibrillation.

Eliminate a possible diagnosis of VF, which may masquerade as asystole, by checking 2 leads perpendicular to each other. In spite of this caveat, Cummins et al found that using a flat-line protocol based on a 3-lead check, occult VF was documented in only 3 (2.5%) of 118 asystolic patients, indicating that VF masquerading as asystole is uncommon.[15] Technical problems were much more common, observed in 10 patients (8%).[15]

Exclude the possibility of lead misplacement by always checking for the presence of a pulse.

Spurious asystole can be seen when using manual defibrillator paddles to monitor the rhythm.[16] This is usually very brief, but nevertheless, can be avoided by switching to monitoring leads, especially after several successive shocks.

 

Treatment

Approach Considerations

Continuous cardiac monitoring is useful during attempts at resuscitation to determine rhythm and effects of intervention. Endotracheal intubation is indicated during resuscitation. Central venous access or intraosseous access may be needed for vascular access.

Emergency Department Care

Mainstays of treatment in the emergency department are providing oxygenation and ventilation via endotracheal intubation and circulation via cardiopulmonary resuscitation (CPR), attempts at transcutaneous or transvenous pacing (that have some small potential to be fruitful in primary asystole that has just occurred), and administration of pharmacologic agents.

There has been a case report of a long but successful resuscitation from asystole of a patient who was hyperkalemic secondary to renal failure.[17] The treatment included calcium chloride to reverse the physiologic effects of hyperkalemia and insulin and glucose to lower serum potassium levels. However, this therapy cannot be recommended routinely for all cases of asystolic arrest.

Some of common reasons to stop or withhold resuscitation efforts include the following:

  • The patient has a a do not resuscitate (DNR) status
  • There is a threat to the safety of rescuers
  • There is family or personal information that precludes resuscitation efforts, such as having living will or advance directive
  • Rigor mortis is present

Electrical defibrillation

Electrical defibrillation should not be applied indiscriminately to the patient in asystole. This is not only fruitless, but also detrimental, eliminating any possibility of recovering a rhythm. Asystole following electrical defibrillation has an even worse outcome than that in a patient whose first documented rhythm was asystole. One caution is that, following defibrillation, a brief spurious asystole can occur using manual monitoring through the defibrillator paddles. This does not occur with the rhythm monitoring leads or hands-off monitor pads. If not taken into consideration, it could lead to a delay in defibrillation, when indeed VF is present.

Admission to Intensive Care Unit

The intensive care unit is the appropriate disposition for the occasional patient who survives bradyasystolic cardiopulmonary arrest and requires further treatment and diagnostic evaluation. In the past decade, survivors who achieved electrical and hemodynamic stability but remained comatose and were modestly cooled to 32-34°C for the first 24 hours showed improvement in overall neurologic outcome.[18] The studies were conducted on prehospital arrests with ventricular fibrillation as the presenting rhythm, but results could be generalized to bradyasystolic survivors.[18]

Testori et al reports an odds ratio of 1.84 for good neurological outcome when bradyasystolic patients with a return of spontaneous rhythm are cooled, especially when the time interval, collapse to return of spontaneous circulation, is brief.[19] Given the prognosis is so poor after cardiac arrest, attempting hypothermia on all adult patients with cardiac arrest, regardless of presenting rhythm, is reasonable.

Prevention of Asystole

Primary asystole may be prevented by the appropriate use of a permanent pacemaker in those patients who have high-grade heart block or sinus arrest. Prevention of secondary asystole requires early recognition and treatment of the preceding event.

Prehospital Care

The only 2 drugs recommended or acceptable by the American Heart Association (AHA) for adults in asystole are epinephrine and vasopressin. Atropine is no longer recommended for young children and infants since 2005, and for adults since 2010 for pulseless electrical activity (PEA) and asystole. In spite of full vagolytic doses of atropine (0.03 mg/kg) and high-dose epinephrine (0.20 mg/kg), or the use of vasopressin 40 units (U), few patients survive to leave the hospital neurologically intact.

Atropine is no longer recommended in young children and infants in asystole but can be considered in adults with slow pulseless electrical activity (PEA) rhythms.

Vasopressin therapy

If spontaneous circulation has not been restored, administering intravenous (IV) vasopressin 40 U for the first 2 doses or followed by epinephrine given at the physician's discretion has showed some promising if not mixed results.

Wenzel et al reported that more patients who were administered vasopressin survived to hospital discharge than those on epinephrine, although the neurologic status of the patients at discharge was not clearly stated.[20] Further analysis suggested a tendency for a worse neurologic outcome in those who received both vasopressin and epinephrine, many of whom ended up in a vegetative state.

Of the 528 patients with asystole in the study, 12 patients in the vasopressin group survived to discharge compared with 4 in the standard therapy group.[20] In this study, the odds ratio stated may not be statistically significant, and there was also a nonstatistically significant trend toward worse results for ventricular fibrillation (VF) and PEA.[20]

In a larger comparison study between epinephrine alone and epinephrine with vasopressin 40 U, Gueugnaiud and colleagues found that there were no significant differences between groups in terms of return of spontaneous circulation, survival to hospital discharge, 1-year survival, or good neurologic recovery among survivors at hospital discharge.[21]

The advanced cardiac life support (ACLS) 2010 guidelines allow vasopressin 40 IU IV as a 1-time dose treatment option in VF and asystole. This treatment can be given either before epinephrine or after the first dose of epinephrine.

Transcutaneous pacing

Transcutaneous pacing (TCP), even when used immediately, has not altered meaningful survival (ie, functional lifestyle) significantly.[13, 22] However, when no metabolic deficit exists, such as in a cardiac arrest preceded by a conduction or impulse generation disorder (ie, primary asystole), immediate use of TCP may be lifesaving.

 

Medication

Medication Summary

Parasympathetic influences during cardiopulmonary arrest have not been elucidated fully, and clinical benefits of atropine have never been confirmed.

Atropine is no longer recommended by the American Heart Association (AHA) for asystole and pulseless electrical activity (PEA).

High-dose epinephrine (0.20 mg/kg) may improve the hemodynamics of cardiopulmonary resuscitation (CPR), thereby increasing the rate of return to spontaneous circulation; however, this agent has not been demonstrated to influence the final clinical outcome. Therefore, high doses are no longer are recommended for children or adults.

Adenosine antagonists, such as aminophylline,[23] have been investigated but have not been shown to be clinically useful.

Anticholinergic agents

Class Summary

The goal in using anticholinergic agents is to enhance sinoatrial (SA) activity and to improve conduction through the SA or atrioventricular (AV) node by reducing vagal tone via muscarinic receptor blockade. This is effective only if the site of the block is within the SA or AV node. For patients with infranodal block, anticholinergic therapy is ineffective, and it may increase a Mobitz II second-degree block to a higher degree of block or a third-degree block.

Atropine IV/IM (Atropine, Sal-Tropine, AtroPen)

Atropine is a parasympatholytic agent used to eliminate vagal influence on the SA and AV nodes. This agent is not effective for infranodal third-degree heart block, PEA, and asystole.

Adrenergic agonists

Class Summary

Adrenergic agents can produce constriction of skeletal and vascular muscle.

Epinephrine (Adrenaline, EpiPen)

Epinephrine is considered the single most useful drug in cardiac arrest; however, some authorities question its clinical effectiveness in humans This agent is used to increase coronary and cerebral blood flow during cardiopulmonary resuscitation (CPR) and may enhance automaticity during asystole. In addition, epinephrine can be used for bradycardia in adult and pediatric patients.

Vasopressin (Pitressin)

Vasopressin has vasopressor and antidiuretic hormone (ADH) activity. This agent increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed via stimulation of V1 receptors (vasopressor effect). Vasoconstriction is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.