Part 7: Adult Advanced Cardiovascular Life Support

    Key Words:
  • arrhythmia
  • cardiac arrest
  • drugs
  • ventricular arrhythmia
  • ventricular fibrillation
PDF Accessible Version

1
Introduction

Basic life support (BLS), advanced cardiovascular life support (ACLS), and post–cardiac arrest care are labels of convenience that each describe a set of skills and knowledge that are applied sequentially during the treatment of patients who have a cardiac arrest.

2
Oxygen Administration During CPR

Because blood flow is typically the major limiting factor to oxygen delivery during CPR, it is theoretically important to maximize the oxygen content of arterial blood by maximizing inspired oxygen concentration.

When supplementary oxygen is available, it may be reasonable to use the maximal feasible inspired oxygen concentration during CPR. (Class IIb, LOE C-EO) (2015 Part 7)

2.1
Passive Oxygen Delivery During CPR

Some EMS systems have studied the use of passive oxygen flow during chest compressions without positive pressure ventilation, an option known as passive oxygen administration. Evidence regarding this approach includes the passive oxygen flow as part of a bundle of care including opening the airway and emphasis on high-quality, minimally-interrupted chest compressions and a program of continuous quality improvement.

We do not recommend the routine use of passive ventilation techniques during conventional CPR for adults. (Class IIb, LOE C-LD) (2015 Part 5) However, in EMS systems that use bundles of care involving continuous chest compressions, the use of passive ventilation techniques may be considered as part of that bundle. (Class IIb, LOE C-LD) (2015 Part 5)

These updated recommendations do not preclude the 2015 recommendation that a reasonable alternative for EMS systems that have adopted bundles of care is the initial use of minimally interrupted chest compressions (ie, delayed ventilation) for witnessed shockable OHCA. (Class IIb; LOE C-LD) (2017 Adult BLS)

3
Airway and Ventilation

3.1
Overview of Airway Management and Ventilation

The purpose of ventilation during CPR is to maintain adequate oxygenation and sufficient elimination of carbon dioxide.

Research has not identified the optimal tidal volume, respiratory rate, and inspired oxygen concentration required during resuscitation from cardiac arrest.

Both ventilation and chest compressions are thought to be important for victims of prolonged ventricular fibrillation (VF) cardiac arrest and for all victims with other presenting rhythms.

During cardiac arrest with CPR, normal ventilation-perfusion relationships can be maintained with a minute ventilation that is much lower than normal because CPR produces systemic and pulmonary blood flow that is substantially lower than normal (≈ 25% to 33% of normal).

During CPR with an advanced airway in place, a lower rate of rescue breathing reduces risk of hyperventilation.

Advanced airway placement in cardiac arrest should not delay initial CPR
and defibrillation for VF cardiac arrest.
(Class I, LOE C) (2010 Part 8)

3.2
Bag-Mask Ventilation

All healthcare providers should be familiar with the use of the bag-mask device.

Bag-mask ventilation is a challenging skill that requires practice for continuing competency.

Bag-mask ventilation is an acceptable method of providing ventilation and oxygenation during CPR

Bag- mask ventilation is most effective when performed by 2 trained and experienced providers.

Bag-mask ventilation is particularly helpful when placement of an advanced airway is delayed or unsuccessful.

Use an adult (1 to 2 L) bag and deliver approximately 600 mL of tidal volume sufficient to produce chest rise over 1 second.

Be sure to open the airway adequately with a head tilt–chin lift, lifting the jaw against the mask and holding the mask against the face, creating a tight seal.

During CPR give 2 breaths (each 1 second) during a brief (about 3 to 4 seconds) pause after every 30 chest compressions.

It is reasonable that before placement of an advanced airway (supraglottic airway or tracheal tube), EMS providers perform CPR with cycles of 30 compressions and 2 breaths. (Class IIa, LOE B-R) (2017 Adult BLS)

It may be reasonable for EMS providers to use a rate of 10 breaths per minute (1 breath every 6 seconds) to provide asynchronous ventilation during continuous chest compressions before placement of an advanced airway. (Class IIb, LOE B-R) (2017 Adult BLS)

These updated recommendations do not preclude the 2015 recommendation that a reasonable alternative for EMS systems that have adopted bundles of care is the initial use of minimally interrupted chest compressions (ie, delayed ventilation) for witnessed shockable OHCA. (Class IIb, LOE C-LD) (2017 Adult BLS)

Bag-mask ventilation can produce gastric inflation with complications, including regurgitation, aspiration, and pneumonia. Gastric inflation can elevate the diaphragm, restrict lung movement, and decrease respiratory system compliance.

There is inadequate evidence of a difference in survival or favorable neurologic outcome with the use of bag-mask ventilation compared with endotracheal intubation or other advanced airway devices. (2015 Part 7) See, also, Advanced Airways, below.

Either bag-mask ventilation or an advanced airway strategy may be considered during CPR in adult cardiac arrest in any setting. (Class IIb, LOE B-R) (2019 ACLS)

3.3
Airway Adjuncts

3.3.1
Cricoid Pressure

The routine use of cricoid pressure in cardiac arrest is not recommended. (Class III, LOE C) (2010 Part 8)

If cricoid pressure is used in special circumstances during cardiac arrest, the pressure should be adjusted, relaxed, or released if it impedes ventilation or advanced airway placement.

3.3.2
Oropharyngeal and Nasopharyngeal Airways

To facilitate delivery of ventilation with a bag-mask device, oropharyngeal airways can be used in unconscious (unresponsive) patients with no cough or gag reflex and should be inserted only by persons trained in their use. (Class IIa, LOE C) (2010 Part 8)

To facilitate delivery of ventilation with a bag-mask device, the nasopharyngeal airway can be used in patients with an obstructed airway. However, in the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred. (Class IIa, LOE C) (2010 Part 8)

3.4
Advanced Airways

It is important that all healthcare providers be trained in delivering effective oxygenation and ventilation with a bag and mask. Because there are times when ventilation with a bag-mask device is inadequate, ideally ACLS providers also should be trained and experienced in insertion of an advanced airway.

Either bag-mask ventilation or an advanced airway strategy may be considered during CPR for adult cardiac arrest in any setting. (Class IIb, LOE B-R) (2019 ACLS)

Providers must be aware of the risks and benefits of insertion of an advanced airway during a resuscitation attempt. The provider should weigh the need for minimally interrupted compressions against the need for insertion of an endotracheal tube or supraglottic airway,

Although insertion of an endotracheal tube can be accomplished during ongoing chest compressions, intubation can frequently result in undesirable interruption of compressions. As a result, providers must weigh the potential benefit of advanced airway insertion against the potential risk of interruption in chest comressions, as well as the potential risk if misplacement of the advanced airway.

If bag-mask ventilation is judged to be adequate and advanced airway placement will interrupt chest compressions, providers may consider deferring insertion of the airway until the patient fails to respond to initial CPR and defibrillation attempts or demonstrates ROSC. (Class IIb, LOE C) (2010 Part 8)

Effective use of an advanced airway requires maintenance of knowledge and skills through frequent practice.

Providers should have a second (backup) strategy for airway management and ventilation in readiness if unable to establish the first-choice airway adjunct. Bag-mask ventilation may serve as such a backup strategy.

Once an advanced airway is inserted, immediately perform a thorough assessment to ensure that the airway is properly positioned. This assessment should not interrupt chest compressions (see Clinical Assessment of Tracheal Tube Placement, below).

3.4.1
Advanced Airway Choice

Either bag-mask ventilation or an advanced airway strategy may be considered during CPR in adult cardiac arrest in any setting. (Class IIb, LOE B-R) (2019 ACLS)

Bag-mask ventilation requires skill and proficiency. The choice of bag-mask device versus advanced airway insertion, then, is determined by the skill and experience of the provider as well as the needs of the patient (See (Figure 1)).

If an advanced airway is used, the supraglottic airway can be used for adults with out of hospital cardiac arrest in settings with low tracheal intubation success rate or minimal training opportunities for endotracheal tube placement. (Class IIb, LOE B-R) (2019 ACLS)

If an advanced airway is used, either the supraglottic airway or endotracheal tube can be used for adults with out-of-hospital cardiac arrest in settings with high tracheal intubation success rates or optimal training opportunities for endotracheal tube placement. (Class IIa LOE B-R) (2019 ACLS)

If an advanced airway is used in the in-hospital setting by expert providers trained in these procedures, either the supraglottic airway or endotracheal tube can be used. (Class IIa LOE B-R) (2019 ACLS)

Recommendations for advanced airway placement presume that the provider has the initial training and skills as well as the ongoing experience to insert the airway and verify proper position with minimal interruption in chest compressions.

Frequent experience or frequent retraining is recommended for providers who perform endotracheal intubation. (Class I, LOE B-NR) (2019 ACLS)

Emergency Medical Services systems that perform prehospital intubation should provide a program of ongoing quality improvement to minimize complications and to track overall supraglottic airway and endotracheal tube placement success rates. (Class I, LOE C-EO) (2019 ACLS)

Figure 1: Schematic representation of ACLS recommendations for use of advanced airways during CPR.
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3.4.2
Clinical Assessment of Tracheal Tube Placement

For a patient with perfusing rhythm who requires intubation, pulse oximetry and electrocardiographic (ECG) status should be monitored continuously during airway placement. Intubation attempts should be interrupted to provide oxygenation and ventilation as needed.

Attempts at endotracheal intubation during CPR have been associated with unrecognized tube misplacement or displacement as well as prolonged interruptions in chest compression.

Clinical assessment to confirm endotracheal intubation consists of visualizing chest expansion bilaterally and listening over the epigastrum (breath sounds should not be heard) and the lung fields bilaterally (breath sounds should be equal and adequate). A devices should also be used to confirm correct placement of the tube in the trachea.

Continuous waveform capnography is recommended in addition to clinical assessment as the most reliable method of confirming and monitoring correct placement of an endotracheal tube. (Class I, LOE C-LD) (2015 Part 7)

If continuous waveform capnometry is not available, a nonwaveform carbon dioxide (CO2) detector, esophageal detector device, or ultrasound used by an experienced operator is a reasonable alternative. (Class IIa, LOE C-LD) (2015 Part 7)

False-negative readings (ie, failure to detect CO2 despite tube placement in the trachea) may be present during cardiac arrest for several reasons.

  • most common reason: blood flow and delivery of CO2 to the lungs is low. In this case, focus is necessary to improve the quality of CPR (ensuring that compressions are of appropriate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in chest compressions, and voiding excessive ventilation)
  • false negative results also reported with pulmonary embolus, because pulmonary blood fow and delivery of CO2 to the lungs are reduced.

A colorimetric CO2 detection device may display a constant color rather than a breath-to-breath color change if the detector is contaminated with gastric contents.

If CO2 is not detected after endotracheal intubation and the clinical exam suggests that the tube is in place, a second method is needed to confirm tube placement, such as direct visualization or the use of an esophageal detector device.

Given the simplicity of the esophageal detector device, it can be used as the initial method for confirming correct tube placement in addition to clinical assessment in the victim of cardiac arrest when waveform capnography is not available. (Class IIa, LOE B) (2010 Part 8)

The esophageal detector device may yield misleading results in patients with morbid obesity, late pregnancy or status asthmaticus, or when there are copious endotracheal secretions, because the trachea tends to collapse in the presence of these conditions (leading to the incorrect conclusion that the tube is not in the trachea).

3.5
Postintubation Airway Management and Ventilation

After inserting and confirming correct placement of an endotracheal tube, record the depth of the tube as marked at the front teeth or gums and secure it.

The endotracheal tube should be secured with tape or a commercial device. (Class I, LOE C) (2010 Part 8)

Apply devices and tape in a manner that avoids compression of the front and sides of the neck, which may impair venous return from the brain.

Backboards and commercial devices for securing the endotracheal tube may be considered during patient transport. (Class IIb, LOE C) (2010 Part 8)

After tube confirmation and fixation, obtain a chest x-ray (when feasible) to confirm that the end of the endotracheal tube is properly positioned above the carina.

3.5.1
Ventilation After Advanced Airway Placement

Whenever an advanced airway (tracheal tube or supraglottic device) is inserted during CPR, it may be reasonable for providers to perform continuous compressions with positive-pressure ventilation delivered without pausing chest compressions. (Class IIb; LOE C-LD) (2017 Adult BLS) It may be reasonable for the provider to deliver 1 breath every 6 seconds (10 breaths per minute) while continuous chest compressions are being performed. (Class IIb; LOE C-LD) (2017 Adult BLS)

4
Automatic Transport Ventilators

Manually triggered, oxygen-powered, flow limited resuscitators may be considered for the management of patients who do not have an advanced airway in place and for whom a mask is being used for ventilation during CPR. (Class IIb, LOE C) (2010 Part 8)

During prolonged resuscitative efforts the use of an automatic transport ventilator (pneumatically powered and time- or pressure- cycled) may provide ventilation and oxygenation similar to that possible with the use of a manual resuscitation bag, while allowing the EMS team to perform other tasks. (Class IIb, LOE C) (2010 Part 8)

Rescuers should avoid using the automatic mode of the oxygen-powered, flow-limited resuscitator during CPR because it may generate high positive end-expiratory pressure (PEEP) that may impede venous return during [and between] chest compressions and compromise forward blood flow. (Class III, LOE C) (2010 Part 7)

5
Suction Devices

Both portable and installed suction devices should be available for resuscitation emergencies.

Portable units should provide adequate vacuum and flow for pharyngeal suction.

The suction device should be fitted with large- bore, nonkinking suction tubing and semirigid pharyngeal tips.

Several sterile suction catheters of various sizes should be available for suctioning the lumen of the advanced airway, along with a nonbreakable collection bottle and sterile water for cleaning tubes and catheters.

The installed suction unit should be powerful enough to provide an airflow of >40 L/min at the end of the delivery tube and a vacuum of >300 mm Hg when the tube is clamped.

The amount of suction should be adjustable for use in children and intubated patients.

6
Overview of the Management of Cardiac Arrest

The management of adult cardiac arrest is depicted in the Adult Cardiac Arrest Algorithm (see Figure 2) and the Adult Cardiac Arrest Circular Algorithm (see Figure 3) as a series of actions that will be performed in sequence by the single rescuer until the arrival of additional rescuers. Once two or more rescuers are present, many of the actions can be performed simultaneously.

Figure 2: Adult Cardiac Arrest Algorithm
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Figure 3: ACLS Cardiac Arrest Circular Algorithm
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The proper sequence of resuscitation actions are determined by the arrest rhythm. The four arrest rhythms are:

  • ventricular fibrillation (VF): disorganized electrical activity with no organized contraction of the ventricle
  • pulseless ventricular tachycardia (pVT): organized electrical activity of the myocardium that does not allow sufficient time for ventricular filling and does not generate significant forward flow of blood or a pulse
  • pulseless electrical activity (PEA): this term encompasses a heterogeneous group of organized electric rhythms that occur at rates that should produce pulses, but do not. The reason can be that the rhythm is not associated with ventricular contraction, or the ventricular contraction is too weak to generate a palpable pulse, or there are other circumstances such as massive hemorrhage that compromise circulation even with a normally beating heart.
  • asystole (or brady-asystole or ventricular asystole): absence of detectable ventricular electric activity (or where ventricular beats are very few and far between) with or without atrial electric activity

Because successful high-quality CPR forms the basis for treatment of cardiac arrest with any presenting rhythm, interventions during resuscitation are organized around two-minute periods of uninterrupted CPR. If VF/pVT is present, rhythm checks and shock delivery occur between these 2-minute periods of CPR, with attempts made to minimize interruptions in chest compressions.

Rhythm checks should be brief, and if an organized rhythm is observed, a pulse check should be performed. If there is any doubt about the presence of a pulse, chest compressions should resume immediately.

Once cardiac arrest is identified, CPR begins and rescuers attach a monitor/defibrillator to determine the arrest rhythm. The treatment will then follow either the “Ventricular Fibrillation (VF)/Pulseless Ventricular Tacyhycardia (pVT)” left branch of the algorithm or the “Asystole/Pulseless Electrical Activity (PEA)” right branch of the algorithm (see Figure 2).

  • VF/pVT: emphasis is on delivering high-quality CPR and shocks. IV epinephrine and an antiarrhythmic are given for shock-refractory VF/pVT
  • Asystole/PEA: emphasis is on delivering high-quality CPR and administration of epinephrine

Note that patients who present with VF/pVT may become asystolic or develop PEA, requiring a change in treatment that is depicted in the Asystole/PEA branch of the algorithm. Patients who present with Asystole/PEA may develop ventricular fibrillation during the course of the resuscitation, requiring a change in treatment to that depicted in the VF/pVT branch of the algorithm (see Figure 2).

The Adult Cardiac Arrest Circular Algorithm (see Figure 3) depicts the same actions shown in the Adult Cardiac Arrest Algorithm in a slightly different way. The circle of actions applies to the care of patients with both VF/pVT and Asystole/PEA arrest rhythms.

In all ACLS algorithms, drug doses and specific details about skills are provided in boxes located to the right side of the algorithms.

7
Access for Parenteral Medications During Cardiac Arrest

7.1
Timing of Intravenous/Intraosseous Access

During cardiac arrest, provision of high-quality CPR and rapid defibrillation are of primary importance and drug administration is of secondary importance.

Although time to drug treatment appears to have importance, the exact time parameters or the precise sequence with which drugs should be administered during cardiac arrest is not known.

7.2
Peripheral Intravenous (IV) Drug Delivery

A resuscitation drug, administered by a peripheral venous route, should be administered by bolus injection and followed with a 20-mL bolus of IV fluid.

Briefly elevating the extremity during and after drug administration may recruit the benefit of gravity to facilitate delivery to the central circulation, although the evidence to support such an effect has not been evaluated.

7.3
Intraosseous (IO) Drug Delivery

It is reasonable for providers to establish intraosseous (IO) access if intravenous (IV) access is not readily available. (Class IIa, LOE C) (2010 Part 8)

7.4
Central Intravenous Drug Delivery

Most in-hospital cardiac arrests should take place in an intensive care unit. As a result, many patients may already have a central IV catheter in place. If central IV access is not in place, an appropriately trained provider may attempt such access if it doesn’t interfere with high-quality CPR (especially compressions).

The appropriately trained provider may consider placement of a central intravenous catheter (internal jugular or subclavian) during cardiac arrest, unless there are contraindications. (Class IIb, LOE C) (2010 Part 8)

7.5
Endotracheal Drug Delivery

If IV or IO access cannot be established, epinephrine, vasopressin, and lidocaine may be administered by the endotracheal route during cardiac arrest. (Class IIb, LOE B) (2010 Part 8)

The optimal endotracheal dose of most drugs is unknown, but typically the dose given by the endotracheal route is 2 to 2½ times the recommended IV dose.

Dilute the dose in 5 to 10 mL of sterile water (or normal saline) and inject the drug as a rapid spray (aerosolized) directly into the endotracheal tube.

Whenever anyone in cardiac arrest fails to respond to initial efforts, providers should consider potential reversible causes, which may be recalled as the Hs and Ts (see Table 1).

Table 1: Treatable Causes of Cardiac Arrest: The H's and T's

8
Management of Cardiac Arrest with Ventricular Fibrillation/Pulseless Ventricular Tachyardia (ie, “shockable” rhythms)

Note: Although providers identify ventricular fibrillation (VF) and pulseless VT (pVT), the rhythm analysis detects VF or VT; the determination that the VT is pulseless is a clinical assessment.

The keys to management pf VF/pVT arrest are:

  • Immediate delivery of high-quality CPR until defibrillator is available and after each shock
  • rapid defibrillation
  • if the VF/pVT is refractory to shocks, then vasopressors and antiarrhythmics are delivered as needed.
  • Providers should search for and treat reversible causes if cardiac arrest fails to respond

8.1
Attempted Defibrillation

Attempted defibrillation with an AED

  • When the initial rhythm check reveals VF/VT, the AED will typically prompt rescuers to charge the device (if it doesn’t do so automatically), quickly “clear” the victim for shock delivery, and then deliver a shock.
  • Resume CPR (beginning with chest compressions) immediately after shock delivery, without a rhythm or pulse check, and and continue for 2 minutes before the next rhythm check.

Attempted defibrillation with a manual defibrillator

  • When the initial rhythm check reveals VF/VT, the first provider resumes CPR while the second provider charges the defibrillator. After this first rhythm analysis and shock, the defibrillator is ideally charged to the correct subsequent dose before the next rhythm check so if VF/VT persists at the next rhythm check, the shock can be delivered without delay.
  • Once the defibrillator is charged, CPR is paused to “clear” the patient for shock delivery.
  • After the patient is “clear,” the second provider gives a single shock as quickly as possible to minimize the interruption in chest compressions (“hands-off interval”).
  • The first provider resumes CPR beginning with compressions immediately after shock delivery (without a rhythm or pulse check) and continues CPR for 2 minutes.
  • After 2 minutes of CPR the sequence is repeated, beginning with a rhythm check.

The provider giving chest compressions should switch at every 2-minute cycle to minimize fatigue.

When possible, CPR quality should be monitored based on mechanical or physiologic parameters.

8.1.1
Defibrillation Strategies for VF/pVT: Waveform Energy and First-Shock Success

Defibrillators (using Biphasic Truncated Exponential, Rectilinear biphasic, or monophasic waveforms) are recommended to treat atrial and ventricular arrhythmias. (Class I, LOE B-NR) (2015 Part 7)

Based on their greater success in arrhythmia termination, defibrillators using biphasic waveforms (Biphasic Truncated Exponential or Rectilinear biphasic) are preferred to monophasic defibrillators for treatment of both atrial and ventricular arrhythmias. (Class IIa, LOE B-R) (2015 Part 7)

In the absence of conclusive evidence that 1 biphasic waveform is superior to another in termination of VF, it is reasonable to use the manufacturer’s recommended energy dose for the first shock. If this is not known, defibrillation at the maximal dose may be considered. (Class IIb, LOE C-LD) (2015 Part 7)

8.1.2
Defibrillation Strategies for VF/pVT: Energy Dose for Subsequent Shocks

It is reasonable that selection of fixed versus escalating energy for subsequent shocks be based on the specific manufacturer’s instructions. (Class IIa, LOE C-LD) (2015 Part 7)

If using a manual defibrillator capable of escalating energies, higher energy for second and subsequent shocks may be considered. (Class IIb, LOE C-LD) (2015 Part 7)

8.1.3
Defibrillation Strategies for VF/pVT: Single Shocks Versus Stacked Shocks

A single-shock strategy (as opposed to stacked shocks) is reasonable for defibrillation. (Class IIa, LOE B-NR) (2015 Part 7)

8.1.4
Automatic Versus Manual Modes for Multimodal Defibrillators

The benefit of using a multimodal defibrillator in manual instead of automatic mode during cardiac arrest is uncertain. (Class IIb, LOE C) (2010 Part 8)

8.1.5
VF Waveform Analysis to Predict Defibrillation Success

The value of VF waveform analysis to guide management of defibrillation in adults with in-hospital and out-of-hospital cardiac arrest is uncertain. (Class IIb, LOE C) (2010 Part 8)

8.2
Vasopressor Therapy for VF/pVT Cardiac Arrest

The primary goal of pharmacologic therapy during cardiac arrest is to facilitate restoration and maintenance of a perfusing spontaneous rhythm. The α-adrenergenic vasoconstrictive effects can improve coronary perfusion pressure and myocardial perfusion, as well as cerebral perfusion.

The timing of drug administration for VF/pVT or Asystole/PEA cardiac arrest is based on the consensus of experts (see Table 2).

Table 2: Timing and sequence of drug administration during cardiac arrest—the knowns and unknowns.

8.2.1
Standard Dose Epinephrine for VF/pVT Cardiac Arrest

The alpha-adrenergic effects of epinephrine can improve the diastolic (relaxation) pressure in the aorta and ultimately improve coronary perfusion pressure. Although epinephrine has not been shown definitively to improve survival with favorable neurological outcome, it has been shown to increase 30-day survival and survival to hospital discharge.

We recommend that epinephrine be administered to patients in cardiac arrest. (Class I, LOE B-R) (2019 ACLS)

On the basis of protocols used in clinical trials, it is reasonable to administer 1 mg every 3-5 minutes. (Class IIa, LOE C-LD) (2019 ACLS)

The optimal timing of epinephrine, particularly in relation to defibrillation when cardiac arrest is due to a shockable rhythm, is not known.

With respect to timing, for cardiac arrest with a shockable rhythm, It may be reasonable to administer epinephrine after initial defibrillation attempts have failed. (Class IIb, LOE C-LD) (2019 ACLS)

Based on the consensus of experts, epinephrine is administered every 3-5 minutes during resuscitation. In practical terms, that means it is typically administered during every other 2-minute period of CPR when VF/pVT persists despite delivery of shocks and high-quality CPR.

High-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III: No Benefit, LOE B-R) (2019 ACLS)

8.2.2
No Advantage to Vasopressin Alone or in Combination with Epinephrine for VF/pVT Cardiac Arrest

Vasopressin may be considered in a cardiac arrest but offers no advantage as a substitute for epinephrine in cardiac arrest. (Class IIb, LOE C-LD) (2019 ACLS)

Vasopressin in combination with epinephrine may be considered during cardiac arrest but offers no advantage as a substitute for epinephrine alone. (Class IIb, LOE C-LD) (2019 ACLS)

8.2.3
More Evidence Needed Regarding Use of Steroids Combined with Vasopressin and Epinephrine

In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post- arrest hydrocortisone may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy. (Class IIb, LOE C-LD) (2015 Part 7)

For patients with OHCA, use of steroids during CPR is of uncertain benefit. (Class IIb, LOE C-LD) (2015 Part 7)

8.3
Antiarrhythmic Drugs During VF/pVT Cardiac Arrest

When VF/pVT persists despite shocks and epinephrine, either amiodarone of lidocaine may be administered.

The principal objective of antiarrhythmic drug therapy in shock-refractory VF/pVT is to facilitate the restoration and maintenance of a spontaneous perfusing rhythm in concert with the shock termination of VF.

Do not compromise the quality of CPR or timely defibrillation to establish vascular access to enable drug administration.

Amiodarone or lidocaine may be considered for VF/pVT that is unresponsive to defibrillation. These drugs may be particularly useful for patients with witnessed arrest, for whom time to drug administration may be shorter. (Class IIb; LOE B-R) (2018 ACLS)

The routine use of magnesium for cardiac arrest is not recommended in adult patients (Class III: No Benefit; LOE C-LD). Magnesium may be considered for torsades de pointes (ie, polymorphic VT associated with long-QT interval). (Class IIb; LOE C-LD) (2018 ACLS)

Recommendations for the use of antiarrhythmic medications in cardiac arrest are based primarily on the potential for improvement in short-term outcome.

8.4
Subsequent Rhythm Check Reveals no VF/pVT

If the next rhythm check indicates that no shockable rhythm is present, look for an organized rhythm on the defibrillator screen.

When a rhythm check in a patient in cardiac arrest reveals an organized rhythm, perform a pulse check.

  • If a pulse is detected and an adequate blood pressure confirmed, post–cardiac arrest care should be initiated immediately (see Part 8, Post-Cardiac Arrest Care)
  • If the pulse is absent (eg, PEA) or the rhythm is asystole, resume CPR immediately, beginning with chest compressions, and provide care that is consistent wth the Asystole/PEA (right) branch of the cardiac arrest algorithm (see Figure 2).
    • If epinephrine was administered during previous 2 minutes of CPR, join the Asystole/PEA (right) side of the algorithm at Box 11.
    • If epinephrine was not administered during the previous 2 minutes of CPR, join the Asystole/PEA (right) side of the algorithm at box 10.

9
Management of Cardiac Arrest with PEA/Asystole

The key to treatment of cardiac arrest associated with Asystole or PEA is

  • delivery of high-quality CPR
  • epinephrine administration as soon as possible and then every 3-5 minutes (typically during every other 2-minute period of CPR)
  • Identification and treatment of reversible causes (see Table 1, above)

First Rhythm analysis:

  • When the first rhythm check in an patient in cardiac arrest reveals a nonshockable rhythm, resume CPR immediately, beginning with chest compressions, and treat the patient according to the Asystole/PEA (right) branch of the Adult Cardiac Arrest Algorithm (see Figure 2), beginning at box/step 10. Continue CPR for 2 minutes before the rhythm check is repeated.

Subsequent rhythm analysis:When a rhythm check in a patient in cardiac arrest reveals no shockable rhythm, look for an organized rhythm on the monitor screen. If an organized rhythm is present,perform a pulse check.

  • If a pulse is detected and an adequate blood pressure confirmed, post–cardiac arrest care should be initiated immediately (see Part 8, Post-Cardiac Arrest Care).
  • If the pulse is absent (eg, PEA) or the rhythm is asystole, resume CPR immediately, beginning with chest compressions, and continue for 2 minutes before the rhythm check is repeated.

If the patient who presented with Asystole/PEA cardiac arrest ever demonstrates a “shockable” rhythm (VF/VT), treat the patient according to the VF/pVT (left) side of the Adult Cardiac Arrest algorithm (see Figure 2).

  • If the patient received epinephrine during the previous 2 minutes of CPR, join the algorithm at step 7, delivering a shock and immediately resuming CPR, beginning with compressions.
  • If the patient did not receive epinephrine during the previous 2 minutes of CPR, join the algorithm at step 5, delivering a shock and immediately resuming CPR, beginning with compressions.

9.1
Critical Role of High-Quality CPR

The provider performing chest compressions should switch every 2 minutes.

If monitoring devices are in place, monitor CPR quality on the basis of mechanical or physiologic parameters.

9.2
Epinephrine Administration

Epinephrine administration can improve aortic diastolic (relaxation) pressure and improve coronary perfusion. If the myocardium is better perfused, administration of a shock may be more likely to eliminate VF/VT.

We recommend that epinephrine be administered to patients in cardiac arrest. (Class I, LOE B-R) (2019 ACLS)

On the basis of protocols used in clinical trials, it is reasonable to administer 1 mg every 3-5 minutes. (Class IIa, LOE C-LD) (2019 ACLS)

Post-hoc analysis from a recent out-of-hospital cardiac arrest trial of epinephrine administration demonstrated an association of earlier epinephrine administration for arrest associated with Asystole/PEA and survival.

With respect to timing, for cardiac arrest with a non- shockable rhythm, it is reasonable to administer epinephrine as soon as feasible. (Class IIa, LOE C-LD) (2019 ACLS)

High-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III: No Benefit, LOE B-R) (2019 ACLS)

9.3
No Advantage to Vasopressin Alone or in Combination with Epinephrine for Asystole/PEA

Vasopressin may be considered in cardiac arrest but offers no advantage as a substitute for epinephrine in cardiac arrest. (Class IIb, LOE C-LD) (2019 ACLS)

Vasopressin in combination with epinephrine may be considered during cardiac arrest but offers no advantage as a substitute for epinephrine alone. (Class IIb, LOE C-LD) (2019 ACLS)

9.4
Atropine Unlikely to be Beneficial for Asystole/PEA

Available evidence suggests that the routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit. (Class IIb, LOE B) (2010 Part 8)

9.5
More Evidence Needed Regarding Use of Steroids Combined with Vasopressin and Epinephrine

In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post- arrest hydrocortisone may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy. (Class IIb, LOE C-LD) (2015 Part 7)

For patients with OHCA, use of steroids during CPR is of uncertain benefit. (Class IIb, LOE C-LD) (2015 Part 7)

9.6
Treating Potentially Reversible Causes of PEA/Asystole

During each 2-minute period of CPR recall the H’s and T’s to identify factors that may have caused the arrest or may be complicating the resuscitative effort; treat those conditions as soon as possible.

The association of PEA with hypoxemia makes placement of an advanced airway theoretically more important than during VF/pulseless VT and might be necessary to achieve adequate oxygenation or ventilation.

PEA caused by severe volume loss or sepsis may benefit from administration of empirical IV/IO crystalloid.

PEA caused by severe blood loss may benefit from a blood transfusion.

When pulmonary embolism is presumed or known to be the cause of cardiac arrest, empirical fibrinolytic therapy can be considered. (Class IIa, LOE B) (2010 Part 8)

If tension pneumothorax is clinically suspected as the cause of PEA, initial management includes needle decompression.

Echocardiography can be used to guide management of PEA because it provides information about:

  • intravascular volume status
  • cardiac tamponade
  • mass lesions (tumor, clot)
  • left ventricular contractility
  • regional wall motion.

See “Part 10: Special Circumstances of Resuscitation” for management of toxicological causes of cardiac arrest.

10
Monitoring Physiologic Parameters During CPR

Monitoring both provider performance and patient physiologic parameters during CPR is essential to optimizing CPR quality.

Although no clinical study has examined whether titrating resuscitative efforts to physiologic parameters during CPR improves outcome, it may be reasonable to use physiologic parameters (quantitative waveform capnography, arterial relaxation diastolic pressure, arterial pressure monitoring, and central venous oxygen saturation) when feasible to monitor and optimize CPR quality, guide vasopressor therapy, and detect ROSC. (Class IIb, LOE C-EO) (2015 Part 7)

10.1
Ultrasound During Cardiac Arrest

Ultrasound (cardiac or noncardiac) may be considered during the management of cardiac arrest, although its usefulness has not been well established. (Class IIb, LOE C-EO) (2015 Part 7)

If a qualified sonographer is present and use of ultrasound does not interfere with the standard cardiac arrest treatment protocol, then ultrasound may be considered as an adjunct to standard patient evaluation. (Class IIb, LOE C-EO) (2015 Part 7)

11
Prognostication During CPR:End-Tidal CO2

In intubated patients, failure to achieve an End-Tidal CO2 of greater than 10 mm Hg by waveform capnography after 20 minutes of CPR may be considered as one component of a multimodal approach to decide when to end resuscitative efforts, but it should not be used in isolation. (Class IIb, LOE C-LD) (2015 Part 7)

In nonintubated patients, a specific ETCO2 cutoff value at any time during CPR should not be used as an indication to end resuscitative efforts. (Class III: Harm, LOE C-EO) (2015 Part 7)

12
Extracorporeal CPR

ECPR refers to venoarterial extracorporeal membrane oxygenation during cardiac arrest, including extracorporeal membrane oxygenation and cardiopulmonary bypass. These techniques require adequate vascular access and specialized equipment.

There is insufficient evidence to recommend the routine use of Extracorporeal CPR for patients with cardiac arrest. (2019 ACLS)

Extracorporeal CPR may be considered for selected patients as rescue therapy when conventional CPR efforts are failing in settings in which it can be expeditiously implemented and supported by skilled providers. (Class IIb, LOE C-LD) (2019 ACLS)

13
Interventions Not Recommended for Routine Use During Cardiac Arrest

13.1
Atropine

Routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit. (Class IIb, LOE B) (2010 Part 8)

13.2
Sodium Bicarbonate

The mainstays of restoring acid-base balance during cardiac arrest includes the restoration of oxygen delivery with high-quality CPR and appropriate ventilation with oxygen.

Routine use of sodium bicarbonate is not recommended for patients in cardiac arrest. (Class III, LOE B) (2010 Part 8)

In some special resuscitation situations, such a spreexisting metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose, administration of sodium bicarbonate can be beneficial (see Part 10: Special Circumstances in Resuscitation).

If sodium bicarbonate is administered, whenever possible, bicarbonate therapy should be guided by the bicarbonate concentration or calculated base deficit obtained from blood gas analysis or laboratory measurement. To minimize the risk of iatrogenically induced alkalosis, do not attempt complete correction of the calculated base deficit.

13.3
Calcium

Routine administration of calcium for treatment of in-hospital and out-of-hospital cardiac arrest is not recommended. (Class III, LOE B) (2010 Part 8)

13.4
Fibrinolysis

Fibrinolytic therapy should not be routinely used in cardiac arrest. (Class III, LOE B) (2010 Part 8)

13.5
Pacing

Electric pacing is not recommended for routine use in cardiac arrest. (Class III, LOE B) (2010 Part 8)

13.6
Precordial Thump and Percussion Pacing

The precordial thump may be considered for termination of witnessed monitored unstable ventricular tachyarrhythmias when a defibrillator is not immediately ready for use (Class IIb, LOE B), but should not delay CPR and shock delivery. (2010 Part 8)

There is insufficient evidence to recommend for or against the use of the precordial thump for witnessed onset of asystole. (2010 Part 8)

There is insufficient evidence to recommend percussion pacing during typical attempted resuscitation from cardiac arrest. (2010 Part 8)

14
Return of Spontaneous Circulation (ROSC)

Once there is return of spontaneous circulation, providers begin post-cardiac arrest care, focusing on support of :

  • Neurologic function, including Targeted Temperature Management
  • Circulation, including treatment of possible acute coronary occlusion (ie, ST-elevation myocardial infarction), arrhythmias andshock, and support of fluid balance
  • Oxygenation and Ventilation

For further information, see Part 8: Post-Cardiac Arrest Care.

15
When Should Resuscitative Efforts Stop?

The final decision to stop resuscitative efforts can never rest on a single parameter, such as duration of resuscitative efforts.

In the out-of-hospital setting, cessation of resuscitative efforts in adults should follow system-specific criteria under direct medical control (see Part 3: Ethical Issue in Resuscitation).

16
Overview of Management of Symptomatic Bradycardia and Tachycardia

  • Electrocardiographic (ECG) and rhythm information should be interpreted within the context of total patient assessment.
  • Errors in diagnosis and treatment are likely to occur if treatment decisions neglect clinical evaluation and are based solely on rhythm interpretation.
  • Evaluate the patient’s symptoms and clinical signs, including ventilation, oxygenation, heart rate, blood pressure, level of consciousness, and signs of inadequate organ perfusion.
  • When an arrhythmia causes a patient to be unstable (vital organ function is acutely impaired or cardiac arrest is ongoing or imminent), immediate intervention is indicated.
  • When an arrhythmia is causing symptoms (e.g. palpitations, lightheadedness, or dyspnea) but the patient is stable and not in imminent danger, more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases make an assessment as to whether the arrhythmia itself is causing the patient to be unstable or symptomatic. Tachycardias, for example, can be a compensatory response to another patient condition (such as hemorrhage or sepsis) at which treatment should instead be directed.
  • It is critically important to determine the cause of the patient’s instability in order to properly direct treatment.
  • In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself.

17
Bradyarrhythmias

The goals of management of bradyarrhythmias in adults are to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the bradyarrhythmia. Drugs (beginning with atropine) or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia.

If bradycardia produces signs and symptoms of instability (eg, acutely altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock that persist despite adequate airway and breathing), the initial treatment is atropine. (Class IIa, LOE B) (2010 Part 8)

If bradycardia is unresponsive to atropine, intravenous (IV) infusion of β-adrenergic agonists with rate-accelerating effects (dopamine, epinephrine) or transcutaneous pacing (TCP) can be effective (Class IIa, LOE B) while the patient is prepared for emergent transvenous temporary pacing if required. (2010 Part 8)

Figure 4: Adult Bradycardia With a Pulse Algorithm
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17.1
Evaluation of the Adult with Bradycardia and a Pulse

Bradycardia is defined as a heart rate <60/minute, but symptomatic bradycardia generally is <50/minute. Bradycardias include sinus bradycardia and sinus rhythms with heart block; but can also occur with any rhythm (such as atrial fibrillation) for which the rate is inappropriately slow.

The Bradycardia Algorithm (see Figure 4) focuses on management of clinically significant bradycardia (ie, bradycardia that is inappropriate for the clinical condition).

  • Focus initial evaluation on signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) and oxyhemoglobin saturation as determined by pulse oximetry (Box 2).
  • If oxygenation is inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen.
  • Attach a monitor to the patient, evaluate blood pressure, and establish IV access.
  • If possible, obtain a 12-lead ECG to better define the rhythm.
  • While initiating treatment, evaluate the patient’s clinical status and identify potentially reversible causes.
  • Identify signs and symptoms of poor perfusion and determine if those signs are likely to be caused by the bradycardia (Box 3).
  • If the signs and symptoms are not due to bradycardia, reassess the underlying cause of the patient’s symptoms.
  • Signs and symptoms of bradycardia may be mild; asymptomatic or minimally symptomatic patients do not necessarily require treatment (Box 4) unless there is suspicion that the rhythm is likely to progress to symptoms or become life-threatening (eg, Mobitz type II second-degree AV block in the setting of acute myocardial infarction [AMI]).
  • If the bradycardia is suspected to be the cause of acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock, timmediate treatment is needed.

17.2
Therapy for Bradyarrhythmias (Figure 4 Box 5)

17.2.1
Atropine

Atropine remains the first-line drug for acute symptomatic bradycardia. (Class IIa, LOE B) (2010 Part 8)

  • Recommended atropine dose for bradycardia: 0.5 mg IV every 3 to 5 minutes to a maximum total dose of 3 mg.
  • Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate.
  • Atropine administration should not delay implementation of external pacing for patients with poor perfusion.
  • Use atropine cautiously in the presence of acute coronary ischemia or MI; increased heart rate may worsen ischemia or increase infarction size.
  • Atropine will likely be ineffective in patients who have undergone cardiac transplantation because the transplanted heart lacks vagal innervation.

NOTE: Providers should not rely on atropine in type II second-degree or third-degree AV block or in patients with third-degree AVmblock with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system). These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with transcutaneous pacing (TCP) or β- adrenergic support as temporizing measures while the patient is prepared for transvenous pacing (see Figure 4, Box 6).

17.2.2
Pacing

Transcutaneous pacing is painful in conscious patients, and, it is at best a temporaizing measure. Whether it is effective or not (ie, achieving inconsistent capture), prepare the patient for transvenous pacing and obtain expert consultation.

It is reasonable for healthcare providers to initiate transcutaneous pacing in unstable patients who do not respond to atropine. (Class IIa, LOE B) (2010 Part 8)

Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. (Class IIb, LOE C) (2010 Part 8) If the patient does not respond to drugs or transcutaneous pacing, transvenous pacing is probably indicated. (Class IIa, LOE C) (2010 Part 8) See Figure 4, Box 6.

17.2.3
Alternative Drugs to Consider

Dopamine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, in whom atropine may be inappropriate or after atropine fails. (Class IIb, LOE B) (2010 Part 8)

Begin the dopamine infusion at 2-10 mcg/kg per minute and titrate to patient response.

Epinephrine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, for whom atropine may be inappropriate or after atropine fails. (Class IIb, LOE B) (2010 Part 8)

Begin the infusin at 2 to 10 mcg per minute.

Isoproterenol is a beta-adrenergic agent with beta-1 and beta-2 effects, resulting in an increase in heart rate and vasodilation. The recommended adult dose is 2 to 10 mcg/min by IV infusion, titrated according to heart rate and rhythm response.

18
Tachyarrhythmias

The goal of therapy for tachycardia is to rapidy identify and treat patients who are hemodynamically unstabe or symptomatic due to the arrhythmia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia.

Management of patients with symptomatic tachyarrhythmias is summarized in the algorithm (see Figure 5).

If the tachycardic patient is unstable with severe signs and symptoms related to a suspected arrhythmia (eg, acute altered mental status, ischemic chest discomfort, decompensated heart failure, hypotension, or other signs of shock), immediate cardioversion should be performed (with prior sedation in the conscious patient). (Class I, LOE B) (2010 Part 8)

In select cases of regular narrow-complex tachycardia with unstable signs or symptoms, a trial of adenosine before cardioversion is reasonable to consider. (Class IIb, LOE C) (2010 Part 8)

The principles of management of tachyarrhythmias is requires identification of the unstable patient and determining if the tachycardia is narrow-complex or wide-complex tachycardia, has a regular or irregular rhythm, and, for wide complex tachycardia, whether the QRS morphology is monomorphic or polymorphic.

Figure 5: Adult Tachycardia With a Pulse Algorithm
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18.1
Classification of Tachyarrhythmias

Tachycardias can be classified in several ways, based on appearance of the QRS complex, and on the heart rate and regularity. ACLS providers should be aware that most wide-complex tachycardias are ventricular in origin.

Narrow–QRS-complex (SVT) tachycardias (QRS <0.12 second), in order of frequency:

  • Sinus tachycardia
  • Atrial fibrillation
  • Atrial flutter
  • AV nodal reentry
  • Accessory pathway–mediated tachycardia
  • Atrial tachycardia (including automatic and reentry forms)
  • Multifocal atrial tachycardia
  • Junctional tachycardia (rare in adults)

Wide–QRS-complex tachycardias (QRS ≥0.12 second)

  • Ventricular tachycardia (VT) and ventricular fibrillation (VF)
  • SVT with aberrancy
  • Pre-excited tachycardias (Wolff-Parkinson-White [WPW] syndrome)
  • Ventricular paced rhythms

Irregularly irregular (meaning the interval between successive beats is variable or chaotic) narrow-complex tachycardias are likely atrial fibrillation or multi-focal atrial tachycardia; occasionally atrial flutter is irregular.

18.2
Initial Evaluation and Management of Tachyarrhythmias

Attempt to determine whether the tachycardia is the primary cause of the presenting symptoms or secondary to an underlying condition that is causing both the presenting symptoms and the faster heart rate.

When a heart rate is <150 beats per minute, it is unlikely that symptoms of instability are caused primarily by the tachycardia unless there is impaired ventricular function.

  • Focus initial evaluation of any patient with tachycardia on signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) and oxyhemoglobin saturation as determined by pulse oximetry (Box 2).
  • If oxygenation is inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen.
  • Attach a monitor to the patient, evaluate blood pressure, and establish IV access.
  • Obtain a 12-lead ECG, if available, to better define the rhythm, but do not delay immediate cardioversion if the patient is unstable.
  • While initiating treatment, evaluate the patient’s clinical status and identify potential reversible causes of the tachycardia.
  • If signs and symptoms persist despite provision of supplementary oxygen and support of airway and ventilation, assess the patient’s degree of instability and determine if the instability is related to the tachycardia (Box 3).
  • If the patient demonstrates rate-related cardiovascular compromise with signs and symptoms such as acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock suspected to be due to a tachyarrhythmia, proceed to immediate synchronized cardioversion (Box 4).
  • With ventricular rates <150 beats per minute in the absence of ventricular dysfunction, it is more likely that the tachycardia is secondary to another underlying condition rather than the primary cause of the instability.

If not hypotensive, the patient with a regular narrow-complex SVT (likely due to suspected reentry, paroxysmal supraventricular tachycardia, as described below) may be treated with adenosine while preparations are made for synchronized cardioversion. (Class IIb, LOE C) (2010 Part 8)

If the patient is stable, there is time to obtain a 12-lead ECG, evaluate the rhythm, and determine if the QRS complex is truly narrow or wide (≥0.12 seconds); the QRS width may not always be evident in a single lead rhythm tracing. Stable patients may await expert consultation because treatment has the potential for harm.

18.3
Electrical Cardioversion

If the patient is conscious, if possible, establish IV access and administer sedation before cardioversion.

Do not delay cardioversion if the patient is extremely unstable.

18.3.1
Synchronized Cardioversion and Unsynchronized Shocks

Refer to Figure 5: Tachycardia Algorithm – Box 4.

Synchronized cardioversion is recommended to treat (1) unstable SVT, (2) unstable atrial fibrillation, (3) unstable atrial flutter, and (4) unstable monomorphic (regular) VT. Shock can terminate the arrhythmias by interrupting the underlying re-entrant pathway that is responsible for them.

If cardioversion is needed and it is impossible to synchronize a shock, use high-energy unsynchronized shock (at a defibrillation dose).

The recommended initial biphasic energy dose for cardioversion of atrial fibrillation is 120 to 200 J. (Class IIa, LOE A) (2010 Part 8) Recommended dose will vary based on the waveform. Check with the manufacturer regarding recommended dose for a specific defibrillator and its waveform.

Increase the dose in a stepwise fashion if the initial shock fails.

Cardioversion of atrial flutter and other supraventricular tachycardias generally requires less energy; an initial energy of 50J to 100J is usually sufficient. If the initial shock fails, increase the dose in a stepwise fashion.Cardioversion of atrial fibrillation with monophasic waveforms should begin at 200 J and increase in stepwise fashion if not successful. (Class IIa, LOE B) (2010 Part 8)

Monomorphic VT (regular form and rate) with a pulse responds well to monophasic or biphasic waveform cardioversion (synchronized) shocks at initial energies of 100 J.If there is no response to the first shock, it may be reasonable to increase the dose in a stepwise fashion. This recommendation represents expert opinion. (Class IIb, LOE C) (2010 Part 8)

Treat a polymorphic VT as VF and deliver high-energy unsynchronized shocks (ie, defibrillation doses). Polymorphic QRS appearance will be virtually impossible to permit synchronization. In addition, although the patient may initially have a pulse, it typically deteriorates quickly to a pulseless VT.See the ACLS Adult Cardiac Arrest Algorithm, Figure 2.

If there is any doubt whether monomorphic or polymorphic VT is present in the unstable patient, do not delay shock delivery to perform detailed rhythm analysis: provide high-energy unsynchronized shocks (ie, defibrillation doses) and CPR.

18.4
Regular Narrow-Complex Tachycardia—Sinus Tachycardia

Sinus tachycardia is defined as a heart rate >100 per minute.

The upper rate of sinus tachycardia is age-related (calculated as approximately 220 per minute, minus the patient’s age in years) and may be useful in judging whether an apparent sinus tachycardia falls within the expected range for a patient’s age.

No specific drug treatment is required for sinus tachycardia. Direct therapy toward identification and treatment of the underlying cause of the tachycardia.

When cardiac function is poor, stroke volume is limited so cardiac output can be dependent on a rapid heart rate; “normalizing” the heart rate can be detrimental.

18.5
Regular Narrow-Complex Tachycardia—Supraventricular Tachycardia (Reentry SVT)

Most SVTs are regular tachycardias that are caused by reentry, an abnormal rhythm circuit that allows a wave of depolarization to repeatedly travel in a circle in cardiac tissue.

The rhythm is considered to be of supraventricular origin if the QRS complex is narrow (<0.12 second) or if the QRS complex is wide (broad) and preexisting bundle branch block or rate-dependent aberrancy is known to be present.

Reentry circuits resulting in SVT can occur in atrial myocardium (resulting in atrial fibrillation, atrial flutter, and some forms of atrial tachycardia). The ventricular rate of reentry arrhythmias based in atrial myocardium will be slowed but not terminated by drugs that slow conduction through the AV node.

In another form of re-entry tachycardia, the reentry circuit may also reside in the AV node itself. These arrhythmias are characterized by abrupt onset and termination and a regular rate that exceeds the typical upper limits of sinus tachycardia at rest (usually >150 per minute).

  • if both limbs of the reentry circuit involve AV nodal tissue an AV nodal reentry tachycardia (AVNRT) may result; this form of reentry tachycardia is often characterized by absence of readily identifiable P waves
  • if one limb of the reentry circuit involves an accessory pathway and the other involves the AV node it may result in AV reentry tachycardia (AVRT)
  • AVNRT and AVRT are both called paroxysmal supraventricular tachycardia (PSVT)
  • These reentry arrhythmias, with at least one limb of the circuit residing in the AV node can be terminated by drugs that slow conduction through the AV node.

A third group of SVTs is referred to as automatic tachycardias are due to an excited automatic focus and includes ectopic atrial tachycardia, multi-focal atrial tachycardia, and junctional tachycardia.

  • The characteristic onset and termination of automatic tachyarrhythmias are more gradual and analogous to how the sinus node behaves in gradually accelerating and slowing heart rate.
  • Automatic arrhythmias can be difficult to treat, are not responsive to cardioversion, and are usually controlled acutely with drugs that slow conduction through the AV node and thereby slow ventricular rate.

18.5.1
Vagal Maneuvers

Vagal maneuvers and adenosine are the preferred initial therapeutic choices for the termination of stable PSVT (Figure 5: Tachycardia Algorithm, Box 7).

For other SVTs, vagal maneuvers and adenosine may transiently slow the ventricular rate and potentially assist rhythm diagnosis but will not usually terminate such arrhythmias.

See Table 3 for drug doses, effects and potential side effects.

Table 3: IV Drugs Used for Tachycardia

18.5.2
Adenosine

If paroxysmal supraventricular tachycardia does not respond to vagal maneuvers, give 6 mg of IV adenosine as a rapid IV push through a large (eg, antecubital) vein catheter [use injection port nearest the vein] followed by a 20 mL saline flush. (Class I, LOE B) (2010 Part 8) If the rhythm does not convert within 1 to 2 minutes, give a 12 mg rapid IV push using the method above.

  • Continuous ECG recording to provide written documentation is strongly encouraged as close attention to varying responses to treatment may help to diagnose the underlying rhythm even if after the fact.
  • Because there is the possibility of initiating atrial fibrillation with rapid ventricular rates in a patient with WPW, a defibrillator should be available when adenosine is administered to any patient in whom WPW is a consideration.

After conversion, monitor the patient for recurrence and treat any recurrence of PSVT with adenosine or a longer-acting AV nodal blocking agent (eg, diltiazem or β-blocker).

If adenosine or vagal maneuvers disclose another form of SVT (such as atrial fibrillation or flutter), treatment with a longer-acting AV nodal blocking agent should be considered to afford more lasting control of ventricular rate.

18.5.3
Calcium Channel Blockers and β-Blockers

If adenosine or vagal maneuvers fail to convert paroxysmal supraventricular tachycardia, the paroxysmal supraventricular tachycardia recurs after such treatment, or these treatments disclose a different form of SVT (such as atrial fibrillation or flutter), it is reasonable to use longer-acting AV nodal blocking agents, such as the nondihydropyridine calcium channel blockers (verapamil and diltiazem) (Class IIa, LOE B) or beta-blockers. (Class IIa, LOE C) (2010 Part 8)

The longer-acting AV nodal blocking agents act primarily on nodal tissue either to terminate the re-entry paroxysmal supraventricular tachycardias that depend on conducation through the AV node or to slow the ventricular response to other SVTs by blocking conduction through the AV node.

Verapamil should be given only to patients with narrow-complex re-entry SVT or arrhythmias known with certainty to be of supraventricular origin. Verapamil should not be given to patients with wide-complex tachycardias patients with impaired ventricular function or heart failure. It should not be use in infants without expert consultation (see Part 12, Pediatric Advanced Life Support).

Use caution when encountering pre-excited atrial fibrillation or flutter that conducts to the ventricles via both the AV node and an accessory pathway. Treatment with an AV nodal blocking agent (including adenosine, calcium blockers, beta-blockers, or digoxin) is unlikely to slow the ventricular rate and in some instances may accelerate the ventricular response. Seek expert consultation under such circumstances.

AV nodal blocking drugs should not be used for pre-excited atrial fibrillation or flutter. (Class III, LOE C) (2010 Part 8)

Caution is also advised to avoid the combination of AV nodal blocking agents that have a longer duration of action, as their effects may overlap, producing profound bradycardia.

Antiarrhythmic medications (eg, amiodarone, procainamide, or sotalol) in patients with atrial-based supraventricular arrhtyhmias (such as atrial fibrillation and flutter) may provide rate control and can result in termination of the arrhythmia, but such rhythm conversion can result in thromboembolic complications unless suitable precautions have been taken.

18.6
Wide-Complex Tachycardia

Wide-complex tachycardias are defined as those with a QRS ≥0.12 second.

18.6.1
Evaluation

The first step in the management of any tachycardia is to determine if the patient’s condition is stable or unstable (Figure 5, Box 3).

  • If the patient is unstable, proceed with immediate cardioversion (see Therapy for Regular Wide-Complex Tachycardias, below)
  • If the patient is stable, continue evaluation by determining if rhythm is regular (vs irregular)

The most common forms of wide- complex tachycardia are:

  • VT or VF
  • SVT with aberrancy
  • Pre-excited tachycardias (associated with or mediated by an accessory pathway)
  • Ventricular paced rhythms

Determine if the rhythm is regular or irregular.

  • A regular wide-complex tachycardia is likely to be VT or SVT with aberrancy.
  • An irregularly irregular wide-complex tachycardia with uniform QRS complexes from beat-to-beat may be atrial fibrillation with aberrancy. Conversely an irregular wide complex tachycardia in which QRS complexes differ in their appearance (morphology) between beats could be pre-excited atrial fibrillation (ie, atrial fibrillation using both the AV node and an accessory pathway for antegrade conduction), or polymorphic VT/torsades de pointes.
  • Consider the need for expert consultation when treating wide-complex tachycardias.

18.6.2
Therapy for Regular Wide-Complex Tachycardias

18.6.2.1
Unstable Patient

An unstable patient with a wide-complex tachycardia should be presumed to have VT, and immediate synchronized cardioversion should be performed (Figure 5, Box 4 and see Electrical Cardioversion, above).

  • If the patient becomes unstable proceed with synchronized cardioversion.
  • Deliver an unsynchronized higher-dose defibrillation shock if the arrhythmia deteriorates to VF or a polymorphic or irregular VT is present, preventing synchronization of the shock.

Precordial thump may be considered for patients with witnessed, monitored, unstable ventricular tachycardia if a defibrillator is not immediately ready for use. (Class IIb, LOE C) (2010 Part 8)

18.6.2.2
Stable Patient

If the patient is stable:

  • obtain a 12-lead ECG (Boxes 6 and 7) to further evaluate the rhythm and help establish a diagnosis.
  • consider the need to obtain expert consultation.

If the etiology of the rhythm cannot be determined, the rate is regular, and the QRS is monomorphic, IV adenosine is relatively safe for both treatment and diagnosis. (Class IIb, LOE B) (2010 Part 8)

  • If the wide-complex tachycardia proves to be SVT with aberrancy it will likely be transiently slowed or converted by adenosine to sinus rhythm.
  • If the wide-complex tachycardia is VT there will be no effect on rhythm (except in rare cases of idiopathic VT), and the brevity of the transient adenosine effect should be reasonably tolerated hemodynamically.
  • Continuous ECG recording to provide written documentation is strongly encouraged as close attention to varying responses to treatment may help to diagnose the underlying rhythm even if after the fact.
  • Typically, adenosine is administered in a manner similar to treatment of PSVT: as a 6 mg rapid IV push; providers may follow the first dose with a 12 mg bolus and a second 12 mg bolus if the rate fails to convert.
  • When adenosine is given for undifferentiated wide-complex tachycardia, a defibrillator should be available.

Adenosine should not be given for unstable or for irregularly irregular or polymorphic wide-complex tachycardias, as it may cause degeneration of the arrhythmia to VF. (Class III, LOE C) (2010 Part 8)

Verapamil is contraindicated for wide-complex tachycardias unless known to be of supraventricular origin. (Class III, LOE B) (2010 Part 8)

For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy.

If IV antiarrhythmics are administered [for patients who are stable with likely VT], procainamide, (Class IIa, LOE B) amiodarone, or sotalol can be considered. (Class IIb, LOE B) (2010 Part 8)

Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation. (Class III, LOE B) (2010 Part 8) Procainamide should be avoided in patients with prolonged QT and congestive heart failure.

If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered. (Class IIa, LOE C) (2010 Part 8)

18.7
Irregular Tachycardias

An irregularly irregular narrow-complex or wide-complex tachycardia (meaning the interval between successive beats is variable or chaotic) is most likely atrial fibrillation (with or without aberrant conduction) with an uncontrolled ventricular response. Other diagnostic possibilities include MAT or sinus rhythm/tachycardia with frequent atrial premature beats.

When there is doubt about the rhythm diagnosis and the patient is stable, a 12-lead ECG with expert consultation is recommended.

18.7.1
Therapy for Atrial Fibrillation and Flutter

General management of atrial fibrillation focuses on control of the rapid ventricular rate (rate control), conversion of hemodynamically unstable atrial fibrillation to sinus rhythm (rhythm control), or both.

Patients with an atrial fibrillation duration of >48 hours are at increased risk for cardioembolic events, although shorter durations of atrial fibrillation do not exclude the possibility of such events. Electric or pharmacologic cardioversion (conversion to normal sinus rhythm) should not be attempted in these patients unless the patient is unstable.

An alternative strategy is to perform cardioversion following anticoagulation with heparin and performance of transesophageal echocardiography to ensure the absence of a left atrial thrombus;

See the ACC/AHA Guidelines for Management of Patients with Atrial Fibrillation.

18.7.1.1
Rate Control

Patients who are hemodynamically unstable should receive prompt electric cardioversion. More stable patients require pharmacologic interventions to achieve ventricular rate control, based on patient symptoms and hemodynamics.

IV beta-blockers and nondihydropyridine calcium channel blockers such as diltiazem are the drugs of choice for acute rate control in most individuals with atrial fibrillation and rapid ventricular response. (Class IIa, LOE A) (2010 Part 8)

Digoxin and amiodarone may be used for rate control in patients with congestive heart failure; however, the potential risk of conversion to sinus rhythm with amiodarone should be considered before treating with this agent.

A wide-complex irregularly irregular rhythm should be considered pre-excited atrial fibrillation. Expert consultation is advised.

  • Avoid AV nodal blocking agents such as adenosine, calcium channel blockers, digoxin and possibly β-blockers in patients with pre-excitation atrial fibrillation because these drugs may cause a paradoxical increase in the ventricular response.
  • Typically, patients with pre-excited atrial fibrillation present with very rapid heart rates and require emergent electric cardioversion. When electric cardioversion is not feasible or effective, or atrial fibrillation is recurrent, use of rhythm control agents (discussed below) may be useful for both rate control and stabilization of the rhythm.
18.7.1.2
Rhythm Control

Expert consultation is recommended.

18.7.2
Polymorphic (Irregular) VT

Polymorphic (irregular) VT requires immediate defibrillation with the same strategy used for VF.

Pharmacologic treatment to prevent recurrent polymorphic VT should be directed by the underlying cause of VT and the presence or absence of a long QT interval during sinus rhythm.

Long QT interval observed during sinus rhythm (ie, the VT is torsades de pointes):

  • stop medications known to prolong the QT interval
  • correct electrolyte imbalance and other acute precipitants (eg, drug overdose or poisoning—see Part 12: Cardiac Arrest Associated With Toxic Ingestions)
  • polymorphic VT associated with long QT syndrome may be treated with IV magnesium
  • polymorphic VT associated with known familial long QT may also be treated with pacing and/or β-blockers
  • isoproterenol should be avoided in polymorphic VT associated with known familial long QT
  • the addition of pacing or IV isoproterenol may be considered when polymorphic VT is accompanied by bradycardia or appears to be precipitated by pauses in rhythm.

In the absence of a prolonged QT interval, the most common cause of polymorphic VT is myocardial ischemia. In this situation IV amiodarone and beta-blockers may reduce the frequency of arrhythmia recurrence. (Class IIb, LOE C) (2010 Part 8)

Myocardial ischemia should be treated with beta-blockers and consideration be given to expeditious cardiac catheterization with revascularization.

Magnesium is unlikely to be effective in preventing polymorphic VT in patients with a normal QT interval, but amiodarone may be effective. (Class IIb, LOE C) (2010 Part 8)

Other causes of polymorphic VT apart from ischemia and long QT syndrome are catecholaminergic VT (which may be responsive to beta-blockers) and Brugada syndrome (which may be responsive to isoproterenol).

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20
Authorship and Disclosures

20.1
2015 Writing Team

Mark S. Link, Chair; Lauren C. Berkow; Peter J. Kudenchuk; Henry R. Halperin; Erik P. Hess; Vivek K. Moitra; Robert W. Neumar; Brian J. O’Neil; James H. Paxton; Scott M. Silvers; Roger D. White; Demetris Yannopoulos; Michael W. Donnino

Table 4: Part 7: Adult Advanced Cardiovascular Life Support: 2015 Guidelines Update Writing Group Disclosures

20.2
2010 Writing Team

Robert W. Neumar, Chair; Charles W. Otto; Mark S. Link; Steven L. Kronick; Michael Shuster; Clifton W. Callaway; Peter J. Kudenchuk; Joseph P. Ornato; Bryan McNally; Scott M. Silvers; Rod S. Passman; Roger D. White; Erik P. Hess; Wanchun Tang; Daniel Davis; Elizabeth Sinz; Laurie J. Morrison

Table 5: 2010 - Guidelines Part 7: CPR Techniques and Devices: Writing Group Disclosures

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Footnotes

The American Heart Association requests that this document be cited as follows:

American Heart Association. Web-based Integrated Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 7: Adult Advanced Cardiovascular Life Support. ECCguidelines.heart.org

© Copyright 2015 American Heart Association, Inc.

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